Arteriosclerosis and Hypertension, with Chapters on Blood Pressure
by Louis M. Warfield · English · Gutenberg #37675 · 445,522 chars · public domain (US)
The Project Gutenberg eBook of Arteriosclerosis and Hypertension, with Chapters on Blood Pressure
This eBook is for the use of anyone anywhere in the United States and
most other parts of the world at no cost and with almost no restrictions
whatsoever. You may copy it, give it away or re-use it under the terms
of the Project Gutenberg License included with this eBook or online
at www.gutenberg.org. If you are not located in the United States,
you will have to check the laws of the country where you are located
before using this eBook.
Title: Arteriosclerosis and Hypertension, with Chapters on Blood Pressure
Author: Louis M. Warfield
Release date: October 9, 2011 [eBook #37675]
Language: English
Other information and formats: www.gutenberg.org/ebooks/37675
Credits: Produced by Bryan Ness, Julia Neufeld and the Online
Distributed Proofreading Team at http://www.pgdp.net (This
file was produced from images generously made available
by The Internet Archive/American Libraries.)
*** START OF THE PROJECT GUTENBERG EBOOK ARTERIOSCLEROSIS AND HYPERTENSION, WITH CHAPTERS ON BLOOD PRESSURE ***
Produced by Bryan Ness, Julia Neufeld and the Online
Distributed Proofreading Team at http://www.pgdp.net (This
file was produced from images generously made available
by The Internet Archive/American Libraries.)
Transcriber's Notes: Passages in italics are indicated by _underscores_.
Passages in bold are surrounded by =.
Small caps have been replaced by ALL CAPS.
ERRATUM
Page 75, Figure shown is not the Brown sphygmomanometer described in the
text, but the Baumanometer manufactured by W. A. Baum Co., Inc., New
York. It is claimed that the Baumanometer is made with particular care
and hence the readings are said to be more accurate than other mercury
instruments. It is apparently a good instrument. The author has had no
personal experience with it.
ARTERIOSCLEROSIS
AND
HYPERTENSION
With Chapters on Blood Pressure
BY
LOUIS M. WARFIELD, A.B., M.D., (Johns Hopkins),
F.A.C.P.
FORMERLY PROFESSOR OF CLINICAL MEDICINE, MARQUETTE UNIVERSITY MEDICAL
SCHOOL; CHIEF PHYSICIAN TO MILWAUKEE COUNTY HOSPITAL; ASSOCIATE
MEMBER ASSOCIATION AMERICAN PHYSICIANS; MEMBER AMERICAN
ASSOCIATION PATHOLOGISTS AND BACTERIOLOGISTS;
AMERICAN MEDICAL ASSOCIATION, ETC., FELLOW
AMERICAN COLLEGE OF PHYSICIANS
_THIRD EDITION_
ST. LOUIS
C. V. MOSBY COMPANY
1920
COPYRIGHT, 1912, 1920, BY C. V. MOSBY COMPANY
_Press of
C. V. Mosby Company
St. Louis_
TO
MY MOTHER
THIS VOLUME IS AFFECTIONATELY
DEDICATED
PREFACE TO THIRD EDITION
Several years have elapsed since the appearance of the second edition of
this book. During this time there has been considerable experimentation
and much writing on arteriosclerosis. The total of all work has not been
to add very much to our knowledge of the etiology of arterial
degeneration. Points of view and opinions change from time to time. It
is so with arteriosclerosis. In this edition arteriosclerosis is not
regarded as a disease with a definite etiologic factor. Rather it is
looked upon as a degenerative process affecting the arteries following a
variety of causes more or less ill defined. It is not considered a true
disease. Possibly syphilitic arteritis may be viewed as an entity, the
cause is known and the lesions are characteristic.
Much new material and many new figures have been added to this edition.
Some rearranging has been done. The chapter on Blood Pressure has been
much expanded and some original observations have been included. The
literature has been selected rather than indiscriminately quoted. Much
that is written on the subject is of little value.
It has always seemed to the author that there is not enough of the
personal element in medical writings. At the risk of being severely
criticized, he has attempted to make this book represent largely his own
ideas, only here and there quoting from the literature.
New chapters on Cardiac Irregularities Associated with Arteriosclerosis,
and Blood Pressure in Its Clinical Application have been added.
The fact that the book has passed through two editions is very
gratifying and seems to show that it has met with favor. The author
takes this opportunity of thanking those who have loaned him
illustrations. Wherever figures are borrowed due credit is given.
It is hoped that the kind of reception accorded to the first and second
editions will also not be withheld from this present edition.
LOUIS M. WARFIELD.
Milwaukee, Wisc.
PREFACE TO THE SECOND EDITION
In this second edition so many changes and additions have been made that
the book is practically a new one. All the chapters which were in the
previous edition have been carefully revised. Two chapters, "Pathology"
and "Physiology," have been completely rewritten and brought up to date.
It was thought best to add some references for those who had interest
enough to pursue the subject further. These references have been
selected on account of the readiness with which they may be procured in
any library, public or private. Two new chapters have been added--one on
"The Physical Examination of the Heart and Arteries," the other on
"Arteriosclerosis in Its Relation to Life Insurance," and it is hoped
that these will add to the practical value of the book.
Arteriosclerosis can scarcely be considered apart from blood pressure,
and in the view expressed within, with which some may not concur, high
tension is considered to be a large factor in the production of
arteriosclerosis. As the data on blood pressure have increased, the
importance of it has become more evident. The chapter on "Blood
Pressure" has been wholly rewritten, expanded so as to give a
comprehensive grasp of the essential features, and several illustrations
have been added in order to elucidate the text more fully. The chief
objects in view were to make clear to the physician the technique and
the necessity for estimating both systolic and diastolic pressures.
The author is grateful for the kindly reception accorded the first
edition. No one is more keenly aware of the imperfections than he. The
necessity for a second edition is taken to mean that the book has found
a place for itself and has been of use to some.
The author hopes that this new edition will fulfill adequately the
purpose for which he prepared the book--namely, as a practical guide to
the knowledge and appreciation of a most important and exceedingly
common disease.
LOUIS M. WARFIELD.
Milwaukee, May, 1912.
PREFACE TO THE FIRST EDITION
It is hoped that this small volume may fill a want in the already
crowded field of medical monographs. The author has endeavored to give
to the general practitioner a readable, authoritative essay on a disease
which is especially an outcome of modern civilization. To that end all
the available literature has been freely consulted, and the newest
results of experimental research and the recent ideas of leading
clinicians have been summarized. The author has supplemented these with
results from his own experience, but has thought it best not to burden
the contents with case histories.
The stress and strain of our daily life has, as one of its consequences,
early arterial degeneration. There can be no doubt that arterial disease
in the comparatively young is more frequent than it was twenty-five
years ago, and that the mortality from diseases directly dependent on
arteriosclerotic changes is increasing. Fortunately, the almost
universal habit of getting out of doors whenever possible, and the
revival of interest in athletics for persons of all ages, have to some
extent counteracted the tendency to early decay. Nevertheless, the
actual average prolongation of life is more probably due to the very
great reduction in infant mortality and in deaths from infectious and
communicable diseases.
The wear and tear on the human organism in our modern way of living is
excessive. Hard work, worry, and high living all predispose to
degenerative changes in the arteries, and so bring on premature old age.
The author has tried to emphasize this by laying stress on the
prevention of arteriosclerosis rather than on the treatment of the fully
developed disease.
No bibliography is given, as this is not intended as a reference book,
but rather as a guide to a better appreciation and understanding of a
most important subject. It has been difficult to keep from wandering off
into full discussions of conditions incident to and accompanied by
arteriosclerosis, but, in order to be clear in his statements and
complete in his descriptions, the author has to invade the fields of
heart disease, kidney disease, brain disease, etc. It is hoped, however,
that these excursions will serve to show how intimately disease of the
arteries is bound up with diseases of all the organs and tissues of the
body.
Some authors have been named when their opinions have been given. Thanks
are extended also to many others to whom the writer is indebted, but of
whom no individual mention has been made.
The author also takes this opportunity of expressing his appreciation of
the kindness of Dr. D. L. Harris, who took the microphotographs, and to
the publishers for their unfailing courtesy and consideration.
LOUIS M. WARFIELD.
St. Louis, August, 1908.
CONTENTS
PAGE
CHAPTER I
ANATOMY 25
Introduction, 25; Definition, 26; General Structure of
the Arteries, 27; Arteries, 29; Veins, 30; Capillaries, 31.
CHAPTER II
PATHOLOGY 32
Syphilitic Aortitis, 44; Experimental Arteriosclerosis, 50;
Arteriosclerosis of the Pulmonary Arteries, 63; Sclerosis
of the Veins, 64.
CHAPTER III
PHYSIOLOGY OF THE CIRCULATION 65
Blood Pressure, 68; Blood Pressure Instruments, 70; Technic,
80; Arterial Pressure, 85; Normal Pressure Variations, 88;
The Auscultatory Blood Pressure Phenomenon, 90; The Maximum
and Minimum Pressures, 94; Relative Importance of the
Systolic and Diastolic Pressures, 97; Pulse Pressure, 100;
Blood Pressure Variations, 102; Hypertension, 106;
Hypotension, 117; The Pulse, 123; The Venous Pulse, 123;
The Electrocardiogram, 126.
CHAPTER IV
IMPORTANT CARDIAC IRREGULARITIES ASSOCIATED WITH
ARTERIOSCLEROSIS 131
Auricular Flutter, 131; Auricular Fibrillation, 133;
Ventricular Fibrillation, 138; Extrasystole, 138;
Heart Block, 140.
CHAPTER V
BLOOD PRESSURE IN ITS CLINICAL APPLICATIONS 147
Blood Pressure in Surgery, 147; Head Injuries, 148; Shock
and Hemorrhage, 148; Blood Pressure in Obstetrics, 152;
Infectious Diseases, 153; Valvular Heart Disease, 155;
Kidney Disease, 155; Other Diseases, Liver, Spleen,
Abdomen, etc., 156.
CHAPTER VI
ETIOLOGY 157
Congenital Form, 157; Acquired Form, 159; Hypertension,
159; Age, Sex, Race, 161; Occupation, 162; Food Poisons,
163; Infectious Diseases, 163; Syphilis, 165; Chronic
Drug Intoxications, 166; Overeating, 167; Mental Strain,
168; Muscular Overwork, 169; Renal Disease, 169; Ductless
Glands, 171.
CHAPTER VII
THE PHYSICAL EXAMINATION OF THE HEART AND ARTERIES 172
Heart Boundaries, 172; Percussion, 174; Auscultation,
176; The Examination of the Arteries, 177; Estimation
of Blood Pressure, 179; Palpation, 180; Precautions When
Estimating Blood Pressure, 181; The Value of Blood
Pressure, 181.
CHAPTER VIII
SYMPTOMS AND PHYSICAL SIGNS 183
General, 183; Hypertension, 185; The Heart, 188; Palpable
Arteries, 189; Ocular Signs and Symptoms, 190; Nervous
Symptoms, 191.
CHAPTER IX
SYMPTOMS AND PHYSICAL SIGNS 194
Special, 194; Cardiac, 195; Renal, 199; Abdominal or
Visceral, 201; Cerebral, 203; Spinal, 205; Local or
Peripheral, 207; Pulmonary Artery, 209.
CHAPTER X
DIAGNOSIS 210
Early Diagnosis, 210; Differential Diagnosis, 215;
Diseases in Which Arteriosclerosis is Commonly Found, 216.
CHAPTER XI
PROGNOSIS 218
CHAPTER XII
PROPHYLAXIS 224
CHAPTER XIII
TREATMENT 229
Hygienic Treatment, 230; Balneotherapy, 233; Personal
Habits, 234; Dietetic Treatment, 235; Medicinal, 238;
Symptomatic Treatment, 245.
CHAPTER XIV
ARTERIOSCLEROSIS IN ITS RELATION TO LIFE INSURANCE 249
CHAPTER XV
PRACTICAL SUGGESTIONS 256
ILLUSTRATIONS
FIG. PAGE
1. Cross section of a large artery 28
2. Cross section of a coronary artery 36
3. Arteriosclerosis of the thoracic and abdominal aorta 39
4. Arteriosclerosis of the arch of the aorta 40
5. Normal aorta 41
6. Radiogram showing calcification of both radial and ulnar
arteries 42
7. Syphilitic aortitis of long standing 44
8. Diagrammatic representation of strain hypertrophy 48
9. Strain hypertrophy 49
10. Cross section of small artery in the mesentery 56
11. Enormous hypertrophy of left ventricle 58
12. Aortic incompetence with hypertrophy and dilatation of
left ventricle 61
13. Cook's modification of Riva-Rocci's blood pressure
instrument 72
14. Stanton's sphygmomanometer 73
15. The Erlanger sphygmomanometer with the Hirschfelder
attachments 74
16. Desk model Baumanometer 75
17. Faught blood pressure instrument 76
18. Rogers' "Tycos" dial sphygmomanometer 77
19. Detail of the dial in the "Tycos" instrument 78
20. Faught dial instrument 79
21. Detail of the dial of the Faught instrument 79
22. The Sanborn instrument 80
23. Method of taking blood pressure with a patient in sitting
position 81
24. Method of taking blood pressure with patient lying down 82
25. Observation by the auscultatory method and a mercury
instrument 84
26. Observation by the auscultatory method and a dial instrument 85
27. Schema to illustrate decrease in pressure 86
28. Chart showing the normal limits of variation in systolic
blood pressure 89
29. Tracing of auscultatory phenomena 94
30. Tracing of auscultatory phenomena 95
31. Clinical determination of diastolic pressure, fast drum 96
32. Clinical determination of diastolic pressure, slow drum 96
33. Venous blood pressure instrument 121
34. New venous pressure instrument 122
35. Events in the cardiac cycle 124
36. Simultaneous tracings of the jugular and carotid pulses 125
37. Jugular and carotid tracings 125
38. Right side of the heart showing distribution of the
two vagus nerves 127
39. Normal electrocardiogram 128
40. Auricular flutter 132
41. Auricular fibrillation 134
42. Auricular fibrillation 134
43. Pulse deficit 135
44. Ventricular fibrillation 137
45. Auricular extrasystoles 139
46. Ventricular extrasystole 139
47. Delayed conduction 141
48. Partial heart block 141
49. Complete heart block 142
50. Alternating periods of sinus rhythm and
auriculoventricular rhythm 144
51. Auriculoventricular or "nodal" rhythm 144
52. Influence of mechanical pressure on the right vagus nerve 144
53. Schematic distribution of right and left vagus 145
54. Blood pressure record from a normal reaction to ether 149
55. Chart showing the method of recording blood pressure
during an operation 150
56. Method of using blood pressure instrument during operation 151
57. Finger-tip palpation of the radial artery 178
58. Finger-tip palpation of the radial artery 178
59. Aneurysm of the heart wall 196
60. Large aneurysm of the aorta eroding the sternum 198
ARTERIOSCLEROSIS AND HYPERTENSION
CHAPTER I
ANATOMY
With the increased complexity of our modern life comes increased wear
and tear on the human organism. "A man is as old as his arteries" is an
old dictum, and, like many proverbs, the application to mankind today
is, if anything, more pertinent than it was when the saying was first
uttered. Notwithstanding the fact that the average age of mankind at
death has been materially lengthened--the increase in years amounting to
fourteen in the past one hundred years of history--clinicians and
pathologists are agreed that the arterial degeneration known as
arteriosclerosis is present to an alarming extent in persons over forty
years of age. Figures in all vital statistics have shown us that all
affections of the circulatory and renal systems are definitely on the
increase. "Arterial diseases of various kinds, atheroma, aneurysm, etc.,
caused 15,685 deaths in 1915, or 23.3 per 100,000. This rate, although
somewhat lower than the corresponding ones for 1912 and 1913, is higher
than that for 1914, and is very much higher than that for 1900, which
was 6.1."
The great group of cases of which cardiac incompetence, aneurysm,
cerebral apoplexy, chronic nephritis, emphysema, and chronic bronchitis
are the most frequent and important appear as terminal events in which
arteriosclerosis has probably played an important part.
Thus, in the sense in which we speak of tuberculosis or pneumonia as a
distinct disease, we can not so designate the diseased condition of the
arteries.
Arteriosclerosis is not a disease =sui generis=. It is best viewed as a
degeneration of the coats of the arteries, both large and small
resulting in several different more or less distinct types.
These types blend one into the other and in the same patient all types
may be found. Thus the sclerosis of the arteries is the result of a
variety of causes, none of which is definitely known in the sense of a
bacterial disease. As we shall see later, one type of arteriosclerosis
has a special pathology and etiology, the syphilitic arterial changes.
Bearing in mind that arteriosclerosis (called by some "arteriocapillary
fibrosis," by others "atherosclerosis") is not a true disease, it may,
for convenience be defined as a chronic disease of the arteries and
arterioles, characterized anatomically by increase or decrease of the
thickness of the walls of the blood vessels, the initial lesion being a
weakening of the middle layer caused by various toxic or mechanical
agencies. This weakness of the media leads to secondary effects, which
include hypertrophy or atrophy of the inner layer--and not infrequently
hypertrophy of the outer layer--connective tissue formation and
calcification in the vessels, and the formation of minute aneurysms
along them. The term arteriocapillary fibrosis has a broader meaning,
but is a cumbersome phrase, and conveys the idea that the capillary
changes are an essential feature of the process, whereas these are for
the most part secondary to the changes in the arteries. The veins do not
always escape in the general morbid process, and when these are affected
the whole condition is sometimes called vascular sclerosis or
angiosclerosis.
Upon the anatomical structure of the arteries depends, as a rule, the
character and extent of the arteriosclerotic lesions. For the clear
comprehension of the process, it is necessary to keep in mind the
essential histological differences between the aorta and the larger and
smaller branches of the arterial tree.
The vascular system is often likened to a central pump, from which
emanates a closed system of tubes, beginning with one large
distributing pipe, which gives rise to a series of tubes, whose number
is constantly increasing at the same time that their caliber is
decreasing in size. From the smallest of these tubes, larger and larger
vessels collect the flowing blood, until, at the pump, two large trunks
of approximately the same area as the one large distributing trunk empty
the blood into the heart, thus completing the circle. This is but a
rough illustration, and, while possibly useful, takes into account none
of the vital forces which are constantly controlling every part of the
distributing system.
General Structure of the Arteries
The aorta and its branches are highly elastic tubes, having a smooth,
glistening inner surface. When the arteries are cut open, they present a
yellowish appearance, due to the large quantity of elastic tissue
contained in the walls. The elasticity is practically perfect, being
both longitudinal and transverse. The essential portion of any blood
vessel is the endothelial tube, composed of flat cells cemented together
by intercellular substance and having no stomata between the cells. This
tube is reinforced in different ways by connective tissue, smooth muscle
fibers, and fibroelastic tissue. Although the gradations from the larger
to the smaller arteries and from these to the capillaries and veins are
almost insensible, yet particular arteries present structural characters
sufficiently marked to admit of histological differentiation.
The whole vascular system, including the heart, has an endothelial
lining, which may constitute a distinct inner coat, the tunica intima,
or may be without coverings, as in the case of the capillaries. The
intima (Fig. 1) consists typically of endothelium, reinforced by a
variable amount of fibroelastic tissue, in which the elastic fibers
predominate. The tunica media is composed of intermingled bundles of
elastic tissue, smooth muscle fibers, and some fibrous tissue. The
adventitia or outer coat is exceedingly tough. It is usually thinner
than the media, and is composed of fibroelastic tissue. This division
into three coats is, however, somewhat arbitrary, as in the larger
arteries particularly it is difficult to discover any distinct
separation into layers.
[Illustration: Fig. 1.--Cross section of a large artery showing the
division into the three coats; intima, media, adventitia. The intima is
a thin line composed of endothelial cells. The wavy elastic lamina is
well seen. The thick middle coat is composed of muscle fibers and
fibroelastic tissue. The loose tissue on the outer (lower portion of
cut) side of the media is the adventitia. (Microphotograph, highly
magnified.)]
The muscular layer varies from single scattered cells, in the
arterioles, to bands of fibers making up the body of the vessel in the
medium-sized arteries and veins.
There is elastic tissue in all but the smallest arteries, and it is also
found in some veins. It varies in amount from a loose network to dense
membranes. In the intima of the larger arteries the elastic tissue
occurs as sheets, which under the microscope appear perforated and
pitted, the so-called fenestrated membrane of Henle.
The nutrient vessels of the arteries and veins, the vasa vasorum, are
present in all the vessels except those less than one millimeter in
diameter. The vasa vasorum course in the external coat and send
capillaries into the media, supplying the outer portion of the coat and
the externa with nutritive material. The nutrition of the intima and
inner portion of the media is obtained from the blood circulating
through the vessel. Lymphatics and nerves are also present in the middle
and outer layers of the vessels.
Arteries
The structure of the arteries varies notably, depending upon the size of
the vessel. A cross section of the thoracic aorta reveals a dense
network of elastic fibers, occupying practically all of the space
between the single layer of endothelial cells and the loose elastic and
connective tissue network of the outer layer. Smooth muscle fibers are
seen in the middle coat, but, in comparison with the mass of elastic
tissue, they appear to have only a limited function.
In a cross section of the radial artery one sees a wavy outline of
intima, caused by the endothelium following the corrugations of the
elastica. The endothelium is seen as a delicate line, in which a few
nuclei are visible. The media is comparatively thick, and is composed of
muscle cells, arranged in flat bundles, and plates of elastic tissue.
Between the media and the externa the elastic tissue is somewhat
condensed to form the external elastic membrane. The adventitia varies
much in thickness, being better developed in the medium-sized than in
the large arteries. It is composed of fibrous tissue mixed with elastic
fibers.
"Followed toward the capillaries, the coats of the artery gradually
diminish in thickness, the endothelium resting directly upon the
internal elastic membrane so long as the latter persists, and afterward
on the rapidly attenuating media. The elastica becomes progressively
reduced until it entirely disappears from the middle coat, which then
becomes a purely muscular tunic, and, before the capillary is reached,
is reduced to a single layer of muscle cells. In the precapillary
arterioles the muscle no longer forms a continuous layer, but is
represented by groups of fiber cells that partially wrap around the
vessel, and at last are replaced by isolated elements. After the
disappearance of the muscle cells the blood vessel has become a true
capillary. The adventitia shares in the general reduction, and gradually
diminishes in thickness until, in the smallest arteries, it consists of
only a few fibroelastic strands outside the muscle cells." (Piersol's
Anatomy.)
The large arteries differ from those of medium size mainly in the fact
that there is no sharp line of demarcation between the intima and the
media. There is also much more elastic tissue distributed in firm
bundles throughout the media, and there are fewer muscle fibers, giving
a more compact appearance to the artery as seen in cross section. The
predominance of elastic tissue permits of great distention by the blood
forced into the artery at every heartbeat, the caliber of the tube being
less markedly under the control of the vasomotor nerves than is the case
in the small arteries, where the muscle tissue is relatively more
developed. The adventitia of the large arteries is strong and firm, and
is made up of interlacing fibroelastic tissue, of which some of the
bundles are arranged longitudinally.
Veins
The walls of the veins are thinner than those of the arteries; they
contain much less elastic and muscular tissue, and are, therefore, more
flaccid and less contractile. Many veins, particularly those of the
extremities, are provided with cup-like valves opening toward the heart.
These valves, when closed, prevent the return of the blood to the
periphery and distribute the static pressure of the blood column. The
bulgings caused by the valves may be seen in the superficial veins of
the arm and leg. There are no valves in the veins of the neck, where
there is no necessity for such a protective mechanism, gravity sufficing
to drain the venous blood from the cranial cavity.
Capillaries
These are endothelial tubes in the substance of the organs, the tissue
of the organ giving them the necessary support. They are the final
subdivisions of the blood vessels, and the vast capillary area offers
the greatest amount of resistance to the blood flow, thus serving to
slow the blood stream and allowing time for nutritive substances or
waste products to pass from and to the blood. Usually the capillaries
are arranged in the form of a network, the channels in any one tissue
being of nearly uniform size, and the closeness of the mesh depending
upon the organ.
As far back as 1865, Stricker observed contraction of the capillaries.
This observation was apparently forgotten until revived again by Krogh
recently. The latter finds that the capillaries are formed of cells
which are arranged in strands encircling the vessel. The capillaries are
rarely longer than 1 mm., and, according to Krogh, are capable of
enormous dilatation.
The rate of flow through any capillary area is very inconstant, and the
usual explanation has been that the capillaries were endothelial tubes
the blood flow of which was dependent upon the contraction or dilatation
of the terminal arterioles. The actual fact that in an observed
capillary area some capillaries are empty renders the above explanation
untenable. The color of a tissue depends upon the state of filling of
the capillaries with blood.
It would seem that all the evidence now leads us to believe that the
capillaries themselves are contractile and it is even possible that they
may be under vasomotor control. If the anatomic structure as stated
above, is correct, it would take but a slight contraction of the
encircling cell to shut off completely the capillary. When the enormous
capillary bed is considered, it is not inconceivable that circulating
poisons may act on large areas and produce a true capillary resistance
to the onflow of blood which might express itself, if long continued, in
actual hypertrophy of the heart.
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 laminae
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 lamellae 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. =Spirochetae pallidae= 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 fibrillae 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 laminae 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 role 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
role. 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 im
Showing first 200,000 characters. Full text: gutenberg.org/ebooks/37675