Arteriosclerosis and Hypertension: - with Chapters on Blood Pressure, 3rd Edition.

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Title: Arteriosclerosis and Hypertension: - with Chapters on Blood Pressure, 3rd Edition.
Author: Warfield, Louis Marshall
Language: English
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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

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

_Press of
C. V. Mosby Company
St. Louis_

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.

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.)

[Illustration: Fig. 2.--Cross-section of a coronary artery, x50, 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.)

[Illustration: 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.]

[Illustration: 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.)]

[Illustration: 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.)

[Illustration: 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=

[Illustration: 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.

[Illustration: 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.

[Illustration: 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.)

[Illustration: 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.)

[1] Longcope and McClintock, however, conclude that permanent
constriction of the superior mesenteric artery and celiac axis, as well
as gradual occlusion of one or both of these vessels, may be present in
dogs for at least five months without giving rise to definite and
constant elevation of blood pressure or to hypertrophy of the heart.
Further, they have been unable to find at autopsy on man a definite
association between sclerosis of the abdominal aorta and great
splanchnic vessels and cardiac hypertrophy.

[Illustration: 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. x2/3.]

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.

[Illustration: 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.

[2] Warthin, A. S.: Am. Jour. Syph., 1918, i, 693.

=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.

[Illustration: 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.

[Illustration: 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.

[Illustration: 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.

[Illustration: 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.

[Illustration: 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.

[Illustration: 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.

[Illustration: Fig. 19.--Detail of the dial in the "Tycos" instrument.]

[Illustration: Fig. 20.--Faught dial instrument.]

[Illustration: 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.

[Illustration: 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.

[Illustration: Fig. 23.--Method of taking blood pressure with a patient
in sitting position.]

[Illustration: 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.

[3] A firm makes a stethoscope so that the bell is clamped on the arm
leaving both the operator's hands free.

[Illustration: Fig. 25.--Observation by the auscultatory method and a
mercury instrument. One hand regulates the stop cock which releases air
gradually.]

[Illustration: 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.

[Illustration: 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.)

[Illustration: 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.

The tones vary greatly in different hearts. A very strong third tone
phase or prolongation of this phase usually means that the heart which
produces the tone is a strongly acting one, although allowances must be
made for a sclerosed artery in which there is a tendency to the
production of a sharp third phase.

Weakness of the third phase, as a rule, indicates weakness of the heart
and this dulling of the third phase may be so excessive that no sound is
produced. Goodman and Howell have carried this method further by
measuring the individual phases and calculating the percentage of each
phase to the pulse pressure. Thus, if in a normal individual the
systolic pressure is 130 mm., the diastolic 85 mm., and the pulse
pressure 45 mm., the first phase lasts from 130 to 116 or 14 mm., the
second from 116 to 96, or 20 mm., the third from 96 to 91 or 5 mm., the
fourth from 91 to 85, or 6 mm. The first phase would then be 31.1 per
cent of the total pulse pressure, the second phase 44.4 per cent, the
third phase 11.1 per cent, and the fourth phase 13.3 per cent. They
consider that the second and third phases represent cardiac strength (C.
S.) and the first and fourth represent cardiac weakness (C. W.). They
believe that C. S. should normally be greater than C. W. In the example
above C. S.:C. W. = 55.5:44.4. In weak hearts, especially in
uncompensated hearts, the conditions are reversed and C. W. > C. S. This
is often the case. As a heart improves C. S. again tends to become
greater than C. W. They think that the phases should be studied in
respect to the sounds and also to the encroachment of one sound upon
another.

These observations are interesting but we have not found the division
into phases as helpful as it was thought to be. We spent a great deal of
time on this question. All that can be said, in my opinion, is that a
loud, long third phase is usually evidence of cardiac strength.

A further interesting feature which can be heard in all irregular hearts
is a great difference in intensity of the individual sounds. Goodman and
Howell call this phenomenon tonal arrhythmia. Irregularities can be made
out by the auscultatory method which can not be heard at the heart.

In anemia the sounds are very loud and clear and do not seem to
represent the actual strength of the heart.

The general lack of vasomotor tone in the blood vessels together with
some atrophy and flabbiness of the coats probably explains the loud
sounds.

In polycythemia the sounds have a curious, dull, sticky character and
can not be differentiated accurately into phases, a condition which was
predicted from the knowledge of the sharp sounds in anemia.

In not all cases can all phases be made out. It is usually the fourth
phase which fails to be heard.

In such cases the loud third tone almost immediately passes to the fifth
phase or no sound phase. The importance of this will later be taken up.

"In arteriosclerosis, with hardening and loss of elasticity of the
vessel walls, the auscultatory phenomena, according to Krylow, are apt
to be more pronounced, since the back pressure at the cuff probably
causes some dilatation of the vessel above it, while the lumen of the
vessel is smaller than normal. Both of these factors cause an increased
rapidity in the transmission of the blood wave when pressure in the cuff
is released, which in time favors the vibration of the vessel walls.

"In high grade thickening of the arterial walls, however, especially
where calcification had occurred, Fischer found that the sounds were
distinctly less loud than normal, the more so in the arm, which showed
the greater degree of hardening. According to Ettinger's experience, the
rapidity of the flow distinctly increases the auscultatory phenomenon."
(Gittings.)

The sounds depend upon the resonating character of the cuff, upon the
size and accessibility of the vessel, upon the force of the heart beat,
and upon the velocity of the blood.

=The Maximum and Minimum Pressures=

The maximum (systolic) pressure is read at the point where the first
audible click is heard after the cuff is blown up and the pressure
gradually reduced by means of the needle valve in the hand bulb or on
the upright of the glass containing the mercury. All are agreed upon
this point. There has been some dispute as to the place where the
diastolic pressure should be read. Korotkov considered that the
diastolic pressure should be read at the fourth phase when the loud tone
suddenly becomes dulled. Others held that the diastolic pressure should
be read at the fifth phase, the absence of all sound. Experiments
carried out to determine this point were made by me with the assistance
of Prof. Eyster and Dr. Meek at the Physiological Laboratory of the
University of Wisconsin. We arranged apparatus making it possible to
hold the pressure in the carotid artery of dogs at maximum or minimum. A
femoral artery was then dissected and an instrument devised to compress
the artery with a water jacket. The whole was connected up with a
kymograph. A time marker was put in so as to record the place where
changes in sound were heard while listening below the cuff around the
femoral artery. Two sets of records were taken. One with pressure
greater than minimum pressure and a falling pressure over the femoral
artery (Fig. 29), the other with pressure at zero and gradually raised
to minimum pressure (Fig. 30). Both sets of records showed the same
result; viz., that at a point corresponding to the sudden change of tone
the pressure on the artery corresponded to the minimum pressure. It was
therefore concluded that experimentally in dogs the point where
diastolic pressure should be read is at the tone change from clear to
dull, not at the point where all sound disappears.

[Illustration: Fig. 29.--Tracing of auscultatory phenomena. (See
explanation in legend of Fig. 30.)]

[Illustration: Fig. 30.--Figures are to be read from left to right. The
top line records the points where sounds were heard, the figures above
the short vertical lines refer to tones (see text). Mx. B. P., maximum
blood-pressure. M. B. P., minimum blood-pressure. P. B., pressure bulb
recorder. It was impossible to lower and raise this bulb by hand without
obtaining the great irregular oscillations of the attached lever above
the mercury manometer. B. L., base line.]

Erlanger showed some years ago, that with his instrument, the point at
which diastolic pressure should be read was at the instant when the
maximum oscillation of the lever suddenly became smaller. While
checking up the graphic with the auscultatory method using Erlanger's
instrument, it was noticed that the disappearance of all sound did not
correspond with the sudden diminution of the oscillation of the lever
connected with the brachial artery. A series of records were carefully
made on patients. It was seen that during the period of the third tone
phase the oscillations of the lever on the drum reached a maximum (Fig.
31) and remained at approximately the same height for some millimeters
while the pressure was gradually falling. At a point at which the third
tone, clear and distinct, became dull, there was an appreciable decrease
in the height of the pulse wave. From this point to the disappearance of
all sound there was a gradual diminution of the size of the pulse
waves.

[Illustration: Fig. 31.--Fast drum. Sudden decrease in size of pulse
wave at 4, marking the change from clear sharp tone to dull tone.]

[Illustration: Fig. 32.--Slow drum. Sudden decrease in amplitude at 4.]

For normal pressures the difference between the fourth (dull) tone and
the fifth (disappearance of all tone) phase, amounted to 4 to 10 mm.
Occasionally the difference was so little, the change from sharp third
tone through fourth dull tone to disappearance of all sound was so
abrupt, that one could take the disappearance of all sound as the
diastolic pressure, with an error of not more than 2 to 4 mm. This is
within the limits of normal error and practically may be used by those
who have difficulty in noting the change from third to fourth phase. For
high pressures, however, the difference between fourth and fifth phases
was never less than 8 mm., and was found as much as 16 mm. The
diastolic, therefore, should always be taken at the fourth phase if
possible.

It was found that with the dial instrument the greatest fling of the
lever corresponded to the third phase and the sudden lessened amplitude
of the oscillation was at the fourth phase and was coincident with the
change of tone from sharp to dull. Thus the diastolic pressure may be
read off on the dial scale by watching the fling of the hand and with
some practice one might acquire considerable accuracy. It is better,
simpler, and, for most observers, more accurate to use the stethoscope
and hear the change of sound.

=The Relative Importance of the Systolic and Diastolic Pressures=

The systolic pressure represents the maximum force of the heart. It is
measured by noting the first sound audible over the brachial artery
using the auscultatory method. It is the summation of two factors
largely; the force expended in opening the aortic valves (potential) and
the force expended from that point to the end of systole, the force
which is actually driving the blood to the periphery (kinetic). To start
the blood in motion, the heart must overcome a dead weight equal to the
sum of all the forces holding the aortic valves closed. This sum of
factors, called the peripheral resistance, must be reached and passed by
the force of the ventricular beat before one drop of blood is set in
motion along the aorta. This factor of resistance assumes a great
importance.

The systolic pressure is always fluctuating as it depends upon so many
conditions, and the calls of the body except during sleep are many and
various. In a study of diurnal variations in arterial blood pressure it
has been found that--(1) A rise of maximum pressure averaging 8 mm. of
Hg. occurs immediately on the ingestion of food. A gradual fall then
takes place until the beginning of the next meal. There is also a slight
general rise of the maximum pressure during the day. (2) The range of
maximum pressure varies considerably in different individuals, but the
highest and lowest maximum pressures are practically equidistant from
the average pressure of any one individual.[4]

[4] Weyse, A. W., and Lutz, B. R.: Diurnal Variations in Arterial
Blood Pressure, Am. Jour. Physiol., 1915, xxxvii, 330.

The pressure is lowest during sleep and gradually rises near the end of
sleep, so that on awakening the pressure was the same as before sleep.

Physiologically there are many conditions which modify the systolic
pressure. Sleep, position, meals, exercise, emotional states cause often
wide fluctuations which may be very sudden. It should be constantly
borne in mind, that the systolic pressure reading which is made, is the
maximum effort of the heart at that moment only.

The diastolic pressure measures the peripheral resistance. It measures
the work of the heart, the potential energy, up to the moment of the
opening of the aortic valves. It is the actual pressure in the aorta.
The diastolic pressure is not very variable; it is not subject to the
same influences which disturb the systolic pressure. It fluctuates as a
rule, within a small range. It is not affected by diet, by mental
excitement, by subconscious psychic influences, to anything like the
extent to which the systolic pressure is affected by the action of
these factors. The diastolic pressure is determined by the tone in the
arterioles and is under the control of the vasomotor sympathetic system.
Any agent which causes chronic irritation of the whole vasomotor system
produces increase in the peripheral resistance with consequent rise in
the diastolic pressure. Any agent which acts to produce thickening of
the walls of the arterioles, narrowing their lumina, produces the same
effect.

Such states naturally result in increased work on the part of the heart,
which as a result, hypertrophies in the left ventricle. The increase in
size and strength is a compensatory process in order to keep the tissues
supplied with their requisite quota of blood. Conversely, paralysis of
the vasomotor system produces fall of diastolic pressure which, if long
continued, results in death.

The diastolic pressure then is of importance for the following reasons:

1. It measures peripheral resistance.

2. It is the measure of the tonus of the vasomotor system.

3. It is one of the points to determine pulse pressure.

4. Pulse pressure measures the actual driving force, the kinetic energy
of the heart.

5. It enables us to judge of the volume output, for pulse pressure which
is only determined by measuring both systolic and diastolic pressure, is
such an index.

6. It is more stable than the systolic pressure, subject to fewer more
or less unknown influences.

7. It is increased by exercise.

8. It is increased by conditions which increase peripheral resistance.

9. The gradual increase of diastolic pressure means harder work for the
heart to supply the parts of the body with blood.

10. Increased diastolic pressure is always accompanied by increased
pulse pressure, and increased size of the left ventricle, temporarily
(exercise) or permanently.

11. Decreased diastolic pressure goes hand in hand with vasomotor
relaxation, as in fevers, etc.

12. Low diastolic pressure is frequently pathognomonic of aortic
insufficiency.

13. When the systolic and diastolic pressures approach, heart failure is
imminent either when pressure picture is high or low.

When all these factors are taken into consideration, it becomes apparent
that the diastolic pressure is most important, if not the most important
part of the pressure picture.

Up to within a very brief time all the statistical evidence of blood
pressure was based on systolic readings alone. This data is most
valuable and much has been learned as to diagnosis and prognosis, but it
is a mass of data based on a one-sided picture and can not be as
valuable as the statistics which will undoubtedly be published later
when all the pressure picture figures can be analyzed.

=Pulse Pressure=

The pulse pressure is the actual head of pressure which is forcing the
blood to the periphery. At every systole a certain amount of blood 75-90
c.c. (Howell) is thrown violently into an already comfortably filled
aorta. The sudden ejection of this blood instigates a wave which rapidly
passes down the arteries as the pulse wave. The elastic recoil of the
aorta and large arteries near the heart contract upon the blood and keep
it moving during diastole. Normally the blood-vessels are highly elastic
tubes with an almost perfect coefficient of elasticity. The pulse
pressure varies under normal conditions from 30 to 50 mm. Hg. There is a
very definite relationship between the velocity of blood and the pulse
pressure which is expressed thus; velocity = pulse rate x pulse
pressure.[5]

Further it has been demonstrated that under normal conditions and during
various procedures--the pulse pressure is a reliable index of the
systolic output.[6]

[5] Erlanger and Hooker: An Experimental Study of Blood Pressure and
of Pulse Pressure in Man, Johns Hopkins Hosp. Rep., 1904, xii, 145.

[6] Dawson and Gorham: The Pulse Pressure as an Index of Systolic
Output, Jour. Exper. Med., 1908, x, 484.

Increased pulse pressure therefore goes hand in hand with greater
systolic output. Physiologically this is most ideally seen during
exercise. Following exercise the pulse rate increases, the systolic
pressure rises greatly, the diastolic slightly or not at all. The pulse
pressure therefore is increased. The velocity also is much increased.
The call comes for more blood and the heart responds. In the chronic
high pulse pressures there are four correlated conditions which, so far
as I have studied them, are always present. These are: (1) An increase
in size of the cavity of the left ventricle. The ventricle actually by
measurement contains more blood than normal, and therefore throws out
more blood at every systole. The volume output is greater per unit of
time. (2) There is actual permanent increase in diameter of the arch of
the aorta. This is a compensating process to accommodate the increased
charge from the left ventricle. (3) There are on careful auscultation
over the manubrium, particularly the lower half, breath sounds which
vary from bronchial to intensely tubular, depending upon the anatomic
placing of the aorta, the shape of the chest, and the degree of
dilatation. Often there is very slight impairment of the percussion note
as well. (4) There is increase in size of all the large distributing
arteries, carotids, brachials, femorals, renals, celiac axis, etc., with
fibrous changes in the media, loss of some elasticity, and increase in
size of the pulse wave. Increased pulse pressure means increased volume
output, but does not always mean increased velocity. The proper
distribution of blood to the various organs of the body is regulated by
the vasomotor system acting upon the small arteries which contain
considerable unstriated muscle. When fibrous arteriosclerosis is present
there is loss of elasticity in the distributing arteries and a greater
volume of blood must be thrown out by the ventricle at every systole in
order that every organ shall have its full quota of blood. A force which
is sufficient to send blood through elastic normal distributing tubes
becomes totally insufficient to send the same amount of blood through
tortuous and more or less inelastic tubes.

It is evident then that pulse pressure is exceedingly important. It can
only be determined by measuring both the _systolic_ and _diastolic_
pressure. The pulse rate must also be known in order to compute the
velocity. It is essential to have the whole pressure picture for all
cases if correct conclusions are to be drawn.

In an irregular heart, especially in the cases due to myocardial
disease, it is quite impossible to determine the true diastolic
pressure. One can only approximate it and say that the pulse pressure is
low or high. As a matter of fact the real systolic pressure can not be
determined. For this figure the place on the scale where most of the
beats are heard may be taken for the average systolic pressure. No one
can seriously maintain that he can measure the diastolic pressure under
all circumstances.

By means of the auscultatory method of measuring blood pressure we are
able to determine irregularities of force in the heart beats more easily
than by listening to the heart sounds. A pulsus alternans is readily
made out. The irregular tones heard over the brachial artery in cases of
irregular heart action have been called "tonal arrhythmias."

=Blood Pressure Variations=

A recent study of diurnal variations in blood pressure has shown that
while the maximum pressure rises after the ingestion of food and
steadily rises slightly throughout the day, the minimum blood pressure
is very uniform throughout the day, and is little affected by the
ingestion and digestion of meals. When it is affected, a rise or a fall
may take place. Throughout the day, it tends to become slightly lower.
The pulse pressure then is greater towards evening.

Weysse and Lutz in a study of this question draw the following
conclusions:

1. A rise of maximum pressure averaging 8 mm. of Hg occurs immediately
on the ingestion of food. A gradual fall then takes place until the
beginning of the next meal. There is also a slight general rise of the
maximum pressure during the day.

2. The average maximum blood pressure for healthy young men in the
neighborhood of 20 years of age is 120 mm. of Hg. This pressure obtains
commonly one hour after meals. The higher maximum pressures occur
immediately after meals, and the lower, as a rule, immediately before
meals.

3. The range of maximum pressure varies considerably in different
individuals, but the highest and lowest maximum pressures are
practically equidistant from the average pressure of any one individual.

4. The minimum blood pressure is very uniform throughout the day, and is
little affected by the ingestion and digestion of meals. When it is
affected a rise or fall may take place. There is a tendency for a slight
general lowering of the minimum pressure throughout the day.

5. The average minimum blood pressure for healthy young men in the
neighborhood of 20 years of age is 85 mm. of Hg. Thus we get an average
pulse pressure of 35 mm. of Hg.

6. Pulse pressure, pulse rate, and the relative velocity of the blood
flow are increased immediately upon the ingestion of meals. They attain
the maximum, as a rule, in half an hour, and then decline slowly until
the next meal. There is a general increase in each throughout the day.

These measurements were made upon persons at rest. Almost any form of
exercise would have made the variations much greater. No account is
taken of the psychic variations which for the physician are the most
important to bear in mind. Neglect to take this variation into account
will inevitably lead to false conclusions.

THE AVERAGE DIURNAL BLOOD PRESSURE RECORD OF THE TEN SUBJECTS

==========+=======+=======+=======+=======+========+=======+===============
TIME |MAXIMUM|MINIMUM| MEAN | PULSE | PULSE |PP x PR| NOTES
| | | | |PRESSURE| RATE |
----------+-------+-------+-------+-------+--------+-------+---------------
|_mm._Hg|_mm._Hg|_mm._Hg|_mm._Hg| | |
4:30 p.m. | 119.5 | 84.1 | 101.8 | 35.4 | 72.0 | 2549 |
5:00 p.m. | 117.7 | 83.5 | 100.6 | 34.2 | 71.1 | 2432 |
6:00 p.m. | 118.0 | 84.0 | 101.0 | 34.0 | 74.9 | 2547 |Before dinner
6:45 p.m. | 127.2 | 88.2 | 107.7 | 39.0 | 78.1 | 3046 |After dinner
7:00 p.m. | 124.7 | 87.7 | 106.2 | 37.0 | 76.0 | 2812 |
7:30 p.m. | 122.0 | 83.4 | 102.7 | 38.6 | 76.0 | 2934 |
8:00 p.m. | 122.4 | 85.5 | 103.4 | 36.9 | 71.2 | 2527 |
8:30 p.m. | 120.0 | 85.0 | 102.5 | 35.0 | 69.7 | 2439 |
9:00 p.m. | 120.5 | 84.7 | 102.5 | 35.8 | 65.2 | 2334 |
9:30 p.m. | 118.2 | 84.4 | 101.6 | 33.8 | 64.4 | 2177 |
7:30 a.m. | 118.4 | 87.6 | 103.0 | 30.8 | 70.3 | 2165 |
8:00 a.m. | 116.4 | 86.4 | 101.4 | 30.0 | 69.8 | 2094 Before breakfast
8:30 a.m. | 124.2 | 85.4 | 104.8 | 38.8 | 79.4 | 3081 |After breakfast
9:00 a.m. | 123.8 | 84.4 | 104.1 | 39.4 | 84.1 | 3313 |
10:00 a.m.| 118.2 | 83.6 | 100.9 | 34.6 | 70.7 | 2446 |
11:00 a.m.| 116.2 | 84.8 | 100.5 | 31.4 | 67.7 | 2126 |
12:00 m | 114.4 | 83.2 | 98.8 | 31.2 | 66.2 | 2065 |Before luncheon
12:30 p.m.| 122.8 | 83.2 | 103.0 | 39.6 | 70.9 | 2808 |After luncheon
1:00 p.m. | 122.3 | 82.0 | 102.1 | 40.3 | 79.7 | 3212 |
2:00 p.m. | 118.4 | 81.4 | 99.9 | 37.0 | 77.6 | 2871 |
3:00 p.m. | 118.8 | 82.6 | 100.7 | 36.2 | 75.1 | 2719 |
4:00 p.m. | 115.8 | 82.0 | 98.9 | 33.8 | 71.9 | 2420 |
5:00 p.m. | 117.2 | 83.4 | 100.3 | 33.8 | 69.6 | 2352 |
6:00 p.m. | 117.4 | 84.4 | 100.9 | 33.0 | 72.8 | 2402 |Before dinner
6:45 p.m. | 124.6 | 83.1 | 103.8 | 41.5 | 80.4 | 3337 |After dinner
7:00 p.m. | 125.2 | 84.2 | 104.7 | 41.0 | 76.1 | 3120 |
7:30 p.m. | 122.0 | 84.0 | 103.0 | 38.0 | 73.7 | 2801 |
8:00 p.m. | 119.6 | 85.0 | 102.3 | 34.6 | 72.3 | 2502 |
8:30 p.m. | 119.7 | 84.0 | 101.3 | 34.7 | 69.0 | 2394 |
9:00 p.m. | 120.0 | 86.2 | 103.1 | 33.8 | 68.0 | 2298 |
+-------+-------+-------+-------+--------+-------+
Average | 120.0 | 85.0 | 102.5 | 35.0 | 72.0 | 2550 |
----------+-------+-------+-------+-------+--------+-------+---------------
(Taken from Weysse and Lutz.)

In some experiments to determine the changes upon the blood pressure
induced by hot and cold applications on and within the abdomen, Hammett,
Tice and Larson found that heat applied to the outside of the abdomen
raises the blood pressure. The application of cold produces no change.
Either hot or cold saline introduced within the abdomen causes a fall in
blood pressure.

Experimentally, certain drugs such as adrenalin, barium chloride,
nicotine, digitalis, strophanthus and the infundibular portion of the
pituitary body known as pituitrin raise the maximum pressure. In the
clinic it is difficult to conclude always whether the drug alone is
responsible for rise in maximum pressure. Adrenalin given intravenously
will raise the pressure. So will digitalis and strophanthus. I have
watched the maximum pressure rise within three minutes following an
intravenous injection of gr. 1/100 (0.0006 gm.) strophanthin 20 mm. of
Hg: I have seen the subcutaneous injection of 10 minims of adrenalin
repeated several times daily for six months fail to have the least
effect on the blood pressure picture.

Elevation of the foot of the bed about nine inches proved so efficacious
in steadying failing hearts in acute infectious diseases, particularly
typhoid, that a study was made of the effect upon blood pressure. Many
observations were made, but no instrumental proof of rise in blood
pressure could be adduced.

Exercise always raises blood pressure, the maximum much more than the
minimum. In athletes the minimum pressure may actually fall, the maximum
rise so that a greater volume output results from the greater pulse
pressure.

Shock and hemorrhage lower it. Hemorrhage lowers also the pulse
pressure, and it may be possible to prognosticate internal hemorrhage by
frequent estimations of the systolic and diastolic pressures (Wiggers).
Compression of the superior mesenteric artery or the celiac axis in dogs
raises the blood pressure measured in the carotid artery for a period of
at least an hour. This seems to be dependent on purely mechanical
causes, and is not a reflex vasomotor phenomenon. (Longcope and
McClintock.)

Experimentally blood pressure can be increased by direct compression of
the brain as Cushing has shown. It was thought at one time that in man
the same effect would result from tumor of the brain or especially from
subdural or extradural hemorrhage following head injuries. This,
however, is not the case. No information of great value can be obtained
by the measurement of blood pressure in these states. We do know that
too high and too prolonged compression of the medulla brings about
exhaustion of the cardiac center accompanied with rapid pulse, low
pressure and eventual death.

=Hypertension=

All the conflict during the past few years over the subject of blood
pressure has revolved around this much overworked word. Hypertension
means high pressure, and yet it carries with it a suggestion of high
pressure which is harmful to the individual. As a matter of fact
hypertension is a compensatory process, it is often a saving process in
spite of the fact that it carries possibilities of harm in its
possessor. It has been made a fetish, a god to fall down before and
worship and it has been the means of holding a torch of fear over a
patient which has not been lost on the charlatans. Popularization of
blood pressure has brought its crop of evils, no one of which has been
as fruitful in dollars to unprincipled quacks as hypertension.

Hypertension is the expression on the part of the circulation to meet
new conditions in the tissues so that all tissues will be nourished and
all will be enabled to function. Looked at from that point of view it is
a conservative process and in many cases it is. It is not an average
normal state, but it is normal state for the man who has it in chronic
form. Hypertension should be viewed rationally and its proper place in
the whole make-up of the patient determined. Hypertension is a relative
term. What might be high pressure in a man of sedentary habits who
reaches the age of fifty, might not be high pressure in a full blooded
formerly athletic man of the same age. Temporary hypertension due to
excitement, exercise, etc., must be kept in mind. It is not intended to
convey the impression that hypertension is of no moment. It is a matter
for investigation, but not a matter to worship as the all-in-all.

Hypertension is, after all, a physiologic response on the part of the
organism in order to maintain the circulation in equilibrium in the face
of conditions which tend to produce vasoconstriction in large areas and,
therefore tend to deprive these areas of blood. That there must be some
substance in the blood stream which causes this constriction seems
certain. What it is, is not at present known. Recently, Voegtlin and
Macht[7] have isolated a crystalline substance from the blood of man and
other mammals which they regard as a lipoid and closely related to
cholesterin. This substance was recovered by them from the cortex of the
adrenal gland. This becomes of added interest in the light of
observations made by Gubar (quoted by Voegtlin and Macht). He noted
"that the vasoconstricting properties of blood serum vary in different
pathologic conditions, being increased in nephritis, for instance, and
diminished in others." In some experiments made in the summer of 1913,
we found there was no marked difference in the anaphylactic shock
produced in half-grown rabbits by the injection of normal and uremic
blood serum. As lipoids do not cause anaphylaxis, there should be no
difference in the reaction of normal and uremic sera unless in one there
was some form of protein not in the other. This does not seem to be the
case. The presence of something in the circulation, therefore, produces
constriction of vessels. This calls for more force in contraction on the
part of the heart. This substance may be of lipoid nature. The continued
presence of this hypothetical substance naturally would lead to
hypertrophy of the heart.

[7] Isolation of a New Vasoconstrictor Substance from the Blood and
the Adrenal Cortex, Jour. Am. Med. Assn., 1913, lxi, 2136.

What makes hypertension of significance is not the hypertension itself,
but the fact that it is the expression of processes going on in the
body which demand exhaustive investigation. To attach a blood pressure
cuff to the arm, find the pressure, and diagnose hypertension is like
putting a thermometer under the tongue, noting a rise in the mercury,
and diagnosing fever. What causes the hypertension? Can the causes be
removed? Those are the really vital questions after the symptom
hypertension has been discovered.

All states of hypertension are accompanied by more or less increase of
pulse pressure. In other words the systolic pressure is always increased
to greater degree than the diastolic pressure. In studies carried out in
the wards and Pathological Laboratory of the Milwaukee County Hospital,
Milwaukee, we found that in all of the cases of chronic high blood
pressure with resulting high pulse pressure four correlated factors were
found. If any one of these factors is present, the other three are
found.

1. In all high pulse pressure cases there is increase in the size of the
cavity of the left ventricle. The ventricle actually contains more blood
when it is full, and throws out, therefore, more blood at each systole.
The actual volume output is greater per unit of time. Such hearts always
show increase in thickness of the ventricular wall. I quite agree with
Stone,[8] who says, "It is merely to be emphasized that when the pulse
pressure persistently equals the diastolic pressure (high pressure
pulse, in other words) with a resulting 50 per cent, _overload_, which
means the expenditure of double the normal amount of kinetic energy on
the part of the heart muscle, cardiac hypertrophy has occurred." They
are found in aortic insufficiency, in chronic nephritis, in the diffuse
fibrous type of arteriosclerosis, and in some cases of exophthalmic
goiter. Such a condition occurs temporarily after exercise.

[8] Stone, W. J.: The Differentiation of Cerebral and Cardiac Types of
Hyperarterial Tension in Vascular Diseases, Arch. Int. Med., November,
1915, p. 775.

2. In all high pulse pressure cases there is actual permanent increase
in diameter of the arch of the aorta. This is a compensating process to
accommodate the increased charge from the left ventricle. Smith and
Kilgore[9] have shown this to be true in cases of chronic nephritis with
hypertension. Their research confirms my own observations. They found
dilatation of the arch in (1) syphilis (that is, aortitis); (2) age over
50 (that is, probable factor of arteriosclerosis); (3) other serious
cardiac enlargement, and (4) hypertension (with more or less
hypertrophy, as in chronic nephritis).

[9] Smith, W. H., and Kilgore, A. R.: Dilatation of the Arch of the
Aorta in Chronic Nephritis with Hypertension, Am. Jour. Med. Sc.,
1915, cxlix, 503.

In ten cases showing arches at the upper limit of normal (that is, 6 cm.
in diameter) and hypertrophy of the heart, three were chronic mitral
endocarditis; one was chronic aortic endocarditis; three were chronic
mitral and aortic endocarditis, and there was one each of
hyperthyroidism, pericarditis and adherent pericardium.

In fourteen cases of hypertension (highest systolic 270 mm., average
systolic, 215 mm.), all showed cardiac hypertrophy. "All but three of
these cases had great vessels whose transverse diameters measured over
the normal limit of 6 cm., and in one of those measuring 6 cm. the
Roentgen-ray diagnosis was 'slight dilatation' of the arch." Smith and
Kilgore are at a loss to explain the three exceptions. They did not give
diastolic pressures, so pulse pressures are not known. Possibly the
three exceptions were cases of high diastolic pressure in which the
pulse pressure possible was not over 60 mm. Such cases might show
"slight dilatation of the arch," but not marked dilatation, such as was
found in the other, evidently high pulse pressure cases.

We have found that only the high pulse pressure cases show dilatation of
the arch. Certain high tension cases which have had a very high
diastolic pressure do not reveal any accurately measurable dilatation of
the aortic arch. An empty aorta after death is quite different from a
functionating aorta during life. Hence the dilatation which is found
postmortem must have been considerable during life. And conversely, a
dilatation which was present during life might not be looked on as such
after death.

3. In all high pulse pressure cases one will find on careful
auscultation over the manubrium, particularly its lower half, breath
sounds which vary from bronchial to intensely tubular. At times the
percussion note will be slightly impaired, as McCrae[10] has shown in
dilatation of the arch of the aorta. This auscultatory sign is evidence
of some more or less solid body in the anterior mediastinum which is
lying on the trachea and permits the normal tubular breathing in the
trachea to be audible over the upper part of the sternum. It is found in
cases of dilated aortic arch. Fluoroscopic examination has confirmed the
findings on auscultation.

[10] McCrae, Thomas: Dilatation of the Arch of the Aorta, Am. Jour.
Med. Sc., 1910, cxl, 469.

4. In all high pulse pressure cases, in which the pulse pressure is over
70 mm. of mercury, there is increase in the size of all large
distributing arteries, carotids, brachials, femorals, renals, celiac
axis, etc., with fibrous changes in the media, loss of some of the
elasticity, and in the palpable superficial arteries, increase in size
of the pulse wave.

Increased pulse pressure means increased volume output, but does not
always mean increased velocity. The proper distribution of blood to the
various organs of the body is regulated by the vasomotor system acting
on the small arteries which contain considerable unstriated muscle. In
order that there may be enough blood at all times and under varying
conditions of rest and function, there must be a proper supply coming
through the distributing vessels, the large arteries, those containing
much elastic tissue, and only a very small amount of unstriated muscle
tissue or none whatever. Fibrous sclerosis of these vessels causes them
to become enlarged and tortuous and to lose much of their elasticity,
which is essential for the even distribution of blood. A greater blood
volume is therefore necessary in order that the organs may receive their
quota of blood. A force which is sufficient to send blood through
elastic normal distributing tubes becomes totally insufficient to send
the same amount of blood through tortuous and more or less inelastic
tubes. As a compensatory process the pulse pressure increases. For this
to increase, the left ventricular cavity dilates, the arch dilates, and
as a greater force must be exerted to keep the increased mass in motion,
the heart responds by hypertrophy of its left ventricle and becomes
itself the subject of fibrous changes in the myocardium. The mass
movement of blood is therefore greater in high pulse pressure cases than
in cases of normal pulse pressure.

In cases of chronic interstitial nephritis--contracted granular
kidney--it may well be that the sclerosis of the arteries is a secondary
process caused, as Adami thinks, by the hypertension itself. In aortic
insufficiency the situation is somewhat different. The high pulse
pressure is due to a very low diastolic pressure, for in my experience
with uncomplicated aortic insufficiency the systolic pressure is, as a
rule, not much increased above the normal for the individual's age. Here
peripheral resistance is so low that a capillary pulse is common. The
volume output per unit of time is greatly increased, the arch of the
aorta is dilated, and the pulse is large. The fact that a large part of
the blood regurgitates during diastole back into the ventricle, and the
fact that the diastolic pressure is low means that there is no increased
resistance to overcome, and the systolic pressure is not raised.

Stone[11] has divided the cases of hypertension into the cerebral and
cardiac types. He finds that there is a difference in prognosis and in
the mode of death in the two groups. He has further attempted to judge
of the work placed upon the heart by calculating what he calls the
heart load or pressure-ratio. For example, he takes a normal pressure at
120-80-40. The relation between 80 and 40 is 1/2 or 50 per cent. That he
considers normal. When the heart load increases so that the pulse
pressure equals or exceeds the diastolic pressure, the heart load is 100
per cent or more, he considers the danger of myocardial exhaustion
graver than when the heart load is normal or less than 50 per cent.

[11] Stone, W. J.: Arch. Int. Med., 1915, xvl, 775.

It is his opinion, in which I heartily concur, "that an individual with
a systolic pressure of 200 and a diastolic pressure of 140, is in
greater danger of cerebral death than an individual with a systolic
pressure of 200 and a diastolic pressure of 100." He is "likewise
certain that the individual with a systolic pressure of 200 and a
diastolic of 90 to 100 is in greater danger of a cardiac death. It is
apparently the constant high diastolic pressure rather than the
intermittently high systolic pressure which predisposes to cerebral
accident."

I have not been able to confirm all of Stone's conclusions. His
contention holds good for some cases, but not, in my experience, for the
great majority of the hypertension cases. I feel that in the
classification of the chronic high pressure case we can go one step
farther and split his first group into two usually differentiable
groups. Syphilis is not an etiological factor in any of these groups. It
is not considered that these groups are absolutely distinct and can
always be rigidly separated. There are variations and combinations which
render an exact separation impossible. But bearing this in mind the
following classification is proposed as a working classification.

Group A. Chronic nephritis.

Group B. Essential hypertension.

Group C. Arteriosclerotic hypertension.

Group A. _Chronic Nephritis._ These are the cases with a high-pressure
picture, that is to say, high systolic (200+) and high diastolic
(120-140+). The pulse pressure is much increased. The palpable arteries
are hard and fibrous. There is puffiness of the under eyelids, which is
more pronounced in the morning on arising. Polyuria with low specific
gravity and nycturia are present. There are almost constant traces of
albumin in the urine, with hyaline and finely granular casts.

Functionally these kidneys are much under normal. The functional
capacity determined by Mosenthal's modification of the Schlayer-Hedinger
method shows a marked inability to concentrate salts and nitrogen. The
phthalein output is below normal. As the case advances the phthalein
output becomes less and less, until a period is reached when there are
only traces or complete suppression at the end of a two-hour period.
Such patients may live for ten weeks (one of our cases) or longer, all
the time showing mild uremic symptoms, and suddenly pass into coma and
die.

The natural end of patients in this group is either uremia or cardiac
decompensation (so-called cardiorenal disease). Cerebral accidents may
happen to a small number. It is only to this group, in my opinion, that
the term cardiorenal disease should be applied. Formerly I believed that
all high systolic pressure cases were cases of chronic nephritis of some
definite degree. From the purely pathologic standpoint that is true, but
from the important, functional standpoint it is far from being the true
state of the cases.

In this group there is marked hypertrophy and moderate dilatation of the
left ventricle with dilatation and nodular sclerosis of the aorta. The
kidneys are firm, red, small, coarsely granular, the cortex much
reduced, the capsule adherent. Cysts are common. It is the familiar
primary contracted kidney. Mallory calls this capsular-glomerulonephritis.
The etiology is obscure. Often no cause can be found. Again, there is a
history of some kidney involvement following one of the acute infectious
diseases, or it may follow the nephritis of pregnancy. Usually, however,
these cases fall into the group of secondary contracted kidneys, chronic
parenchymatous nephritis.

Illustrative Case.--R. Z., a woman, aged thirty-six years, was seen
July 26, 1916, in coma. There was a history of typhoid fever at
nineteen years, but no other disease. She had had nine full-term
pregnancies, the last one thirteen months previously. For a week
before the onset of the present illness she had complained of severe
headaches and dizziness. There were no heart symptoms. For the past
year she has had nycturia. Physical examination revealed tubular
breathing beneath the manubrium, a few rales in the chest, an
enlarged heart (left side), with a systolic murmur over the aortic
area. Blood pressure was 178-125-53, the pulse rate 96, leucocytes
27,250. Venesection of 500 c.c. of blood and intravenous injections
of 500 c.c. of 5 per cent NaHCO_3 in normal saline were employed.
Lumbar puncture withdrew 60 c.c. of clear fluid under pressure with
6 cells per cubic millimeter. The eye grounds showed distinct
haziness of the disks and dilatation of the veins. Blood pressure
after venesection was 164-122-42, pulse 76, but in a few days rose
to 222-142-80, pulse 70. A second venesection of 400 c.c. and
proctoclysis of 1000 c.c. saline solution was tried. The
blood-pressure now was 198-140-58. The pH of the blood was 7.6, the
alkaline reserve was 35 volume per cent (van Slyke), and the CO_2
tension of the alveolar air (Marriott) was 25 mm. The phthalein on
the day following the second venesection was 45 per cent in two
hours. The urine at first showed 500 c.c. in twenty-four hours,
specific gravity 1016, albumin and casts. Later she passed 1300 to
1600 c.c. with specific gravity around 1010. The blood-pressure
fluctuated considerably, reaching as low as 138-98-40, pulse 88. She
was discharged improved September 10, 1916. She had constant
headache but managed to keep up. In June, 1917, she suddenly died in
an uremic coma.

Group B. This one might designate as the hereditary type, although there
is not always a history in the antecedent. This group includes the
robust, florid, exuberantly healthy people. They often are heard to
boast that they have never had a doctor in their lives. They are usually
thick-set or very large, fleshy people. The pressure picture is
exceedingly high. The pulse pressure is moderately increased. The
arteries are rather large, fibrous, and often quite tortuous, although
this is not always the case. Some persons have hard, small, fibrous
arteries. There is no puffiness beneath the eyes, no polyuria, and no
nycturia as a rule. The urine is of normal amount, color, and specific
gravity. Albumin is only rarely found and then in traces, but careful
search of a centrifuged specimen invariably reveals a few hyaline
casts. The phthalein excretion is normal or only slightly reduced. The
kidneys excrete salt and nitrogen normally. It is in this group that
apoplexy is found most frequently. The rupture of the vessel occurs when
the victim is in perfect health, often without any warning. Occasionally
when such a case recovers sufficiently to be around, cardiac
decompensation sets in later and he dies then of the cardiac
complications.

Pathologically the hearts of such persons are found to have the most
enormous hypertrophy of the wall of the left ventricle. The cavity is
somewhat enlarged, as is always the case when the pulse-pressure is
increased, but the size of the cavity is not the striking feature. The
aorta is fibrous, thick walled, and the arch is slightly dilated. There
are patches of arteriosclerosis. One such case seen only at autopsy had
a rupture of the aorta just above the sinus of Valsalva and died of
hemopericardium. The kidneys are of normal size, dark red, firm, the
capsule strips readily, the surface is smooth or finely granular, the
cortex is not decreased. The pyramids are congested and red streaks
extend into the cortex. Microscopically the capsules of the glomeruli
are a trifle thickened; a few show hyaline changes. There is rather
diffuse, mild, round-cell infiltration between the tubules. The tubular
epithelium shows little or no demonstrable changes. The arterioles are
generally the seat of a moderate thickening of the intima and media, but
it is not usual to find obliterating endarteritis. There is evidently a
diffuse fibrous change which has not affected either the tubules or
glomeruli to any great extent.

Illustrative Case.--L. C., a man, aged fifty-six years, stonemason
by trade, is a stocky, thick-necked individual. He had never been
ill in his life until a year ago, when he fell from his chair
unconscious. He had a right-sided hemiplegia which has cleared up so
completely that except for a very slight drag to his foot he walks
perfectly well. He came in complaining of shortness of breath and
cough. There was no swelling of the feet. Here evidently was
left-heart decompensation. Examination showed the blood pressure to
be 240-130-110, pulse irregular, 104 to the minute. There were
cyanosis and rales throughout both chests. The urine was normal in
color, specific gravity 1025, small amount of albumin, few casts,
hyaline and granular. The phthalein elimination was 65 per cent in
two hours. Under rest, purgatives, and digitalis he was much
improved. He has since had two other apoplectic strokes, the last of
which was fatal.

When these patients are seen with acute cardiac decompensation, there
are, of course, much albumin and many casts in the urine, and the
phthalein output is, for the time being, decreased.

Group C. This might be called the arteriosclerotic high-tension group
(Stone's cardiac group). The cases are usually over fifty years old.
They are men and women who have lived high and thought hard. Often they
have had periods of great mental strain. Many men in this group were
athletes in their young manhood. Many have been fairly heavy drinkers,
although never drinking to excess. They are usually well nourished and
inclined to stoutness. The pressure picture is high systolic with normal
or only slightly increased diastolic and large pulse pressure. The
arteries are large, full, fibrous, usually tortuous. The heart is very
large, the apex far down and out. There is no polyuria; nycturia is
uncommon, quite the exception. The urine is normal in color, amount, and
specific gravity. Albumin is only rarely found and hyaline casts are not
invariably present. The phthalein excretion is quite normal and the
excretions of salt and nitrogen are also normal. The terminal condition
in most of the patients in this group is cardiac decompensation. They
may have several attacks from which they recover, but after every attack
the succeeding one is produced by less exertion than the preceding one,
and it becomes more and more difficult to control attacks. Eventually
the patients become bed- or chair-ridden, and finally die of acute
dilatation of the heart.

Occasionally patients in this group may have a cerebral attack, but in
my experience this is uncommon. Pathologically the heart is large, at
times true _cor bovinum_, dilated and hypertrophied. The cavity of the
left ventricle is much dilated. The aorta is dilated and sclerosed.

The kidneys are increased in size, are firm, dark red in color, with
fatty streaks in the cortex. The capsule strips readily and the cortex
is normal in thickness or only slightly increased. The organ offers some
resistance to the knife. The microscope shows small areas scattered
throughout where the glomeruli are hyalinized, the stroma full of small
round cells, the tubules dilated, and the cells are almost bare of
protoplasm. Naturally the tubules are full of granular cast material.
Also the arterioles show extensive intimal thickening, fibrous in
character, with occasional obliterating endarteritis. One gets the
impression that the small sclerotic lesions are the result of anemia and
gradual replacement of scattered glomeruli by fibrous tissue. For the
most part the kidney, except for the chronic passive congestion, appears
quite normal. One can readily understand that in such a kidney function
could not have been much interfered with.

Illustrative Case.--C. K., an active, stout, business man, aged
fifty-six years, consulted me on account of shortness of breath and
swelling of the feet in May, 1915. He had just returned from a
hospital in another city, where he had gone with what was apparently
cardiac decompensation. In his early manhood he had been a gymnast
and a prize winner. He has worked hard, often given way to violent
paroxysms of temper, has eaten heavily but drunk very moderately.
The heart was greatly enlarged, the arch of the aorta dilated, a
mitral murmur was audible at the apex. The radials and temporals
were large, tortuous, and fibrous. The blood pressure picture ranged
around 180-90-90. He was easily made dyspneic and had a tendency to
swelling of the lower legs. The urine was acid, of normal specific
gravity, normal in amount, normal phthalein, normal concentration of
salt and nitrogen, contained albumin only when he was suffering from
decompensation of the heart. Casts were always found. He finally
died, after sixteen months, with all the symptoms of chronic
myocardial insufficiency. The heart was enormous, a true _cor
bovinum_. The kidneys were typical of this condition, possibly
somewhat larger than usual.

=Hypotension=

When the pressure is constantly below the normal, it is called
hypotension. This may be transient--as in fainting--it may be a normal
state of the individual, it occurs in most fevers and in a great
variety of diseases, including anemias.

In arteriosclerosis, especially the diffuse (senile) type, the blood
pressure is invariably low, and may be spoken of as hypotension. The
heart in such a case is small, the muscle is flabby, there is brown
atrophy of the fibers, and some replacement of the muscle cells by
connective tissue. The same causes which have produced general
arteriosclerosis have also produced sclerosis of the coronary arteries,
and probably the lessened blood supply accounts for much of the atrophy
of the heart muscle.

In typhoid fever the maximum blood pressure during beginning
convalescence may be as low as 65 mm. Hg. I have frequently seen
hypotension of 80 mm. This is common.

Meningitis is the only acute infectious disease in which the blood
pressure is more often high than low. This is accounted for by the
increased intracranial tension.

Following large hemorrhages the blood pressure is reduced. In
venesection the withdrawal of blood may not affect the blood pressure.
The procedure is done to relieve overdistension of the heart.

In pleurisy with effusion and in pericarditis with effusion there is
hypotension.

Collapse, whether from poisoning by drugs or as the result of dysentery,
cholera, or profuse vomiting from whatever cause, reduces the blood
pressure.

In cachectic states, such as cancer, the blood pressure is low. General
wasting of the whole musculature includes that of the heart and the
heart muscle shows the condition known as "brown atrophy."

A most interesting and important condition in which hypotension occurs
is pulmonary tuberculosis. Haven Emerson has recently gone over the
whole subject in a careful piece of work and his summary is as follows:

"Hypotension or subnormal blood pressure is universally found in
advanced pulmonary tuberculosis, in which condition emaciation may play
a part in its causation. Hypotension is found in almost all cases of
moderately advanced tuberculosis, or in early cases in which the toxemia
is marked except when arteriosclerosis, the so-called arthritic or gouty
diathesis, chronic nephritis, or diabetes complicate the tuberculosis
and bring about a normal pressure or a hypertension. Occasionally the
period just preceding a hemoptysis or during a hemoptysis may show
hypertension in a patient whose usual condition is that of hypotension.

"Hypotension has been found by so many observers in early, doubtful or
suspected cases with or before physical signs of the disease in the
lungs, and is considered by competent clinicians so useful a
differential sign between various conditions and tuberculosis, that it
should be sought for as carefully as it is the custom at present to
search for pulmonary signs.

"Hypotension when found persistently in individuals or families or
classes living under certain unhygienic conditions should put us on our
guard against at least a predisposition to tuberculosis. Most unhygienic
conditions, overwork, undernourishment and insufficient air, are of
themselves causes of a diminished resistance, and it seems likely that a
failure of normal cardiovascular response to exercise or change of
position may be found to indicate this stage of susceptibility,
especially to tuberculous infection.

"... Hypotension, when it is present in tuberculosis, increases with an
extension of the process. Recovery from hypotension accompanies arrest
or improvement. Return to normal pressure is commonly found in those who
are cured. Continuation of hypotension seems never to accompany
improvement. Prognosis can as safely be based on the alteration in the
blood pressure as on changes in the pulse or temperature...."

There are a few drugs which lower the blood pressure, but, as a rule,
their effects are more or less transitory. We know of no drug, unless it
be iodide of potassium, which has the property of causing changes in the
blood (decrease in viscosity?), which tends to reduce the blood pressure
when it is excessive. This drug fails us many times.

SOME DRUGS WHICH INFLUENCE THE BLOOD PRESSURE

=Pressure Raisers=

Adrenalin, when injected directly
into a vein or deep into the muscles.
The action is transitory.

Caffeine, preferably in the form
of caffeine-sodium-benzoate. A good
drug.

Strychnine, which does not act directly
but seemingly through the
higher centers.

Ergot, somewhat uncertain.

Nicotine, not used therapeutically.

Camphor, used in sterile olive oil
and injected deeply into the muscles.

Digitalis, when the cardiac tone is
low and decompensation is present.
Its action is prolonged but slow. Injections
of the infundibular portion
of the pituitary body. Not in use
clinically.

=Pressure Depressors=

Nitroglycerine and amyl nitrite,
action transitory but rapid.

Sodium nitrite and erythrol tetranitrate.
Action somewhat more prolonged.

Aconite, veratrum viride, chloral,
etc. These depress the heart.

Purgatives, drastic and hydragogue.

Potassium and sodium iodide may
lower blood pressure. When they do,
the action is prolonged.

Diuretin and theocin-sodium-acetate.

=Venous Pressure=

Comparatively little work has been done upon the determination of the
pressure in the veins in man. It is conceivable that this procedure may,
at times, be of great value. A number of attempts have been made to
measure the venous pressure by compressing the arm veins and noting on a
manometer the force necessary to obliterate the vein. As the pressure is
so slight, water is used instead of mercury, and readings have been
given in centimeters of water.

[Illustration: Fig. 33.--Apparatus for estimating the venous blood
pressure in man, devised by Drs. Hooker and Eyster. The small figure is
the detail of the box B. See explanation in text.]

In the apparatus shown in the figure (Fig. 33), Drs. Hooker and Eyster
succeeded in making estimations of the venous pressure. The box _B_ is
held in position by the tapes _A_, so that the vein is visible through
the rectangular opening in the thin rubber covering the bottom. The box
is connected with the water manometer _G_, by a rubber tube, from which
a T-tube enters the rubber bulb _E_. When the bulb _E_ is compressed
between the plates _D_, by the coarse thumbscrew _C_, air is forced
into the box _B_, exerting a pressure on the vein lying exposed beneath.
This pressure is transmitted directly to the manometer =G=, and may be
read off in centimeters of water on the accompanying scale. The veins of
the back of the hand are used and there must be no obstruction between
them and the heart. The rubber-covered box is accurately and lightly
fitted over a vein and pressure made until it is obliterated. By
measuring the distance above or below the heart level that the hand was
when the observation was made, and subtracting or adding these figures
to the manometer reading, we obtain the venous pressure at the heart
level.

Eyster has modified this instrument so that it is now much simpler to
operate. He uses a small glass cup with a flaring edge and a diameter of
about 2 cm. This is sealed to the skin directly over a vein on the back
of the hand by means of collodion. The stem of the cup has a rubber tube
leading to a small hand bulb and to the manometer tube which contains
colored water. Slight compression of the hand bulb obliterates the vein
which can be seen through the glass cup. The pressure in centimeters of
water is then read off. (Fig. 34.) The principle is the same as in the
earlier instrument, but the application is easier.

[Illustration: Fig. 34.--New venous pressure instrument. (After
Eyster.)]

Practically Hooker and Eyster found that the normal variation in healthy
subjects was from 3 to 10 cm. of water. The pressure rose in cases of
decompensated hearts with dyspnea and venous stasis, and returned to
normal with improvement in the condition of the patient. It might be
possible with this instrument to foretell an oncoming decompensation by
the rise in venous pressure.

The venous pressure may also be estimated roughly by slowly elevating
the arm and noting the instant at which a particular vein collapses. By
measuring the height of the vein above the heart some idea may be
obtained of the pressure within the right auricle.

=The Pulse=

There is nothing characteristic about the pulse of a person suffering
from arteriosclerosis, except it be the difference in the pulse of high
tension and of low tension. The pulse of high tension has a gradual
rise, a more or less rounded apex, and the dicrotic wave is slightly
marked and occurs about half-way down on the descending limb. In
arteriosclerosis with low tension the radial artery is usually so rigid
that very little pulse wave can be obtained. The general form of a low
tension pulse is a sharp upstroke, a pointed summit, and a secondary
wave on the base line, which corresponds to the dicrotic wave. Such a
pulse can be easily palpated, and is known as a dicrotic pulse. However,
such a pulse can occur only when the artery still retains all or a large
part of its elasticity; hence in arteriosclerotic low tension we would
never see such a pulse as the typical dicrotic.

=The Venous Pulse=

It would carry us too far to discuss fully the character of the venous
pulse, but a brief summary of the essential features of the normal
venous pulse is presented. The venous pulse is a term used to express
the tracing obtained from the internal or external jugular vein at the
root of the neck. Normally a very characteristic curve is produced,
which can be readily analyzed into a series of waves corresponding to
the fluctuations in the cardiac cycle. To understand these waves and
their values, the accompanying figure is helpful. (Fig. 35.)

[Illustration: Fig. 35.--Semidiagrammatic representation of the events
in the cardiac cycle: Jug., pulse in the jugular vein; Aur., contraction
of auricle; V. Pr., intraventricular pressure; Pap. M., contraction of
the papillary muscles; Car., carotid pulse. Below are given the times of
occurrence of the heart sounds and of the opening and closing of the
heart valves. (After Hirschfelder.)]

Bachmann summarizes the normal waves in the venous pulse tracing as
follows:

"The physiological or so-called venous pulse consists of three positive
and three negative waves, bearing a more or less definite relation to
the events of the cardiac cycle, and having their origin in the various
movements of the chambers and structures of the right heart. The first
positive wave (_a_) is presystolic in time, and is due to the
contraction of the auricle, causing a slowing of the venous current and
producing a centrifugal wave through a sudden arrest of the inflowing
blood. The second positive wave (_S_) is presystolic in time, and
originates in the sudden projection of the tricuspid valve into the
cavity of the auricle during the quick, incipient rise in the
intraventricular pressure occurring in the protosystolic period. The
third positive wave (_v_) occurs toward the end of ventricular systole.
It consists of two lesser waves separated by a shallow notch. The
factors entering into its formation are the relaxation of the papillary
muscle at a time when the intraventricular is still higher than the
intraauricular pressure, resulting in an upward movement of the
tricuspid leaflets and a return of the auriculoventricular septum to its
position of rest.

"The first negative wave (between positive wave _a_ and _S_) is due to
the relaxing auricle. The second negative wave (_Af_) occurs during the
diastole of the auricle. It is due to the dilatation of its walls, to
the displacement of the auriculoventricular septum toward the apex
occurring at the time of ventricular systole, and to the pull of the
papillary muscles on the tricuspid valve leaflets. The third negative
wave (_Vf_) appears during ventricular diastole and in the common pause
of the heart chambers. Its cause is found in the passage of the blood
from the auricle into the ventricle. It is somewhat modified possibly by
the continual ascent of the auriculoventricular septum and by a wave of
stasis due to the accumulation of blood coming from the periphery."
(Fig. 36.)

[Illustration: Fig. 36.--Simultaneous tracings of the jugular and
carotid pulses showing normal waves in the venous pulse and relation to
carotid pulse. (After Bachmann.)]

Hirschfelder has described another wave which he calls the "h" wave,
which is due to the floating up of the tricuspid valve by the blood in
the ventricle before the complete filling of the ventricle following the
auricular systole. (Fig. 37.)

[Illustration: Fig. 37.--Jugular and carotid tracing from a normal
individual with a well-marked third heart sound showing a large "h" and
a smaller pre-auricular wave "w." ? indicates a small wave in
mid-diastole following the "h" wave, occasionally found though perhaps
an artefact. (After Hirschfelder.)]

=The Electrocardiogram=

In the past few years an immense amount of work has been done by
numerous observers on the changes in the electrical potential of the
various portions of the heart during contraction. The very elaborate and
delicate electrocardiograph with the string galvanometer devised by
Einthoven is used. It has been definitely determined that the impulse to
cardiac contraction originates in the sinus node, a collection of
differentiated nerve cells situated at the junction of the superior vena
cava with the right auricle. From there the impulse travels in certain
fibers in the interauricular wall, passes through another node, the
auriculoventricular or Tawara node, situated in the auricular wall just
above the auriculoventricular ring, thence via the Y-bundle, or bundle
of His to the ventricles. This sequence is orderly, regular, and
normally invariable. (Fig. 38.)

[Illustration: Fig. 38.--Right side of the heart showing
diagrammatically the distribution of the two vagus nerves to different
parts of the viscus. The impulse to contraction originates at the
sino-auricular node and passes over the wall of the auricle to Tawara's
node, and thence over His' bundle across the auriculoventricular septum
to be distributed throughout the ventricular wall. If the upper,
sino-auricular, node is damaged, or if its impulses fail to get across
the wall of the auricle, Tawara's node acts in its place to start off
the ventricle. If a lesion at the base of the mesial segment of the
tricuspid valve damages His' bundle, so that Tawara's node is cut off
from the ventricle, then the ventricle may originate its own impulses to
contraction. (Hare's Practice of Medicine.)]

The sino-auricular (s-a) node is the most irritable portion of the
heart, it is endowed with the greatest amount of rhythmicity as well.
It is under the control of the vagus nerve. Its inherent rate of
rhythmicity is probably more rapid than the usual numbers of impulses
per minute, but it is inhibited by the vagus. Paralysis of the vagus
endings increases the rate of impulse formation and therefore the rate
of the heart.

The electrocardiogram is a graphic representation on a photographic film
or sensitive bromide paper of the changes of electrical potential during
muscular activity. The lines are made by the highly magnified string of
the galvanometer as it moves across the slit in the photographic
apparatus in response to the induction currents set up in the heart
magnified by the special galvanometer.

The record is made in three so-called Leads.

Lead I

The electrodes are attached to right arm and left arm.

Lead II

The electrodes are attached to right arm and left leg.

Lead III

The electrodes are attached to left arm and left leg.

A series of regular figures is normally obtained in which are
depressions and elevations and regular spacing of these elevations and
depressions. The waves so-called have been arbitrarily designated _P_,
_Q_, _R_, _S_, _T_. There is some difference in the three leads. "The
wave _P_ is positive in _all leads_. _P_ to _R_ interval varies slightly
in the _three leads_. All the waves of _Lead II_ are greater than those
of _Leads I_ and _III_. The wave _R_ is positive in _all leads_. _T_ is
usually positive in _all leads_, but is occasionally negative in Lead
III. Even in normal individuals there is a considerable range of
variation in the electrocardiogram which is within the limits of the
normal." (Hart.) (Fig. 39.)

[Illustration: Fig. 39.--Normal electrocardiogram. (After Hart.)]

The _P_ wave is admitted to be the wave of auricular contraction. _Q_,
_R_, _S_, is the ventricular complex caused, it is thought, by the
current passing over the ventricles. _T_ wave is not yet definitely
settled. It has been thought by some that it represented actual
ventricular contraction and its height and shape had some meaning in
heart force. This is denied by others. Hart defines it as "The final
activity of the ventricle." The _T_ wave is usually increased in size
during exercise.

The _P-R_ interval is almost the most important feature of the tracing.
It is the actual conduction time in fractions of a second of the impulse
from s-a node to the ventricles. Normally this is about 0.2 second or
slightly less. Much that was hoped for from the electrocardiograph in
the clinic has not been forthcoming. Its greatest value is in states of
abnormal conductivity, such as various grades of heart block,
extrasystoles, whether originating in auricles or in either ventricle,
abnormalities of rhythm, as flutter and fibrillation. It has, however,
aided materially in the intelligent interpretation of many phenomena
heretofore not well understood, and has enormously increased our
knowledge of the physiology and pathologic physiology of the heart.

It is not possible to enter farther into the subject here. This brief
discussion must suffice. The reader is referred to works on this subject
in connection with diseases of the heart.

CHAPTER IV

IMPORTANT CARDIAC IRREGULARITIES ASSOCIATED WITH ARTERIOSCLEROSIS

Arteriosclerosis of the aorta, of the coronary arteries, or of both, is
practically always found in cases dying of various cardiac
irregularities other than those the result of rheumatic cardiac lesions.
It is not that arteriosclerosis causes the cardiac lesions (although the
thickening of the walls of the coronary arteries does interfere
mechanically with the nutrition of the heart muscle), but the
arteriosclerosis is a part of the tissue reaction in the arteries to
some set of causes affecting the whole body. It is true when one boils
down the question to its last analysis, general arteriosclerosis may
mechanically so interfere with the blood supply to tissues that the
tissue is thrown out of function either in the reduction or even loss of
function. So it may be that occasionally the arteriosclerosis in the
arteries supplying the heart is really responsible for the cardiac
irregularity. The past few years have been fruitful ones in increasing
our knowledge of the various irregularities of the heart. We can do no
more than sketch briefly some of them in relation to arteriosclerosis.

The chief irregularities are (1) auricular flutter, (2) auricular
fibrillation, (3) ventricular fibrillation, (4) auricular extrasystole,
(5) ventricular extrasystole, (6) heart block, partial or complete.

=Auricular Flutter=

Auricular flutter is an abnormal rhythm characterized by very rapid, but
rhythmic auricular contractions usually 250 to 300 per minute. The
auricular contractions are so rapid that the ventricle can not respond,
so that an electrocardiagram of a heart in such a state (Fig. 40) shows
the ventricle beating regularly but at a much slower rate than the
auricle.

[Illustration: Fig. 40.--(After Hart.)]

The majority of cases exhibiting this peculiar rhythm are over 40 years
of age. In many cases sclerosis of the coronary arteries as a part of
general arteriosclerosis has been found. Auricular flutter can be
suspected when the pulse is regular or not particularly irregular and a
fluttering, rapid pulsation is seen in the jugular vein on the right
side. One can only be sure of the condition by making graphic records of
the heart.

Attacks usually come on suddenly and may disappear as suddenly,
suggesting paroxysmal tachycardia. The patient feels a commotion in his
chest, dyspnea, precordial distress, etc. The attack may last for weeks
or months, in which case the patient may carry on his usual work but be
conscious of palpitation in his chest. One may safely assume that the
flutter is a sign of a failing myocardium and sooner or later the heart
will pass to the graver stage of auricular fibrillation.

=Auricular Fibrillation=

In this condition the auricle is widely dilated and over its surface are
countless twitchings of individual muscles giving to the auricle the
appearance of a squirming bunch of worms. Such a condition may be
readily produced in a dog's exposed heart by direct faradization of the
auricle. It should be seen by every physician in order fully to
appreciate the passive, dilated sac part which the auricle plays when in
such a state. There is no auricular wave on the electrocardiogram (Figs.
41 and 42) only a series of fine tremulous lines, and the ventricles
beat irregularly with many dropped beats and variations in the size and
force of individual beats. Extrasystoles are also frequent. The heart is
absolutely irregular. Such a condition is readily recognizable as the
state of broken compensation. Graphic records are not essential as in
auricular flutter to establish the condition. Inspection of the root of
the neck for jugular pulsations and examination of the pulse with the
patient's evident dyspneic, cyanotic, edematous condition settles the
diagnosis.

[Illustration: Fig. 41.--Electrocardiogram showing auricular
fibrillation in Leads I (upper) and II (middle and lower). (Courtesy of
Dr. G. C. Robinson.)]

[Illustration: Fig. 42.--Auricular fibrillation. (After Hart.)]

In no case of auricular fibrillation is the heart muscle free from
extensive fibrous changes. These may be the result of general
arteriosclerotic changes or may result from toxic changes. It is the
general consensus of opinion that auricular fibrillation may persist for
months or even years. Some hold that the state of perpetual irregular
pulse is associated with auricular fibrillation. If that is true, then
auricular fibrillation may last for many years. Patients may go about
their work but always live with the imminent danger of a sudden
dilatation of the ventricle and symptoms of acute cardiac
decompensation.

In these cases the blood pressure is of particular interest. It is often
stated that the blood pressure is lowered as compensation returns and
digitalis has exhibited its full action. As a matter of fact this
statement needs some modification. If one takes the highest pressure at
the strongest beat, which may be only one in a dozen or more, that may
be true, but that does not represent the action of the much embarrassed
heart. We know that the circulation is much interfered with, that there
is hypostatic congestion, that the mass action is slow. The pulse
pressure is greatly disturbed and the head of pressure which should
force the blood to the periphery is so little that the circulation
almost ceases.

A count of the cardiac contractions heard with the stethoscope and a
count of the pulse shows a great discrepancy in number. This has been
called the "pulse deficit" (Hart). In order to arrive at the true
average systolic pressure the following procedure is done. "The apex and
radial are counted for one minute, at the same time by two observers,
(if possible) then a blood pressure cuff is applied to the arm, and the
pressure raised until the radial pulse is completely obliterated; the
pressure is then lowered 10 mm., and a second radial count is made; this
count is repeated at intervals of 10 mm. lowered pressure until the
cuff-pressure is insufficient to cut off any of the radial waves
(between each estimation the pressure on the arm should be lowered to
zero). From the figures thus obtained the average systolic blood
pressure is calculated by multiplying the number of radial beats by the
pressures under which they came through, adding together these products
and dividing their sum by the number of apex-beats per minute, the
resulting figure is what we have called the 'average systolic blood
pressure.'" (Fig. 43.)

[Illustration: Fig. 43.--The shaded area represents the pulse deficit;
the upper edge is the apex rate, the lower edge the radial rate. The
broken line indicates the "average systolic blood pressure." (Compare
these values with the figures at the bottom of the chart, which show the
systolic blood pressure determined by the usual method.) (After Hart.)]

For example: "B. S., April 29, 1910, Apex 131; radial, 101; deficit, 30.

BRACHIAL PRESSURE RADIAL COUNT
100 mm. Hg. 0
90 mm. 13 13 x 90 = 1170
80 mm. 47 - 13 = 34 x 80 = 2720
70 mm. 75 - 47 = 28 x 70 = 1960
60 mm. 82 - 75 = 7 x 60 = 420
50 mm. 101 - 82 = 19 x 50 = 950
----
Apex = 131) 7220
----
Average systolic blood-pressure 55 plus

B. S., May 11, 1910, Apex 79; radial, 72; deficit 7.

BRACHIAL PRESSURE RADIAL COUNT
120 mm. Hg. 0
110 mm. 44 44 x 110 = 4840
100 mm. 64 - 44 = 20 x 100 = 2000
90 mm. 72 - 64 = 8 x 90 = 720
----
Apex = 79) 7560
----
Average systolic blood-pressure 95 plus"

The diastolic pressure in these cases can not be determined except
approximately. This may be done by using an instrument with a dial and
noting the pressure where the oscillations of the dial hand show the
maximum excursion. The diastolic pressure is not at all important under
such conditions of acute cardiac breakdown. It would make no difference
in treatment whether the case was one of pure cardiac disease or one
of the hypertension groups. After the heart has rallied and the
circulation is reestablished, then a careful determination of the
diastolic pressure can be made and the prognosis will rest on what is
found at the compensated stage.

=Ventricular Fibrillation=

Ventricular fibrillation as its name implies, is fibrillation of the
ventricle analogous to that of the auricle, but the condition is rarely
observed as it is incompatible with life. It has been shown that hearts
at the time of death at times enter a state of fibrillation of the
ventricles and that cases of sudden death may be due to this condition.
Recently G. Canby Robinson[12] has seen and made electrocardiograms of a
case of ventricular fibrillation. (Fig. 44.) The case was that of a
woman forty-five years old, "who had a series of attacks of prolonged
cardiac syncope, closely resembling Stokes-Adams syndrome, from which
she recovered." During an attack of unconsciousness in which there was
no apex beat for about four minutes, the electrocardiogram was taken.
Following this the tracings showed an almost regular heart beating at
the rate of 85 to 100 per minute. The patient had three convulsions and
died with edema of lungs about 30 hours after the attack of ventricular
fibrillation.

[12] Robinson, G. C., and Bredeck, J. F.: Arch. Int. Med., 1917, xx,
725.

[Illustration: Fig. 44.--Upper curve. Record obtained during period of
cardiac syncopy at 2:48 p.m., Lead II. Lower curve from dog. Ventricular
fibrillation observed in the exposed heart. Lead from right foreleg and
left hind leg. (Courtesy of Dr. G. C. Robinson.)]

Autopsy revealed chronic fibrous endocarditis of aortic and mitral
valves, arteriosclerosis, bilateral carcinoma of the ovaries, and signs
of general chronic passive congestion.

It is possible that the syncopal attacks in this case were the result of
sclerosis of the vessels supplying the heart muscle although careful
microscopical examination did not throw much light on the ultimate
cause.

=Extrasystole=

Whenever there is a dropped beat or an intermittent pulse one may be
sure that it is the result of an extrasystole. Such extrasystoles are
produced in the ventricle at some point other than the regular path of
conduction of impulses. The extrasystole may have its origin in either
the auricle or the ventricle. If there is auricular extrasystole it can
not usually be recognized except by graphic methods. (Fig. 45.) The
ventricular extrasystole on the contrary is commonly seen and readily
recognized. Most of those seen in the clinic have their origin in some
part of the ventricular wall. Their two characteristics are that they
occur too early and that they are followed by a pause longer than the
normal diastolic pause. (Fig. 46.)

[Illustration: Fig. 45.--Electrocardiogram showing auricular
extrasystoles (P). (Courtesy of Dr. G. C. Robinson.)]

[Illustration: Fig. 46.--Electrocardiogram showing ventricular
extrasystole. Heart rate 56-60 beats per minute. Note that diastolic
pause in which extrasystole occurs is practically equal to two normal
diastolic pauses. (Courtesy of Dr. G. C. Robinson.)]

When one listens over the chest to a heart when extrasystoles are
occurring, one suddenly hears a weak beat which has taken place rather
too early after the previous systole to be strong enough to effect the
opening of the aortic valves. Consequently there is no pulse, the blood
does not move, and that beat is lost to the circulation. Moreover, when
the next regular stimulus comes from the s-a node it finds the ventricle
in a refractory condition, having just ceased a contraction, and it is
not until the next sinus impulse that the ventricle responds normally.
(Fig. 46.)

Patients who have occasional extrasystoles will say that all of a sudden
the heart turns upside down in the chest. Sometimes there is slight
sharp twinge of pain. Patients are at times quite alarmed about their
condition. Provided there is no evidence of gross myocardial lesion, the
extrasystole itself is of no great significance.

While many cases showing pathologic causes for extrasystoles have more
or less marked arteriosclerosis, there are other states in which no
arteriosclerosis is found where the extrasystole is present.

=Heart Block=

As heart block occurs frequently in cases characterized by extensive
arteriosclerosis, a brief discussion of the essential features will be
given. It is, however, probable that arteriosclerosis is not the cause
of any of the cases of heart block directly, but it is only a result of
the same etiological conditions which produce the lesion or lesions
which result in heart block. We may define heart block as the condition
in which the auricles and ventricles beat independently of each other.
There may be delayed conduction (Fig. 47), partial (Fig. 48), or
complete heart block (Fig. 49). In the former there are ventricular
silences, during which the auricles beat two, three, four, five, even up
to nine times, with only one ventricular contraction. It is believed by
most physiologists that the essential factor in the production of heart
block is an interference in the conduction of impulses from the
auricles to the ventricles through the band of tissue known as the
auriculoventricular bundle.

[Illustration: Fig. 47.--Electrocardiogram showing delayed conduction
(lengthening of P-R interval). These P-R intervals are quite regular.
When irregular there is apt to be extrasystole of ventricle or
occasional blocking of impulse going to ventricle. (Courtesy of Dr. G.
C. Robinson.)]

[Illustration: Fig. 48.--Electrocardiogram showing partial heart-block
in the three leads. Note the variability of P-R interval calculated in
seconds in Lead II. (Courtesy of Dr. G. C. Robinson.)]

[Illustration: Fig. 49.--Complete heart block. (Courtesy of Dr. G. C.
Robinson.)]

The bundle of muscles described by His in 1905, connecting the auricles
and ventricles, has been definitely shown to be the path through which
impulses having their origin in the orifices of the great veins pass to
the ventricles. The situation and size of this bundle has been thus
described in man by Retzer:

"When viewed from the left side, the bundle lies just above the muscular
septum of the ventricles and below the membranous septum. In some hearts
the muscular septum is so well developed that it envelops the bundle. It
is then difficult to find, but occasionally it can be seen directly by
means of transmitted light. From the left side the bundle can be
followed no farther posteriorly than the right fibrous trigone, for here
the connective tissue becomes so dense that it is difficult to dissect
it away. The impression is, therefore, received that this mass of
connective tissue forms the insertion of the bundle. The bundle may be
followed anteriorly until it becomes intimately mixed with the
musculature of the ventricles.

"When viewed from the right side of the heart, the bundle can not be
seen, because it is covered by the mesial leaflet of the tricuspid
valve, whose line of attachment passes obliquely over the membranous
septum. Then, if the endocardium is removed from the posterior part of
the septum of the auricle up to the membranous septum, the posterior
part of the auriculoventricular bundle will be exposed. If, in addition,
the membranous septum be removed, the bundle may be traced from the
point to which it could be followed when viewed from the left side as it
passes posteriorly over the muscular septum. In the region of the
auriculoventricular junction it loses its compactness, the fibers
divide, and the bundle seems to fork. One branch passes into the
superficial part of the valve musculature which descends from the
auricles, and the other branch passes directly into the musculature of
the auricle.

"Briefly, the auriculoventricular bundle runs posteriorly in the septum
of the ventricles about 10 mm. below the posterior leaflet of the aortic
semilunar valves; with a gentle curve it passes posteriorly just over
the upper edge of the muscular septum and sends its fibers into the
musculature of the right auricle and of the auricular valves. In the
heart of the adult the bundle is 18 mm. long, 2.5 mm. wide, and 1.5 mm.
thick." (Erlanger.)

All normal impulses have their origin in the sino-auricular node at the
junction of the superior vena cava with the right auricle (Fig. 50).
From there the impulse travels in the wall of the auricle in the
interauricular septum to the node of Tawara or A-V node (Fig. 51),
thence through the bundle of His to be distributed to the fibers of the
right and left ventricles. This sequence is orderly and perfectly
regular.

[Illustration: Fig. 50.--Showing alternating periods of sinus rhythm and
auriculoventricular rhythm. (After Eyster and Evans.)]

[Illustration: Fig. 51.--Period of auriculoventricular or "nodal" rhythm
following exercise in sitting posture. (After Eyster and Evans.)]

It has also been shown that the independent auricular and ventricular
rates vary somewhat, that of the auricle being in general faster than
that of the ventricle. A strip of mammalian ventricle placed outside of
the body in proper surroundings will begin to beat automatically at the
rate of about 40 beats a minute. Experimentally various grades of heart
block have been produced in the dog's heart by more or less compression
of the bundle at the A-V ring. The block may be partial, when two to
nine auricular beats occur to every one of the ventricle, up to
absolute complete block when the auricles and ventricles beat
independently of one another.

In any stage of partial block, pressure on the vagus nerve in the neck
produces certain specific changes. (Fig. 52.) Robinson and Draper[13]
have found qualitative differences in the two vagi. The right vagus
sends most of its fibers to the s-a node (Fig. 53) and has a more
evident influence on the rate and force of the cardiac contractions. The
majority of fibers from the left vagus are distributed to the A-V node
so that its most evident action is upon the conductivity of the impulse.
Pressure then on the right vagus will have a tendency to slow the whole
heart. Pressure on the left vagus will have a tendency to prolong the
P-R interval until even complete block occurs. Even when the heart block
is complete, stimulation of the accelerator nerve, as a rule, increases
the rate of both auricles and ventricles.

[Illustration: Fig. 52.--Influence of mechanical pressure on the right
vagus nerve. (After Eyster and Evans.)]

[Illustration: Fig. 53.--Schematic distribution of right and left vagus.
(After Hart.)]

[13] Jour. Exper. Med., 1911, xiv, 217.

If the block is functional, depending upon some temporary
overstimulation of the vagus nerve, atropin, which paralyzes the endings
of the vagus, will naturally lift the block. If the block is due to some
actual lesion of the bundle of His, such as fibrosis, gumma, or other
lesion, then atropin will have no influence to terminate the block. In
this manner we are able to distinguish between functional and organic
heart block.

CHAPTER V

BLOOD PRESSURE IN ITS CLINICAL APPLICATIONS

It is well to bear constantly in mind the point made over and over in
this work, that blood pressure is only one of many methods of acquiring
information. He who worships his sphygmomanometer as a thing apart and
infallible will sooner or later come to grief. Judgment must be used in
interpreting changes in blood pressure just as judgment is essential in
properly evaluating any instrumental help in diagnosis. One must not
forget the personal equation which enters into even accurate
instrumental recording in medicine and surgery.

In this chapter there will be no attempt to quote largely from what
others have said or thought. Every one has his own opinion as to the
value of certain methods after he has worked with them for a long time.
The ideas here expressed, except in cases where no opportunity has
offered to make personal studies, are those gathered from personal
experience.

=Blood Pressure in Surgery=

Careful estimation of the blood pressure in surgical cases has, at
times, great value. In all surgical diseases the most important fact to
know is not the systolic pressure, but the pulse pressure. If the pulse
pressure keeps within the range of normal, does not drop much below 30
mm. in an adult, then so far as we can tell the circulation is being
carried on. When the systolic pressure is gradually falling and the
diastolic remains the same, the circulation is failing and unless the
pulse pressure can be established again the patient will die. Again we
see the value of the pulse pressure.

All prolonged febrile diseases tend to produce a lowering of the blood
pressure picture. The diastolic does not fall to the same extent as the
systolic so that there is a pulse pressure smaller than normal. This is
to be expected from what we know of the general depression of the
circulation in fevers. The blood pressure reading is only a graphic
record of what we have long known, and enables us from day to day
accurately to measure the general circulation.

=Head Injuries=

It was claimed that in fracture of the skull or in concussion much could
be gained by frequent estimations of the blood pressure. This seemed
probable in the light of experiments on compressing the brains of dogs
by the use of bags inserted through trephine openings (Cushing). In the
clinic, however, it has not been found of any material value. It has a
value in differentiating a simple fracture, let us say, from a case of
uremia which is picked up on the street with a bump on the head. There
the high pressure usually found would at once direct attention to the
kidneys and the newer methods of blood examination would at once settle
the question. Naturally uremics may also have skull fracture. There the
diagnosis would be complicated. A decompression done at once would be
indicated. If the skull fracture happened in a uremic, the decompression
would probably do no harm. In fact, there are some who advise
decompression for uremia.

=Shock and Hemorrhage=

In shock the blood pressure picture is low but the pulse pressure drops
to abnormally low figures. It seems to me that the blood pressure
instrument has its greatest value in surgery in the warning it gives to
the operating surgeon in cases of impending shock.

It is well known that the first effect of ether, the commonly used
anesthetic, is to raise the blood pressure and quicken the pulse rate.
The whole blood pressure picture is at first elevated (Fig. 54). Soon
the whole pressure falls slightly but continues at a higher level than
normal. The diastolic pressure drops back nearly to normal and the
increased pulse pressure is due almost entirely to the slight rise in
the systolic pressure. Now the whole duty of the anesthetist is to
administer the ether so that this ratio of systolic and diastolic is
maintained throughout the operation. Warning comes to him of impending
shock before it comes to any one in the neighborhood (Fig. 55). Any
sudden change in the pressure is a signal for increased watchfulness.
Should the pressure all at once drop he can immediately notify the
surgeon and institute measures to resuscitate the patient.

[Illustration: Fig. 54.--Blood pressure record from a normal reaction to
ether. Note that the systolic and diastolic rise and fall together. At
the end of the anesthetization the pulse pressure is practically the
same as at the beginning. Compare this with the record in Fig. 55, where
the operation had to be discontinued on account of the onset of shock.]

[Illustration: Fig. 55.--Beginning of operative shock. Chart showing the
method of recording blood pressure during operation.

Note that the pulse and respiration show no remarkable changes, but the
blood pressure steadily fell, the systolic more than the diastolic so
that the pulse pressure was gradually reaching the danger point. Further
work on this case was stopped following the warning given by the blood
pressure. The patient was returned to the ward and a week later
anesthesia was again given, the operation was completed, and the patient
had a satisfactory convalescence.]

A method which is widely used is as follows: The anesthetist wraps the
cuff of one of the dial instruments around the patient's arm, and
arranges the dial so that it can easily be seen by him at all times.
This does not in any way interfere with the work of the surgeon. Over
the brachial artery below the cuff is the bell of a binaural stethoscope
held in place by the strap attachment now on the market. The tubes of
the stethoscope are long enough to reach conveniently to the ear pieces.
A watch is pinned to the sheet of the table. He has a chart, as
illustrated (Fig. 56) on a board and makes a dot in every space for five
minute intervals. By joining the lines a curve is obtained which tells
at a glance what the circulation is doing. I feel sure that more
attention and care exercised on the part of the anesthetist would be the
means of conserving many lives lost from shock following operation.

[Illustration: Fig. 56.--Showing method of using blood pressure
instrument during operation without interfering with the operator or
assistants. Sheet thrown back to show cuff on arm of patient.
Anesthetist has chart on table beside him, dial pinned to pad in full
view, bulb near hand. Extra tubing must be put on the blood pressure
instrument.]

A sudden drop in the pressure picture may mean a large hemorrhage. The
gradual return of the pressure picture means that the vasomotor
mechanism has acted to keep up the pulse pressure. Should the diastolic
pressure continually fall, it may mean that the hemorrhage is still
taking place (Wiggers).

=Blood Pressure in Obstetrics=

One might affirm almost without fear of contradiction that the constant
determination of blood pressure during pregnancy is more important than
the examination of the urine. Within recent years a number of observers
having access to a large material, have given the results of their
findings. There is a striking unanimity of opinion, although now and
then a difference in minor details.

The blood pressure should be taken frequently during pregnancy. The
usual and highly essential precautions in taking pressure in general
apply most particularly in these cases. Towards the end of pregnancy the
pressure should if possible be taken daily and oftener if necessary.

Pressure in women is usually below 120 mm. Many patients have a
temporary rise in blood pressure during pregnancy, due oftenest to
constipation, without developing other symptoms. This is common to all
conditions and has no significance. Some think that an abnormally low
pressure, that is, a systolic below 90 mm., suggests that the patient is
likely to react unduly to the strain of labor. This is denied by others.
Among 1000 cases (Irving) the pressure was below 90 in only one case. A
gradually rising pressure precedes albuminuria, as a rule. If there is
albumin without change in pressure the albumin may usually be
disregarded. Some think that a pressure over 130 mm. systolic should be
carefully watched. The danger limit is set by some at 150 mm. If the
blood pressure from the very first is high, it may mean only that that
was the patient's normal pressure. This calls for increased
watchfulness. It is held by some that high blood pressure favors
hemorrhage and probably explains the hemorrhagic lesions in the placenta
and some viscera in eclampsia and albuminuria.

All are agreed that the most significant change is the gradual but sure
rise from a low pressure. When this is combined with albuminuria the
danger of toxemia is imminent. The high blood pressure in those under
thirty years of age seems to be a more certain sign of approaching
toxemia than the same pressure in those older. The pressure falls within
a few days to its normal after delivery in the toxic cases.

Although the emesis gravidarum is held to be a sign of a toxemia of some
unknown nature, the blood pressure is never raised even in the
pernicious form.

=Infectious Diseases=

In all infectious diseases the blood pressure tends to be lower than
normal. During chills the systolic may rise to great height due to the
violent muscular contractions.

We found the blood pressure of great value in giving information
concerning the circulation. Again we repeat that it is not the systolic
alone or the diastolic alone but the pulse pressure which we wish to
keep informed about. In pneumonia we have tried out Gibson's law only to
discard it. This so-called law is that in pneumonia the systolic
pressure in millimeters should remain above the figure for the pulse
rate. When the figure in mm. of pressure is equalled by or exceeded by
the pulse rate the prognosis is grave.

In typhoid fever we have made many estimations at various stages of the
disease. We can only say that the pressure picture tends to fall during
the course. The systolic falls more than the diastolic so that it is not
uncommon to see pulse pressures of 20 mm. at the beginning of
convalescence in spite of the high caloric feeding practiced. At the
time of perforation the systolic pressure may be raised. This is only
the reflex from the initial pain. Soon the pressure falls and if
peritonitis sets in, the pressure is exceedingly low and the pulse
pressure gradually falls until the circulation can no longer be carried
on. In large hemorrhage the pressure suddenly falls. If only one
hemorrhage has occurred a gradual rise takes place, but the general
pressure picture remains at a lower level for days, gradually returning
where it was before the hemorrhage.

In beginning failure of the circulation we found elevation of the foot
of the bed about nine inches to be of such value that we felt there must
be some increase in blood pressure. Numerous readings were made covering
a period of several months. Although we felt certain that the
circulation was improved, we rarely needed cardiac stimulation, we never
could prove any increase of blood pressure with the sphygmomanometer.

In all infectious diseases there is no help offered by blood pressure
estimations in diagnosis. The sole and important use is that of keeping
track of the circulation.

=Valvular Heart Disease=

No rules can be laid down for blood pressure in valvular heart disease.
Aortic stenosis, the rarest of the valvular lesions, is practically
always accompanied by high pressure picture. Mitral stenosis on the
contrary usually shows a low pressure picture. Mitral insufficiency may
show an exceedingly low picture or an exceedingly high picture. Aortic
insufficiency also may be accompanied by a high systolic or by a normal
systolic pressure. It depends on the etiology. Practically all the
rheumatic cases have low pressure, the syphilitic cases have a high
pressure. It is characteristic of all cases of aortic insufficiency that
the diastolic pressure is low, even as low as 30 mm. The pulse pressure
is invariably high. Usually there is no difficulty in determining the
diastolic pressure. The intense third tone suddenly becomes dull at the
point of diastolic pressure and frequently the dull sound can be
distinctly heard over the artery down to the zero of the scale. If
difficulty is found in reading the diastolic as the pressure is reduced,
the estimation may be reversed and the pressure gradually increased from
zero to the point where the dull tone suddenly becomes loud and clear.
These points always coincide.

=Kidney Diseases=

This has already been discussed somewhat fully in Chapter III and will
receive more consideration later. It might be remarked in passing that
in a case of seeming coma where albumin is found in the urine but where
the blood pressure is low or normal, I have found at autopsy in several
cases pyonephrosis and not chronic nephritis. The blood pressure may be
useful in differentiating uremic coma from the coma of pyonephrosis.
Also in the cases of coma with anasarca, either the acute, subacute or
chronic form the blood pressure is not raised as a rule. Other diseases
of the kidney, as tuberculosis, cancer, infection with pyogenic
organisms, are not accompanied with any notable changes in blood
pressure.

=Other Diseases, Liver, Spleen, Abdomen, etc.=

Blood pressure is only of value in the above diseases in affording
information concerning the state of the circulation. There is nothing
characteristic about the pressure in any of these diseases.

CHAPTER VI

ETIOLOGY

The causes of arteriosclerosis are many and varied. No two persons have
the same resisting power toward poisons that circulate in the blood.
Some go through life exposed to all the infectious diseases without ever
becoming infected, while others fall easy victims to every disease that
comes, no matter how careful they may be, and it is quite the same in
regard to the resistance of the arterial tissues. If the tubing is of
first class quality and the individual does not place too much strain on
it, he may live to the biblical three-score years and ten, and possess
arteries which have undergone such slight changes that they are not
palpable. Such a person is, however, the exception. On the other hand,
if the tissue is of poor quality, even the ordinary wear and tear of
life causes early changes in the vessels, and a person of forty may have
hard arteries.

We have described in a previous chapter the changes which normally occur
in the arteries as age advances. An artery that is normal for a man of
fifty years would be distinctly abnormal for a boy of fifteen.

Two broad divisions of arteriosclerosis may be made: (1) congenital, or
the result of inherited tendency; (2) acquired.

=Congenital Form=

When Dr. O. W. Holmes was asked how to live to the age of seventy, he
replied that a man should begin to pick his ancestors one hundred years
before he was born. Our parents determine the character of the tissues
with which we start in life, and this determines our general resistance.
We might properly speak of congenital arteriosclerosis where the
affected individual had poor arterial tissue with which to begin life,
for that, in a sense, is a congenital defect, and arterial tissue that
is poor in quality is prone to disease.

The author is more and more impressed with the part that heredity plays
in the determination of arterial degeneration. Especially does syphilis
in the parents or grandparents leave its stigma in the succeeding
generations in the shape of poor arterial tissue which is prone to early
degeneration. Recently W. W. Graves has called attention to a
malformation of the vertebral border of the scapula which consists in a
concavity instead of the normal convexity of the bone. To this
malformation he has given the name, scaphoid scapula. He considers this
to be but one manifestation of a general lack of development in the
individual. He speaks of this maldevelopment as a blight and considers
that syphilis in the ancestors is responsible for the condition in the
offspring. He finds that even in children, the subjects of the scaphoid
scapula, the arteries are very definitely thickened. While confirmation
of his observations is lacking, there is no doubt that we must lay the
blame for much of the arteriosclerosis in our patients to the poor
quality of arterial tissue transmitted by ancestors who have acquired
some constitutional disease. It may have been syphilis, it may have been
the degeneration produced by alcohol or other drug. We can not ignore
the part which heredity plays. The various factors to be considered in
the production of the acquired form of arteriosclerosis appear to me to
be but contributory factors to a very great extent, the essential and
fundamental factor being the quality of arterial tissue with which the
individual is endowed.

Arteriosclerosis may occur in infants. Cases have been reported of
calcification of the arteries in infants and children. The
arteriosclerosis may occur without nephritis or rise of blood pressure.
Cerebral hemorrhage in a child of two years has been seen. Heredity in
these cases plays a most important rôle. In many of the reported cases
there was no question of congenital syphilis. Aneurysms, single or
multiple, have been found in the arteries of children, and even the
pulmonary artery may show sclerotic changes.

=Acquired Form=

As a rule the cases usually seen belong in this group because it seems
as if a connection could be established almost always between one or
more of the etiologic factors to be described and the disease. While
this apparently is the case, we must never lose sight of the part which
the quality of the tissue plays. When we leave this out of our
calculations we undoubtedly make many false deductions. When two men of
the same age who have been exposed to the same conditions as far as we
can learn, are found to have quite different arteries, the one normal,
the other thickened, we must postulate congenitally poor tissue on the
part of the latter. Such tissue readily becomes diseased following
conditions which would very likely have produced no noticeable effect on
perfectly normal, healthy tissue.

=Hypertension=

Hypertension must still be reckoned with in the etiology of
arteriosclerosis although the rôle that it was thought to play does not
seem so important. Changes of blood pressure alone are not considered by
many to be sufficient for the production of arteriosclerosis. This may
play some part, but there are many other factors mostly unknown which
determine in any case the production of arterial lesions.

With every systole of the heart, blood is forced out into the arterial
system against a certain amount of resistance represented by the
tonicity of the capillary area, and the amount of cohesion between the
viscous blood and the walls of arterioles. When a dilatation of the
capillaries over any large area takes place, the blood pressure falls,
provided there is no compensatory contraction in other areas to make up
for the decreased resistance in the dilated vessels. The viscosity of
the blood, as such, probably has very little effect on the resistance to
the flow. With the systole of the heart there is a sudden dilatation of
the arch of the aorta, and a wave of expansion follows, which is
transmitted to the periphery and is lost only in the capillaries.

The blood pressure is constantly changing. Physiologically there are
relatively wide variations in the pressure in a perfectly normal
individual. There are some persons who have hypotension, a blood
pressure much below the normal. Such persons have usually small hearts,
small aortas, and they seem to have but little resistance to disease.
Many diseases, especially the prolonged fevers, diminish markedly the
blood pressure. Whether the hypertension is the cause of the structural
changes that are found in the walls of the vessels, or is the result of
the diminished area of the arterial tree through which the same amount
of blood has to be driven as before the vessel walls became narrowed, is
still disputed. As has been stated, experimental evidence would tend to
place the initial blame upon the poisons circulating in the blood, which
first damage the vessel walls. The subsequent changes then produce
thickening and inelasticity. Some think (Allbutt) that the hypertension
is primary. There are cases seen clinically that lend support to this
view and there is experimental evidence also (v. Chap. II). Not
infrequently individuals in middle life begin to show increase of
arterial blood pressure without discoverable cause. In such case it may
be that there is slowly progressing chronic nephritis. The urine if
examined only superficially in single specimens may not reveal any
abnormalities. Careful functional examination by means of the newer
tests may reveal functional deficiency. It must not be supposed that
all cases of increasing hypertension are cases of chronic nephritis. The
opinion has already been expressed (Chap. III) concerning this point.
Experience has convinced me that the opinion expressed in former
editions is not altogether correct.

=Age=

No age is exempt from the lesions of arteriosclerosis if we consider the
two groups. However, the disease is seen for the most part in persons
past middle life. The relative frequency with which it is found in the
different decades depends on so many factors that it is of no value to
tabulate them. As has been stated, arteriosclerosis of all types is an
involution process that advances with age. Longevity is a question of
the integrity of the arterial tissue, and no one can tell what sort of
"vital rubber" (Osler) any one of us has. However, many with poor tubing
may make such use of it that it will outlast good tubing that is badly
treated. Unfortunately we have no way of telling early enough with just
what sort of arterial tissue we are starting life.

=Sex=

There is no doubt that men are far more prone to arterial disease than
women are; all statistics are in accord on this point. This is explained
by the greater exposure of men to those conditions of life which tend to
produce circulatory strain, and so to produce arteriosclerosis, or vice
versa. Arteriosclerosis in women is not often seen until after the
fiftieth year. Cases of the most extreme grade of pipe stem arteries
are, however, seen in old women, and calcified arteries are not hard to
find among the inmates of an old woman's home.

=Race=

Some of the most beautiful examples of arteriosclerosis in this country
are seen in the negro. Not only is this disease more frequent in the
black race, but the age of onset is much earlier than in the Caucasian.
The accidents of arteriosclerosis, viz., aneurysm, cerebral hemorrhage,
etc., are more common among the negro males. The etiologic factors that
are most often found in the history are the prevalence of syphilis and
hard physical labor.

=Occupation=

Certain occupations have a distinct causal relationship to
arteriosclerosis; among such are particularly those entailing prolonged
muscular exercise, especially if much lifting is necessary. Every one is
familiar with the phenomena accompanying the exertion of lifting. The
breath is drawn in, the glottis is closed, and the muscles of the chest
wall are held rigidly while the exertion lasts. This causes a great
increase in blood pressure, and constant repetition of this will produce
permanent high tension. In hospitals, the stevedores as a class have
marked arteriosclerosis, and, almost without exception, they are
comparatively young men. Occupations that are accompanied with prolonged
mental strain, such as now occur to the heads of large manufacturing and
financial institutions, also predispose to early arterial changes.
Psychic activity, especially when it is accompanied by worry, is a
potent factor in the production of the increased blood pressure which is
the chief factor in producing arterial disease. It has been suggested
that sexual continence in high-strung men produces changes in the
nervous system which can conceivably lead to the production of high
tension and further to arteriosclerosis. This, however, I can not think
has any foundation in fact except in so far as such men are prone to
live at high speed and wear themselves out sooner than the normal
person. The sexual continence _per se_ is not harmful. There are,
however, men who seem not to be harmed by the constant wear and tear of
our modern life. These are the exceptions.

Workers in factories where paint is made and the ingredients
hand-mixed, are prone to develop arteriosclerosis early in life. It has
been found that the laborers most apt to be victims of lead intoxication
are those who are careless in their habits of cleanliness, particularly
in regard to the fingernails. The continuous absorption of lead into the
system, brings about a condition of hypertension that has its inevitable
results.

The fact is that any occupation which entails either the absorption of
toxic substances, or prolonged muscular labor, will hasten markedly the
onset of arterial disease.

=Food Poisons=

The opinion that arteriosclerosis is due in large part to poisoning by
end products or by-products of protein digestion is now receiving much
support. Experiments on dogs and rabbits have lent some confirmation to
chemical observations. It has been shown that dogs fed for a long time
on putrefied meat developed inflammation and degeneration of the
adventitia and media, with hyperplasia and calcification of the intima
of many arteries. In the pulmonary and carotid arteries, in the vena
cavas and myocardium, there were extensive necroses and hyaline
degeneration. Moreover, injections of sodium urate and ergot caused
necroses in the muscularis and elastica of the aorta, pulmonary artery,
vena cavas inferior and heart muscle, but there was no calcification.
Guinea pigs which were fed indol in small doses by the mouth over a long
period showed atheromatous degeneration of the aorta.

=Infectious Diseases=

As more study has been given to the arteries in persons who have died of
the acute infectious diseases, more has come to light concerning the
effects of the toxins of these diseases on the vessel walls. In the
arteries of children who have died of measles, scarlet fever,
diphtheria, cerebrospinal meningitis, etc., degenerative changes in the
arteries occur, modified only by the length of time that the toxins have
acted.

Thayer has shown that the arteries of those who have passed through an
attack of moderately severe or severe typhoid fever are as a rule more
readily palpable than are the vessels of persons of corresponding years
who have never had the disease. Clinically the typhoid toxin appears to
cause the early production of arteriosclerosis. The changes in the
arteries occur for the most part, and always earlier, in the peripheral
arteries, and the media is chiefly affected. Minute yellowish patches
are found on the aorta, carotids, and coronaries. In persons who have
passed through an attack of one of the fevers, and have later died from
some other cause, regenerative changes are sometimes found to have taken
place in the arteries, consisting of an ingrowth of elastic fibers from
the intact adventitia to the diseased media.

That there are some other factors than the infectious disease which are
concerned in the production of arterial changes seems evident from a
study[14] made recently among a group of almshouse inmates ranging in
age from 38 to 90 years. The study included 500 persons of both sexes.
Careful histories were taken to determine the presence of antecedent
infectious disease. The radial artery was palpated to determine the
presence of sclerosis. Among the cases giving a history of one
infectious disease the following table gives the results:

-------------------------------------------------------------
DISEASE NO. + ++ +++ POSITIVE NEGATIVE
-------------------------------------------------------------
Measles 47 10 6 12 28 19
Infectious arthritis 38 9 6 4 19 19
Pneumonia 30 5 8 5 18 12
Typhoid 27 6 8 3 17 10
Scarlet fever 10 0 0 4 4 6
Smallpox 14 1 4 0 5 9
Miscellaneous 12 2 5 2 9 3
-------------------------------------------------------------
178 33 37 30 100 78
-------------------------------------------------------------

[14] Warfield, L. M.: Jour. Lab. and Clin. Med., November, 1917.

A summary of the cases showed: 252 cases without sclerosis; 248 with
sclerosis; 147 cases with infections but no sclerosis; 180 cases with
infections and sclerosis.

This study failed to throw any positive light on the question.
Infectious diseases undoubtedly play a certain rôle, particularly those
continuing a long time and certain particular infectious diseases, as
measles.

=Syphilis=

Syphilis is one of the most important of the etiologic factors in the
production of arteriosclerosis. It has been shown that in 85 per cent of
cases of aortic insufficiency in persons, usually males, over forty-five
years, who did not have chronic infective endocarditis, the Wassermann
reaction was positive. Acute aortitis affecting the ascending and
transverse portions of the arch of the aorta is very commonly seen, and
the irregular, scattered, slightly raised, yellowish-white patches of
sclerosis in the arch which are found years after the syphilitic lesion,
are considered by some to be very characteristic of syphilis.
Mesaortitis is the primary lesion and acts as a _locus minoris
resistentiæ_ where an aneurysm forms.

Hypertensive cardiovascular cases have been serologically studied, and a
positive Wassermann reaction found in a large percentage of one series.
In fifty cases, 90 per cent either gave a positive Wassermann reaction
or luetin test, were known to have syphilis, or had children with
hereditary syphilis. This suggests what might be called "familial
cardiovascular syphilis."

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

=Chronic Drug Intoxications=

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

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

=Overeating=

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

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

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

=Mental Strain=

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

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

=Muscular Overwork=

Muscular overwork is to be reckoned with as an etiologic factor. One
sees it especially among the laboring class in both whites and negroes.
Possibly other factors, as alcohol and coarse heavy food, contribute to
the early arterial degeneration. Hypertrophy of the heart occurs in
athletes, and statistics gathered among the oarsmen especially, show a
relatively high mortality at the different decades traceable to the high
tension produced while in training. This question deserves more
consideration than has been accorded it.

=Renal Disease=

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

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

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

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

=Ductless Glands=

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

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

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

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

CHAPTER VII

THE PHYSICAL EXAMINATION OF THE HEART AND ARTERIES

=Heart Boundaries=

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

It is frequently stated that the right limit of cardiac dullness is
normally, in the adult, just at the right border of the sternum. This is
not strictly accurate. Careful dissections at the autopsy table and
x-ray plates of the chest made at a distance of two meters from the tube
show that the border of the right auricle is from one to one and a half
and even two centimeters from the edge of the sternum at the level of
the fourth rib, and on the living subject this can be also demonstrated.
The right border of the heart usually is from 3 to 4 cm. from the
midsternal line at the level of the fourth rib.

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

Normally, then, the cardiac dullness, the so-called relative cardiac
dullness, begins above at the upper border of the third costal
cartilage, as a rule, and taking a somewhat curved line with the
concavity inward, descends to the fifth interspace or beneath the fifth
rib from 9 to 10 cm. from a line drawn through the center of the sternum
parallel to its length, the midsternal line. This seems to me to be a
better method of recording the size of the heart than by the lines
commonly used; viz., the nipple, or midclavicular, or parasternal line.
Below, the cardiac dullness is merged into the tympany from the stomach
and the dullness from the liver. At the sixth right costosternal
articulation there is a sharp turn upwards forming at that point with
the liver the cardiohepatic angle. At the fourth right cartilage or the
third interspace, the dullness is from one to two centimeters from the
edge of the sternum. We have then a somewhat pear-shaped area or
triangular area with the apex at the apex of the heart. The so-called
absolute cardiac dullness does not appear to me to be of any great
significance. In reality it is the limit of lung resonance and may be
greater or less, not so much on account of variations in the size of the
heart, as of variations in size of the lungs and shape of the chest
wall.

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

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

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

=Percussion=

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

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

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

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

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

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

=Auscultation=

In auscultating the heart I prefer the binaural stethoscope of the Ford
pattern. The recent substitution of an aluminum bell for the hard rubber
bell is an improvement. Personally I do not favor the phonendoscope or
any of the new patent non-roaring instruments now for sale by urgent
instrument makers. The phonendoscope has its uses, for example in
auscultating the back when a patient is lying in bed or in listening to
the heart sounds when a patient is under an anesthetic; but for
differentiating the murmurs and for heart diagnosis, I much prefer the
regular bell stethoscope.

In arteriosclerosis the two places over which it is important to listen
are the apex and the second right cartilage, the aortic area. Over the
former, one gains data in regard to the strength of the heart as
indicated by the first sound, over the latter point, one learns of the
tension in the aorta by the character of the sound produced when the
aortic valves close.

The hypertrophy of the heart in arteriosclerosis is invariably due to
the enlargement and thickening of the left ventricle. From the nature of
the position which the heart assumes in the thorax, this enlargement is
downward and to the left. The apex beat will therefore be found in the
fifth or sixth interspace, and definitely at an increased distance from
the midsternal line. As stated above, it is most important that this
distance be accurately measured and put down in the notes of the case
for future reference. No satisfactory prognosis can be given unless this
is done, for the gradual increase or the decrease under treatment in the
size of the heart can thus be definitely known, and, knowing the other
factors, a prognosis may be given which will be of some value to the
patient.

=The Examination of the Arteries=

It is exceedingly difficult at times to affirm definitely that an
artery, the radial for example, is actually sclerosed. Much depends on
the sensitiveness of the fingers of him who palpates, and much upon the
relation of the palpated artery to the surrounding, chiefly underlying,
structures. In the examination of arteries it is well to inspect the
body for the pulsations caused by them. Frequently an exceedingly
tortuous artery, such as the brachial, may be seen throughout its whole
extent and yet the radial appear little, if any, thickened by palpation.
Again the artery of a pulse of high tension which is small in size but
full between the beats, may not be as sclerosed as one which collapses
and feels much softer. It is difficult to obtain accurate data in regard
to the tension in an artery by feeling it with the fingers of one hand.
One should use both hands. With the middle finger of the right (left)
hand the artery is compressed peripherally, that is, nearest the wrist.
The blood is then pressed out of the artery with the middle finger of
the left (right) hand, so as to obliterate completely the pulse wave and
the two or three inches between the middle fingers are felt with the
index fingers. By holding the finger firmly on the artery near the wrist
so as to block any wave that may come through the palmar arch by
anastomosis with the ulnar artery and by releasing pressure on the
proximal middle finger, some idea may be had of the degree of pulse
tension. However, no amount of practice can more than approximate the
tension and when one is surest that he can tell how many millimeters of
pressure there are, he is apt to be farthest wrong when he checks his
guess with the sphygmomanometer.

Much may be learned from carefully palpating the peripheral arteries,
and, as a rule, the sclerosis of these arteries means general
arteriosclerosis, although there are many exceptions to this.

A more recent method, and one which in the author's hands has been found
to be valuable, is that proposed by Wertheim-Salomonson who palpates the
artery not with the ball of the finger but with the fingernail. The
finger is held so that the nail is perpendicular to the surface of the
skin and the artery is felt with the end of the nail. The sensation is
perceived at the root and makes use of all the sensitive nerve endings
there. In this way it is possible to feel the arterial wall distinctly,
and a little practice will enable one to determine whether or not the
vessel wall is thickened. It is also possible to determine with a
considerable degree of accuracy the diameter of the artery and the size
of the wall when the current is cut off by pressure on the proximal side
of the artery. It is best to have a firm background when this
"fingernail" palpation is used. This may be obtained by palpating the
radial artery against the lower end of the radius.

Probably the best method of palpating the arteries, especially the
radial, to determine the degree of sclerosis and thickening, is to use
the tip of the finger and roll it carefully over the artery. The tip of
the finger is exceedingly sensitive and, moreover, it is a firmer
palpating surface than the ball, thus enabling one to appreciate degrees
of sclerosis which could not be differentiated by palpation with the
soft yielding ball. This finger tip palpation is well illustrated in the
figures here shown. (Figs. 57 and 58.)

[Illustration: Fig. 57.--A method of finger-tip palpation of the radial
artery. (Graves.)]

[Illustration: Fig. 58.--Another method of finger-tip palpation of the
radial artery. (Graves.)]

=Estimation of Blood Pressure=

It must be borne in mind at the outset that arteriosclerosis and high
blood pressure are not always associated. As a matter of fact in the
severest grades of senile arteriosclerosis the blood pressure is usually
below the normal for the individual's years. However, as high tension is
a frequent factor in the production of arterial thickening, blood
pressure readings are of importance.

The instrument which one uses is of minor importance provided it is
properly standardized. The most important feature of the instrument is
the cuff. This must be 12 cm. wide and be long enough to wrap around the
arm several times so that the pressure is evenly distributed over the
whole arm and not over a small portion. One mercury instrument we had in
the hospital was reported to be at great variance with a dial
instrument. This mercury instrument was provided with a cuff which was
short and was tied around the arm by means of a piece of tape. This
caused a tight constriction over a small area and rendered the
estimation too high. A new, long tailed cuff easily remedied the
apparent defect in the instrument.

In taking blood pressures the difference from day to day of 10 or even
15 mm. of systolic pressure has no great significance. Fluctuations of
the systolic pressure alone, it is insisted upon, have very little
meaning. One must take the whole pressure picture into consideration and
determine how the picture changes in order to draw any conclusion in
regard to the state of the blood pressure. Failure to pay attention to
this evident point has caused much futile work to be written and
published.

It is well to emphasize again the point that the blood pressure picture
consists of the systolic, the diastolic, the pulse pressure and the
pulse rate.

=Palpation=

Hoover has called attention to the direct palpation of the femoral
artery just below Poupart's ligament as a more accurate index of the
pressure in the aorta than the palpation of the radial artery. Possibly
one can obtain a more accurate estimate of the blood pressure in this
way. This, however, is open to dispute. To estimate the blood pressure
by palpating the radial artery is most deceptive. In about 75 per cent
of cases one can tell fairly well whether the pressure is abnormally
high or abnormally low. Small variations are impossible to determine.
Unquestionably it is most advantageous to get into the habit of
palpating the femoral artery and checking the result with the
sphygmomanometer so that the fingers may be trained to appreciate as
accurately as possible changes of pressure.

It may be that one day when the instrument is needed it is not at hand.
A well-trained touch then becomes a great asset.

=Precautions When Estimating Blood Pressure=

There are certain precautions which must be strictly observed when
deductions are drawn from the manometer readings. The psychic factor
must be reckoned with. Any emotion may cause marked variations in the
pressure. Excitement and anger are especial sources of error. Even the
slight excitement arising from taking the first blood pressure on a
nervous patient especially is apt to give false values. Usually the
readings must be taken many times at the first sitting and the first few
may have to be set aside. Worry is a potent factor in raising the
pressure. A walk to the physician's office, especially if rapid, has its
effect.

The position of the patient when the blood pressure is taken is
important. Usually in the office the pressure is taken when the patient
sits in a chair. He should assume a relaxed, comfortable attitude. The
readings should be made at the same time of day and at the same interval
between meals. The pressure in both arms should be measured and
comparisons should be made only between readings on the same arm. These
precautions may seem useless and even somewhat trivial, and the
conditions difficult to control. But unless they are carefully observed
the readings will be false, no comparisons can be drawn between the
readings on different days, and the instrument will most probably be
blamed. I have known this to happen so often that I can not emphasize
too strongly the importance of controlling all the essential conditions
which go to make accurate work.

=The Value of Blood Pressure=

In the past few years there has been a veritable avalanche of blood
pressure instrument salesmen who have covered the country, sold
instruments, and have made many startling claims for the instrument.
They have emphasized its value out of proportion to what the instrument
can do even in the hands of one familiar will all the defects.
Consequently it is not necessary to emphasize the value of blood
pressure. It seems best to utter a few words of caution in regard to its
interpretation.

The value lies not in the occasional estimation compared with some other
one reading, but in the frequent estimation and in the visualization of
the blood pressure picture. For the great majority of diseases the blood
pressure has no particular value except to show that the circulation is
not materially disturbed. The limits of normal are rather wide, so that
consideration of the patient's age, sex, build, etc., will give us some
idea of a base line, so to speak, for any one person. Wide departures
from relatively normal figures are important, but are not diagnostic or,
rather, pathognomonic. I can not help but feel that the diastolic
pressure is _the_ most important part of the blood pressure picture.
Persistent high diastolic pressure means increased work for the heart,
which, if acting for a long time against the high peripheral resistance,
must eventually hypertrophy. The arteries become thickened, lose their
wonderful elasticity, fibrous tissue is deposited in their walls, and
the vicious circle is established which leads to pathologic
hypertension.

Blood pressure readings must be intimately mixed with brains in order to
be of any great value in diagnosis or prognosis.

CHAPTER VIII

SYMPTOMS AND PHYSICAL SIGNS

=General=

Well developed arteriosclerosis shows four pathognomonic signs: (1)
hypertrophy of the heart; (2) accentuation of the aortic second sound;
(3) palpable thickening of the arteries; and (4) heightened blood
pressure. However, it must not be inferred that these signs must be
present in order to diagnose arteriosclerosis. It has already been said
that a very marked degree of thickening, with even calcification of the
palpable arteries, may occur with absolutely no increase of blood
pressure, and at autopsy a small flabby heart may be found.

While arteriosclerosis is usually a disease which is of slow maturation,
nevertheless cases are occasionally seen which develop rather rapidly.
The peripheral arteries have been noticed to become stiff and hard in as
relatively brief a time as two years from the recognized onset of the
disease.

Since involution processes are physiologic, as has been described (vide
infra), arteriosclerosis may assume an advanced grade and run its course
devoid of symptoms referable to diseased arteries. It is doubtful
whether the sclerosis itself could produce symptoms, except in cases
later to be described, were it not that the organs supplied by the
diseased arteries suffer from an insufficient blood supply and the
symptoms then become a part of the symptom-complex of any or all the
affected organs.

There are cases, however, in comparatively young persons where a
combination of certain ill-defined symptoms gives a clue to the
underlying pathologic processes. These symptoms of early
arteriosclerosis are the result of slight and variable disturbances in
the circulation of the various organs. Normally there are frequent
changes in the blood pressure in the organs, but the vasomotor control
of normal elastic vessels is so perfect that no symptoms are noted by
the individual. When the arteries are sclerosed, they are less elastic
and the blood supply is, therefore, less easily regulated. At times
symptoms occur only after effort. The patient may tire more readily than
he should for a given amount of mental or bodily exercise; he is weary
and depressed, and occasionally there is noted an unusual intolerance of
alcohol or tobacco. Vertigo is common, especially on rising in the
morning or in suddenly changing from a sitting to a standing position.
Some complain of constant roaring or ringing in the ears. There may be
dull headache that the accurate fitting of glasses does not alleviate.
Unusual irritability or somnolency with a disinclination to commence a
new task may be present. Sometimes the effort of concentrating the
attention is sufficient to increase the headache. This has been called
"the sign of the painful thought." Numbness and tingling in the hands,
feet, arms, or legs are also complained of, and neuralgias, not
following the course of the nerves but of the arteries, also occur. It
is important to remember that the train of symptoms resembling
neurasthenia in a person over forty-five years old may be due to
incipient arteriosclerosis. This tardy neurasthenia frequently
accompanies cancer, tuberculosis, diabetes, and incipient general
paralysis, as well as incipient arteriosclerosis.

Bleeding from the nose, epistaxis, taking place frequently in a
middle-aged person, sometimes is an early symptom. The bleeding may be
profuse, but is rarely so large as to be positively harmful. In fact, it
may do much good in relieving tension. Slight edema of the ankles and
legs is seen. Dyspnea on slight exertion is not uncommon. Dyspeptic
symptoms are not infrequent, pyrosis (heartburn), a feeling of fullness
after meals with belching or a feeling of weight in the epigastrium.
The dyspeptic symptoms may be so marked that one might almost speak of a
variety of arteriosclerosis, the dyspeptic type. For quite a while
before any symptoms that would definitely fix the case as one of
undoubted arteriosclerosis, the patient complains that foods which
previously were digested with no difficulty now give him gastric
distress. The examination of the stomach contents of a patient
presenting gastric symptoms reveals usually a subacidity. The total
acidity measured after the Ewald test meal may be only 20 and the free
HCl may be absent. Attention has been called to an unnatural pallor of
the face in early arteriosclerosis. Progressive emaciation is sometimes
seen in cases of arteriosclerosis and may be the only symptom of which
the patient complains.

=Hypertension=

Not all cases of arteriosclerosis are accompanied by increased arterial
tension. As has been stated in a previous chapter, the blood pressure in
the arterial system depends chiefly on two factors; viz., the degree of
peripheral (capillary) resistance, and the force of the ventricular
contraction. The highest arterial pressures recorded with the
sphygmomanometer occur not in pure arteriosclerosis but in cases where
there is concomitant chronic interstitial disease of the kidneys. When
this is found there is always arteriosclerosis more or less marked. In
cases where the arteries are so sclerosed that they feel like pipe stems
there may be an actual decrease in the blood pressure. Hence the
clinical measuring of the pressure in the brachial artery alone is not
sufficient for a diagnosis of arteriosclerosis. A persistent high blood
pressure even with normal urinary findings is not a sign of
arteriosclerosis. The high tension later may lead to the production of
sclerosis of the arteries, but in these cases the kidney may be
primarily at fault.

The impression must not be gained that hypertension in itself always
constitutes a disease or even a symptom of disease. Hypertension itself
is practically always a compensatory process. That is to say, it is the
attempt on the part of the body to equalize the distribution of blood in
the body when there is some poison causing constriction of the small
arteries. In this sense hypertension is not only essential, but actually
life-saving. A heart which is so diseased that it can not respond to the
call for increased action by hypertrophy of its fibers, would shortly
wear out. The very fact that the heart becomes enlarged and the tension
in the arteries becomes high, indicates that in such a heart there was
great reserve power. But while hypertension is largely an effort at
adjustment among the various parts of the circulation, it nevertheless
tends to increase, provided the cause or causes which produced it act
continuously. Moreover, as has been said (Chap. II), the arterioles do
not respond to increased work on the part of the heart by expanding, but
by contracting. A vicious circle is thus maintained which eventually
must lead to serious consequences.

Hypertension is then, if anything, only a symptom which may or may not
demand treatment. That hypertension leads to the production of sclerosis
of the arteries has been repeatedly affirmed here. In certain cases it
is good and should not be experimented with. In other cases it is bad
and some treatment to reduce the tension must be tried. The main point
is to regard hypertension as one regards a compensated heart lesion.

Prof. T. Clifford Allbutt divides the causes of arteriosclerosis
clinically into three classes: (1) The toxic class--the results of
poisons of the most part of extrinsic origin, chiefly those of certain
infections. In some of these diseases, the blood pressures, as for
example, in syphilis, are ordinarily unaffected; in others, as in lead
poisoning, they are raised. (2) The class he calls hyperpietic,[15] in
which an arteriosclerosis is the consequence of tensile strength, of
excessive arterial blood pressure persisting for some years. A
considerable example of this class is the arteriosclerosis of granular
kidney, but in many cases kidney disease is, clinically speaking,
absent. (3) The involutionary class, in which the change depends upon a
senile, or quasisenile degradation. This may be no more than wear and
tear, a disposition of all or of certain tissues to premature
failure--partly atrophic, partly mechanical--under ordinary stresses; or
it also may be toxic, a slow poisoning by the "faltering rheums of age."
In ordinary cases of this class the blood pressures for the age of the
patient are not excessive. Although the toxins of the specific fevers,
notably typhoid, as stated above, and influenza, have been shown to
produce arteriosclerosis, this, under favorable circumstances he
believes tends to disappear. This has been shown by Wiesel.

[15] From piesô to squeeze, oppress or distress. Hyperpiesis,
therefore, signifies excessive pressure.

As the blood pressure is dependent on the resistance offered by the
capillaries and arterioles, there are only two ways in which increased
pressure can be brought about; either by rendering the blood more
viscous, or by the generation of some poison from the food taken into
the body which, acting on the vasomotor center or directly on the finer
vessels, arteriolar or capillary, sets up a constriction over any large
area, and mainly in the splanchnic area. In regard to the liability to
arteriosclerosis, this area stands second only to the aortic and
coronary areas. He believes that arteriosclerosis itself has little
effect in raising arterial pressure. Many cases are seen in which with
extreme arteriosclerosis there was no rise in blood pressure, and some
in which pressures have been rising even long before the appearance of
arterial disease. Prof. Allbutt also believes that in the hyperpietic
cases the arteries undergo a transient thickening, which can be removed
if the causes can be reached and overcome.

Clinically speaking, then, hyperpietic arteriosclerosis is not a
disease, but a mechanical result of disease. If the narrowing of the
arterioles is brought about by thickening due to arteriosclerosis, then
it would seem _a priori_ that such obliteration should cause a rise in
pressure. Were the vascular system a mere mechanical set of tubes and a
pump, this would happen, but other factors of great importance must be
taken into consideration besides the mechanical factors; viz., chemical
and biological factors. Thus, whole parts may be closed and with
compensatory dilatation in other parts there would be little or no
change in pressure, unless there were hyperpiesis. In established
hyperpiesis, we note two conditions in the radial artery: first, a
comparatively straight vessel with a small diameter; secondly, a larger,
more tortuous vessel, "the large leathery artery." In the cases of the
first group, hyperpiesis is often more marked, although not appearing so
to the examining finger, than in the second class. In view of the
difficulty of estimating by touch alone the amount of hyperpiesis in a
contracted hard artery, it is often overlooked until a ruptured vessel
in the brain startles us to a realization of our mistake. The "narrow"
artery is more dangerous than the tortuous one, for with every change in
pressure the passive vessels of the brain must receive blood that under
normal conditions would go to other parts of the circulation.

In involutionary sclerosis there is a gradual thickening and tortuosity
of the vessel, which although it may be greater than in the hyperpietic
cases, yet is never so dangerous to life. The heart in hyperpiesis
hypertrophies and dilates, but such a heart is the result, not an
integral part, of the arterial disease.

=The Heart=

When the arterial tree becomes narrowed and the resistance offered to
the flow of blood thereby is increased, more muscular work is required
of the left ventricle and according to the general laws which govern
muscles the ventricle hypertrophies. There is an actual increase in
number of fibers as well as an increase in the size of the individual
fibers. Some of the best examples of simple hypertrophy of the left
ventricle are found under such circumstances. The chambers as a rule do
not dilate until the resistance becomes greater than the contraction can
overcome, when symptoms of broken compensation of the heart take place.
The hypertrophy of the left ventricle brings more of this portion of the
heart toward the anterior chest wall. The enlargement is toward the
left, also, consequently the apex-beat is found below and to the left of
its usual site, even an inch or more beyond the nipple line. The impulse
is heaving, pushing the palpating hand forcibly up from the chest wall.
The visible area of pulsation may occupy three interspaces and the
precordium is seen to heave with every systole. On auscultation the
second sound at the aortic cartilage is ringing, clear, and accentuated.
Not infrequently, too, the first sound is loud and booming, but has a
curious muffled sound that may even be of a murmurish quality. The
leaflets of the mitral valve may be the seat of sclerosis, the edges are
slightly thickened and do not quite approximate, thus causing a definite
murmur with every systole. This murmur may be transmitted out into the
axilla and be heard at the inferior angle of the left scapula.

=Palpable Arteries=

Not every artery that can be felt is the subject of arteriosclerosis,
and, as has been stated, palpable arteries being more or less a
condition of advancing years, judgment as to whether the artery is
pathologically or physiologically thickened may be a matter of
individual opinion. A radial artery that lies close to the lower end of
the radius and can actually be seen to pulsate when the hand is held
slightly extended on the back of the wrist, is easily felt, but must
not, therefore, be considered a sclerosed artery. The radial may be so
deeply situated in the wrist of a fat subject that it is difficultly
palpable. Yet the two cases just described may have arteries of
identical structure, there being no more retrogressive changes in the
one than in the other. "Experience is fallacious and judgment
difficult."

The small, contracted, wiry artery of a chronic nephritic may feel like
a pipe stem, but if properly felt the mistake will not be made of
considering such an artery an unusually sclerosed one. When the wave is
pressed out of such a high tension artery, it is found that what seemed
to be a firm sclerosed vessel, was in reality an artery tightly
stretched over the column of blood.

=Ocular Signs and Symptoms=

It would not exaggerate too much to say that the examination of the eye
grounds with the ophthalmoscope is the most important aid in the early
diagnosis of arteriosclerosis. Long before there are any subjective
symptoms, changes can be seen in the blood vessels of the retina which,
while not always diagnostic, at least call attention to a beginning
chronic disease. As I become more proficient in the use of the
ophthalmoscope, I am impressed with the importance of the ocular signs
of arterial disease. I would urge practitioners to familiarize
themselves with this instrument. The electrically lighted instruments on
the market now have so simplified the technic that any physician should
be able to see the grosser changes which take place in the arteries and
veins of the retina and in the disc. Frequently the ophthalmologist is
the first to recognize early arteriosclerosis. In the fundus are seen
increased tortuosity of the retinal vessels and their terminal twigs
with more or less bending of the vessels at their crossings. The
arteries are terminal ones, and small patches of retinitis are therefore
found. The changes have been divided into (1) suggestive, (2)
pathognomonic.

Under (1) are:

(a) Uneven caliber of the vessels,

(b) Undue tortuosity,

(d) An unusually light color of the breadth of the artery.

Under (2) are:

(a) Changes in size and breadth of the retinal arteries so that they
look beaded,

(b) Distinct loss of translucency,

(d) Most important of all, the indentation of the veins by the stiffened
arteries.

There is yet another sign which appears to be pathognomonic. The
arteries are pale, appear rigid and through the center, parallel to the
course, is a rather bright, fine threadlike line. The appearance is
known as the "silverwire" artery. It is particularly constant in
hypertension where the most beautiful examples are seen.

Moreover, there is the arcus senilis, the fine translucent to opaque
circle surrounding the outer portion of the iris. Practically every one
with a well-marked arcus senilis has arteriosclerosis, but vice versa
not every one with even marked arteriosclerosis has an arcus senilis.

In general, the symptoms are gradual loss of acute vision, and attacks
of transient loss of vision. The explanation which has been offered for
these phenomena is the contraction in a diseased central artery.

=Nervous Symptoms=

The onset of arteriosclerosis is, in the majority of cases, so insidious
that certain nervous manifestations, due in all probability to
disturbances in blood pressure, are present long before the actual
sclerosis of the arteries can be felt. These nervous symptoms are at
times the sign posts to show us the way to accurate diagnosis. There may
be gradual increase in irritability of temper, inability to sleep,
vertigo even extending to transient attacks of unconsciousness. Loss of
memory for details frequently is an early symptom of sclerosis of the
cerebral arteries. Nervous indigestion may be present. Various
paresthesias as numbness, tingling, a sense of coldness or of heat or
burning, a sense of stiffness or even actual stiffness or weakness may
occur in the arms and legs, more frequently in the legs. The pain
complained of may be due to occlusion of an artery, although evidence
for this is lacking. It has been thought by some that the pain in angina
pectoris might be due to this cause.

Several curious and interesting diseases which have been thought by some
to have arteriosclerosis as a basis are accompanied by pain. Such are
erythromelalgia, Raynaud's disease, "dead fingers," and intermittent
claudication.

Erb has reported a large series of intermittent limp (claudication) from
his private practice. He finds that the large majority of the cases
occur in men. The abuse of tobacco was evidently the main etiologic
factor in about half of the cases. Repeated exposure to cold and the
abuse of alcohol were responsible for most of the other cases. Curiously
enough he finds that a history of syphilis was present in only a small
proportion of his cases. It is his firm conviction that intermittent
limping--which he thinks should be called angiosclerotic dysbasia--is
frequently incorrectly diagnosed. It is mistaken for other troubles and
treated wrongly. As gangrene may develop this is particularly dangerous.
The affection generally develops gradually, although he has seen cases
where the onset was rather acute. The partial or complete lack of the
pulse in the foot is the one striking sign, together with the varying
behavior of the pulse, its disappearance when the feet are cold and its
return after a warm foot bath or under other treatment. Signs of general
arteriosclerosis were present in nearly every case. When there is a
tendency to the development of intermittent limp he finds that a
valuable sign is the manner in which the leg blanches when it is lifted
repeatedly while the patient is recumbent and becomes hyperemic later
when placed horizontally. In health this change occurs more rapidly.

CHAPTER IX

SYMPTOMS AND PHYSICAL SIGNS

=Special=

Our conception of arteriosclerosis as a degenerative process affecting
the vascular tree rather than a disease, removes the possibility of
discussing special symptoms. As a matter of fact, we know of very few
organs where even profound pathologic changes in the vascular system
produced during life any symptoms which could be laid to these arterial
changes. Kind nature has given to us such an excess of organs of every
kind that the destruction of large portions of any organ seems to affect
the function but little. So only particular groups of organs, which show
symptomatic changes as the result of arteriosclerotic processes, will be
discussed. It is realized that this may not give Teutonic completeness
to the discussion, but it certainly saves paper and has a distinct
practical value to the long suffering reader.

Although arteriosclerosis is a disease which affects the whole arterial
system, it nevertheless never reaches the same grade all over the body.
The difference in the structure and functions of the various organs
determines to great extent the eventual symptomatology. Endarteritis
obliterans of a small sized artery in the liver or leg would lead to no
marked symptoms, as the circulation is so rich that the anastomoses of
the blood vessels would soon establish a collateral circulation that
would be perfectly competent to sustain the function of the part. Quite
different would it be should one of the small arteries of the brain, the
lenticulo-striate, for example, which supplies the corpus striatum,
become the seat of a thrombosis or embolism caused by arteriosclerosis.
The arteries of the brain are terminal arteries and the blood supply
would be cut off entirely with a resulting anemic necrosis of the part
supplied by the artery and a loss of function of the part. What would be
of no moment in the leg or arm might prove even fatal in the brain.

The further symptomatology, therefore, of arteriosclerosis depends
entirely on the organ or organs most affected by the interference with
the blood supply. The following groups may be recognized:

1. Cardiac.

2. Renal.

3. Abdominal.

4. Cerebral.

5. Spinal.

6. Local vasomotor effects.

7. Pulmonary.

=Cardiac=

Most cases of arteriosclerosis sooner or later present symptoms
referable to the heart. When the organ is hypertrophied and is already
working against an enormous peripheral resistance, a slight excess of
work put upon it may cause a dilatation of the chambers with the
resulting broken compensation. There is dyspnea on slight exertion,
possibly some precordial distress, slight edema of the ankles and lower
legs and possibly scanty urine. With proper care, a patient with such
symptoms may recover, but the danger of another break in compensation is
enhanced. The next attack is more severe. The edema is greater, there
may be signs of edema of the lungs, effusions into the serous cavities
may occur. The heart shows marked dilatation. There is gallop or canter
rhythm and there are loud murmurs at the apex. When a patient is first
seen in this stage, it may be quite impossible to state whether or not
there is true valvular disease of the heart. The muscle is usually
diseased in that there is fibroid degeneration of more or less
extensive character. This factor causes the heart to lose much of its
elasticity and increases the tendency to permanent dilatation. Such
cases must be watched before one can say that true valvular
insufficiency is not present. The fatal termination of such a case is
quite like that of true valvular disease. There is increasing dyspnea,
increasing anasarca, and the patient usually succumbs to edema of the
lungs, drowned in his own secretions.

[Illustration: Fig. 59.--Aneurysm of the heart wall. (Milwaukee County
Hospital.)]

A very rare complication of the fibroid degeneration of the heart muscle
is aneurysm of the heart wall. (Fig. 59.) The apex of the left
ventricle is most commonly the site of the aneurysm and rupture
occasionally occurs. Such an accident is rapidly fatal. In the
arteriosclerotic process which occurs at the root of the aorta, the
coronary arteries become involved both at the openings and along the
courses of the vessels. A branch or branches or even one artery may
become blocked as a result of obliterating endarteritis. The arteries of
the heart are not terminal vessels but as a rule blocking of a large
branch leads to anemic infarct. These areas become replaced by fibrous
tissue which in the gross specimen appears as streaks of whitish or
yellowish color in the musculature. Anemic infarcts may not occur. In
such cases the anastomosis between branches of the coronary arteries is
unusually free. Through arteriosclerosis of the coronary vessels
extensive fibrous changes may occur that lead to a myocardial
insufficiency with its attending symptoms--dyspnea, irregular and
intermittent heart, gallop rhythm, edema, etc. One of the most
distressing and dangerous results of sclerosis of the coronary arteries
and of the root of the aorta is angina pectoris. While in almost every
case of angina pectoris there is disease of the coronary arteries, the
contrary does not hold true, for most extensive disease, even embolism,
of the arteries is frequently found in persons who never suffered any
attacks of pain. This symptom group is more common in males than in
females and as a rule occurs only in adult life. "In men under
thirty-five syphilitic aortitis is an important factor." (Osler.)

Since the valuable experiments of Erlanger on heart block, considerable
attention has been paid to lesions of the Y-shaped bundle of fibers, a
bundle arising at the auriculoventricular node and extending to the two
ventricles, known also as the auriculoventricular bundle of His.
Interference with the transmission of impulses through this bundle gives
rise to the symptom group known as the Stokes-Adams syndrome, which is
characterized by: (a) slow pulse, (b) cerebral attacks--vertigo,
syncope, transient apoplectiform and epileptiform seizures, (c) visible
auricular impulses in the veins of the neck. Many of the cases which
occur are in elderly people the subjects of arteriosclerosis.

[Illustration: Fig. 60.--Large aneurysm of the aorta eroding the
sternum. Death from rupture through the skin preceded by frequent small
hemorrhages. (Milwaukee County Hospital.)]

So far as we now know all cases of the Stokes-Adams syndrome are caused
by heart block which is only another name for disease in the
auriculoventricular bundle. Of interest here is the fact that besides
gummata, ulcers, and other lesions of the bundle, definite
arteriosclerotic changes have been found.

"The investigation of a typical case of Stokes-Adams disease has shown
that the symptoms of this case are caused by some lesion in the heart
which gives rise to the condition now generally termed heart block.
Practically all degrees of heart block have been observed, namely,
complete heart block and partial block with 4:1, 3:1, and 2:1 rhythm,
and occasionally ventricular silences. These stages occurred during
recovery.

"Experiments testing the reaction of the heart to various extrinsic
influences demonstrate that when the block is complete the ventricles do
not respond to influences presumably of vagus origin, although the
auricles still respond normally to such influences, that effects exerted
upon the heart presumably through the accelerators still influence the
rate of the ventricles as well as that of the auricles.

"When the block is partial the rate of the ventricular contraction
varies proportionally with the rate of the auricular contractions but
only within certain limits. When these limits are exceeded the block
becomes more complete, i. e., a 2:1 rhythm may be changed into a 3:1
rhythm, this into a 4:1 rhythm, and this into complete block, and vice
versa.

"The syncopal attacks are, in all probability, directly dependent upon a
marked reduction of the ventricular rate. Such reductions of the
ventricular rate are always associated with an increase of the auricular
rate, and it is believed that the latter is the cause of the former."
(Erlanger.)

The epileptiform seizures of the syndrome may be caused by the anemia of
the brain resulting from failure of the heart to supply a sufficient
quantity of blood.

The apoplectiform attacks are most probably caused by venous congestion
when the slowing of the ventricular contractions is not sufficient to
cause convulsions, but will just cause complete unconsciousness.

=Renal=

Chronic nephritis, hypertension, arteriosclerosis form a most important
trinity. Some stoutly affirm that in all cases of high tension there is
chronic renal disease. Certainly the very highest blood pressures which
we see occur in the chronic interstitial forms of kidney disease. The
cause is most probably to be sought in some poison which is elaborated
in the kidney, is absorbed into the circulation and acts powerfully
either on the vasoconstrictor center as a stimulus, or directly on the
musculature of the small arteries all over the body. Usually
hypertension is progressive but it may be temporary.

A man, 43 years old, entered the Milwaukee County Hospital in uremic
coma. The systolic blood pressure was 280-290 mm. Hg, the diastolic
pressure 220 mm. (Janeway instrument). Under treatment his blood
pressure gradually became lower, at the same period the albumin and
casts gradually disappeared from the urine. In two weeks from admission
he seemed perfectly well, there were no albumin or casts found in the
urine, and the systolic blood pressure was 136 mm., not a high figure
for a muscular man of the laboring class. It must be admitted, however,
that such cases are the exception, not the rule.

Patients suffering from the association of chronic nephritis with
hypertension die slowly, usually. There is gradual development of
anasarca. Headache is frequent and severe. Pains all over the body may
occur. The sight may suddenly become dim or may even be lost. Dizziness
may be complained of and dyspnea is usually marked. Cyanosis comes on,
the pulse becomes weak, irregular or intermittent, heart failure sets
in, and the patient dies with edema of the lungs.

Another class of renal arteriosclerosis is characterized by a small
granular kidney in which fibrous changes of a patchy character have
taken place. These scattered areas are the result of obliterating
endarteritis of renal arteries here and there with consequent anemia,
death of cells, and replacement by fibrous tissue. It occurs as part of
a generalized arteriosclerosis in which the whole arterial system is the
seat of diffuse (senile) sclerosis. The palpable arteries are usually
beaded or even encircled with calcareous deposits and the aorta is the
seat of an extensive nodular and ulcerating sclerosis. The heart is
usually small, shows extensive fibrous and fatty changes and possibly
the condition known as "brown atrophy;" the blood pressure is low. Such
cases do not show any special symptoms. They are anemic, short of breath
on exertion, have the appearance and show the signs of senility.

In the first group it is, at times, difficult to say whether the kidney
disease or the arterial disease is the most important. From a clinical
standpoint the decision is not essential as the end results are much the
same in both. However, when actual uremic symptoms dominate the picture,
it becomes evident that the disease of the kidney is the chief feature
in the causation of the symptoms.

=Abdominal or Visceral=

There is an important group of cases to which but little attention has
been paid until quite recently. This is the abdominal or visceral type
of arteriosclerosis. It has been stated that arteriosclerosis of the
splanchnic vessels almost invariably causes high tension. Among others,
Janeway has shown that general arteriosclerosis without marked disease
of the splanchnic vessels does not cause as a rule increase of blood
pressure.

There are cases in which the brunt of the lesion falls upon the
abdominal vessels. Such cases have been called "angina abdominalis." It
has been suggested (Harlow Brooks) that this type of arteriosclerosis
may be determined by constant overloading of the stomach with food,
especially rich and spiced food. This causes overwork of the special
arteries connected with digestion and so leads to sclerosis of the
vessels of the stomach, pancreas, and intestines. Personal habits
probably influence to great extent the production of this more or less
=localized= condition.

The organs supplied by the diseased arteries suffer from changes
analogous to those occurring in general or local malnutrition, such as
starvation, old age, or local anemias. These changes are atrophy with
hemachromatosis (brown atrophy) or fatty infiltration and degeneration.
Following the degenerative changes there result connective tissue growth
and further limitation of the functionating power of the affected
organs.

Pain is a more or less constant symptom of visceral sclerosis. In the
early stages there may be only a sense of oppression, of weight, or of
actual pressure in the abdomen or pit of the stomach. There may be only
recurring attacks of violent abdominal pain accompanied by vomiting. In
some cases symptoms of tenderness in the epigastrium, pains in the
stomach after eating, vomiting and backache may suggest gastric ulcer.
There may be dyspnea and a sense of anguish accompanied with a rapid and
feeble pulse. Hematemesis may make the symptom group even more like
ulcer of the stomach, and only the course of the disease with the
failure of rigid ulcer treatment and the substitution of treatment
directed toward relief of the arterial spasm with resulting betterment,
enables one to make a diagnosis. The condition may be present for years
and the symptoms only epigastric tenderness with dizziness and sweating
on lying down after dinner, as in one of Perutz's patients. The attacks
are probably due to spasmodic contraction of the sclerosed intestinal
vessels with a resulting local rise in blood pressure. The pains are
most probably due to the spasm of the intestinal muscles, and some think
they are located in the sympathetic and mesenteric plexuses.

This result of arteriosclerosis is not so uncommon, and by keeping this
cause of obscure abdominal pain in mind we are now and then enabled to
save a patient from operation.

An autopsy on a case which for many years had attacks of abdominal pain
and cramp-like attacks, with high blood pressure and heart hypertrophy,
showed extensive sclerosis of the abdominal aorta, superior mesenteric
and iliacs. These vessels were calcified. Hypertrophy of the left
ventricle was found. The kidneys were microscopically normal. There were
no changes in the ascending aorta but in the descending portion there
were scattered nodules and small calcified plaques.

The attacks of pain from which this patient suffered for many years, the
hypertrophy of the left ventricle and the increased blood pressure were
thought to be directly due to the sclerosis of the abdominal vessels.

=Cerebral=

It has been stated that arteriosclerosis is a general disease, yet
certain systems of vessels may be affected far more than others, and
indeed there may be marked sclerosis at one part of the body and none
demonstrable at another part.

In advanced sclerosis there may be one or more of a series of accidents
due to embolism, thrombosis, or rupture of the vessels. Such conditions
as transient hemiplegia, monoplegia or aphasia may occur. The attacks
may come on suddenly and be over in a few minutes; what Allbutt calls
"Larval apoplexies." They may last from a few hours up to a day, and are
very characteristic. A patient aged 64 years with pipe stem radials and
tortuous hard temporals would be lying quietly in bed when suddenly he
would stiffen, the eyes would become fixed and the breathing cease. In a
few seconds consciousness returned, the patient would shake himself,
pass his hand over his brow and ask, "Where am I? Oh, yes, that's all
right." He had as many as thirty of these attacks in twenty-four hours,
none of them lasting over one minute. To just what such attacks are due,
it is hard to say. Some have attributed them to spasm of the smaller
blood vessels of the brain, but there have never been demonstrated in
the vessels any constrictor fibers.

There is a well recognized form of dementia caused by arteriosclerosis.
In general paralysis of the insane and in senile dementia the blood
vessels are always diseased. Milder grades of psychic disturbances are
accompanied by such symptoms as mental fatigue, persistent headaches,
vertigo, memory weakness and fainting. Aphasia, periods of excitement
and mental confusion occur in some. Later stages are at times
accompanied by inclination to fabulate, loss of judgment,
disorientation, narrowing of the external interests, episodes of
confusion and hallucinatory delirium.

The hemiplegias, monoplegias and paraplegias may occur again and again
and last for one or two days. Unless there has been rupture of the
vessels, there is complete recovery as a rule.

In persons who have arteriosclerosis with high tension attacks of
melancholia are seen. There are at the same time fits of depression,
insomnia, irritability, fretfulness, and a generally marked change in
disposition. When the tension is reduced by appropriate treatment these
symptoms disappear, to recur when the tension again becomes high. On the
contrary, attacks of mania are accompanied by low blood pressure. The
dizziness and vertigo in cerebral arteriosclerosis are probably due to
the stiffness of the vessels which prevents them from following closely
the variations of pressure produced by position, and thus, at times, the
brain is deprived of blood and a transient anemia occurs.

Arteriosclerosis of the cerebral vessels is always a serious condition.
The greatest danger is from rupture of a blood vessel. Another of the
dangers is gradual occlusion of the arteries bringing about necrosis
with softening of the brain substance. The latter is more apt to be
associated with psychic changes, dementia, etc.; the former, with
hemiplegia. It is curious that a small branch of the Sylvian artery, the
lenticulo-striate, which supplies the corpus striatum, should be the one
which most frequently ruptures. Where the motor fibers from the whole
cortex are gathered together in one compact bundle, a very small
hemorrhage may and does cause very serious effects. A comparatively
large hemorrhage in the silent area of the brain may cause few or no
symptoms.

=Spinal=

It is conceivable that arteriosclerosis of the vessels of the spinal
cord might cause symptoms which would be referred to the areas of the
cord where the process was most advanced. The lesions would be scattered
and consequently the symptoms might be protean in character.

True epileptic convulsions dependent on arteriosclerotic changes are
also seen and are not so uncommon.

This is on the whole a rare condition, much less common than
arteriosclerosis of the cerebral vessels. Collins and Zabriskie report
the following typical case:

"H., a fireman, fifty-one years old, was in ordinary good health
until toward the end of 1902. At that time he noticed that his legs
were growing weak and that they tired easily. Later he complained of
a jerking sensation in different parts of the lower extremities and
at times of sharp pain, which might last from several minutes to two
or three hours. The legs were the seat of a heavy, unwieldy
sensation, but there was no numbness or other paresthesia. About the
same time he began to have difficulty in holding the urine, a
symptom which steadily increased in severity. These symptoms
continued until March, 1903, i. e., for three months, then he
awakened one morning to find that he was unable to stand or walk,
and the sphincters of the bowels and bladder relaxed. There was no
complaint of pain in the back or legs, no difficulty in moving the
arms, in swallowing or in speaking. He says he was able to tell when
his lower extremities were touched and he could feel the bed and
clothes. He was admitted to the City Hospital three weeks later and
the following record was made on April 21, 1903.

"The patient was a frail, emaciated man of medium height, who had
the appearance of being 55-60 years of age. He was unable to stand
or walk. When he was lying, he could flex the thigh and the legs
slowly and feebly. There was slight atrophy of the anterior and
inner muscles, more of the left than of the right side. The knee
jerks and ankle jerks were absent. Irritation of the soles caused
quite a typical Babinski phenomenon. The patient had fair strength
in the upper extremities, but the arms tired very soon, he said. The
grip was moderate and alike in each hand. The motility of the face,
head, and neck was not noticeably impaired. There was no difficulty
in swallowing, and articulation was not defective. Tactile
sensibility was slightly disordered in the lower extremities,
although he could feel contact of the finger, the point of a pin,
and the like. Sensibility was not so acute as normal; there was a
quantitative diminution. Sensory perception was not delayed. There
was a distinct zone of slight hyperesthesia about as wide as the
hand above the femoral trochanters. Above that, sensibility was
normal. There was no discernible impairment of thermal sensibility.
No part of the body was particularly tender on pressure. A bedsore
existed over the sacrum, and there was excoriation of the genitals
from constant dribbling of urine.

"Examination of the chest showed shallow respiratory movements. The
heart was regular, weak, there were no murmurs, the second sound was
accentuated. Examination of the abdomen showed that the liver and
spleen were palpable, but were not enlarged. The abdominal reflexes,
both upper and lower, were sluggish. The patient was slow of speech,
likewise apparently of thought. He did not seem to show an adequate
interest in his condition, still he was fully oriented and seemed to
have a fair memory. His mental reflex was slow. There were
indications in the peripheral blood vessels and heart of a moderate
degree of general arteriosclerosis. The peripheral vessels such as
the radial, were palpable, the walls thickened, the blood pressure
increased.

"The patient did not complain of pain while he was in the hospital,
a period of four weeks, nor was there any particular change in the
patient's symptoms, subjective and objective, during this time. His
mental state remained clear until forty-eight hours before death,
when he became sleepy, stuporous, and comatose, dying apparently of
cardiac weakness, which had set in simultaneously with the clouding
of consciousness."

At autopsy, except for a few small hemorrhages in the posterior
horns of the lower dorsal segments on the right side and a similar
condition of the left anterior horns, there was nothing noticed. On
microscopic examination, there was found widespread sclerosis of the
vessels of the cord to a marked degree with only slight thickening
of the vessels of the brain. There were secondary degenerations of
ascending and descending type particularly marked at the ninth
dorsal segment. They included portions of all the tracts, the
pyramidal tract as well. The symptoms in brief were: (1) weakness
and easily induced fatigue of the legs; (2) peculiar sensations in
the lower extremities, described as jerky, numbness, heaviness, and
occasionally sharp pain; (3) progressive incontinence of urine; (4)
progressive paraplegia.

Since one of the chief manifestations of syphilis is sclerosis of the
arteries, neurologic cases characterized by irregular symptoms and signs
which can not be placed in any of the definite system disease groups,
are possibly due to irregularly scattered areas of sclerosis throughout
the spinal cord caused by obliterating arteritis. Such cases are not so
very uncommon. Several have come under my observation. Further studies
of the spinal cords of these cases at autopsy are necessary before a
final opinion can be given as to their dependence on arteriosclerosis of
the spinal vessels.

=Local or Peripheral=

When the arteriosclerosis in the peripheral arteries reaches a stage
where endarteritis obliterans supervenes, there is usually no chance for
a compensatory or collateral circulation to be established. The area
supplied by the vessel undergoes dry gangrene. A portion of a toe or
finger or a whole foot or hand may shrivel up. It is more common to see
the spontaneous amputation take place in the lower extremities. The same
effect may be produced by the plugging of a vessel with a thrombus.
There may be much pain connected with the sudden blocking, whereas the
gradual obliteration of the blood supply of a toe or foot is not as a
rule at all painful. The condition is at times revealed more or less
accidentally when a patient injures his toe or foot and discovers that
there is no sensation in the part and that the wound instead of healing
is inclined to grow larger.

Other interesting vasomotor phenomena are frequently connected with
arteriosclerosis. Such a one is the curious condition known as Raynaud's
disease, a vascular disorder which is divided into three grades of
intensity: (1) local syncope, (2) local asphyxia, (3) local or
symmetrical gangrene. This is not the place to describe this condition
except to say that the condition called "dead fingers" is the most
characteristic feature of the first stage. Chilblains represent the
mildest grade of the second stage. The parts are intensely congested and
there may be excruciating pain. Any one who has ever had chilblains
knows how painful they can be. The general health is not impaired as a
rule, although the attacks are apt to come on when the person is run
down. The third stage may vary from a very mild grade, with only small
necrotic areas at the tips of the fingers, to extensive multiple
gangrene.

Another and very rare condition in which chronic endarteritis was the
only constant finding is the disease described by S. Weir Mitchell and
called by him erythromelalgia (red neuralgia). This is "A chronic
disease in which a part or parts--usually one or more extremities--suffer
with pain, flushing, and local fever, made far worse if the parts hang
down." (Weir Mitchell.)

Probably the most frequently seen result of arteriosclerosis in the leg
arteries is the remarkable condition, first described by Charcot, known
as intermittent claudication. Persons the subject of this disease are
able to walk if they go slowly. If, however, any attempt be made to
hurry the step, there results total disability accompanied at times by
considerable cramp-like pain. The condition is much more prone to occur
in men than in women, and Hebrews seem more frequently affected. The
cause is most probably to be sought in the anemia which results from the
narrowing of the channels through which the blood reaches the part. The
stiff, much narrowed arteries allow sufficient blood to pass along for
the nutrition of the part at rest or in quiet motion. Just as soon as
more violent exercise is taken, calling for more blood, an ischemia of
the part supervenes, for the stiff vessels can not accommodate
themselves to changes in the necessary vascularity of the part. A rest
brings about a gradual return of blood and the function of the part is
restored. Pulsation may be totally absent in the dorsal arteries of the
feet and when the legs are allowed to hang down there is apt to be deep
congestion.

In this connection a curious case reported by Parkes Weber will not be
out of place. The patient, a male, aged 42 years, complained of
cramp-like pains in the sole of the left foot and calf of the leg
occurring after walking for a few minutes and obliging him to rest
frequently. When the legs were allowed to hang over the side of the bed,
the distal portion of the left foot became red and congested looking.
No pulsation could be felt in the dorsal artery of the left foot or in
the posterior tibial artery. There was no evidence of cardiovascular or
other disease. An ulcer on the little toe had slowly healed, but
cramp-like muscular pains still occurred on walking. The disease had
lasted about five years without the appearance of gangrene.

Weber calls this case one of arteritis obliterans with intermittent
claudication.

=Pulmonary Artery=

In the symptomatology of sclerosis of the pulmonary artery the clinical
signs and symptoms are mostly referable to the obliterating endarteritis
of the smaller vessels, while the physical signs are more apt to reveal
the involvement of the main trunk. A history of severe infection in the
past is frequent, especially smallpox, and accompanying aortic sclerosis
with insufficiency of the mitral valve or stenosis of this valve is the
rule. Striking cyanosis is an early symptom, while there is little if
any dyspnea and edema. Intermittent dyspragia is common. There seems to
be no tendency to clubbed fingers. Repeated hemorrhages from the lungs
without the formation of infarcts may occur. There is usually an area of
dullness at the upper left margin of the sternum and nearby parts,
sensitive to pressure and to percussion, and the heart dullness extends
unusually far towards the right. The diagnosis of the right ventricular
hypertrophy may be substantiated by a fluoroscopic examination.

CHAPTER X

DIAGNOSIS

=Early Diagnosis=

Arteriosclerosis is essentially a disease of middle life and old age. It
is not unusual, however, to find evidences of the disease in persons in
the third decade and even in the second decade. Hereditary influences
play a most important rôle, syphilis and the abuse of alcohol in the
family history are particularly momentous. The recognition of the early
changes in the arteries among young persons depends largely upon how
carefully these changes are looked for. The difference in the point of
view of one man who finds many cases in the comparatively young, and
another man who rarely finds such changes early in life, at times,
depends upon the acuity of perception and observation and not upon the
fact that one man has had a series of unusually young arteriosclerotic
subjects. The diagnosis of arteriosclerosis may be so easily made that
the tyro could not fail to make it. It is, however, the purpose of this
volume to lay stress on the earliest possible diagnosis and, if
possible, to point out how the diagnosis may be arrived at. It is
obviously much to the advantage of the patient to know that certain
changes are beginning in his arteries, which, if allowed to go on, will
inevitably lead to one or more of the symptom groups described in the
preceding chapters.

The combination of (1) hypertrophied heart, (2) increased blood
pressure, (3) palpable arteries, and (4) ringing, accentuated second
sound at the aortic cartilage is, in reality, the picture of advanced
arteriosclerosis. If the individual is in good condition much may be
done by judicious advice and treatment to ward off complications and
prolong life with a considerable degree of comfort. But we should not
wait until such signs are found before making a diagnosis and
instituting treatment. As in all forms of chronic disease the early
diagnosis is all important.

The history of the case is the first essential. Often a careful inquiry
into the personal habits of a patient, with the record of all the
preceding infectious diseases will give us valuable information and may
be the means of directing the attention at once to the possible true
condition. Particularly must we inquire into the family history of gout
and rheumatism. An individual who comes of gouty stock is certainly more
prone to arterial degeneration than one who can show a healthy heredity.
Alcoholism in the family also is of importance because of the fact that
the children of alcoholics start in life with a poor quality of tissue,
and conditions that would not affect a man from healthy stock might
cause early degeneration of arterial tissue in one of bad ancestry.

What infectious diseases has the patient had? Even the exanthemata may
cause degenerations in the arteries, but, as has been shown, such
lesions probably heal completely with no resulting damage to the vessel.
Should the patient have passed through a long siege of typhoid fever the
problem is quite different. Here (vide supra) (Thayer), the palpable
arteries do appear to be sclerosed permanently. Probably the length of
time that the toxin has had a chance to act determines the permanent
damage to the vessel wall. More potent than all other diseases to cause
early arteriosclerosis is syphilis, and hence very careful inquiry
should be made in regard to the possibility of infection with this
virus. Not only the fact of actual infection but the duration and
thoroughness of treatment are important matters for the physician to
know.

What is the patient's occupation? Has he been an athlete, particularly
an oarsman? Has he been under any severe, prolonged, mental strain? Is
he a laborer? If so, in what form of manual labor is he engaged? Such
questions as these should never be overlooked, as they form the
foundation stones of an accurate diagnosis, and early, accurate
diagnosis, we repeat, is essential to successful therapy.

We have called attention to the factor of sustained high pressure in the
production of arteriosclerosis. Constant overstretching of the vessels
leads to efforts of the body to increase the strength of the part or
parts. The material which is used to strengthen the weakened walls has a
higher elastic resistance than muscle and elastic tissue, but a lower
limit of elasticity, and is none other than the familiar connective
tissue. In athletes, laborers, brain workers who are under constant
mental strain, and in those whose calling brings them into contact with
such poisons as lead, there is every factor necessary for the production
of high tension and consequently of arteriosclerosis.

Another question in regard to personal habits is how much tobacco does
the patient use and in what form does he use it? Our experience is that
the cigar smoker is more prone to present the symptoms of
arteriosclerosis than the cigarette smoker, the pipe smoker, or the one
who chews the tobacco. A very irritable heart results not infrequently
from cigarette smoking but such is almost always found in young men in
whom the lesions of arteriosclerosis are exceedingly rare. The
probabilities are that the arteriosclerosis in cigar smoking results
from the slowly acting poison which causes a rapid heart rate with an
increase of pressure.

Last but not least, and perhaps the most important question is, has the
patient been a heavy eater? This I believe to be a potent cause of
splanchnic arteriosclerosis with the resulting indigestion, cramp-like
attacks, high blood pressure, etc. In a joking manner we are accustomed
to remark, "Overeating is the curse of the American people." There is,
however, much truth in that sentence. Osler, than whom there is no
keener observer, states that he is more and more impressed with the fact
that overloading the stomach with rich or heavy or spiced foods is today
one of the first causes of arterial degeneration. It stands to reason
that this is true. We know that organs exposed constantly to hard work
undergo hypertrophy, and that the blood tension in those organs is high.
Blood tension is, after all, dependent on capillary resistance, and if
the capillaries are distended with blood, the resistance is great. The
digestive organs can be no exception to this rule. Increased work means
an increase of blood. This inevitably causes distension of the
capillaries with stretching of the arteries and consequent damage to the
walls. Once arteriosclerosis is present a vicious circle is established.

A man about forty-five consults us and says that he has noticed recently
that he gets out of breath easily; in tying his shoes he experiences
some dizziness. He finds that he has palpitation of the heart and
possibly pain over the precordial region now and then. He notices also
that he is irritable, that is, his family tell him he is, and he notices
that things that formerly did not annoy him, now are almost hateful to
him. On examination, one finds a palpable radial, a somewhat
hypertrophied heart and slightly accentuated second aortic sound. The
blood pressure may be high. The urine may or may not reveal any
abnormalities. Not infrequently, although no albumin may be found, there
are hyaline casts. Such a case of arteriosclerosis is evidently not to
be regarded as early. Then the question arises, How are we to recognize
early arteriosclerosis? I do not believe that the solution of this
problem lies entirely in the hands of the physician. Some men are
fortunate enough to come up for an examination for life insurance before
an observant doctor who recognizes the palpable artery, makes out the
beginning heart hypertrophy and the slightly accentuated second aortic
sound. The patient will tell you that he never felt better in his life.
He gets up at seven, works all day, plays golf, drinks his three to six
whiskies, and is proud of his physical development. But the great mass
of people are not fortunate from this standpoint. They do not seek the
advice of the physician until they are stretched out in bed. They boast
of the fact that for twenty years they have never had a doctor. One may
well say that it is a problem how to reach such persons. It seems to me
that there can be but one way to do this. The people must be taught that
the duty of a physician is just as much to keep them in health as it is
to bring them back to health when they are ill. To that end people
should be taught that at least twice a year they should be carefully
examined. I do not mean that the patient should present himself to the
doctor and, after a few questions the doctor say cheerfully, "You are
all right." The patient should be systematically examined. That means a
removal of the clothing and examination on the bare skin. Such
cooperation on the part of patient and doctor would save the patient
years of active life and make of the doctor, what his position entitles
him to be, the benefactor to the community. Too often careless work on
the physician's part lulls the patient into a false sense of security
and he wakes up too late to find that he has wasted months or years of
life. Early diagnosis of arteriosclerosis is only possible in
exceptional cases unless people present themselves to the physician with
the thought in mind that he is the guardian of health as well as the
healer.

There are patients who go to the ophthalmologist for failing vision.
Physically they feel quite well. They have been heavy eaters, hard
workers, men and women who have been under great mental strain. On
examination of the fundus of the eye there is found slight tortuosity of
the vessels with possibly areas of degeneration in the retina. A careful
physical examination will usually reveal the signs of arteriosclerosis
elsewhere. We have mentioned frequently high tension as an early sign.
This must be taken with somewhat of a reservation, for this reason: not
infrequently a persistent high tension is the earliest sign of chronic
nephritis. The arteries may be pipe stem in character and the heart
small and flabby. However, if one watches for the palpably thickened
superficial arteries (always bearing in mind the normal palpability as
age advances) and the high tension, he can not go far wrong in his
treatment whether the case is one of chronic nephritis or of
arteriosclerosis.

There is also this to bear in mind. Arteriosclerosis may be marked in
some vessels and so slight in the peripheral vessels that it can not
with certainty be made out. But when the radials are sclerosed, it is
usually the case that similar changes exist in other parts. Then too,
there may be marked changes at the root of the aorta leading to
sclerosis of the coronary vessels alone, and the first intimation that
the patient or any one else has that there is disease, may be an attack
of angina pectoris. Except for symptoms on the part of the heart there
is no way to make the diagnosis of sclerosis of the coronary arteries.

=Differential Diagnosis=

In arriving at a diagnosis, when the question is whether or not
arteriosclerosis is the main etiologic factor, the most important fact
to know is the age of the patient. Other points that have been dwelt on
fully must of necessity also be borne in mind.

Possibly the chief conditions that may be confused with some of the
results of arteriosclerosis are pseudo angina pectoris which may be
mistaken for true angina pectoris, and ulcer of the stomach,
appendicitis (?) or other inflammatory abdominal condition which may be
mistaken for angina abdominalis.

Differential tables are sometimes of value in fixing the chief points of
difference graphically.

=Pseudo angina pectoris=.

Etiology rather certain; hysteria, neurasthenia, toxic agents, and
reflex irritations.

No age is exempt. Usually in young people, chiefly females.

Paroxysms of pain occur spontaneously, are periodic and often
nocturnal.

Pain, while severe, is diffuse and sensation is of distension of
heart. No sense of real anguish.

Duration may be an hour or more.

Restlessness and emotional symptoms of causative conditions are
prominent.

Usually no increase in arterial tension.

Prognosis favorable.

=True angina pectoris=.

Etiology not certain but almost always associated with
arteriosclerosis of the coronary arteries and also aortic
regurgitation.

Age is important factor. Rare before forty, and males usually
affected.

Paroxysms brought on by overexertions or excessive mental emotion.
Rarely periodic.

Intense pain, radiating down arm; heart felt as in a vise. Sense of
anguish and impending dissolution.

Duration from few seconds to several minutes.

Silent and fixed attitude, rigidity rather than restlessness.

Arterial tension is as a rule increased.

Prognosis most unfavorable.

In differentiating between ulcer of the stomach and angina abdominalis
the following points may be of service:

=Ulcer=.

Occurs as a rule in young persons, more often females.

Pain of boring character increased by food and by certain positions
with food in stomach. Felt through to left of spine.

Occult blood found in stools.

Considerable anemia apt to be present.

Arterial tension usually low.

=Angina abdominalis=.

Only occurs in adults over forty who have been heavy eaters and
drinkers, mostly males.

Pain cramp-like, diffuse, although more localized in epigastrium.
Not necessarily any connection with food.

No occult blood in stools.

Anemia more often absent.

Arterial tension high. (Splanchnic sclerosis.)

=Diseases in Which Arteriosclerosis Is Commonly Found=

There are certain more or less chronic diseases in which
arteriosclerosis is found either as a separate disease or as a result of
the chronic disease itself, or the sclerosis may be the cause of the
disease. As examples of the first class are diabetes mellitus and
cirrhosis of the liver. As examples of the second class are chronic
nephritis, gout, syphilis, and lead poisoning. Examples of the third
class have already been fully described. Then certain rare diseases that
have been briefly described in this chapter, viz.: Raynaud's disease and
erythromelalgia are frequently associated with demonstrable
arteriosclerosis.

CHAPTER XI

PROGNOSIS

In a disease that presents as many vagaries as arteriosclerosis, it is
not possible to give a certain prognosis. Unfortunately we do not as a
rule see the arteriosclerotic until the disease is well advanced, or
even after some of the more serious complications have taken place. By
that time the condition is progressive, and while the prognosis is grave
the individual may live a number of years.

It is fortunate for the arteriosclerotic that mild grades of the disease
are compatible with a fairly active life. The disease in this stage may
become arrested and the patient may live many years. Not only in the
mild grades is this possible. Even patients with advanced sclerosis may
enjoy good health provided the organs have not been so damaged as to
render them unfit to perform their functions. The frequency with which
we see advanced arteriosclerosis at the postmortem table as an
accidental discovery, attests the truth of the foregoing statement. Yet
how often does it happen that individuals, apparently in the best of
health, suddenly succumb to an asthmatic or uremic attack, an apoplexy,
cessation of the heart beat, or a rupture of the heart due to
arteriosclerosis!

In order to arrive at an intelligent opinion in regard to prognosis
certain factors must be taken into consideration, chief of which are:
the seat of the sclerosis; the probable stage; the existing
complications; and, last and most important, the patient himself. The
whole man must be studied and even then our prognosis must be most
guarded.

It is much more dangerous for the patient when the process is in the
ascending portion of the arch of the aorta than when it has attacked the
peripheral arteries. Here, at the root of the aorta, are the openings of
the coronary arteries and the arteries supplying the brain are close
by. The coronary arteries here control the situation. When loud murmurs
are heard at the aortic orifice and the heart is evidently diseased, it
is useful to divide the endocarditis into two types, the
arteriosclerotic and the endocarditic. The etiology of the former is
sclerosis and the prognosis is grave because of the liability, nay the
probability, that the orifices of the coronary arteries will become
narrowed. The etiology of the second type is in most cases rheumatic
fever or some other infectious disease, and the prognosis is far better
than in the first type. True, the two may be combined. In such a case,
the prognosis is entirely dependent upon the course of the
arteriosclerosis.

The involvement of the arteries in the kidneys is of considerable
importance, for it is usually bilateral and widespread. As a rule, the
disease makes but slow progress provided that the general condition of
the patient is good, but at any time from a slight indiscretion or for
no assignable cause, symptoms of renal insufficiency may appear and may
rapidly prove fatal.

It must not be thought that because the localization of the
arteriosclerosis in the peripheral arteries is usually the most
favorable condition that it is therefore devoid of ill effects. On the
contrary, very serious, even fatal, results may be brought about by
interference with the circulation with resultant extensive gangrene of
the part supplied by the diseased arteries. The amputation of a portion
of a leg, for instance, may relieve, to some extent, an overburdened
heart and prove life-saving to the patient, but the neuritic pains are
not necessarily relieved. The torture from these pains may be
excruciating.

No stage of the disease is exempt from its particular danger. In the
early stages of the disease before the artery or arteries have had time
to become strengthened by proliferation of the connective tissue, there
is the danger of aneurysm. Later, the very same protective mechanism
leads to stiffening and narrowing of the arteries and hence to
increased work on the part of the heart with all of its consequences.
Thrombosis is favored, and where atheromatous ulcers are formed,
embolism is to be feared.

As the complications and results of arteriosclerosis come to the front
every one must be considered by itself and as if it were the true
disease. There may be a slight apoplectic attack from which the patient
fully recovers, but the prognosis is now of a grave character, as the
chances are that another attack may supervene and carry off the subject.
Yet, after an apoplectic attack, patients have lived for many years.
Probably the most noted illustration of this is the life of Pasteur. He
had at forty-six hemiplegia with gradual onset. He recovered with a
resulting slight limp, did some of his best work after the stroke, and
lived to be seventy-three years old. Yet the exception but proves the
rule and the prognosis after one apoplectic stroke should always be
guarded.

The first attack of cardiac asthma is to be looked upon as the beginning
of the end. The end may be postponed for some time, but it comes nearer
with every subsequent attack. One may recover from what appears to be a
fatal attack of cardiac asthma accompanied by edema of the lungs and
irregular, intermittent, laboring heart, but the recovery is slow and
the chances that the next attack will be the fatal one are increased.

The significance of albuminuria is difficult to determine. The kidneys
secrete albumin under so many conditions that the mere presence of
albumin in the urine may have but little prognostic value. Many cases
are seen where there is no demonstrable albumin, and yet the patient may
suddenly have a cerebral hemorrhage. As a general rule the urine should
be carefully examined, but not too much stress should be laid on the
discovery of albumin and casts. It is not always possible to determine
the extent of the kidney lesion by the urinary examination, yet at any
time a uremic attack may appear and prove fatal.

After all the most important fact for the patient is not what the
pathologist finds in his kidneys after he is dead, but what the living
functional capacity of the kidneys is. This can now be determined in a
variety of ways as the result of extensive work carried out in quite
recent years. The simplest method of determining the functional capacity
of the kidneys is by the injection into the muscles of the back of a
solution containing 6 mg. of the drug phenolsulphonephthalein in one
c.c. of fluid. This comes already prepared in ampules, with full
directions for its employment.[16] Some clinicians use indigo-carmine in
place of phthalein. The general consensus of opinion is in favor of
phthalein.

[16] I have found the small colorimeter made by Hynson, Westcott and
Dunning, Baltimore, Mo., costing $5.00, a very practical instrument.

The nephritic test meal carefully worked out by Mosenthal[17] gives much
valuable information. The determination of the nonprotein nitrogen or
the creatinin in the blood also reveals the functional capacity of the
kidneys.[18]

[17] Mosenthal, H. O.: Arch. Int. Med., 1915, xvi, 733.

[18] Myers and Lough: Arch. Int. Med., 1915, xvi, 536.

One might say that the appearance of albumin in the urine of an
arteriosclerotic where it had not been before, is a bad sign, and in
making a prognosis this must be taken into consideration.

Bleeding from the nose is not infrequently seen in those who have
arteriosclerosis. It can hardly be called a dangerous symptom as it can
always be controlled by tampons. There are times when epistaxis is
decidedly beneficial as it relieves headache, dizziness, and may avert
the danger of a hemorrhage into the brain substance. It is rare to have
nose bleed except in cases of high tension in plethoric individuals. My
experience has been that it has saved me the trouble of bleeding the
patient. It is always of serious import in that it indicates a high
degree of tension, but there is scarcely ever any immediate danger from
the nose bleed itself.

Intestinal hemorrhage is always a grave sign. As has been shown,
arteriosclerosis of the splanchnic vessels not infrequently occurs, and
an embolus or thrombus may completely occlude the superior mesenteric
artery. The chances of the establishment of a collateral circulation are
small, as the arteries of the intestines are end arteries. Necrosis of
the part follows, blood is found in the stools, and perforation or
gangrene, or both, are apt to follow. There may be blocking of small
branches only, leading to ulceration of the intestine. Under all
conditions the prognosis is serious.

The general condition of the patient, his build, physical strength,
powers of recuperation, etc., must be taken into account in giving a
prognosis. The more powerful the individual, the more favorable, as a
rule, is the prognosis, with this reservation always in mind, that the
greater the body development, the greater is the heart hypertrophy, and
the accidents from high tension must not be overlooked. Many puny
individuals with stiff, calcified arteries go about with more ease than
a robust man with thickened arteries only. The differentiation as
pointed out by Allbutt (page 186), is well to keep in mind in giving a
prognosis. It can not be too strongly emphasized that it is the whole
patient that we must consider and not any one system that at the time
happens to be the seat of greatest trouble, and by its group of symptoms
dominates the picture.

It is evident from what has been said that an accurate prognosis in
arteriosclerosis is no easy matter. Were arteriosclerosis a simple
disease of an acute character there might be grounds for giving a more
or less definite prognosis. The most that can be said is that
arteriosclerosis is always a serious disease from the time that symptoms
begin to make themselves known. The gravity depends altogether on the
seat of the greatest arterial changes, and is necessarily greater when
the seat is in the brain than when it is in the legs or arms.

The attitude of the patient himself also determines to a great extent
the prognosis. Some men, especially those who have always enjoyed good
health, turn a deaf ear to warnings and instead of ordering their lives
according to the advice of the physician, persist in going their own way
in the hope that the luck that has always been with them will continue
to stand at their elbows. Neither firmness nor pleadings avail with some
men. The only salve for the conscience of the physician is that he has
done his best to steer the patient away from the shoals and breakers. In
others who realize their condition and take advantage of the advice
given as to the regulation of their lives, the prognosis is generally
favorable.

To sum up the chapter in a few words, I should say: Always remember that
the patient is a human being; study his habits and character and mode of
life; look at him as a whole; take everything into consideration, and
give always a guarded prognosis.

CHAPTER XII

PROPHYLAXIS

Arteriosclerosis comes to almost every one who lives out his allotted
time of life. As has been noted within, many diseases and many habits of
life are conducive to the early appearance of arterial degeneration.
Decay and degeneration of the tissues are necessary concomitants of
advancing years and none of us can escape growing old. From the period
of adolescence certain of the tissues are commencing a retrograde
metamorphosis, and hand in hand with this goes the deposit of fibrous
tissue which later may become calcified. The arterial tissue is no
exception to this rule, and we have already shown that certain changes
normally take place as the individual grows older, changes which are
arteriosclerotic in type and are quite like those caused in younger
people by many of the etiologic factors of the disease.

We are absolutely dependent upon the integrity of our hearts and blood
vessels for the maintenance of activity and span of life. Respiration
may cease and be carried on artificially for many hours while the heart
continues to beat. Even the heart has been massaged and the individual
has been brought back to life after its pulsations have ceased, but such
cases are few in number. We can not live without the heart beat and the
prophylaxis of arteriosclerosis consists in the adjustment of our lives
to our environment, so that we may get the maximum amount of work
accomplished with the minimum amount of wear and tear on the blood
vessels.

The struggle for existence is keen. Competition in every profession or
trade is exceedingly acute, so much so that to rise to the head in any
branch of human activity requires exceptional powers of mind. Among
those who are entered in this keen competition, the fittest only can
survive for any period of time. The weaklings are bound to succumb. A
scion of healthy stock will stand the wear and tear far better than will
the progeny of diseased parentage.

It is only necessary to call attention to the part that alcohol,
syphilis and insanity play in heredity. These have been discussed fully
in the earlier part of this book.

We live rapidly, burning the candle at both ends. It is not strange that
so many comparatively young men and women grow old prematurely. While
heredity is a factor as far as the prophylaxis of arteriosclerosis is
concerned, of far more importance is the mode of life of the individual.
Scarcely any of us lead strictly temperate lives. If we do not abuse our
bodies by excessive eating and drinking and so wear out our splanchnic
vessels and cause general sclerosis by the high tension thereby induced,
we abuse our bodies by excessive brain work and worry with all their
multitudinous evils. The prophylaxis of arteriosclerosis might well be
labeled, "The plea for a more rational mode of life." Moderation in all
things is the keynote to health, and to grow old gracefully is an art
that admits of cultivation. Excesses of any kind, be they mental, moral,
or physical, tend to wear out the organism.

People habitually eat too much; many drink too much. They throw into the
vascular system excessive fluid combined frequently with toxic products
that cause eventually a condition of high arterial tension. It has been
shown how poisonous substances absorbed from the intestines have some
influence on the blood pressure. Anything that causes constant increase
of pressure should be studiously avoided.

Mild exercise is an essential feature of prophylaxis. One may, by
judicious exercise and diet, make of himself a powerful muscular man
without, at the same time, raising his average blood pressure. The man
who goes to excess and continually overburdens his heart, will suffer
the consequences, for the bill with compound interest will be charged
against him. It is a great mistake for any one to work incessantly with
no physical relaxation of any kind, and yet, after all, it is not so
much physical relaxation that is necessary, as the pursuit of something
entirely different, so that the mind may be carried into channels other
than the accustomed routes. Diversification of interests is as a rule
restful. That is what every man who reaches adult life should aim at.
Hobbies are sometimes the salvation of men. They may be ridden hard, but
even then they are helpful in bearing one completely away from daily
cares and worries. The man who can keep the balance between his mental
and physical work is the man who will, other things being equal, live
the longest and enjoy the best health.

Nowadays the trend of medicine is toward prophylaxis. We give the state
authority to control epidemics so far as it is possible by modern
measures to control them.

We urge over and over again the value of early diagnosis in all chronic
diseases, for we know that many of them, and this applies particularly
to arteriosclerosis, could be prevented from advancing by the
recognition of the condition and the institution of proper hygienic and
medicinal treatment.

_It is the patent duty of every physician to instruct the members of his
clientele in the fundamental rules of health._ Recently the President of
the American Medical Association, in his address before the 1908
meeting, urged the dissemination of accurate knowledge concerning
diseases among the laity. While this may be done by city and state
boards of health, it seems far better for the modern trained physician
to work among his own people. With concise information concerning the
modes of infection and the dangers of waiting until a disease has a firm
hold before consulting the health mender, people should be able to
protect themselves from infections and be able to nip chronic processes
in the bud. But it is difficult to turn the average individual away from
the habit of having a drug-clerk prescribe a dose of medicine for the
ailment that troubles him. It is really unfortunate that most of the
pains and aches and morbid sensations that one has speedily pass away
with little or no treatment. Herein lies the strength of charlatanism
and quackery. Unfortunate, yes, for a man can not tell whether the
trivial complaint from which he suffers is any different from the one
that was so easily conquered six months ago. But instead of recovering,
he grows worse. Hope that springs eternal in the human breast, leads him
to dilly-dally until he at last seeks medical advice, only to find that
the disease has made such progress that little can be done.

_Instruct the public to consult the doctors twice a year._ The dentists
have their patients return to them at stated intervals only to see if
all is well. _How much more rational it would be if men and women past
the age of forty had a physical examination made twice a year to find
out if all is well._

The prophylaxis of arteriosclerosis is moderation in all the duties and
pleasures of life. This in no sense means that a man has to nurse
himself into neurasthenia for fear that something will happen to him. As
one grows in years exercise should not be as violent as it was when
younger, and food should be taken in smaller quantities. Many forms of
exercise suggest themselves, particularly walking and golf. Walking is a
much neglected form of exercise which, in these modern days with our
thousand and one means of locomotion, is becoming almost extinct. There
is no better form of exercise than graded walking. To strengthen the
heart selected hill climbing is one of the best therapeutic methods that
we have. The patient is made to exercise his heart just as he is made to
exercise his legs, and as with exercise of voluntary muscles comes
increase in strength, so by fitting exercise may the heart muscle be
increased in power. A warning should be sounded, however, against over
exercise. This leads naturally to hypertrophy with all its disastrous
possibilities. Men who have been athletes when young should guard
against overeating and lack of exercise as they grow older. Many of the
factors which favor the development of arteriosclerosis are already
there, and a sedentary, ordinary life, such as office all day, club in
afternoon, a few drinks and much rich food, will inevitably lead to
well-advanced arterial disease.

Karl Marx in his famous Socialistic platform said: "No rights without
duties; no duties without rights." So we may paraphrase this and say:
"No brain work without moderate physical exercise in the open air; no
physical exercise without moderate brain work."

There is yet one other point that is important, the combination of
concentrated brain work and constant whiskey drinking. This is most
often seen in men of forty-five to fifty-five, heads of large business
concerns who habitually take from six to twelve drinks of whiskey daily,
and with possibly a bottle of wine for dinner. Such men appear ruddy and
in prime health but, almost invariably, careful examination will reveal
unmistakable signs of arterial disease. There is usually the enlarged
heart and pulse of high tension with or without the trace of albumin in
the urine. The lurking danger of this group of manifestations has so
impressed the medical directors of several of the large insurance
companies that a blood pressure reading must be made on all applicants
over forty years of age. Should high blood pressure be found, the
premium is increased, as the expectation of life is proportionately
shorter in such men than in normal persons.

Therefore, let every physician act his part as guardian of health. Only
in this way is the prophylaxis of arteriosclerosis possible.

CHAPTER XIII

TREATMENT

Although it has been rather dogmatically stated (vide supra) that every
one who reaches old age has arteriosclerosis, it must not be inferred
that absolutely no exceptions to this rule are found. Cases are known
where persons of ninety years even had soft arteries, and we have seen
persons of eighty whose arteries could not be palpated. When infants and
children are seen with considerable sclerosis, it proves that, after
all, it is the quality of the tissue even more than the wear and tear,
that is the determining factor in the production of arteriosclerosis. It
would be well if those who can not bring healthy progeny into the world
were to leave this duty to those who can.

In general the treatment of arteriosclerosis is prophylactic and
symptomatic. In the preceding chapter I had something to say about
prophylaxis in general; I must again refer to it in detail.

Arteriosclerosis is essentially a chronic progressive disease, and the
secret of success in the management of it is not to treat the disease or
the stage of the disease, but to treat the patient who has the disease.
To infer the stage of the disease from the feeling of the sclerosed
artery, may lead to serious mistakes. Persons with calcified arteries
may be perfectly comfortable, while those with only moderate thickening
may have many severe symptoms. The keynote is individualization. It is
manifestly absurd to treat the laboring man with his arteriosclerosis as
one would treat the successful financier. The habits, mode of life,
every detail, should be studied in every patient if we expect to gain
the greatest measure of success in the treatment. One may treat fifty
patients who have typhoid fever by a routine method and all may
recover. Individualizing, while of great value in the treatment of acute
diseases, yet is not absolutely essential in order that good results may
be obtained. Far different is it when treating a disease like
arteriosclerosis. One who relies on textbook knowledge will find himself
at a loss to know what to do. Textbooks can only outline, in the
briefest manner, the average case, and no one ever sees the average book
case. At the bedside with the patients is the place to learn
therapeutics as well as diagnosis. All that can be hoped for in
outlining the treatment of arteriosclerosis is to lay down a few
principles. The tact, the intuition, the subtle something that makes the
successful therapeutist, can not be learned from books. So the man who
treats cases by rule of thumb is a failure from the beginning. There are
certain general principles that will be our sheet anchors at all times
and for all cases. The art of varying the application of these
fundamentals to suit the individual case, is not to be culled from
printed words.

=Hygienic Treatment=

Every man is more or less the arbiter of his own fate. Granted that he
has good tissue to begin life, his own habits and actions determine his
span of comfortable existence. No one cares to live after his brain
begins to fail, and the failing brain is often due to disease of the
cranial arteries. The hygienic treatment resolves itself into advice in
regard to prophylaxis.

First and foremost is exercise. It has seemed to us that the revival of
out-of-door sports is one of the best signs of promise of the
preservation of a virile, hardy race. That women, as well as men,
indulge in the lighter forms of out-of-door exercise should bring it
about that the coming generation will start in life under the most
advantageous conditions of bodily resistance.

Among all the forms of exercise, golf probably is the best. It is not
too violent for the middle-aged man, yet it gives the young athlete
quite enough exercise to tire him. It is played in the open. One is
compelled to walk up and down in pleasant company, for golf is
essentially a companionable game, while he reaps the full benefit of the
invigorating exercise. The blood courses through the muscles and lungs
more rapidly; the contraction of the skeletal muscles serves to compress
the veins and so to aid the return of blood to the heart: the lungs are
rendered hyperemic, deeper and fuller breaths must be taken; oxidation
is necessarily more rapid, and effete products, which if not completely
oxidized would possibly act as vasoconstrictors, are oxidized to
harmless products and eliminated without irritating the excretory
organs.

Other forms of out-door exercise that can be recommended are tennis,
canoeing, rowing, fishing, horseback riding, swimming, etc. Tennis is
the most violent of all the sports mentioned and might readily be
overdone. Rowing as practiced by the eights at college is undoubtedly
too violent a form of exercise, and may be productive in later life of
very grave results. Canoeing is a delightful and invigorating exercise.
The muscles of the arms, shoulders, and trunk are especially used, the
leg muscles scarcely at all. Nevertheless, the deep breathing that
necessarily comes with all chest exercises aerates every portion of the
lungs, and is of great benefit to the whole body.

Swimming as an exercise has much to recommend it. In this sport all the
muscles take part and at the same time the chest is broadened and
deepened.

All these methods of using the muscles to keep oneself in trim, so to
speak, are part and parcel of the general hygienic mode of life that is
conducive to a healthy old age. Exercise can be overdone, as eating can
be overdone. Both are essential and yet both can be the means of
hastening an individual to a premature grave.

When the arteriosclerosis has advanced so far that it is easily
recognizable, certain forms of exercise should be absolutely prohibited.
Such are tennis, rowing and swimming. Horseback riding to be allowed
must be strictly supervised. At times this may be an exceedingly violent
exercise. As an out-of-door sport, there is nothing that equals golf.
The physician, knowing the character of the course, and the length of
it, can say to his patient that he may play six, nine, twelve, or
eighteen holes, depending on the patient's condition.

For those who are not able to get out, exercise in the room with the
windows open must take the place of out-of-door sports. Here the use of
chest weights is a most excellent means of keeping up the tone of the
muscles. By adjusting the weights, the exercise may be made light,
medium, or heavy. Every physician should be familiar with the chest
weight exercises. They are not as good as open air exercise but they
undoubtedly have been the means of saving years of life to many patients
with arterial disease.

There comes a time when all forms of exercise must be prohibited on
account of the dyspnea, edema, dizziness, etc. It seems unwise to keep
such a patient in bed, even though the edema be considerable. Once on
his back in bed he becomes weak, and the danger of edema of the lungs or
hypostatic congestion of the bases, with subsequent bronchopneumonia, is
very great.

Such patients may be allowed to sit up in a comfortable chair with the
legs supported straight out on a stool or other chair. The half
reclining position is not easy to assume in bed. Considerable ingenuity
must often be exercised by the physician in making the patient
comfortable without increasing the symptoms from which the patient
suffers following the least amount of exercise. Although such persons
can not exercise actively, they should have passive exercise in the form
of massage, carefully given, so that no injury is done to the rigid
vessels. It is possible to rupture a vessel, the walls of which are
encrusted with lime salts, and full of small aneurysmal dilatations.
Every patient must be watched carefully and measures instituted for the
individual.

=Balneotherapy=

As a tonic and invigorator, the cold or cool bath (shower or tub), in
the morning on arising can be highly recommended. It promotes skin
activity, is a stimulant to the bowels and kidneys and to the general
circulation, besides being cleansing. We find today that the morning
bath has become such a necessity to the average American that all new
hotels are fitted with private baths, and old hotels, in order to get
patronage, are arranging as many baths connected with sleeping rooms as
is possible. Our generation assuredly is a ruddy, clean-bodied one. What
the actual results of this out-door life and frequent bathing will be
for the race remains to be seen, but one can not but feel that it must
build up a stronger, more resistant race of people, who not only enjoy
better health than did their forefathers, but enjoy it longer.

Not every one can stand a cold bath. It is folly to urge it on one to
whom it is distasteful, or on one who does not feel the comfortable glow
that should naturally result. For the well, or those with a tendency to
arteriosclerosis, or those in whose families there have been several
members who had early arteriosclerosis, such proceedings as recommended
could not be improved upon. However, for the person who has well
recognized sclerosis, only warm baths should be advised, and these not
daily. The water should be at a temperature of 90-95° F. Care should be
taken that persons sent to spas be cautioned against hot baths. It is
not inconceivable that the increased force of the heart beat that
accompanies a hot bath might be sufficient to rupture a small cranial
vessel. Hence, Turkish and Russian baths should be most unqualifiedly
condemned. As a matter of fact, persons vary so in their habits with
regard to bathing that what might suit one person would do another much
harm.

=Personal Habits=

The personal habits of the individual, more than any other factor,
determine whether or not arteriosclerosis sets in early in his life. The
man or woman who is moderate in eating and drinking, sees that the
kidneys are kept in good condition, and attends strictly to regularity
of the bowels, lays a good basis for the measure of health which is so
essential for happiness. It has been shown that sclerosis of the
splanchnic vessels may be due to constant irritation of toxic products
elaborated in digesting constantly enormous meals. In obstinate
constipation, many poisons, the nature of which we do not know, are
absorbed and circulate in the blood. We have not sufficient data to
prove that constipation favors the production of arteriosclerosis, but
our impression has been that it does favor it. Constipation can often be
relieved by a glass of water before breakfast, a regular time to go to
stool, and abdominal massage or exercises. Some maintain that it is a
bad habit only, and can be readily overcome. Whatever is done, avoid
leading the patient into the drug habit, for the last state of the
patient will be worse than the first. Habits of sleep are not of such
great importance. Most persons get enough sleep except when under severe
mental strain. Most adults need from seven to eight hours' sleep,
although some can do all their work and keep in prime health on five or
six hours' sleep.

Tobacco has been accused of causing many ills and has been thereby much
maligned. We can not see that the use of tobacco in any form in
moderation is harmful to most men. Undoubtedly the blood pressure is
raised when mild tobacco poisoning occurs, and individual peculiarities
of reaction to the weed are multitudinous. But to condemn offhand its
use is the height of folly. There is no reason why the arteriosclerotic
who has always used tobacco in moderation, should not continue to use
it, whether he smoke cigarettes, cigars, or pipe. His supply should be
decreased, but there is no sense in depriving a man of one of the
solaces of life, unless, as is sometimes the case, abstinence is easier
for the patient than moderation.

As for alcohol, opinions differ widely.[19] Some see in alcohol one of
the most frequent causes of arteriosclerosis; others do not believe that
the part played by alcohol is a serious one, only in conjunction with
other poisonous substances is it dangerous. Probably unreasoning
fanaticism has had much to do with the wholesale condemnation of
alcoholic beverages. The general effect of alcohol is to lower the blood
pressure by causing marked dilatation of all the vessels of the skin.
True, the alcohol circulates in the blood, and is broken up in the
liver, and this organ would seem to bear the brunt of the harm done.
Alcoholic drinks in moderation, I do not believe have any deleterious
effect on health. On the contrary, I believe that they may in some cases
assist digestion and assimilation. Indiscriminate indulgence is to be
condemned, as is overindulgence in exercise or eating. What may be
moderate for A, might be excessive for B. Every man is then the arbiter
of his own fortune and within his own limits can indulge moderately (a
relative term after all) without fear of doing himself harm. In advanced
arteriosclerosis it is necessary to decrease the supply of alcohol just
as it is necessary to cut down the food supply. This must rest entirely
on the judgment of the physician, who must not act arbitrarily, but must
have his reasons for every one of his orders.

[19] Discussion of alcohol at present has value only as it relates
to the past. The present is dry. The future is in the lap of the gods.

=Dietetic Treatment=

Most persons eat too much. We not only satisfy our hunger, but we
satisfy our palates, and, instead of putting substantial foodstuffs
into our stomachs, we frequently take unto ourselves concoctions that
defy description.

Foodstuffs are composed of one or all of three classes: (1) proteins,
(2) fats, (3) carbohydrates. As examples of the first are beef and white
of egg; of the second, the oils, butter, lard; of the third, sugar,
potato, beet, corn, etc.

The physiologists and chemists have shown us that both endogenous and
exogenous uric acid in excess will cause a rise of blood pressure, but
the bodies most concerned in the production of elevated blood pressure
are the purin bodies, those organic compounds which are formed from
proteins and represent chemically a step in the oxidation of part of the
protein molecule to uric acid. Red meat contains more of the substances
producing purin bodies than any other one common foodstuff, and for this
reason the excessive meat eater is, _ceteris paribus_, more apt to
develop arteriosclerosis comparatively early in life.

The fats and carbohydrates contain practically no substances that react
on the body of the ordinary individual in a deleterious manner during
their digestion. The extra work that is put on the heart by the
formation of many new blood vessels in adipose tissue is the only
harmful effect of overindulgence in these foodstuffs.

It has been found that nitrogen equilibrium can be maintained at a wide
range of levels. Formerly 135-150 gms. of protein daily were considered
necessary for a man doing light work. Now it is known that half that
amount is sufficient to keep one in nitrogenous equilibrium, and to
enable one to keep his weight. A person at rest requires even less than
that. One who is engaged in hard physical labor burns up more fuel in
the muscles, and so must have a larger fuel supply.

Although we habitually eat too much we drink too little water. For those
who have any form of arterial disease an excess of fluid is harmful, as
the vessels become filled up and a condition of plethora results, which
necessarily reacts injuriously on the heart and circulation. The
drinking of a glass of water during meals is, in the author's opinion,
good practice. The water must be taken mouthful at a time, and not
gulped down. If this is done, there results sufficient dilution of the
solid food to enable the gastric juices successfully and rapidly to
reach all parts of the meal.

Some are in favor of a rigid milk diet for those who have
arteriosclerosis. Some men have lived on nothing but milk for several
years and have not only kept in good health, but have actually gained
weight and led at the same time active lives. It has been held by others
that rigid milk diet is positively harmful on account of the relatively
large quantity of calcium salts that are ingested. This was thought to
favor the deposition of calcareous material in the walls of the already
diseased arteries. While possibly there may be some danger of increased
calcification, the majority of clinicians are in favor of a milk cure
given at intervals. Thus the patient is made to take three to four
quarts daily for a period of a month. There is then a gradual return to
a general diet, exclusive of meat, for several weeks, then another rigid
milk diet period.

If we are bold enough to follow Metschnikoff in his theories of
longevity, we might advise resection of the large intestine, on the
ground that it is an enormous culture tube that produces prodigious
amounts of poisonous substances which are thrown into the general
circulation. To combat such a grave (?) condition as the carrying of
several feet of large intestine, we are recommended to take buttermilk
or milk soured by means of the _b. acidus lacticus_. Clinical experience
has taught that in arteriosclerosis buttermilk is of great value,
whether it be the natural product, or made directly from sweet milk by
the addition of the bacilli. The latter is a smoother product and has,
to my mind, a delightful flavor. It may be diluted with Vichy or plain
soda water. Cases that can not take milk or any other food will often
take buttermilk, and do well on this restricted diet. From two to four
quarts daily should be taken. It should be drunk slowly as should milk.

=Medicinal=

It has long been thought that the iodides have some specific effect on
the advancing arteriosclerosis, checking its spread, if not really
aiding nature to a limited restoration of the diseased arteries. It is
possible that the eulogies upon the iodides owe their origin to the
successful treatment of syphilitic arteriosclerosis, in which condition
these drugs have a specific action. However that may be, there is no
doubt that the administration of sodium or potassium iodide is good
therapeutics in cases of arteriosclerosis.

Unfortunately many persons have such irritable stomachs that they can
not take the iodides, even though they be diluted many times. They may
be made less irritating by giving them with essence of pepsin. Unless
the case is syphilitic, it is doubtful whether it is of value to
increase the dose gradually until a dram or even more is taken three
times daily after meals. Usually a maximum dose of ten grains seems to
be quite sufficient. This may be taken three times a day, well diluted,
for three months. There follows a month's rest, then the treatment is
resumed for another period of three months, and so on. Either sodium or
potassium iodide in saturated solution may be given. The sodium salt is
possibly less irritating, and contains more free iodine than the
potassium salt, although the latter is more generally used. The
strontium iodide may also be used.

One sees a patient now and then who can not take the iodides, however
they may be combined. For such patients one may obtain good results with
iodopin, sajodin, or other of the preparations put up by reputable
firms. Personally I have never yet seen a patient who could not take the
ordinary iodides in some form or other, and I am opposed to ready made
drugging.

The action of the iodides is to lower the blood pressure, and they are
of greatest value when the blood pressure is high, and when headache and
precordial pain are present.

When the case is moderately advanced, very mild doses, gr. 1/2, morning
and evening, of the thyroid extract may be given. It is generally
believed that the internal secretion of the thyroid and the adrenal are
antagonistic. That the thyroid secretion lowers blood pressure in
certain forms of hypertension is certain, possibly on account of its
iodine content. Some combinations of iodine and thyroid such as the
iodothyroidin have been used and have had some measure of success
attributed to them.

Hypertension does not always demand active measures for its reduction.
Viewed from the physiologic standpoint, hypertension is but the
expression of a compensating mechanism which is designed to keep the
blood moving through narrowed channels. Heart hypertrophy then is
absolutely essential to the maintenance of life. It has been said that
the highest blood pressures occur in chronic disease of the kidneys. The
poisonous substances produced in the kidneys must exert their action
through absorption into the general blood stream. This toxin may be
completely eliminated, if we accept as our criterion the reduction of
tension to normal together with the complete return of the affected
individual to health. A concrete example is as follows: A man aged 44
years was brought to the Milwaukee County Hospital in coma. His systolic
blood pressure was over 280 mm. Hg, diastolic 170 mm., his urine
contained considerable albumin and many casts. He had general anasarca.
Venesection was done at once and 300 c.c. blood obtained. Immediately
following this operation the pressure was 210-150, but within twelve
hours it was again above 280-170. He was given no medication to reduce
pressure except that he was freely purged. He was given a steam sweat
bath daily. Frequent blood pressure readings were taken. Within seven
days the pressure was 130-86. He had, in the meantime, completely
recovered from his symptoms. He was kept in the hospital for two weeks
longer assisting in the work on the ward, and he was discharged with a
pressure (systolic) between 130 and 136 diastolic 80-84. The treatment
was rest in bed, free purging, venesection, and sweat baths, simple but
exceedingly effective.

Should there be actual indications for reducing the blood pressure, I
must admit that it can not always be done. The majority of cases will do
well on the sodium nitrite or erythrol tetranitrate. However, these do
not always lower blood pressure and keep it within normal limits. When a
man has very high tension we do not wish to reduce it to what it should
normally be for the age of the patient, as symptoms of collapse might
set in at any time under such conditions.

Observations made with the sphygmomanometer[20] show that the effect of
nitroglycerin is transient or of no effect except in doses which are
relatively enormous (one drop of the one per cent solution given every
hour). Sodium nitrite may lower the blood pressure but the effects will
have worn off in two hours. It is the same with erythrol tetranitrate.
Sodium sulphocyanate in doses of from one to three grains three times a
day is highly recommended by some. My own experience with it does not
lead me to believe that it is of any great value in hypertension. It,
however, may be tried. Benzyl benzoate has been used recently to reduce
the high blood pressure of hypertension. Macht has reported some
success. In the author's hands it has been efficacious in a few cases.
As long as the patient takes the drug the pressure may be slightly
reduced, but upon the withdrawal of the drug the pressure returns to its
former level. It is well worth a trial and further experimentation may
reveal better methods of administration. The dose is from 2 to 6 c.c.
mixed with water at intervals.

[20] Miller, Jos. L.: Hypertension and the Value of the Various
Methods for Its Reduction. Jour. Am. Med. Assn., 1910, liv, p. 1666.

In the hypertension of the menopause some have had success with large
doses of corpus luteum extract. As a matter of fact the drug treatment
of hypertension, when it becomes necessary to treat this condition with
drugs, has suffered a notable set-back since more careful control has
been made with the blood pressure instruments. In giving any of the
depressor drugs their action should be controlled by blood pressure
measurements, for only in this way can we be sure that the drug is
exerting its physiological effect and we may expect results. The
individual reaction to these drugs varies greatly and no rule for dosage
can be dogmatically laid down. The only successful therapy is rigid
individualization. This is the keystone to treatment in cases of
arteriosclerosis and high tension.

It must not be inferred from what has been said that the nitrites are of
no value. They are of decided value but they have their limitations. The
most evanescent of these drugs is amyl nitrite. This is put up in the
form of capsules, or pearls, containing from one to three minims. When
it is desired to dilate the peripheral vessels suddenly, one or two of
these capsules are broken in a cloth held to the nose. The effect is
almost instantaneous. There is flushing of the face and other peripheral
vessels, particularly near the head, denoting a relaxation and widening
of the bed of the blood stream, and a consequent decrease in pressure in
the arteries. These effects are over in a short while. It is only used
in attacks of cardiac spasm, as in angina pectoris. Nitroglycerin, the
Spiritus Glonoini of the U. S. P., acts in about the same manner as amyl
nitrite but the effects last usually a trifle longer. One drop of the
one per cent solution may be given every hour until physiologic effects
are produced. It may be given hypodermically. This may be a means of
reducing pronounced high tension. This drug has been found of benefit
especially in cases where arteriosclerosis combined with chronic
nephritis causes cardiac asthma. The other drug which may be of service
in these conditions, one whose sphere of action is somewhat broader,
because its effects are more lasting, is sodium nitrite. This is given
in water in doses of one to three or five grains every four hours. Some
have objected to the use of this drug, but my experience has made me
place considerable confidence in its harmlessness, provided that the
patient is carefully watched. This, however, applies to all of the
nitrite compounds. My experience with erythrol tetranitrate is not
large. It may be used in place of sodium nitrite.

For a mild case, one often finds that sweet spirits of niter is
sufficient to control the pressure and relieve the distressing symptoms,
and it is undoubtedly the least harmful of all the nitrites. Drugs that
are of great value, but of which little is noted in textbooks, are
aconite and veratrum viride. Both of these drugs are well known to be
marked circulatory depressors. Veratrum viride in my experience should
be very cautiously used, and never used unless a trained attendant is
constantly at hand. With regard to aconite I have no such feeling, and a
mixture of tincture of aconite and spiritus etheris nitrosi may be given
for several weeks with no fear of doing any harm. Personally, of all the
drugs mentioned, I prefer the nitrite of sodium or the combination just
given. They may be advantageously alternated.

My own feeling is that the most successful means of treatment of acute
high tension is without the use of drugs. The most important measure is
absolute rest in bed. This often suffices to lower the blood pressure
and to arrest the symptoms produced by high tension. Venesection I
believe is also of value. True the arterioles appear to contract almost
immediately upon the lessened quantity of blood, or there is immediate
interchange of serum from the tissues which brings the blood volume
back to the original amount. Whatever happens the pressure is not
greatly reduced, at times not reduced at all, but often the symptoms are
relieved. Hot packs or sweat baths assuredly do reduce the pressure in
many cases. This seems to me to be an exceedingly valuable measure.
Finally the diet should be nourishing, but very light, not too much
fluid should be ingested, and the bowels should be freely opened.

With the fibrolysin of Merck, I have had no experience. Some men assert
that they have had good results from its use, but on the whole the
evidence is not highly favorable.

Morphine is invaluable. No drug is of such value in the nocturnal
dyspneic attacks that occur in the late stages of arteriosclerosis when
the heart or the kidneys are failing. Morphine not only relaxes spasm
and quiets the cerebral centers, but is an actual heart stimulant under
such conditions, and should never be withheld, as the danger of the
patient's becoming addicted to its use is more fanciful than real.
However, morphine, at times, suppresses the secretion of urine. So that
if after trial the urine becomes scanty and the edema increases,
recourse must be had to other drugs. The various hypnotics may be used
with caution. One which seems to be very useful is adalin.

As heart stimulants, one may use strychnine, spartein, caffein, or
camphor. In desperate cases, where a rapidly diffusible stimulant is
needed, a hypodermic syringeful of ether may be given, and repeated in a
short while.

Several years ago a so-called serum was brought out by Trunecek which
was said to have a favorable effect on the metabolism of the vessel
walls. It was given at first hypodermatically or intravenously but the
former method was painful. It was later stated that given by mouth it
acted just as well. The results with the Trunecek serum have not come up
to the expectations that the early favorable reports promised. The
original serum was composed as follows: NaCl, 4.92 gm.; Na_2SO_4, 0.44
gm.; Na_2CO_3, 0.21 gm.; K_2SO_4, 0.40 gm.; aqua destil. q. s. ad. 100.0
c.c. Later this was modified for internal use to the following
prescription:

R_{x} Natrii chlor. 10. gm.
Natrii sulphat. 1. gm.
Natrii carbonat. 0.40 gm.
Natrii phosphat. 0.30 gm.
Calcii phosphat.
Magnesii phosphat. aa. 0.75 gm.
M. Ft. cachets No. XIII.

The contents of every cachet corresponds to 15 c.c. of the fluid serum
or to 150 c.c. of blood serum. The preparation called antisclerosin
consists of the salts contained in the serum. As to its efficacy, I can
not judge, as I have never felt that it was worth while to use it.
Reports of cases in which it has been tried do not speak very highly of
it.

In the general treatment of arteriosclerosis, there is no one factor of
more importance than the regular daily bowel movement. Attention to this
may save the patient much discomfort and even acute attacks of cardiac
embarrassment. The choice of the purgative is immaterial, with this
reservation only, that the mild ones, such as cascara, rhubarb, licorice
powder and the mineral waters, should be thoroughly tried before we
resort to the more drastic purgatives. Plenolphthalein in 3 to 5 grain
doses acts remarkably well in some people as a pleasant laxative.
Agar-agar with or without cascara may be useful.

Liquid paraffin under a variety of names is a most useful and
efficacious laxative. As its action is purely mechanical it may be taken
indefinitely without doing harm to the intestinal musculature.

The old Lady Webster dinner pill is an excellent tonic aperient. When
the heart is embarrassed and edema of the legs and effusion into the
serous cavities have taken place, then it becomes necessary to use the
drastic purgatives that cause a number of watery movements. Epsom salts
given in concentrated form, elaterin gr. 1-12, the compound cathartic
pill, blue mass and scammony, or even croton oil may be used. Since the
observation of a greatly congested intestine from a patient who had been
given croton oil, I have ceased to use this purgative, and I doubt much
whether its use is ever justifiable in these cases.

The management of the ordinary case of arteriosclerosis resolves itself
into a careful hygienic and dietetic regime with the addition of the
iodides, aconite, or the nitrites. A diet consisting of very little
meat, alcohol in moderation or even absolutely prohibited, and not too
much fluid should be prescribed. Condiments and spices should also be
used sparingly. Cold baths, shower baths, cold and hot sheets
alternating, are of great benefit in assisting the heart to do its best
work by making the large capillary area of the skin more permeable. It
is not true that such baths raise the blood pressure so markedly.
Certain acts, as sneezing, violent coughing, etc., increase the blood
pressure much more than judicious bathing.

=Symptomatic Treatment=

The fact that arteriosclerosis really loses much of its own identity
and, in later stages, becomes merged with the symptomatology of the
diseases of various organs, as the kidney, brain, heart, compels us, for
completeness' sake, to say a few words about the treatment of these
complications.

One of the results of arteriosclerosis of the coronary arteries, angina
pectoris, demands prompt treatment. In the acute attack, the chief
object is to relieve the spasm and pain. Pearls of amyl nitrite should
be inhaled, and morphine sulphate with atropine sulphate given
hypodermatically at the very earliest moment. It is senseless to
withhold morphine. The only possible reason for withholding it would be
uncertainty as to the diagnosis. It is probably better to err on the
safe side, and should the case prove to be one of pseudo angina, in the
next attack sterile water can be given instead of the morphine and
atropine.

When a patient is seen in the condition of broken compensation with the
much dilated heart, anasarca, dyspnea and suppression of urine, there is
no better practice than venesection. Especially is this valuable when
the tension is still fairly high and the individual is robust. Following
the abstraction of six to eight ounces of blood (300-500 c.c.)[21] the
whole picture changes, so that a man who a short while before was
apparently at death's door, notices his surroundings and takes an
interest again in life. This should be followed up with thorough
purgation, and cardiac stimulants should be ordered. In such cases
digitalis is useful, but its action is never so striking as in cases of
this general character due to uncompensated valvular disease. It must be
remembered that in arteriosclerosis the changes in the myocardium must
be of a considerable grade for the heart to give away. Therefore,
digitalis can not be expected to act on a diseased muscle as it acts on
a comparatively healthy muscle. It is only in such cases of broken
compensation that digitalis should ever be used.

[21] I have taken as much as 1700 c.c. from a large man. He
recovered and went back to work.

Digitalis is not a general vasoconstrictor as used to be taught. Its
action on the kidney is actually a vasodilator one. And in its action on
the heart the digitonin dilates the coronary arteries, according to
Macht, while the digitoxin acts on the heart muscle. Overdosing with
digitalis has produced partial heart block in many cases. It is
absolutely contraindicated in Stokes-Adams syndrome.

There are, however, some cases, especially those with transudations,
when digitalis may be carefully tried even though high tension be
present. It is sometimes of advantage to combine digitalis with the
nitrites although they are said to be physiologically incompatible.

Still another drug, that is of great value in conditions such as have
been described, is diuretin. This may be given in capsule or tablets,
grs. x. three times daily. There is only one caution to express in the
use of this drug. It should not be given when the kidneys are the seat
of chronic inflammatory changes; in fact, actual harm may be done by
administering the drug under such conditions.

The same is true even to a greater extent with theocin. This is a
powerful diuretic. If given by mouth it should be well diluted as it is
most irritating to the stomach. It is best given intravenously in doses
of two and a half to three grains dissolved in five to six cubic
centimeters of distilled water. One must be reasonably sure that the
kidneys are not the subject of chronic disease and are functionally,
therefore, below par. The intravenous dose should not be given oftener
than once in four days.

For the pain in aneurysm, nothing (except, of course, morphine) is so
valuable as iodide of potassium. Patients who are suffering agony, when
put to bed and given KI grs. x. three times a day, soon lose all the
distressing symptoms. This applies particularly to aneurysms of the arch
of the aorta.

When the sclerosis has affected the cerebral arteries to such an extent
that symptoms result, the case is, as a rule, exceedingly grave. Not
much can be done except to relieve the headaches and keep down the blood
pressure, if this is high, by means of rest in bed, the iodides,
aconite, or the nitrites. The cases of transient monoplegias or
hemiplegias can be much relieved by careful hygienic measures and
judicious administration of drugs. Much ingenuity is sometimes required
to overcome the idiosyncrasies of patients, but care and patience will
succeed in surmounting all such difficulties.

The treatment of intermittent claudication is the treatment of
arteriosclerosis in general. Sometimes the circulation in the affected
leg or legs is much helped by daily warm foot baths. Light massage might
be tried and the galvanic current may be used once or twice daily.

There are a few distressing symptoms that occur usually late in the
disease, when complications have already occurred, which frequently
baffle the therapeutic skill of the physician. The chief of
these--insomnia, dyspnea, and headache--may not be late manifestations,
but insomnia and headache are frequently associated with the moderately
advanced stages of arteriosclerosis. At times all the symptoms seem to
be due to the high tension, the relief of which causes them to
disappear. There are, unfortunately, times when high tension is not
responsible for the headache and insomnia. Under these circumstances
such drugs as trional, veronal, amylene hydrate, ammonol, etc., may be
tried until one is found which produces sleep. For the headaches,
phenacetin, alone or in combination with caffein and bromide of sodium,
may be tried. Acetanilid, cautiously used, is at times of value. There
have been cases of arteriosclerosis with low blood pressure, accompanied
by severe headaches, that have been relieved by ergot. Codeine should be
used with care, and morphine only as a very last resource.

Great care must always be exercised in giving drugs that depress the
circulation, for it is easily conceivable that more harm than good can
come from injudicious drugging.

CHAPTER XIV

ARTERIOSCLEROSIS IN ITS RELATION TO LIFE INSURANCE

The value of the early recognition of cases of arteriosclerosis and
hypertension has been spoken of within, but it needs to be further
emphasized. There is perhaps no class among physicians to whom is
afforded a better opportunity of seeing early cases than the medical
examiners of life insurance companies.

The relationship between a patient and the physician whom he consults,
and the applicant for life insurance and the examiner are diametrically
opposite. In the former the patient desires to conceal nothing and the
physician is called upon to diagnose and treat disease. In the latter
the applicant, a presumably healthy person, may have much to conceal and
the examiner is there to pass upon the state of health. The question is
this--"Is the applicant now in good health?" It becomes then of vital
importance for the examiner to be able to detect among other abnormal
conditions the incipient signs of arteriosclerosis and of hypertension.
Parenthetically it may be stated that arteriosclerosis and hypertension
are not one and the same disease as has been so frequently insisted upon
within; the former may occur without the latter but the latter can not
from its very nature be present for long without arterial thickening
supervening. It is necessary in discussing the question here to group
the two conditions together in order to prevent needless repetition.

Such a case as the following is common. A successful business man of
forty-four years was brought to me by an agent in 1905 for examination.
The man was six feet tall, weighed 218 pounds, had a ruddy color and
looked to be the picture of health. He was not strictly intemperate, he
never became intoxicated, but every day he drank three or four whiskies
and often he had a bottle of wine for dinner in the evening. When he was
examined his pulse was of good quality and owing to the fleshiness of
the wrist it was difficult to say positively whether the radial artery
was sclerosed or not. In the heart no murmurs were heard, and it was
difficult to be sure that the left ventricle was enlarged. There was,
however, a slight but definite accentuation of the second sound at the
aortic cartilage which might readily have been overlooked had the
patient not been stripped and a careful examination made with the
stethoscope. Upon taking the blood pressure it was found to be from
170-175 mm. of Hg. The urine specimen examined at the visit was normal,
no casts were found. The applicant was seen at his home and the blood
pressure measured. It was again the same. He was seen a third time and
practically the same systolic blood pressure was found. Under protests
from all the agency staff the man was declined. Two years later he died
of apoplexy. The man was angry at being refused. Instead of looking the
matter squarely in the face he thrust aside the idea that there was
anything the matter with him. He had never had one ill day in his life,
his forebears had lived to ripe old age, and he was sure that he knew
more about himself than the examiner.

Had this applicant showed a sense of reasonableness he should have been
grateful to the doctor for calling his attention to a condition which
surely would sooner or later prove either fatal itself or lead to some
fatal lesion. It was learned that this man had gone directly to his
family physician who laughed at such nonsense as had been told the (now)
patient by the examiner.

Another illustration of a slightly different type of case is afforded in
the following history.

A man of fifty years of age, five feet ten in height and 164 lbs. in
weight, was brought for examination. In his youth there was a history
of a mild attack of scarlet fever. He was almost a total abstainer,
rarely taking liquor in any form. Physically he appeared to be an
excellent risk. However, on examining the heart it was found that there
was slight hypertrophy with an accentuated second aortic sound at the
base, and the blood pressure was 180 mm. of Hg. Some sclerosis of the
radial arteries was found. One company had refused him on account of
albumin in the urine. There was none in the first specimen which was
passed while in the office. The specific gravity was 1014. A morning
specimen was obtained and contained a trace of albumin. Several
specimens were then examined. Some contained albumin, some had no
albumin content. The man was declined; no protests from the agent as
albumin had been found. There was something tangible in that. Had the
applicant been refused on account of his high tension, sclerosis of the
radials, and slightly enlarged heart there would undoubtedly have been
protests. And yet an applicant revealing such a state of the
cardiovascular system without albumin in the urine should unhesitatingly
be declined. Attention has been called to hypertension as an early, and
some think an invariable, sign of chronic nephritis. My own experience
has confirmed me in the belief that in hypertension the kidneys are
often the seat of chronic interstitial changes. Careful palpation of the
radial and brachial arteries will in every case reveal more or less
thickening.

There is yet another group of cases which the examiner sees as healthy
subjects, namely those cases of sclerosis of the peripheral arteries
without sclerosis of the aorta and without high tension. In such cases
the radials, brachials, temporals and other superficial arteries are
readily palpable, sometimes even revealing irregularities along the
course of a vessel. Such cases are not subjects for insurance. The
recognition of such a condition is of great importance to the one who
has it and he should be urged to go to his regular physician for
thorough examination. Should the physician ridicule the idea, as has
happened to me more than once when I was actively engaged in insurance
work, the examiner has done his full duty to the company, the applicant,
and himself.

A life insurance examiner has a difficult position to fill. He has four
people to satisfy; the applicant, the agent, the medical director and
himself. The straight and narrow path of strict honesty is his only
salvation. By being honest with himself he necessarily gives a square
deal to the other three parties.

No applicant who has palpable arteries or hypertension can be considered
a first class risk. It can not be denied that men with arteriosclerosis
live to an advanced age and may even outlive those who have apparently
normal arteries, but the average life expectancy at any age for an
arteriosclerotic is less than that for a normal person. The apparently
healthy applicant who learns for the first time when examined for life
insurance that he has the early or moderately advanced signs of arterial
disease, should thank the agent and examiner for showing him the danger
signals ahead. The sensible man then orders his life so that he puts as
little strain on his heart, arteries, and kidneys as possible and may
add many years to his life.

It is on account of this very insidiousness of onset that I have
elsewhere urged as a prophylactic measure the examination every six
months of all persons over forty years of age. I am more and more
convinced that it is of vital importance to the health of the public.

As I have remarked, the average man consults his dentist at least once a
year so that no tooth may be so far diseased that it can not be saved.
It is purely a means of preserving the teeth. Why not do the same with
the whole body? Of what use is it to save the teeth and lose the body?
It seems to me that the great army of life insurance examiners are in an
enviable position in their ability to add years of life to many men and
women. I doubt whether they realize their importance in the campaign for
health. I should urge life insurance companies not to employ recent
graduates unless they have had at least a year's hospital experience.
For the company as well as for the individuals I believe that there is a
prognostic sense which the examiner should have and this can only be
acquired by experience.

I believe that arteriosclerosis and hypertension are increasing for the
reasons which have been given in another chapter. There can be no doubt
that when these conditions are recognized long before symptoms would
naturally supervene, men and women would not only live longer but also
die more comfortably and many very likely would be carried off by some
disease having no relationship whatever to arteriosclerosis. Slight
enlargement of the heart downward and to the left, accentuation of the
second aortic sound at the base, a full pulse, arteries which are
palpably thickened, increased blood pressure are signs to which
attention must be paid.

When the peripheral arteries are palpable they are not always sclerosed.
The radial artery, the one usually palpated, may lie very close to the
bone in a thin person. Under these conditions the artery can be easily
felt. It is better then to palpate for the brachial as it lies beneath
the inner edge of the biceps muscle. Should this artery be felt then
very probably sclerosis is present. Opinion as to whether or not
sclerosis is present, when it is slight, may differ. It is difficult at
times to say definitely. Should such be the case the applicant should be
most carefully questioned as to his family and past history, the heart
should be carefully outlined by percussion and the blood pressure should
be taken, both the systolic and diastolic pressures. The urine should be
examined with particular care. I am aware that the average examination
for life insurance is not made with the care which is bestowed upon a
patient. Yet I see no reason why the same attention to detail should
not be given in one as in the other. The examination of the great
majority of applicants can he made in a short time, as there is no
question of latent chronic disease. When the exception turns up he
should be given a searching examination and a full report should be sent
to the Medical Director. Only in this way will it be possible to weed
out the undesirable risks.

On the surface it does not seem to require any great diagnostic acumen
to be a life insurance examiner. In the old days of many of the
companies there were no examiners. The applicant was brought before the
president or other appointed official and he was passed or rejected on
his general appearance. This has changed, and now the medical department
with its scores of examiners in the field is a well organized
department.

It seems to me that the examiner should be an exceedingly able
diagnostician and prognosticator. There is no telling when he may be
called upon to pass judgment on a borderline case. From personal
experience I know how difficult it is to make a decision in some cases.
These suspicious cases after a careful examination had better be passed
by the examiner and a supplementary report sent to the medical director
containing unbiased details. But no applicant with readily palpable
arteries, even though the blood pressure be normal, should be considered
a first class insurance risk.

The question of the value of the diastolic pressure reading in
examinations for life insurance is not yet settled to the satisfaction
of all medical directors. Certain medical directors with clinical
experience behind them, lay great stress on the increased diastolic
pressure and consider a persistent diastolic of 100 mm. really more
significant as an indication of hypertension than a systolic pressure of
160 mm. Other directors pay little or no attention to the diastolic
reading. Should an applicant show a systolic above the average normal on
several successive readings, he is declined. When one takes into
consideration the psychic effect of knowing that he is being examined
for high blood pressure, it seems unfair to refuse insurance on such
grounds as is constantly done.

Up to the present there are no extensive series of life-expectancy
tables in which hundreds of thousands of cases are analyzed from the
diastolic pressure values. There are many such tables for the systolic
pressures alone. In the tabulation of such statistics one must not lose
sight of the important fact that the figures are taken by thousands of
men of varying capacity and different degrees of intelligence. Such
studies to be of any real value must be taken from records made at the
home offices by capable men. We shall await these tables with interest.
In the meantime we must be permitted to have the impression that the
diastolic pressure has been much neglected. This has no doubt been due
to the difficulty of measuring it with any degree of accuracy. Now with
the auscultatory method and the correct place to read the diastolic
pressure the results of blood pressure estimations should begin to have
some value for statistical data.

Clinically the diastolic is probably more important than the systolic.
Until proof is brought to the contrary we shall believe that in life
insurance examinations it has the same importance.

CHAPTER XV

PRACTICAL SUGGESTIONS

The time spent in obtaining a careful history of a case is time well
spent. Often the diagnosis can be made from the history alone, the
physical examination merely adding confirmation to the data already
obtained.

The younger the patient who has arteriosclerosis, the more probable is
it that syphilis is the etiologic factor. A denial of infection should
have little weight if the history of possible exposure is present.
Miscarriages in a woman should arouse the suspicion of lues in her
husband. The complement-fixation reaction will often clear up an
apparently obscure diagnosis.

There are various ways of examining a patient but there is only one
right way; the examination should be made on the bare skin. However
skillful one may be in the art of physical diagnosis, he can gather few
accurate data by examining over the clothes even if he use a
phonendoscope.

The immoderate eater is laying up for himself a wealth of trouble at the
time when he can least afford to bear it. The ounce of advice in time is
worth more to him than the pounds of medicine later.

It is a wise maxim never to drive a horse too far. Apply that to the
human being and the rule holds equally well.

There may be no symptoms in a case of advanced arteriosclerosis. Do not
on that account neglect to advise a patient in whom the disease is
accidentally discovered.

Many a man owes a debt of gratitude to the life insurance examiner. He
rarely feels grateful.

When a competent ophthalmologist refers a case to a general practitioner
with the statement that he believes from the appearance of the fundus of
the eye that arteriosclerotic changes are present over the body, the
case should be most carefully examined. The earliest diagnoses are not
infrequently made by the ophthalmologist.

It is the part of wisdom never to have such a firmly preconceived idea
of the diagnosis that facts observed are perverted in order to fit into
the diagnosis. Let the facts speak for themselves.

Beware of the snap diagnosis. Even in a case of well-marked
arteriosclerosis when the diagnosis seems to be written in large letters
all over the patient, go through the routine. Nine times out of ten this
may seem needless. The tenth time it saves your conscience and
reputation. Always consider that you are examining a tenth case.

Gradual loss of weight in a person over fifty years old should arouse
the suspicion of arteriosclerosis.

Do not call the nervous symptoms displayed by a middle-aged man or woman
neurasthenia until you have ruled out all organic causes, particularly
arteriosclerosis.

When palpating the radial artery, always use both hands according to the
method already described. Pay attention to the superficial or deep
situation of the artery.

The examination of one specimen of urine does not give much information,
especially if it should be found to contain no abnormal elements. Fairly
accurate data may be gathered from the mixed night and morning urine;
most accurate data from the twenty-four hour specimen. To be of any real
value there should be frequent examinations of the day's excretion.

In measuring the day's output a good rule is as follows: begin to
collect urine after the first morning's micturition and collect all
including the first quantity passed the next morning. It is best to
examine the centrifugated urine for casts even though no albumin be
present. It is useless to look for casts in an alkaline urine.

Casts are not infrequently found in chemically normal urine from a
middle-aged patient. Other things being normal, the finding has no
significance. The kidneys must be carefully tested functionally.

Blood pressure readings should always be taken with the patient in the
same posture at every estimation. At the first examination it is
advisable to take readings from both brachial arteries. Let the patient
sit comfortably and relax all muscles.

Differentiate as soon as possible between the uncompensated heart caused
by valvular disease and that caused by arteriosclerosis. There is a
difference in prognosis. Both give the same symptoms, and are treated
similarly until compensation returns; thereafter the management of the
two forms is different.

Aortic incompetence that comes on late in life is generally the result
of curling of the free margins of the valves caused by syphilitic
arteriosclerosis. Prognosis is grave because of the fact that the heart
muscle also is the seat of degenerative changes and compensatory
hypertrophy is established with difficulty.

When laying down a regime for a patient, consider his disposition, and
individualize the treatment. Remember that exercise is an essential
feature of the hygiene of the patient's life but do not forget to be
explicit about the amount and character of the permissible exercise.

In the prophylaxis of arteriosclerosis, a rational mode of living is the
all-important factor. As a rule, the less meat one eats, the less is the
liability of arterial degeneration as age advances. The exceptions to
this rule are many, and probably depend upon the character of the "vital
rubber" with which the individual begins life.

The diet in well-marked cases of arteriosclerosis should be carefully
selected with regard to its nutritive and non-irritating character.
Animal proteins should be sparingly used. Milk should have an important
place in the dietary.

No drug relieves the pain of uncomplicated aneurysm as surely as iodide
of potassium.

Iodides frequently upset the stomach. Be cautious in the use of them.
The irritable stomach may turn the scales against your patient.

Use cardiac stimulants with care and judgment. If all the valuable
ammunition is used up at first, the fight will be lost.

Use digitalis with especial care. Its chief usefulness is in steadying
the decompensated heart, improving the conduction of impulses, and
increasing the tone of the cardiac muscle. _It should never be given to
patients with very slow pulses, the subjects of Stokes-Adams syndrome._
Digitalis has been found to produce partial to complete heart block when
therapeutically administered.

Remember that in the uncompensated heart morphine not only eases the
oppressive dyspnea, but also steadies and stimulates the heart.

See to it that the patient has a daily movement of the bowels. In the
early stage try the effect of liquid paraffin or of the mineral waters
such as Pluto, or Hunyadi Janos, or artificial Carlsbad salts (Sprudel
salts). These last can be made as follows: Sodium chloride, ounce I;
sodium bicarbonate, ounce II; sodium sulphate, ounce IV. Take two
tablespoonsful of this in a glass of hot water before breakfast. Should
these not succeed, assist the action of the drugs by the use of enemata.
The pill of aloin, strychnine sulphate, and extract of cascara, with the
addition of a small quantity of hyoscyamus, is a mild tonic purgative.
In cases of constipation with high tension, there is no drug as valuable
as calomel or one of the other mercurials given occasionally.

Never give Epsom salts unless copious watery stools are desired to
deplete effusion into the serous cavities or into the subcutaneous
tissue.

Chronic constipation increases the gravity of the prognosis.

In case of suppression of urine and anasarca, hot air packs may be of
value. The patient may be wrapped in a hot wet sheet and covered with
blankets. I do not believe in administering pilocarpine to assist the
sweating.

Remember to treat the patient and not the disease. The careful hygienic
and dietetic treatment, combined with the least amount of drugging, is
the best and most rational method of treatment.

INDEX

Abdominal symptoms, 201

Aconite in treatment, 242

Acquired arteriosclerosis, 159

Adami, effect of syphilis in aorta, 45

Adventitia, 28

Age in arteriosclerosis, 161

Albuminuria, 221

Albutt's classification of arteriosclerosis, 186

Alcohol, 166, 228, 235

Anatomy, 25

Angina abdominalis, 201, 216
pectoris, 197, 216
pseudo, 216

Angiosclerosis, 26, 64

Aorta, 27
anatomical lesions in, 33
Aschoff on, 35
normal, 41
syphilis in, 44
thoracic, 29
thoracic and abdominal, arteriosclerosis of, 39
velocity of blood in, 66

Aortic incompetence, 61, 258
stenosis, 60

Aortitis, acute, 165

Arcus senilis, 191

Arrhythmia, tonal, 92, 102

Arterial pressure, 85
symptoms, 189

Arteries, 29
examination of, 172, 177
general structure of, 27
large, 30
adventitia of, 30
palpable, 189
pulmonary, arteriosclerosis of, 63

Arteriocapillary fibrosis, 26

Arteriosclerotic endocarditis, 60, 219

Artery, coronary, cross-section of, 36
pulmonary, 209
radial, 29

Aschoff on aorta, 35

Atheroma, simple, 32

Atheromatous abscess, 38

Auricular fibrillation, 133
flutter, 131

Auscultation, 176

Auscultatory blood pressure phenomenon, 90
method of taking blood pressure, 83
percussion, 175

Balneotherapy, 233

Basch's blood pressure instrument, 70

Blood, circulation of, 65
velocity of, 65
in animals, 66
in aorta, 66
in capillaries, 66
viscosity of, 68

Blood pressure, 68
auscultatory method of taking, 83
clinical applications of, 147
diurnal variations of, 102
drugs influencing, 120
estimation of, 179
in cancer, 118
in collapse, 118
in exercise, 105
in head injuries, 148
in hemorrhages, 105, 118, 148
in infectious diseases, 153
in kidney diseases, 155
in meningitis, 118
in obstetrics, 152
in pulmonary tuberculosis, 119
in shock, 105, 148
in surgery, 147
in typhoid fever, 118, 154
in valvular heart disease, 155
increase of, 55
instruments, 70
Brown's, 74
Cook's, 71
Erlanger's, 72
Faught's, 75, 80
Hill and Barnard's, 70
Hirschfelder's, 73
K. Vierordt's, 70
Marcy's, 70
Potain's, 70
Riva Rocci's, 70
Roger's, 77
Sanborn's, 80
Stanton's, 72
technique of, 80
"Tycos," 77
v. Basch's, 70
v. Recklinghausen's, 76
mechanism of, 55
normal variations of, 88
phenomenon, auscultatory, 90
precautions when estimating, 181
value of, 181

Bowman's capsules, sclerosis of, 62

Brain, changes in, 62

Brown atrophy, 60, 118, 201

Calcification of media, 43, 59

Cancer, blood pressure in, 118

Capillaries, anatomy of, 27, 31

Capillary pulse, 67

Cardiac dullness, 172
irregularities in arteriosclerosis, 131
symptoms, 195

Cerebral symptoms, 203

Circulation of blood, 65
physiology of, 65

Cirrhosis of liver, 64, 216

Classification of arteriosclerosis, 32, 37
Allbutt's, 186

Collapse, blood pressure in, 118

Congenital arteriosclerosis, 157

Cook's blood pressure instrument, 71

Cor bovinum, 116

Coronary artery, cross section of, 36

Corpus luteum, 241

Definition of arteriosclerosis, 26

Diabetes mellitus, 216

Diagnosis, 210
differential, 215
early, 210
ophthalmic examination in, 214

Diastolic pressure, 69, 83, 85, 94
importance of, 97

Dicrotic pulse, 123

Dietetic treatment, 235

Differential diagnosis, 166, 215

Diffuse arteriosclerosis, 32, 37, 38, 57

Digitalis in treatment, 246, 259

Diuretin in treatment, 246

Drug intoxications, 166

Drugs influencing blood pressure, 105, 120

Ductless glands, 171

Dullness, cardiac, 172

Dyspeptic symptoms, 184

Dyspnea, 184
treatment of, 248

Electrocardiogram, 126

Embolism, 59

Endarteritis deformans, 47
obliterans, 46

Endocarditis, arteriosclerotic, 60, 219

Endothelial lining, 27
tubes, 31

Epistaxis, 184, 221

Erlanger's blood pressure instrument, 72

Erythromelalgia, 192, 208

Estimation of blood pressure, 179

Etiology, 157

Examination of arteries, 172, 177
of heart, 172
of urine, 257

Exercise, blood pressure in, 105
in prophylaxis, 225
in treatment, 230

Experimental arteriosclerosis, 50

Extrasystole, 138

Faught's blood pressure instrument, 75, 80

Fibrillation, auricular, 133
ventricular, 138

Fibrolysin in treatment, 243

Fingernail palpation, 178

Finger tip palpation, 179

Flutter, auricular, 131

Food poisons in arteriosclerosis, 163

Gibson's law, 154

"H" wave, 126

Habits, personal, 234

Head injuries, blood pressure in, 148

Headache, 184
treatment of, 248

Heart block, 140
boundaries, 172
examination of, 172
hypertrophy of, 60
physical examination of, 172
stimulants, 243, 246, 259
symptoms, 188

Hemorrhages, blood pressure in, 118

Henle, membrane of, 29

Hill and Barnard's blood pressure instrument, 70

Hirschfelder's blood pressure instrument, 73

His, bundle of, 141, 197

Hygienic treatment, 230

Hyperpietic arteriosclerosis, 186

Hypertension, 60, 106, 169, 185, 249
cause of arteriosclerosis, 159
classification of cases, 112

Hypertrophy of left ventricle, 58

Hypotension, 117

Incompetence, aortic, 61, 258

Indicanuria, 167

Infants, arteriosclerosis in, 158

Infectious diseases in arteriosclerosis, 163
blood pressure in, 153

Insomnia, treatment of, 248

Intermittent claudication, 192, 208
treatment of, 247

Intoxications, chronic drug, 166

Intracranial tension, 105

Involutionary arteriosclerosis, 187

Iodides in treatment, 238, 247, 259

Kidney diseases, blood pressure in, 155

Kidneys, sclerosis of, 61, 170

Life insurance, relation to, 249

Light percussion, 174
touch palpation, 175

Liver, cirrhosis, 64, 216

Local symptoms, 207

Marey's blood pressure instrument, 70

Maximum pressure, 85, 94

Mean pressure, 85

Media, calcification of, 43, 59

Medicinal treatment, 238

Meningitis, blood pressure in, 118

Mental strain, 168

Mesaortitis, 45, 47, 49, 165

Mesentery, cross-section of small artery in, 56

Milk diet, 237

Minimum pressure, 86, 94

Moenckeberg type of arteriosclerosis, 43

Morphine in treatment, 243

Mosenthal test meal, 221

Muscular overwork, 169

Nervous symptoms, 191

Nitrites in treatment, 240

Nitroglycerin in treatment, 241

Nodular arteriosclerosis, 32, 37

Normal blood pressure variation, 88

Obstetrics, blood pressure in, 152

Occupation in arteriosclerosis, 162

Ocular symptoms, 190

Ophthalmic examination, importance in early diagnosis, 214, 256

Orthodiagraph, 173

Overeating, 167, 212, 225, 235

Overwork, muscular, 169

"P" wave, 129

"P-R" interval, 130

Palpable arteries, 189

Palpation, 174, 180
fingernail, 178
finger tip, 179
light touch, 175

Pathology, 32

Percussion, 174
auscultatory, 175
light, 174

Peripheral symptoms, 207

Personal habits, 234

Phlebosclerosis, 64

Phthalein test, 221

Physical signs, 183

Physiology of the circulation, 65

Potain's blood pressure instrument, 70

Practical suggestions, 256

Pressure, arterial, 85
ausculatory method of determining, 83
diastolic, 83, 94
estimation of, 179
in surgery, 147
maximum, 85, 94
normal variations, 88
pulse, 83, 85, 87, 100
systolic, 82, 85
technique, 80
venous, 120

Prognosis, 218

Prophylaxis, 224
exercise in, 225

Pseudo angina pectoris, 216

Pulmonary artery, 209
arteriosclerosis of, 63
tuberculosis, blood pressure in, 119

Pulse, 123
capillary, 67
deficit, 135
dicrotic, 123
in arteriosclerosis, 123
pressure, 69, 83, 85, 87, 100
rate, 69
venous, 123

Purgatives in treatment, 244, 259

Pyrosis, 184

"Q R S" complex, 129

Rabbits, lesions produced experimentally in, 50

Race in arteriosclerosis, 161

Radial artery, 29

Radials, sclerosis of, 43

Raynaud's disease, 192, 207

Recklinghausen's blood pressure instrument, 76

Renal disease, 169
symptoms, 199

Rest in treatment, 242

Riva-Rocci's blood pressure instrument, 70

Rogers' blood pressure instrument, 77

Sanborn's blood pressure instrument, 80

Scaphoid scapula, 158

Schwellungsperkussion, 174

Sclerosis of veins, 64

Senile arteriosclerosis, 32, 37, 43, 59

Sex in arteriosclerosis, 161

Shock, blood pressure in, 105, 148

Spinal symptoms, 205

Spirochaeta pallida, 45

Stanton's blood pressure instrument, 72

Stenosis, aortic, 60

Stokes-Adams syndrome, 197

Stomach, ulcer of, 216

Strain hypertrophy, 47, 54, 55

Surgery, blood pressure in, 147

Symptomatic treatment, 245

Symptoms, 183
abdominal, 201
arterial, 189
cardiac, 195
cerebral, 203
dyspeptic, 184
dyspnea, 184
general, 183
headache, 184
heart, 188
local, 207
nervous, 191
ocular, 190
peripheral, 207
pyrosis, 184
renal, 199
special, 194
spinal, 205
vertigo, 184
visceral, 201

Syphilis, 165
in aorta, 44

Syphilitic arteriosclerosis, 37

Systolic pressure, 69, 82, 85, 94
importance of, 97

"T" wave, 130

Technique of blood pressure instruments, 80

Thayer and Fabyan, 34

Theocin, 247

Thoma on arteriosclerosis, 33

Thoracic aorta, 29

Thyroid extract in treatment, 239

Tobacco, 167, 212, 234

Tonal arrhythmia, 92, 102

Toxic arteriosclerosis, 186

Treatment, 229
aconite in, 242
balneotherapy in, 233
corpus luteum, 241
dietetic, 235
digitalis in, 246, 259
diuretin in, 246
exercise in, 230
fibrolysin in, 243
heart stimulants in, 243
hygienic, 230
iodides in, 238, 247, 259
medicinal, 238
morphine in, 243
nitrites in, 240
nitroglycerin in, 241
of dyspnea, 248
of headache, 248
of insomnia, 248
of intermittent claudication, 247
personal habits in, 234
purgatives in, 244, 259
rest in, 242
symptomatic, 245
theocin in, 247
thyroid extract in, 239
Trunecek's serum in, 243
venesection in, 242
veratrum viride in, 242

Trunecek's serum in treatment, 243

Tuberculosis, blood pressure in, 119

Tunica intima, 28
media, 28

"Tycos" blood pressure instrument, 77

Typhoid fever as cause of arteriosclerosis, 164
blood pressure in, 118

Ulcer of stomach, 216

Urine, examination of, 257
suppression of, 259

Valvular heart disease, blood pressure in, 155

Vasa vasorum, 29

Veins, anatomy of, 30
sclerosis of, 64

Velocity of blood in animals, 66
of blood in aorta, 66

Venesection in treatment, 242

Venous pressure, 120
pulse, 123

Ventricle, left, hypertrophy of, 58

Ventricular fibrillation, 138

Veratrum viride in treatment, 242

Vertigo, 184

* * * * *

Transcriber's Notes: Irregular hyphenation has been preserved, as in
blood pressure and blood-pressure. Both "Hg" and "Hg." appear.

Minor typographical errors and inconsistencies have been silently
normalized.

The original printed list of illustrations shows the original
locations; they have been moved closer to their discussion area
in the text to not interrupt the flow of reading.

Page 244 Prescription symbol is replaced with R_{x}

Page 259 Apothecaries ounce symbol replaced with "ounce"

*** End of this LibraryBlog Digital Book "Arteriosclerosis and Hypertension: - with Chapters on Blood Pressure, 3rd Edition." ***

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