diff options
Diffstat (limited to '37675-h')
| -rw-r--r-- | 37675-h/37675-h.htm | 10599 | ||||
| -rw-r--r-- | 37675-h/images/fig_001.png | bin | 0 -> 66576 bytes | |||
| -rw-r--r-- | 37675-h/images/fig_002.png | bin | 0 -> 69951 bytes | |||
| -rw-r--r-- | 37675-h/images/fig_003.png | bin | 0 -> 18519 bytes | |||
| -rw-r--r-- | 37675-h/images/fig_004.png | bin | 0 -> 40436 bytes | |||
| -rw-r--r-- | 37675-h/images/fig_005.png | bin | 0 -> 14995 bytes | |||
| -rw-r--r-- | 37675-h/images/fig_006.png | bin | 0 -> 23056 bytes | |||
| -rw-r--r-- | 37675-h/images/fig_007.png | bin | 0 -> 32532 bytes | |||
| -rw-r--r-- | 37675-h/images/fig_008.png | bin | 0 -> 14889 bytes | |||
| -rw-r--r-- | 37675-h/images/fig_009.png | bin | 0 -> 4892 bytes | |||
| -rw-r--r-- | 37675-h/images/fig_010.png | bin | 0 -> 74137 bytes | |||
| -rw-r--r-- | 37675-h/images/fig_011.png | bin | 0 -> 48833 bytes | |||
| -rw-r--r-- | 37675-h/images/fig_012.png | bin | 0 -> 59292 bytes | |||
| -rw-r--r-- | 37675-h/images/fig_013.png | bin | 0 -> 15394 bytes | |||
| -rw-r--r-- | 37675-h/images/fig_014.png | bin | 0 -> 27104 bytes | |||
| -rw-r--r-- | 37675-h/images/fig_015.png | bin | 0 -> 23668 bytes | |||
| -rw-r--r-- | 37675-h/images/fig_016.png | bin | 0 -> 30736 bytes | |||
| -rw-r--r-- | 37675-h/images/fig_017.png | bin | 0 -> 49208 bytes | |||
| -rw-r--r-- | 37675-h/images/fig_018.png | bin | 0 -> 32053 bytes | |||
| -rw-r--r-- | 37675-h/images/fig_019.png | bin | 0 -> 22477 bytes | |||
| -rw-r--r-- | 37675-h/images/fig_020.png | bin | 0 -> 16798 bytes | |||
| -rw-r--r-- | 37675-h/images/fig_021.png | bin | 0 -> 27195 bytes | |||
| -rw-r--r-- | 37675-h/images/fig_022.png | bin | 0 -> 27604 bytes | |||
| -rw-r--r-- | 37675-h/images/fig_023.png | bin | 0 -> 30111 bytes | |||
| -rw-r--r-- | 37675-h/images/fig_024.png | bin | 0 -> 49102 bytes | |||
| -rw-r--r-- | 37675-h/images/fig_025.png | bin | 0 -> 37219 bytes | |||
| -rw-r--r-- | 37675-h/images/fig_026.png | bin | 0 -> 39514 bytes | |||
| -rw-r--r-- | 37675-h/images/fig_027.png | bin | 0 -> 4558 bytes | |||
| -rw-r--r-- | 37675-h/images/fig_028.png | bin | 0 -> 55648 bytes | |||
| -rw-r--r-- | 37675-h/images/fig_029.png | bin | 0 -> 10195 bytes | |||
| -rw-r--r-- | 37675-h/images/fig_030.png | bin | 0 -> 5517 bytes | |||
| -rw-r--r-- | 37675-h/images/fig_031.png | bin | 0 -> 5136 bytes | |||
| -rw-r--r-- | 37675-h/images/fig_032.png | bin | 0 -> 19812 bytes | |||
| -rw-r--r-- | 37675-h/images/fig_033.png | bin | 0 -> 16726 bytes | |||
| -rw-r--r-- | 37675-h/images/fig_034.png | bin | 0 -> 51507 bytes | |||
| -rw-r--r-- | 37675-h/images/fig_035.png | bin | 0 -> 25988 bytes | |||
| -rw-r--r-- | 37675-h/images/fig_036.png | bin | 0 -> 13769 bytes | |||
| -rw-r--r-- | 37675-h/images/fig_037.png | bin | 0 -> 20142 bytes | |||
| -rw-r--r-- | 37675-h/images/fig_038.png | bin | 0 -> 38286 bytes | |||
| -rw-r--r-- | 37675-h/images/fig_039.png | bin | 0 -> 36763 bytes | |||
| -rw-r--r-- | 37675-h/images/fig_040.png | bin | 0 -> 69854 bytes | |||
| -rw-r--r-- | 37675-h/images/fig_041.png | bin | 0 -> 64523 bytes | |||
| -rw-r--r-- | 37675-h/images/fig_042.png | bin | 0 -> 31998 bytes | |||
| -rw-r--r-- | 37675-h/images/fig_043.png | bin | 0 -> 25280 bytes | |||
| -rw-r--r-- | 37675-h/images/fig_044.png | bin | 0 -> 31175 bytes | |||
| -rw-r--r-- | 37675-h/images/fig_045.png | bin | 0 -> 8707 bytes | |||
| -rw-r--r-- | 37675-h/images/fig_046.png | bin | 0 -> 7291 bytes | |||
| -rw-r--r-- | 37675-h/images/fig_047.png | bin | 0 -> 9856 bytes | |||
| -rw-r--r-- | 37675-h/images/fig_048.png | bin | 0 -> 42766 bytes | |||
| -rw-r--r-- | 37675-h/images/fig_049.png | bin | 0 -> 33279 bytes | |||
| -rw-r--r-- | 37675-h/images/fig_050.png | bin | 0 -> 8883 bytes | |||
| -rw-r--r-- | 37675-h/images/fig_051.png | bin | 0 -> 28687 bytes | |||
| -rw-r--r-- | 37675-h/images/fig_052.png | bin | 0 -> 8792 bytes | |||
| -rw-r--r-- | 37675-h/images/fig_053.png | bin | 0 -> 18897 bytes | |||
| -rw-r--r-- | 37675-h/images/fig_054.png | bin | 0 -> 30470 bytes | |||
| -rw-r--r-- | 37675-h/images/fig_055.png | bin | 0 -> 42204 bytes | |||
| -rw-r--r-- | 37675-h/images/fig_056.png | bin | 0 -> 56844 bytes | |||
| -rw-r--r-- | 37675-h/images/fig_057.png | bin | 0 -> 34329 bytes | |||
| -rw-r--r-- | 37675-h/images/fig_058.png | bin | 0 -> 27185 bytes | |||
| -rw-r--r-- | 37675-h/images/fig_059.png | bin | 0 -> 42038 bytes | |||
| -rw-r--r-- | 37675-h/images/fig_060.png | bin | 0 -> 41146 bytes |
61 files changed, 10599 insertions, 0 deletions
diff --git a/37675-h/37675-h.htm b/37675-h/37675-h.htm new file mode 100644 index 0000000..0069e32 --- /dev/null +++ b/37675-h/37675-h.htm @@ -0,0 +1,10599 @@ +<!DOCTYPE html PUBLIC "-//W3C//DTD XHTML 1.0 Strict//EN" + "http://www.w3.org/TR/xhtml1/DTD/xhtml1-strict.dtd"> + +<html xmlns="http://www.w3.org/1999/xhtml" xml:lang="en" lang="en"> + <head> + <meta http-equiv="Content-Type" content="text/html;charset=iso-8859-1" /> + <meta http-equiv="Content-Style-Type" content="text/css" /> + <title> + The Project Gutenberg eBook of Arteriosclerosis and Hypertension with Chapters on Blood Pressure, by Louis M. Warfield. + </title> + <style type="text/css"> + +body { + margin-left: 10%; + margin-right: 10%; +} + + h1,h2,h3,h4 { + text-align: center; /* all headings centered */ + clear: both; +} + +p { + margin-top: .75em; + text-align: justify; + margin-bottom: .75em; +} + + .hanging {margin-left: 2em; text-indent: -2em;} + + + +hr { + margin: 3em auto 3em auto; + height: 0px; + border-width: 1px 0 0 0; + border-style: solid; + border-color: #dcdcdc; + width: 500px; + clear: both; +} + +hr.hr2 { + width: 250px; + margin: 3em auto 3em auto; +} + + .toc { + margin: 0 25% auto 25%; + padding: 0; +} + + p.toc { + font-size: 60%; + margin-bottom: 0; + padding-bottom: 0; +} + .toc li { + list-style-type: none; +} + .toc li p { + margin-top: 0; + padding-top: 0; + text-indent: -1em; + text-align: justify; padding-right: 2em; +} + .toc .num { + position: absolute; + right: 25%; + top: auto; + text-indent: 0; +} + .tocdesc { + padding-right: 2.2em; +} + + + .pgnum-contents { + position: absolute; + left: 90%; + text-align: right; +} + + .pagenum { /* uncomment the next line for invisible page numbers */ + /* visibility: hidden; */ + position: absolute; + left: 92%; + font-size: smaller; + text-align: right; + color: #999; +} /* page numbers */ + + + .blockquot { + margin-left: 5%; + margin-right: 10%; +} + + + .bbox {border: solid 2px;} + + .center {text-align: center;} + + .smcap {font-variant: small-caps;} + + .u {text-decoration: underline;} + + .caption {font-weight: bold;} + + .gap { margin-top: 1em; } + + table { + width: auto; + border-collapse: collapse; + margin-left: auto; + margin-right: auto +} + + table.leftside { + margin-left: 2em; + margin-right: auto +} + td { + padding-bottom: 0em; + padding-left: 1em; + padding-right: 1em; + padding-top: 0em +} + th { + padding-bottom: 0em; + padding-left: 1em; + padding-right: 1em; + padding-top: 0em +} + .tdouble { + border-bottom: black; + border-left: black; + border-top: black double; + border-right: black +} + .bdouble { + border-bottom: black double; + border-left: black; + border-top: black; + border-right: black +} + .bb { + border-bottom: black 2px solid +} + .bl { + border-left: black 1px solid +} + .bt { + border-top: black 2px solid +} + .br { + border-right: black 1px solid +} + ol.upper-roman { + list-style-type: upper-roman +} + ol.upper-alpha { + list-style-type: upper-alpha +} + ol.lower-alpha { + list-style-type: lower-alpha +} + ol.decimal { + list-style-type: decimal +} + ol.none { + list-style-type: none +} + ul { + list-style-type: none +} + li.pad { + padding-top: 3% +} + + + +/* Images */ + .figcenter { + margin: auto; + text-align: center; +} + .bord img { + padding: 1px; + border: 1px solid black; +} + + p.caption { + margin-top: 0; + font-size: 70%; + text-align: left; +} + +/* Transcriber Notes */ +div.tn { + background-color: #EEE; + border: dashed 1px; + color: #000; + margin-left: 20%; + margin-right: 20%; + margin-top: 5em; + margin-bottom: 5em; + padding: 1em; +} + +/* Footnotes */ +div.fn { + background-color: #EEE; + border: dashed 1px; + color: #000; + margin-left: 20%; + margin-right: 20%; + margin-top: 5em; + margin-bottom: 5em; + padding: 1em; +} + + .footnote { + margin-left: 10%; + margin-right: 10%; + font-size: 0.9em; +} + + .footnote .label { + position: absolute; + right: 84%; + text-align: right; +} + + .fnanchor { + vertical-align: super; + font-size: .8em; + text-decoration: none; +} + + .signature { + text-align: right; + margin-right: 5%; +} + +/* INDEX */ +ul.index { list-style-type: none; + width: 20em; + margin: 2em auto; +} + +ul.index2 { list-style-type: none; } + +li.pad { padding-top: 2.0%; } + + </style> + </head> +<body> + + +<pre> + +The Project Gutenberg EBook of Arteriosclerosis and Hypertension:, by +Louis Marshall Warfield + +This eBook is for the use of anyone anywhere 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 + + +Title: Arteriosclerosis and Hypertension: + with Chapters on Blood Pressure, 3rd Edition. + +Author: Louis Marshall Warfield + +Release Date: October 12, 2011 [EBook #37675] + +Language: English + +Character set encoding: ISO-8859-1 + +*** START OF THIS PROJECT GUTENBERG EBOOK ARTERIOSCLEROSIS AND HYPERTENSION: *** + + + + +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.) + + + + + + +</pre> + + + + + + +<h4><span class="smcap">Erratum</span></h4> + + +<p>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.<br /><br /></p> +<hr style="width: 45%;" /> +<h1> +ARTERIOSCLEROSIS<br /> +<br /> +AND<br /> +<br /> +HYPERTENSION</h1> +<h3> +With Chapters on Blood Pressure<br /> +<br /> +BY<br /> + +</h3> + + +<h2>LOUIS M. WARFIELD, A.B., M.D., (Johns Hopkins),<br /> +F.A.C.P.</h2> +<div class="center"><br /> +<br /> +FORMERLY PROFESSOR OF CLINICAL MEDICINE, MARQUETTE UNIVERSITY MEDICAL<br /> +SCHOOL; CHIEF PHYSICIAN TO MILWAUKEE COUNTY HOSPITAL; ASSOCIATE<br /> +MEMBER ASSOCIATION AMERICAN PHYSICIANS; MEMBER AMERICAN<br /> +ASSOCIATION PATHOLOGISTS AND BACTERIOLOGISTS;<br /> +AMERICAN MEDICAL ASSOCIATION, ETC., FELLOW<br /> +AMERICAN COLLEGE OF PHYSICIANS<br /> +<br /><br /> +<i>THIRD EDITION</i><br /> +<br /><br /> +ST. LOUIS<br /> +<br /> +C. V. MOSBY COMPANY<br /> +<br /> +1920<br /> +<br /> +</div> +<hr style="width: 45%;" /> +<div class="center"><span class="smcap">Copyright, 1912, 1920, by C. V. Mosby Company</span><br /> +<br /> +<i>Press of<br /> +C. V. Mosby Company<br /> +St. Louis</i><br /> +<br /> +</div> +<hr style="width: 65%;" /> + +<div class="center">TO<br /> +<br /> +MY MOTHER<br /> +<br /> +THIS VOLUME IS AFFECTIONATELY<br /> +<br /> +DEDICATED<br /> +</div> + +<hr style="width: 65%;" /> + +<p><span class="pagenum"><a name="Page_15" id="Page_15">[15]</a></span></p> +<h2>PREFACE TO THIRD EDITION</h2> + + +<p>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.</p> + +<p>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.</p> + +<p>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.</p> + +<p>New chapters on Cardiac Irregularities Associated with +Arteriosclerosis, and Blood Pressure in Its Clinical Application +have been added.</p> + +<p>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.</p> + +<p><span class="pagenum"><a name="Page_16" id="Page_16">[16]</a></span>It is hoped that the kind of reception accorded to the first +and second editions will also not be withheld from this present +edition.</p> + +<div class="signature"><span class="smcap">Louis M. Warfield.</span></div> +<p> +Milwaukee, Wisc. +</p> + + + +<hr style="width: 65%;" /> +<h2>PREFACE TO THE SECOND EDITION</h2> + + +<p>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.</p> + +<p>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.</p> + +<p>The author is grateful for the kindly reception accorded +the first edition. No one is more keenly aware of the imperfections<span class="pagenum"><a name="Page_17" id="Page_17">[17]</a></span> +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.</p> + +<p>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.</p> + +<div class="signature"><span class="smcap">Louis M. Warfield.</span></div> + +<p>Milwaukee, May, 1912.<br /> +</p> + + + +<hr style="width: 65%;" /> +<h2>PREFACE TO THE FIRST EDITION</h2> + + +<p>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.</p> + +<p>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.</p> + +<p><span class="pagenum"><a name="Page_18" id="Page_18">[18]</a></span>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.</p> + +<p>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.</p> + +<p>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.</p> + +<p>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.</p> + +<div class="signature"> +<span class="smcap">Louis M. Warfield.</span></div> + +<p>St. Louis, August, 1908.<br /> +</p> + +<hr style="width: 65%;" /> +<p><span class="pagenum"><a name="Page_19" id="Page_19">[19]</a></span></p> +<h2>CONTENTS</h2> + +<blockquote> + +<p><span class="pgnum-contents"><span class="smcap">page</span></span></p> + +<h3><a href="#CHAPTER_I">CHAPTER I.</a></h3> + +<p><span class="smcap">Anatomy</span><span class="pgnum-contents">25</span></p> + +<p class="hanging">Introduction, 25; Definition, 26; General Structure of the Arteries, +27; Arteries, 29; Veins, 30; Capillaries, 31.</p> + +<h3><a href="#CHAPTER_II">CHAPTER II.</a></h3> + +<p><span class="smcap">Pathology</span><span class="pgnum-contents">32</span></p> + +<p class="hanging">Syphilitic Aortitis, 44; Experimental Arteriosclerosis, 50; Arteriosclerosis +of the Pulmonary Arteries, 63; Sclerosis of the Veins, 64.</p> + +<h3><a href="#CHAPTER_III">CHAPTER III.</a></h3> + +<p><span class="smcap">Physiology of the Circulation</span><span class="pgnum-contents">65</span></p> + +<p class="hanging">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.</p> + +<h3><a href="#CHAPTER_IV">CHAPTER IV.</a></h3> + +<p><span class="smcap">Important Cardiac Irregularities Associated With Arteriosclerosis</span> <span class="pgnum-contents">13</span></p> + +<p class="hanging">Auricular Flutter, 131; Auricular Fibrillation, 133; Ventricular +Fibrillation, 138; Extrasystole, 138; Heart Block, 140.</p> + +<h3><a href="#CHAPTER_V">CHAPTER V.</a></h3> + +<p><span class="smcap">Blood Pressure in Its Clinical Applications</span><span class="pgnum-contents">147</span></p> + +<p class="hanging">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.</p> + +<h3><a href="#CHAPTER_VI">CHAPTER VI.</a></h3> + +<p><span class="smcap">Etiology</span><span class="pgnum-contents">157</span></p> + +<p class="hanging">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.</p> +<p><span class="pagenum"><a name="Page_20" id="Page_20">[20]</a></span></p> +<h3><a href="#CHAPTER_VII">CHAPTER VII.</a></h3> + +<p><span class="smcap">The Physical Examination of the Heart and Arteries</span><span class="pgnum-contents">172</span></p> + +<p class="hanging">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.</p> + +<h3><a href="#CHAPTER_VIII">CHAPTER VIII.</a></h3> + +<p><span class="smcap">Symptoms and Physical Signs</span><span class="pgnum-contents">183</span></p> + +<p class="hanging">General, 183; Hypertension, 185; The Heart, 188; Palpable Arteries, +189; Ocular Signs and Symptoms, 190; Nervous Symptoms, 191.</p> + +<h3><a href="#CHAPTER_IX">CHAPTER IX.</a></h3> + +<p><span class="smcap">Symptoms and Physical Signs</span><span class="pgnum-contents">194</span></p> + +<p class="hanging">Special, 194; Cardiac, 195; Renal, 199; Abdominal or Visceral, 201; +Cerebral, 203; Spinal, 205; Local or Peripheral, 207; Pulmonary +Artery, 209.</p> + +<h3><a href="#CHAPTER_X">CHAPTER X.</a></h3> + +<p><span class="smcap">Diagnosis</span><span class="pgnum-contents">210</span></p> + +<p class="hanging">Early Diagnosis, 210; Differential Diagnosis, 215; Diseases in Which +Arteriosclerosis is Commonly Found, 216.</p> + +<h3><a href="#CHAPTER_XI">CHAPTER XI.</a></h3> + +<p><span class="smcap">Prognosis</span><span class="pgnum-contents">218</span></p> + +<h3><a href="#CHAPTER_XII">CHAPTER XII.</a></h3> + +<p><span class="smcap">Prophylaxis</span><span class="pgnum-contents">224</span></p> + +<h3><a href="#CHAPTER_XIII">CHAPTER XIII.</a></h3> + +<p><span class="smcap">Treatment</span><span class="pgnum-contents">229</span></p> + +<p class="hanging">Hygienic Treatment, 230; Balneotherapy, 233; Personal Habits, +234; Dietetic Treatment, 235; Medicinal, 238; Symptomatic Treatment, +245.</p> + +<h3><a href="#CHAPTER_XIV">CHAPTER XIV.</a></h3> + +<p><span class="smcap">Arteriosclerosis in Its Relation to Life Insurance</span><span class="pgnum-contents">249</span></p> + +<h3><a href="#CHAPTER_XV">CHAPTER XV.</a></h3> + +<p><span class="smcap">Practical Suggestions</span><span class="pgnum-contents">256</span></p> +</blockquote> + + + + +<hr style="width: 65%;" /> +<p><span class="pagenum"><a name="Page_21" id="Page_21">[21]</a></span></p> +<h2>ILLUSTRATIONS</h2> + + + +<div class="center"> +<table border="0" cellpadding="4" cellspacing="0" summary="LIST OF ILLUSTRATIONS"> +<tr><td align="left">FIG.</td><td><span class="smcap">page</span></td></tr> +<tr><td align="left"><a href="#Cross_section_of_a_large_artery">1. Cross section of a large artery</a></td><td align="right">28</td></tr> +<tr><td align="left"><a href="#Cross_section_of_a_coronary_artery">2. Cross section of a coronary artery</a></td><td align="right">36</td></tr> +<tr><td align="left"><a href="#Arteriosclerosis_of_the_thoracic_and_abdominal_aorta">3. Arteriosclerosis of the thoracic and abdominal aorta</a></td><td align="right">39</td></tr> +<tr><td align="left"><a href="#Arteriosclerosis_of_the_arch_of_the_aorta">4. Arteriosclerosis of the arch of the aorta</a></td><td align="right">40</td></tr> +<tr><td align="left"><a href="#Normal_Aorta">5. Normal Aorta</a></td><td align="right">41</td></tr> +<tr><td align="left"><a href="#Radiogram_showing_calcification_of_both_radial_and_ulnar_arteries">6. Radiogram showing calcification of both radial and ulnar arteries</a></td><td align="right">42</td></tr> +<tr><td align="left"><a href="#Syphilitic_aortitis_of_long_standing">7. Syphilitic aortitis of long standing</a></td><td align="right">44</td></tr> +<tr><td align="left"><a href="#Diagrammatic_representation_of_strain_hypertrophy">8. Diagrammatic representation of strain hypertrophy</a></td><td align="right">48</td></tr> +<tr><td align="left"><a href="#Strain_hypertrophy">9. Strain hypertrophy</a></td><td align="right">49</td></tr> +<tr><td align="left"><a href="#Cross_section_of_small_artery_in_the_mesentery">10. Cross section of small artery in the mesentery</a></td><td align="right">56</td></tr> +<tr><td align="left"><a href="#Enormous_hypertrophy_of_left_ventricle">11. Enormous hypertrophy of left ventricle</a></td><td align="right">58</td></tr> +<tr><td align="left"><a href="#Aortic_incompetence_with_hypertrophy_and_dilatation_of_left_ventricle">12. Aortic incompetence with hypertrophy and dilatation of left ventricle</a></td><td align="right">61</td></tr> +<tr><td align="left"><a href="#Cooks_modification_of_Riva-Roccis_blood_pressure_instrument">13. Cooks modification of Riva-Roccis blood pressure instrument</a></td><td align="right">72</td></tr> +<tr><td align="left"><a href="#Stantons_sphygmomanometer">14. Stanton's sphygmomanometer</a></td><td align="right">73</td></tr> +<tr><td align="left"><a href="#The_Erlanger_sphygmomanometer_with_the_Hirschfelder_attachments">15. The Erlanger sphygmomanometer with the Hirschfelder attachments</a></td><td align="right">74</td></tr> +<tr><td align="left"><a href="#Desk_model_Baumanometer">16. Desk model Baumanometer</a></td><td align="right">75</td></tr> +<tr><td align="left"><a href="#Faught_blood_pressure_instrument">17. Faught blood pressure instrument</a></td><td align="right">76</td></tr> +<tr><td align="left"><a href="#Rogers_Tycos_dial_sphygmomanometer">18. Rogers' "Tycos" dial sphygmomanometer</a></td><td align="right">77</td></tr> +<tr><td align="left"><a href="#Detail_of_the_dial_in_the_Tycos_instrument">19. Detail of the dial in the "Tycos" instrument</a></td><td align="right">78</td></tr> +<tr><td align="left"><a href="#Faught_dial_instrument">20. Faught dial instrument</a></td><td align="right">79</td></tr> +<tr><td align="left"><a href="#Detail_of_the_dial_of_the_Faught_instrument">21. Detail of the dial of the Faught instrument</a></td><td align="right">79</td></tr> +<tr><td align="left"><a href="#The_Sanborn_instrument">22. The Sanborn instrument</a></td><td align="right">80</td></tr> +<tr><td align="left"><a href="#Method_of_taking_blood_pressure_with_a_patient_in_sitting_position">23. Method of taking blood pressure with a patient in sitting position</a></td><td align="right">81</td></tr> +<tr><td align="left"><a href="#Method_of_taking_blood_pressure_with_patient_lying_down">24. Method of taking blood pressure with patient lying down</a></td><td align="right">82</td></tr> +<tr><td align="left"><a href="#Observation_by_the_auscultatory_method_and_a_mercury_instrument">25. Observation by the auscultatory method and a mercury instrument</a></td><td align="right">84</td></tr> +<tr><td align="left"><a href="#Observation_by_the_auscultatory_method_and_a_dial_instrument">26. Observation by the auscultatory method and a dial instrument</a></td><td align="right">85</td></tr> +<tr><td align="left"><a href="#Schema_to_illustrate_decrease_in_pressure">27. Schema to illustrate decrease in pressure</a></td><td align="right">86</td></tr> +<tr><td align="left"><a href="#Chart_showing_the_normal_limits_of_variation_in_systolic_blood_pressure">28. Chart showing the normal limits of variation in systolic blood pressure</a></td><td align="right">89</td></tr> +<tr><td align="left"><a href="#Tracing_of_auscultatory_phenomena">29. Tracing of auscultatory phenomena</a></td><td align="right">94</td></tr> +<tr><td align="left"><a href="#Tracings_of_auscultatory_phenomena">30. Tracings of auscultatory phenomena</a></td><td align="right">95</td></tr> +<tr><td align="left"><a href="#Clinical_determination_of_diastolic_pressure_fast_drum">31. Clinical determination of diastolic pressure fast drum</a></td><td align="right">96</td></tr> +<tr><td align="left"><a href="#Clinical_determination_of_diastolic_pressure_slow_drum">32. Clinical determination of diastolic pressure slow drum</a></td><td align="right">96</td></tr> +<tr><td align="left"><a href="#Venous_blood_pressure_instrument">33. Venous blood pressure instrument</a></td><td align="right">121</td></tr> +<tr><td align="left"><a href="#New_venous_pressure_instrument">34. New venous pressure instrument</a></td><td align="right">122</td></tr> +<tr><td align="left"><a href="#Events_in_the_cardiac_cycle">35. Events in the cardiac cycle</a></td><td align="right">124</td></tr> +<tr><td align="left"><a href="#Simultaneous_tracings_of_the_jugular_and_carotid_pulses">36. Simultaneous tracings of the jugular and carotid pulses</a></td><td align="right">125</td></tr> +<tr><td align="left"><a href="#Jugular_and_carotid_tracings">37. Jugular and carotid tracings</a></td><td align="right">125</td></tr> +<tr><td align="left"><a href="#Right_side_of_the_heart_showing_distribution_of_the_two_vagus_nerves">38. Right side of the heart showing distribution of the two vagus nerves</a></td><td align="right">127</td></tr> +<tr><td align="left"><a href="#Normal_electrocardiogram">39. Normal electrocardiogram</a></td><td align="right">128</td></tr> +<tr><td align="left"><a href="#Auricular_flutter">40. Auricular flutter</a></td><td align="right">132</td></tr> +<tr><td align="left"><a href="#Auricular_fibrillation">41. Auricular fibrillation</a></td><td align="right">134</td></tr> +<tr><td align="left"><span class="pagenum"><a name="Page_22" id="Page_22">[22]</a></span></td></tr> +<tr><td align="left"><a href="#Auricular_fibrillations">42. Auricular fibrillation</a></td><td align="right">134</td></tr> +<tr><td align="left"><a href="#Pulse_deficit">43. Pulse deficit</a></td><td align="right">135</td></tr> +<tr><td align="left"><a href="#Ventricular_fibrillation">44. Ventricular fibrillation</a></td><td align="right">137</td></tr> +<tr><td align="left"><a href="#Auricular_extrasystoles">45. Auricular extrasystoles</a></td><td align="right">139</td></tr> +<tr><td align="left"><a href="#Ventricular_extrasystole">46. Ventricular extrasystole</a></td><td align="right">139</td></tr> +<tr><td align="left"><a href="#Delayed_conduction">47. Delayed conduction</a></td><td align="right">141</td></tr> +<tr><td align="left"><a href="#Partial_heart_block">48. Partial heart block</a></td><td align="right">141</td></tr> +<tr><td align="left"><a href="#Complete_heart_block">49. Complete heart block</a></td><td align="right">142</td></tr> +<tr><td align="left"><a href="#Alternating_periods_of_sinus_rhythm_and_auriculoventricular_rhythm">50. Alternating periods of sinus rhythm and auriculoventricular rhythm</a></td><td align="right">144</td></tr> +<tr><td align="left"><a href="#Auriculoventricular_or_nodal_rhythm">51. Auriculoventricular or "nodal" rhythm</a></td><td align="right">144</td></tr> +<tr><td align="left"><a href="#Influence_of_mechanical_pressure_on_the_right_vagus_nerve">52. Influence of mechanical pressure on the right vagus nerve</a></td><td align="right">144</td></tr> +<tr><td align="left"><a href="#Schematic_distribution_of_right_and_left_vagus">53. Schematic distribution of right and left vagus</a></td><td align="right">145</td></tr> +<tr><td align="left"><a href="#Blood_pressure_record_from_a_normal_reaction_to_ether">54. Blood pressure record from a normal reaction to ether</a></td><td align="right">149</td></tr> +<tr><td align="left"><a href="#Chart_showing_the_method_of_recording_blood_pressure_during_an">55. Chart showing the method of recording blood pressure during an</a></td></tr> +<tr><td align="left">operation</td><td align="right">150</td></tr> +<tr><td align="left"><a href="#Method_of_using_blood_pressure_instrument_during_operation">56. Method of using blood pressure instrument during operation</a></td><td align="right">151</td></tr> +<tr><td align="left"><a href="#Finger-tip_palpation_of_the_radial_artery">57. Finger-tip palpation of the radial artery</a></td><td align="right">178</td></tr> +<tr><td align="left"><a href="#Finger-tip_palpations_of_the_radial_artery">58. Finger-tip palpation of the radial artery</a></td><td align="right">178</td></tr> +<tr><td align="left"><a href="#Aneurysm_of_the_heart_wall">59. Aneurysm of the heart wall</a></td><td align="right">196</td></tr> +<tr><td align="left"><a href="#Large_aneurysm_of_the_aorta_eroding_the_sternum">60. Large aneurysm of the aorta eroding the sternum</a></td><td align="right">198</td></tr> +</table></div> + +<p><span class="pagenum"><a name="Page_24" id="Page_24"></a></span><span class="pagenum"><a name="Page_23" id="Page_23"></a></span></p> + +<hr style="width: 65%;" /> +<p><span class="pagenum"><a name="Page_25" id="Page_25">[25]</a></span></p> +<h2>ARTERIOSCLEROSIS AND HYPERTENSION</h2> + +<hr style="width: 65%;" /> +<h2><a name="CHAPTER_I" id="CHAPTER_I"></a>CHAPTER I.</h2> + + +<h3>ANATOMY</h3> + + +<p>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."</p> + +<p>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.</p> + +<p>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.</p> + +<p>Arteriosclerosis is not a disease <b>sui generis</b>. It is best<span class="pagenum"><a name="Page_26" id="Page_26">[26]</a></span> +viewed as a degeneration of the coats of the arteries, both +large and small resulting in several different more or less +distinct types.</p> + +<p>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.</p> + +<p>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.</p> + +<p>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.</p> + +<p>The vascular system is often likened to a central pump, +from which emanates a closed system of tubes, beginning<span class="pagenum"><a name="Page_27" id="Page_27">[27]</a></span> +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.</p> + + +<h4>General Structure of the Arteries</h4> + +<p>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.</p> + +<p>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<span class="pagenum"><a name="Page_28" id="Page_28">[28]</a></span> +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.</p> + +<div class="figcenter bord" style="width: 415px;"><a name="Cross_section_of_a_large_artery" id="Cross_section_of_a_large_artery"></a> +<img src="images/fig_001.png" width="415" height="500" alt="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.)" title="Fig. 1.—Cross section of a large artery showing the division into the three coats; intima, +media, adventitia... (Microphotograph, highly magnified.)" /> +<span class="caption">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.)</span> +</div> + +<p>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.</p> + +<p>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.</p> + +<p>The nutrient vessels of the arteries and veins, the vasa +vasorum, are present in all the vessels except those less<span class="pagenum"><a name="Page_29" id="Page_29">[29]</a></span> +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.</p> + + +<h4>Arteries</h4> + +<p>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.</p> + +<p>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.</p> + +<p>"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<span class="pagenum"><a name="Page_30" id="Page_30">[30]</a></span> +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.)</p> + +<p>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.</p> + + +<h4>Veins</h4> + +<p>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.</p> + +<p><span class="pagenum"><a name="Page_31" id="Page_31">[31]</a></span></p> +<h4>Capillaries</h4> + +<p>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.</p> + +<p>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.</p> + +<p>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.</p> + +<p>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.</p> + +<hr style="width: 65%;" /> +<p><span class="pagenum"><a name="Page_32" id="Page_32">[32]</a></span></p> +<h2><a name="CHAPTER_II" id="CHAPTER_II"></a>CHAPTER II.</h2> + +<h3>PATHOLOGY</h3> + + +<p>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.</p> + +<p>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.</p> + +<p>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<span class="pagenum"><a name="Page_33" id="Page_33">[33]</a></span> +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.</p> + +<p>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.</p> + +<p>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<span class="pagenum"><a name="Page_34" id="Page_34">[34]</a></span> +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.</p> + +<p>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.</p> + +<p>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<span class="pagenum"><a name="Page_35" id="Page_35">[35]</a></span> +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.)</p> + +<div class="figcenter bord" style="width: 434px;"> +<a name="Cross_section_of_a_coronary_artery" id="Cross_section_of_a_coronary_artery"></a> + +<img src="images/fig_002.png" width="434" height="500" alt="Fig. 2.—Cross section of a coronary artery, ×50, showing nodular sclerosis. Note the +heaping up of cells in the intima, the fracture of the elastica, and the destruction of the +media beneath the nodule. The primary lesion evidently was in the media. The thickened +intima is the effort on the part of nature to heal the breach. At such places as +shown here aneurysms may form. (Microphotograph.)" title="Fig. 2.—Cross section of a coronary artery, ×50, showing nodular sclerosis. Note the +heaping up of cells in the intima, the fracture of the elastica, and the destruction of the +media beneath the nodule.... (Microphotograph.)" /> +<span class="caption">Fig. 2.—Cross section of a coronary artery, ×50, showing nodular sclerosis. Note the +heaping up of cells in the intima, the fracture of the elastica, and the destruction of the +media beneath the nodule. The primary lesion evidently was in the media. The thickened +intima is the effort on the part of nature to heal the breach. At such places as +shown here aneurysms may form. (Microphotograph.)</span> +</div> + +<p>Aschoff's studies of the aorta show that, "in infancy the +elastic laminæ of the media stand out sharply defined, well +separated from each other by the muscle layers, which are +well developed.... From childhood there is to be observed +a slowly progressive increase in the elastic elements of the +media. Not only do the individual lamellæ seen in cross-sections +become thicker, but also they afford an increasing +number of fine secondary filaments feathering off from these +and crossing the muscle layer, so that now they are no +longer sharply defined, but more ragged upon cross-section. +This progressive increase attains its maximum at or about<span class="pagenum"><a name="Page_36" id="Page_36">[36]</a></span> +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.</p> + +<p><span class="pagenum"><a name="Page_37" id="Page_37">[37]</a></span>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.</p> + +<p>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.</p> + +<p>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<span class="pagenum"><a name="Page_38" id="Page_38">[38]</a></span> +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.)</p> + + +<div class="figcenter bord" style="width: 201px;"><a name="Arteriosclerosis_of_the_thoracic_and_abdominal_aorta" id="Arteriosclerosis_of_the_thoracic_and_abdominal_aorta"></a> +<img src="images/fig_003.png" width="201" height="500" alt="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." title="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...." /> +<span class="caption">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.</span> +</div> + +<div class="figcenter" style="width: 359px;"> +<a name="Arteriosclerosis_of_the_arch_of_the_aorta" id="Arteriosclerosis_of_the_arch_of_the_aorta"></a> +<img src="images/fig_004.png" width="359" height="500" alt="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.)" title="Fig. 4.—Arteriosclerosis of the arch of the aorta.... (Milwaukee County Hospital.)" /> +<span class="caption">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.)</span> +</div> + +<div class="figcenter bord" style="width: 200px;"> +<a name="Normal_Aorta" id="Normal_Aorta"></a> + +<img src="images/fig_005.png" width="200" height="500" alt="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." title="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...." /> +<span class="caption">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.</span> +</div> + +<p>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.</p> + +<p>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<span class="pagenum"><a name="Page_39" id="Page_39">[39]</a></span> +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<span class="pagenum"><a name="Page_40" id="Page_40">[40]</a></span> +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<span class="pagenum"><a name="Page_41" id="Page_41">[41]</a></span> +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<span class="pagenum"><a name="Page_43" id="Page_43">[43]</a></span><span class="pagenum"><a name="Page_42" id="Page_42"></a></span> +of the media is found and is said to be preceded by hypertrophy +of the middle coat.</p> + +<p>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.</p> + +<p>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.)</p> + +<div class="figcenter bord" style="width: 290px;"> +<a name="Radiogram_showing_calcification_of_both_radial_and_ulnar_arteries" id="Radiogram_showing_calcification_of_both_radial_and_ulnar_arteries"></a> +<img src="images/fig_006.png" width="290" height="500" alt="Fig. 6.—Radiogram of a man aged seventy-five, showing calcification of both radial and +ulnar arteries." title="Fig. 6.—Radiogram of a man aged seventy-five, showing calcification of both radial and +ulnar arteries." /> +<span class="caption">Fig. 6.—Radiogram of a man aged seventy-five, showing calcification of both radial and +ulnar arteries.</span> +</div> + +<p>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.</p> +<p><span class="pagenum"><a name="Page_44" id="Page_44">[44]</a></span></p> + +<h4>Syphilitic Aortitis</h4> + +<div class="figcenter" style="width: 375px;"> + +<a name="Syphilitic_aortitis_of_long_standing" id="Syphilitic_aortitis_of_long_standing"></a> + +<img src="images/fig_007.png" width="375" height="500" alt="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.)" title="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.)" /> +<span class="caption">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.)</span> +</div> + +<p>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,<span class="pagenum"><a name="Page_45" id="Page_45">[45]</a></span> +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. <b>Spirochetæ pallidæ</b> 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.</p> + +<p>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<span class="pagenum"><a name="Page_46" id="Page_46">[46]</a></span> +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.</p> + +<p>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<span class="pagenum"><a name="Page_47" id="Page_47">[47]</a></span> +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.</p> + +<p>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.</p> + +<p>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<span class="pagenum"><a name="Page_48" id="Page_48">[48]</a></span> +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.</p> + +<div class="figcenter" style="width: 308px;"> +<a name="Diagrammatic_representation_of_strain_hypertrophy" id="Diagrammatic_representation_of_strain_hypertrophy"></a> + +<img src="images/fig_008.png" width="308" height="500" alt="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.)" title="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.)" /> +<span class="caption">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.)</span> +</div> + +<p>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.</p> + +<div class="figcenter" style="width: 171px;"> + +<a name="Strain_hypertrophy" id="Strain_hypertrophy"></a> + +<img src="images/fig_009.png" width="171" height="500" alt="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.)" title="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.)" /> +<span class="caption">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.)</span> +</div> + +<p>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<span class="pagenum"><a name="Page_49" id="Page_49">[49]</a></span> +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.</p> +<p><span class="pagenum"><a name="Page_50" id="Page_50">[50]</a></span></p> + +<h4>Experimental Arteriosclerosis</h4> + +<p>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.</p> + +<p>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<span class="pagenum"><a name="Page_51" id="Page_51">[51]</a></span> +(yolk of egg, brain tissue) and +pure cholesterin and found changes in the intima and inner +portion of the media consisting of fatty infiltration between +the muscle and elastic fibres, advent of small round cells +and large phagocytic cells containing fat droplets of cholesterin +esters. The elastic fibres were dissolved, broken up +into fibrillæ and these seemed to be absorbed. The internal +elastic lamina as such disappeared and the inner layer of +the aorta fused with the middle coat. He considers these +changes to be quite analogous to those found in human +aortas.</p> + +<p>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.</p> + +<p>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<span class="pagenum"><a name="Page_52" id="Page_52">[52]</a></span> +by injections of adrenalin. The degree of disease of +the circulatory system increases with the duration of the +experiment."</p> + +<p>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.</p> + +<p>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.</p> + +<p>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.</p> + +<p>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.</p> + +<p>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<span class="pagenum"><a name="Page_53" id="Page_53">[53]</a></span> +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.</p> + +<p>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.</p> + +<p>Experimentally, the changes caused by the toxins above +noted are proliferations of cells in the intima and subintimal +tissues, and a breaking up of the internal elastic laminæ +into several parallel layers which stretch themselves among +the proliferating cells. The diphtheria toxin, on the contrary, +produces a lesion more like that caused by adrenalin. +All pathologists are not agreed as to whether the experimental +lesions produced by blood pressure raising drugs +are similar to the arteriosclerotic changes in the arteries +of man.</p> + +<p>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.<span class="pagenum"><a name="Page_54" id="Page_54">[54]</a></span> +They differ macroscopically in that the lesion is usually +limited to a few foci near the origin of the aorta.</p> + +<p>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.</p> + +<p>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.</p> + +<p>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<span class="pagenum"><a name="Page_55" id="Page_55">[55]</a></span> +the condition produced experimentally by the toxin of the +typhoid bacillus, for example.</p> + +<p>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.</p> + +<p>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.</p> + +<p>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<span class="pagenum"><a name="Page_56" id="Page_56">[56]</a></span> +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.)</p> + +<div class="figcenter bord" style="width: 417px;"> +<a name="Cross_section_of_small_artery_in_the_mesentery" id="Cross_section_of_small_artery_in_the_mesentery"></a> +<img src="images/fig_010.png" width="417" height="500" alt="Fig. 10.—Cross-section of a small artery in the mesentery. Note that the vessel appears +capable of being much widened. The internal elastic lamina is thrown into folds +somewhat resembling the convolutions of the brain. Note also that the middle coat +of the artery is composed almost entirely of muscle. The enormous number of such +vessels in the mesentery and intestines explains the ability of the splanchnic area to +accommodate the greater part of the blood in the body. Universal constriction of these +vessels would naturally render the intestines anemic. The vasomotor control of these +vessels plays an important rôle in the distribution of the blood. Small arteries in the +skin and in other organs, possibly the brain, have a similar function. (Microphotograph, +highly magnified".)" title="Fig. 10.—Cross-section of a small artery in the mesentery... (Microphotograph, +highly magnified.)" /> +<span class="caption">Fig. 10.—Cross-section of a small artery in the mesentery. Note that the vessel appears +capable of being much widened. The internal elastic lamina is thrown into folds +somewhat resembling the convolutions of the brain. Note also that the middle coat +of the artery is composed almost entirely of muscle. The enormous number of such +vessels in the mesentery and intestines explains the ability of the splanchnic area to +accommodate the greater part of the blood in the body. Universal constriction of these +vessels would naturally render the intestines anemic. The vasomotor control of these +vessels plays an important rôle in the distribution of the blood. Small arteries in the +skin and in other organs, possibly the brain, have a similar function. (Microphotograph, +highly magnified.)</span> +</div> + +<p>It is conceivable that in one section of the body the vessels<span class="pagenum"><a name="Page_57" id="Page_57">[57]</a></span> +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.</p> + +<p>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.</p> + +<p>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.<a name="FNanchor_1_1" id="FNanchor_1_1"></a><a href="#Footnote_1_1" class="fnanchor">[1]</a> 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.)</p> + +<div class="figcenter" style="width: 500px;"> +<a name="Enormous_hypertrophy_of_left_ventricle" id="Enormous_hypertrophy_of_left_ventricle"></a> + +<img src="images/fig_011.png" width="500" height="357" alt="Fig. 11.—Enormous hypertrophy of left ventricle probably due to prolonged increased +peripheral resistance. Note that the whole anterior surface of the heart is occupied +by the left ventricle. The right ventricle does not appear to be much affected. +× ⅔." title="Fig. 11.—Enormous hypertrophy of left ventricle probably due to prolonged increased +peripheral resistance. Note that the whole anterior surface of the heart is occupied +by the left ventricle. The right ventricle does not appear to be much affected. +× ⅔." /> +<span class="caption">Fig. 11.—Enormous hypertrophy of left ventricle probably due to prolonged increased +peripheral resistance. Note that the whole anterior surface of the heart is occupied +by the left ventricle. The right ventricle does not appear to be much affected. +× ⅔.</span> +</div> + +<p>In diffuse arteriosclerosis accompanied by chronic nephritis +the heart is always hypertrophied. This is a result, not<span class="pagenum"><a name="Page_58" id="Page_58">[58]</a></span> +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.</p> + +<p><span class="pagenum"><a name="Page_59" id="Page_59">[59]</a></span>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.</p> + +<p>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.</p> + +<p>There is, as a rule, no increase in arterial tension; on the<span class="pagenum"><a name="Page_60" id="Page_60">[60]</a></span> +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.</p> + +<p>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.</p> + +<p>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<span class="pagenum"><a name="Page_61" id="Page_61">[61]</a></span> +only when all factors, including the typical pulse +tracings, are taken into consideration.</p> + +<div class="figcenter" style="width: 500px;"> +<a name="Aortic_incompetence_with_hypertrophy_and_dilatation_of_left_ventricle" id="Aortic_incompetence_with_hypertrophy_and_dilatation_of_left_ventricle"></a> +<img src="images/fig_012.png" width="500" height="451" alt="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.)" title="Fig. 12.—Aortic incompetence with hypertrophy and dilatation of left ventricle, the +result of arteriosclerosis affecting the aortic valves.... (Reduced +one-half.)" /> +<span class="caption">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.)</span> +</div> + +<p>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<span class="pagenum"><a name="Page_62" id="Page_62">[62]</a></span> +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.</p> + +<p>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.</p> +<p><span class="pagenum"><a name="Page_63" id="Page_63">[63]</a></span></p> + +<h4>Arteriosclerosis of the Pulmonary Arteries</h4> + +<p>There have been a number of cases of sclerosis of the +pulmonary arteries, either alone, or associated with general +systemic arteriosclerosis.</p> + +<p>A primary and a secondary form are recognized, the former +in conjunction with congenital malformations of the +heart, the latter as the result of severe infection or of mitral +stenosis. These two causes seem to be the most important +in the production of the arterial changes. The cases +thus far described have revealed widespread thickening +of the pulmonary arteries. If one may judge by the description +of the pathologic changes, the condition is quite +similar to that produced in a vein by transplantation along +the course of an artery. The diffuse form with connective +tissue thickening of all coats has been generally described. +There is also obliterating endarteritis of the smaller vessels. +In the etiology of the condition severe infection seems +to play a prominent rôle. The constant presence of right +ventricular hypertrophy is interesting, the heart dullness +extends, as a rule, far to the right of the sternum. In some +of the cases no demonstrable changes were observed in the +bronchial arteries or in the pulmonary veins.</p> + +<p>Sanders has described a case of primary pulmonary arteriosclerosis +with hypertrophy of the right ventricle.</p> + +<p>Recently Warthin<a name="FNanchor_2_2" id="FNanchor_2_2"></a><a href="#Footnote_2_2" class="fnanchor">[2]</a> 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.</p> +<p><span class="pagenum"><a name="Page_64" id="Page_64">[64]</a></span></p> + +<h4>Sclerosis of the Veins</h4> + +<p>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.)</p> + +<p>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.</p> + +<hr style="width: 65%;" /> +<p><span class="pagenum"><a name="Page_65" id="Page_65">[65]</a></span></p> +<h2><a name="CHAPTER_III" id="CHAPTER_III"></a>CHAPTER III.</h2> + +<h3>PHYSIOLOGY OF THE CIRCULATION</h3> + + +<p>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.</p> + +<p>"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.)</p> + +<p>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<span class="pagenum"><a name="Page_66" id="Page_66">[66]</a></span> +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.</p> + +<p>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<span class="pagenum"><a name="Page_67" id="Page_67">[67]</a></span> +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."</p> + +<p>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.</p> + +<p>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.</p> + +<p>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.</p> + +<p>It has been calculated that the average amount of blood +thrown into the aorta at every systole of the heart is from<span class="pagenum"><a name="Page_68" id="Page_68">[68]</a></span> +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.</p> + +<p>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.</p> + + +<h4>Blood Pressure</h4> + +<p>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.</p> + +<p><span class="pagenum"><a name="Page_69" id="Page_69">[69]</a></span>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.</p> + +<p>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 <i>all</i> 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.</p> + +<p>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 <i>moment when it was taken</i>. 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.</p> +<p><span class="pagenum"><a name="Page_70" id="Page_70">[70]</a></span></p> + +<h4>Blood Pressure Instruments</h4> + +<p>There are several instruments which are in common use +for the purpose of recording blood pressure in man.</p> + +<p>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.</p> + +<p>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.</p> + +<p>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<span class="pagenum"><a name="Page_71" id="Page_71">[71]</a></span> +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.</p> + +<p>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.</p> + +<p>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.</p> + +<p>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<span class="pagenum"><a name="Page_72" id="Page_72">[72]</a></span> +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.</p> + +<div class="figcenter" style="width: 500px;"> +<a name="Cooks_modification_of_Riva-Roccis_blood_pressure_instrument" id="Cooks_modification_of_Riva-Roccis_blood_pressure_instrument"></a> + +<img src="images/fig_013.png" width="500" height="386" alt="Fig. 13.—Cook's modification of Riva-Rocci's blood pressure instrument." title="Fig. 13.—Cook's modification of Riva-Rocci's blood pressure instrument." /> +<span class="caption">Fig. 13.—Cook's modification of Riva-Rocci's blood pressure instrument.</span> +</div> + +<p>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.</p> + +<div class="figcenter" style="width: 386px;"> + +<a name="Stantons_sphygmomanometer" id="Stantons_sphygmomanometer"></a> + +<img src="images/fig_014.png" width="386" height="500" alt="Fig. 14.—Stanton's sphygmomanometer." title="Fig. 14.—Stanton's sphygmomanometer." /> +<span class="caption">Fig. 14.—Stanton's sphygmomanometer.</span> +</div> + +<p>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<span class="pagenum"><a name="Page_73" id="Page_73">[73]</a></span> +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.</p> +<p><span class="pagenum"><a name="Page_74" id="Page_74">[74]</a></span></p> +<div class="figcenter" style="width: 362px;"> +<a name="The_Erlanger_sphygmomanometer_with_the_Hirschfelder_attachments" id="The_Erlanger_sphygmomanometer_with_the_Hirschfelder_attachments"></a> + +<img src="images/fig_015.png" width="362" height="500" alt="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." title="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." /> +<span class="caption">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.</span> +</div> + +<p>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<span class="pagenum"><a name="Page_75" id="Page_75">[75]</a></span> +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.</p> + +<div class="figcenter" style="width: 271px;"> + +<a name="Desk_model_Baumanometer" id="Desk_model_Baumanometer"></a> + +<img src="images/fig_016.png" width="271" height="500" alt="Fig. 16.—Desk model Baumanometer." title="Fig. 16.—Desk model Baumanometer." /> +<span class="caption">Fig. 16.—Desk model Baumanometer.</span> +</div> + +<p>The Faught instrument (Fig. 17) is larger than the +Brown, but is less easily broken and is not too cumbersome<span class="pagenum"><a name="Page_76" id="Page_76">[76]</a></span> +to carry around. The substitution of a metal air pump for +the rubber makes the apparatus more durable.</p> + +<div class="figcenter" style="width: 483px;"> + +<a name="Faught_blood_pressure_instrument" id="Faught_blood_pressure_instrument"></a> + +<img src="images/fig_017.png" width="483" height="500" alt="Fig. 17.—The Faught blood pressure instrument. An excellent instrument which is +quite easily carried about and is not easily broken." title="Fig. 17.—The Faught blood pressure instrument. An excellent instrument which is +quite easily carried about and is not easily broken." /> +<span class="caption">Fig. 17.—The Faught blood pressure instrument. An excellent instrument which is +quite easily carried about and is not easily broken.</span> +</div> + +<p>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.</p> + +<p>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.</p> + +<p>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.</p> + +<p>There is, however, the inertia of the mercury to be overcome,<span class="pagenum"><a name="Page_77" id="Page_77">[77]</a></span> +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.</p> + +<div class="figcenter" style="width: 500px;"> + +<a name="Rogers_Tycos_dial_sphygmomanometer" id="Rogers_Tycos_dial_sphygmomanometer"></a> + +<img src="images/fig_018.png" width="500" height="341" alt="Fig. 18.—Rogers' "Tycos" dial sphygmomanometer." title="Fig. 18.—Rogers' "Tycos" dial sphygmomanometer." /> +<span class="caption">Fig. 18.—Rogers' "Tycos" dial sphygmomanometer.</span> +</div> + +<p>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<span class="pagenum"><a name="Page_78" id="Page_78">[78]</a></span> +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<span class="pagenum"><a name="Page_79" id="Page_79">[79]</a></span> +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<span class="pagenum"><a name="Page_80" id="Page_80">[80]</a></span> +"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.</p> + +<div class="figcenter" style="width: 297px;"> + +<a name="Detail_of_the_dial_in_the_Tycos_instrument" id="Detail_of_the_dial_in_the_Tycos_instrument"></a> + +<img src="images/fig_019.png" width="297" height="500" alt="Fig. 19.—Detail of the dial in the "Tycos" instrument." title="Fig. 19.—Detail of the dial in the "Tycos" instrument." /> +<span class="caption">Fig. 19.—Detail of the dial in the "Tycos" instrument.</span> +</div> + +<div class="figcenter" style="width: 500px;"> + +<a name="Faught_dial_instrument" id="Faught_dial_instrument"></a> + +<img src="images/fig_020.png" width="500" height="323" alt="Fig. 20.—Faught dial instrument." title="Fig. 20.—Faught dial instrument." /> +<span class="caption">Fig. 20.—Faught dial instrument.</span> +</div> + +<div class="figcenter" style="width: 282px;"> + +<a name="Detail_of_the_dial_of_the_Faught_instrument" id="Detail_of_the_dial_of_the_Faught_instrument"></a> + +<img src="images/fig_021.png" width="282" height="500" alt="Fig. 21.—Detail of the dial of the Faught instrument." title="Fig. 21.—Detail of the dial of the Faught instrument." /> +<span class="caption">Fig. 21.—Detail of the dial of the Faught instrument.</span> +</div> + +<p>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.</p> + +<div class="figcenter bord" style="width: 500px;"> + +<a name="The_Sanborn_instrument" id="The_Sanborn_instrument"></a> + +<img src="images/fig_022.png" width="500" height="246" alt="Fig. 22.—The Sanborn instrument." title="Fig. 22.—The Sanborn instrument." /> +<span class="caption">Fig. 22.—The Sanborn instrument.</span> +</div> + +<p>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.</p> + + +<h4>Technic</h4> + +<p>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<span class="pagenum"><a name="Page_81" id="Page_81">[81]</a></span> +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 <i>0</i> 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<span class="pagenum"><a name="Page_82" id="Page_82">[82]</a></span> +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.</p> + +<div class="figcenter bord" style="width: 500px;"> +<a name="Method_of_taking_blood_pressure_with_a_patient_in_sitting_position" id="Method_of_taking_blood_pressure_with_a_patient_in_sitting_position"></a> +<img src="images/fig_023.png" width="500" height="417" alt="Fig. 23.—Method of taking blood pressure with a patient in sitting position." title="Fig. 23.—Method of taking blood pressure with a patient in sitting position." /> +<span class="caption">Fig. 23.—Method of taking blood pressure with a patient in sitting position.</span> +</div> + +<div class="figcenter bord" style="width: 500px;"> + +<a name="Method_of_taking_blood_pressure_with_patient_lying_down" id="Method_of_taking_blood_pressure_with_patient_lying_down"></a> + + +<img src="images/fig_024.png" width="500" height="349" alt="Fig. 24.—Method of taking blood pressure with patient lying down." title="Fig. 24.—Method of taking blood pressure with patient lying down." /> +<span class="caption">Fig. 24.—Method of taking blood pressure with patient lying down.</span> +</div> + +<p>The pressure is now allowed to fall, until the palpating<span class="pagenum"><a name="Page_83" id="Page_83">[83]</a></span> +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.</p> + +<p>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.</p> + +<p>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. <i>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.</i></p> + +<p>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<span class="pagenum"><a name="Page_84" id="Page_84">[84]</a></span> +cuff.<a name="FNanchor_3_3" id="FNanchor_3_3"></a><a href="#Footnote_3_3" class="fnanchor">[3]</a> 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<span class="pagenum"><a name="Page_85" id="Page_85">[85]</a></span> +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.</p> + +<div class="figcenter bord" style="width: 500px;"> + +<a name="Observation_by_the_auscultatory_method_and_a_mercury_instrument" id="Observation_by_the_auscultatory_method_and_a_mercury_instrument"></a> + + +<img src="images/fig_025.png" width="500" height="484" alt="Fig. 25.—Observation by the auscultatory method and a mercury instrument. One hand +regulates the stop cock which releases air gradually." title="Fig. 25.—Observation by the auscultatory method and a mercury instrument. One hand +regulates the stop cock which releases air gradually." /> +<span class="caption">Fig. 25.—Observation by the auscultatory method and a mercury instrument. One hand +regulates the stop cock which releases air gradually.</span> +</div> + +<div class="figcenter bord" style="width: 500px;"> +<a name="Observation_by_the_auscultatory_method_and_a_dial_instrument" id="Observation_by_the_auscultatory_method_and_a_dial_instrument"></a> + +<img src="images/fig_026.png" width="500" height="485" alt="Fig. 26.—Observation by the auscultatory method and a dial instrument. The right +hand holds the bulb and regulates the air valve." title="Fig. 26.—Observation by the auscultatory method and a dial instrument. The right +hand holds the bulb and regulates the air valve." /> +<span class="caption">Fig. 26.—Observation by the auscultatory method and a dial instrument. The right +hand holds the bulb and regulates the air valve.</span> +</div> + + +<h4>Arterial Pressure</h4> + +<p>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 <b>maximum</b> or <b>systolic pressure</b>. It +practically equals the intraventricular pressure. The minimum +pressure in the artery, the pressure at the end of diastole, +is called the <b>diastolic pressure</b>. The difference between +the systolic and diastolic pressures is known as the +<b>pulse pressure</b>. There is yet another term known as the +<b>mean pressure</b>. For convenience, this may be said to be the<span class="pagenum"><a name="Page_86" id="Page_86">[86]</a></span> +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.</p> + +<div class="figcenter" style="width: 500px;"> +<a name="Schema_to_illustrate_decrease_in_pressure" id="Schema_to_illustrate_decrease_in_pressure"></a> + +<img src="images/fig_027.png" width="500" height="193" alt="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.)" title="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.)" /> +<span class="caption">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.)</span> +</div> + +<p>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.</p> + +<p>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<span class="pagenum"><a name="Page_87" id="Page_87">[87]</a></span> +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.</p> + +<p>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.</p> + +<p>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.</p> + +<p>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<span class="pagenum"><a name="Page_88" id="Page_88">[88]</a></span> +vessels without actually carrying on the circulation adequately.</p> + + +<h4>Normal Pressure Variations</h4> + +<p>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.)</p> + +<div class="figcenter" style="width: 441px;"> + +<a name="Chart_showing_the_normal_limits_of_variation_in_systolic_blood_pressure" id="Chart_showing_the_normal_limits_of_variation_in_systolic_blood_pressure"></a> + + +<img src="images/fig_028.png" width="441" height="500" alt="Fig. 28.—Chart showing the normal limits of variation in systolic blood pressure. (After +Woley.)" title="Fig. 28.—Chart showing the normal limits of variation in systolic blood pressure. (After +Woley.)" /> +<span class="caption">Fig. 28.—Chart showing the normal limits of variation in systolic blood pressure. (After +Woley.)</span> +</div> + +<p>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.</p> + +<p>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<span class="pagenum"><a name="Page_89" id="Page_89">[89]</a></span> +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<span class="pagenum"><a name="Page_90" id="Page_90">[90]</a></span> +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.</p> + + +<h4>The Auscultatory Blood Pressure Phenomenon</h4> + +<p>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<span class="pagenum"><a name="Page_91" id="Page_91">[91]</a></span> +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.)</p> + +<p>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.</p> + +<p>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.</p> + +<p>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.</p> + +<p>The fourth phase is a transition from the third and becomes +duller in sound as the artery approaches the normal +size.</p> + +<p>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.</p> + +<p>It is generally conceded that the sounds heard are produced +in the artery itself and not at the heart.</p> + +<p>The tones vary greatly in different hearts. A very +strong third tone phase or prolongation of this phase usually<span class="pagenum"><a name="Page_92" id="Page_92">[92]</a></span> +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.</p> + +<p>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.</p> + +<p>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.</p> + +<p>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<span class="pagenum"><a name="Page_93" id="Page_93">[93]</a></span> +the auscultatory method which can not be heard at the +heart.</p> + +<p>In anemia the sounds are very loud and clear and do not +seem to represent the actual strength of the heart.</p> + +<p>The general lack of vasomotor tone in the blood vessels +together with some atrophy and flabbiness of the coats +probably explains the loud sounds.</p> + +<p>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.</p> + +<p>In not all cases can all phases be made out. It is usually +the fourth phase which fails to be heard.</p> + +<p>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.</p> + +<p>"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.</p> + +<p>"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.)</p> + +<p>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.</p> +<p><span class="pagenum"><a name="Page_94" id="Page_94">[94]</a></span></p> + +<h4>The Maximum and Minimum Pressures</h4> + +<p>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<span class="pagenum"><a name="Page_95" id="Page_95">[95]</a></span> +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.</p> + +<div class="figcenter bord" style="width: 500px;"> +<a name="Tracing_of_auscultatory_phenomena" id="Tracing_of_auscultatory_phenomena"></a> + +<img src="images/fig_029.png" width="500" height="479" alt="Fig. 29.—Tracing of auscultatory phenomena. (See explanation in legend of Fig. 30.)" title="Fig. 29.—Tracing of auscultatory phenomena. (See explanation in legend of Fig. 30.)" /> +<span class="caption">Fig. 29.—Tracing of auscultatory phenomena. (See explanation in legend of Fig. 30.)</span> +</div> + +<div class="figcenter" style="width: 500px;"> + +<a name="Tracings_of_auscultatory_phenomena" id="Tracings_of_auscultatory_phenomena"></a> + + +<img src="images/fig_030.png" width="500" height="260" alt="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." title="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)...." /> +<span class="caption">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.</span> +</div> + +<p>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<span class="pagenum"><a name="Page_96" id="Page_96">[96]</a></span> +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.<span class="pagenum"><a name="Page_97" id="Page_97">[97]</a></span></p> + +<div class="figcenter" style="width: 500px;"> + +<a name="Clinical_determination_of_diastolic_pressure_fast_drum" id="Clinical_determination_of_diastolic_pressure_fast_drum"></a> + + +<img src="images/fig_031.png" width="500" height="83" alt="Fig. 31.—Fast drum. Sudden decrease in size of pulse wave at 4, marking the change +from clear sharp tone to dull tone." title="Fig. 31.—Fast drum. Sudden decrease in size of pulse wave at 4, marking the change +from clear sharp tone to dull tone." /> +<span class="caption">Fig. 31.—Fast drum. Sudden decrease in size of pulse wave at 4, marking the change +from clear sharp tone to dull tone.</span> +</div> + +<div class="figcenter" style="width: 500px;"> + +<a name="Clinical_determination_of_diastolic_pressure_slow_drum" id="Clinical_determination_of_diastolic_pressure_slow_drum"></a> + + +<img src="images/fig_032.png" width="500" height="315" alt="Fig. 32.—Slow drum. Sudden decrease in amplitude at 4." title="Fig. 32.—Slow drum. Sudden decrease in amplitude at 4." /> +<span class="caption">Fig. 32.—Slow drum. Sudden decrease in amplitude at 4.</span> +</div> + +<p>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.</p> + +<p>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.</p> + + +<h4>The Relative Importance of the Systolic and Diastolic Pressures</h4> + +<p>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<span class="pagenum"><a name="Page_98" id="Page_98">[98]</a></span> +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.</p> + +<p>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.<a name="FNanchor_4_4" id="FNanchor_4_4"></a><a href="#Footnote_4_4" class="fnanchor">[4]</a></p> + +<p>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.</p> + +<p>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.</p> + +<p>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<span class="pagenum"><a name="Page_99" id="Page_99">[99]</a></span> +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.</p> + +<p>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.</p> + +<p>The diastolic pressure then is of importance for the following +reasons:</p> + +<p>1. It measures peripheral resistance.</p> + +<p>2. It is the measure of the tonus of the vasomotor system.</p> + +<p>3. It is one of the points to determine pulse pressure.</p> + +<p>4. Pulse pressure measures the actual driving force, the +kinetic energy of the heart.</p> + +<p>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.</p> + +<p>6. It is more stable than the systolic pressure, subject to +fewer more or less unknown influences.</p> + +<p>7. It is increased by exercise.</p> + +<p>8. It is increased by conditions which increase peripheral +resistance.</p> + +<p>9. The gradual increase of diastolic pressure means +harder work for the heart to supply the parts of the body +with blood.</p> + +<p>10. Increased diastolic pressure is always accompanied +by increased pulse pressure, and increased size of the left +ventricle, temporarily (exercise) or permanently.</p> + +<p><span class="pagenum"><a name="Page_100" id="Page_100">[100]</a></span>11. Decreased diastolic pressure goes hand in hand with +vasomotor relaxation, as in fevers, etc.</p> + +<p>12. Low diastolic pressure is frequently pathognomonic +of aortic insufficiency.</p> + +<p>13. When the systolic and diastolic pressures approach, +heart failure is imminent either when pressure picture is +high or low.</p> + +<p>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.</p> + +<p>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.</p> + + +<h4>Pulse Pressure</h4> + +<p>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 × pulse pressure.<a name="FNanchor_5_5" id="FNanchor_5_5"></a><a href="#Footnote_5_5" class="fnanchor">[5]</a></p> +<p><span class="pagenum"><a name="Page_101" id="Page_101">[101]</a></span></p> +<p>Further it has been demonstrated that under normal conditions +and during various procedures—the pulse pressure +is a reliable index of the systolic output.<a name="FNanchor_6_6" id="FNanchor_6_6"></a><a href="#Footnote_6_6" class="fnanchor">[6]</a></p> + +<p>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<span class="pagenum"><a name="Page_102" id="Page_102">[102]</a></span> +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.</p> + +<p>It is evident then that pulse pressure is exceedingly important. +It can only be determined by measuring both the +<i>systolic</i> and <i>diastolic</i> 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.</p> + +<p>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.</p> + +<p>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."</p> + + +<h4>Blood Pressure Variations</h4> + +<p>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<span class="pagenum"><a name="Page_103" id="Page_103">[103]</a></span> +take place. Throughout the day, it tends to become slightly +lower. The pulse pressure then is greater towards evening.</p> + +<p>Weysse and Lutz in a study of this question draw the following +conclusions:</p> + +<p>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.</p> + +<p>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.</p> + +<p>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.</p> + +<p>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.</p> + +<p>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.</p> + +<p>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.</p> + +<p>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.</p> +<div class="center"><span class="smcap">The Average Diurnal Blood Pressure Record of the Ten Subjects</span></div> + + + + +<table summary="Diurnal blood Pressure"> + + <tr> + <th class="tdouble">TIME</th> + <th class="tdouble">MAXIMUM</th> + <th class="tdouble">MINIMUM</th> + <th class="tdouble">MEAN</th> + <th class="tdouble">PULSE</th> + <th class="tdouble">PULSE</th> + <th class="tdouble">PP x PR</th> + <th class="tdouble">NOTES</th></tr> + + +<tr> +<th class="bdouble bb"> </th> +<th class="bdouble bb"> </th> +<th class="bdouble bb"> </th> +<th class="bdouble bb"> </th> +<th class="bdouble bb">PRESSURE</th> +<th class="bdouble bb">RATE</th> +<th class="bdouble bb"> </th> +<th class="bdouble bb"> </th> +</tr> + + +<tr><td align="left"> </td><td align="left"><i>mm.</i>Hg</td><td align="left"><i>mm.</i>Hg</td><td align="left"><i>mm.</i>Hg</td><td align="left"><i>mm.</i>Hg</td></tr> +<tr><td align="left">4:30 p.m.</td><td align="left">119.5</td><td align="left">84.1</td><td align="left">101.8</td><td align="left">35.4</td><td align="left">72.0</td><td align="left">2549</td></tr> +<tr><td align="left">5:00 p.m.</td><td align="left">117.7</td><td align="left">83.5</td><td align="left">100.6</td><td align="left">34.2</td><td align="left">71.1</td><td align="left">2432</td></tr> +<tr><td align="left">6:00 p.m.</td><td align="left">118.0</td><td align="left">84.0</td><td align="left">101.0</td><td align="left">34.0</td><td align="left">74.9</td><td align="left">2547</td><td align="left">Before dinner</td></tr> +<tr><td align="left">6:45 p.m.</td><td align="left">127.2</td><td align="left">88.2</td><td align="left">107.7</td><td align="left">39.0</td><td align="left">78.1</td><td align="left">3046</td><td align="left">After dinner</td></tr> +<tr><td align="left">7:00 p.m.</td><td align="left">124.7</td><td align="left">87.7</td><td align="left">106.2</td><td align="left">37.0</td><td align="left">76.0</td><td align="left">2812</td></tr> +<tr><td align="left">7:30 p.m.</td><td align="left">122.0</td><td align="left">83.4</td><td align="left">102.7</td><td align="left">38.6</td><td align="left">76.0</td><td align="left">2934</td></tr> +<tr><td align="left">8:00 p.m.</td><td align="left">122.4</td><td align="left">85.5</td><td align="left">103.4</td><td align="left">36.9</td><td align="left">71.2</td><td align="left">2527</td></tr> +<tr><td align="left">8:30 p.m.</td><td align="left">120.0</td><td align="left">85.0</td><td align="left">102.5</td><td align="left">35.0</td><td align="left">69.7</td><td align="left">2439</td></tr> +<tr><td align="left">9:00 p.m.</td><td align="left">120.5</td><td align="left">84.7</td><td align="left">102.5</td><td align="left">35.8</td><td align="left">65.2</td><td align="left">2334</td></tr> +<tr><td align="left">9:30 p.m.</td><td align="left">118.2</td><td align="left">84.4</td><td align="left">101.6</td><td align="left">33.8</td><td align="left">64.4</td><td align="left">2177</td></tr> +<tr><td align="left">7:30 a.m.</td><td align="left">118.4</td><td align="left">87.6</td><td align="left">103.0</td><td align="left">30.8</td><td align="left">70.3</td><td align="left">2165</td></tr> +<tr><td align="left">8:00 a.m.</td><td align="left">116.4</td><td align="left">86.4</td><td align="left">101.4</td><td align="left">30.0</td><td align="left">69.8</td><td align="left">2094</td><td align="left">Before breakfast</td></tr> +<tr><td align="left">8:30 a.m.</td><td align="left">124.2</td><td align="left">85.4</td><td align="left">104.8</td><td align="left">38.8</td><td align="left">79.4</td><td align="left">3081</td><td align="left">After breakfast</td></tr> +<tr><td align="left">9:00 a.m.</td><td align="left">123.8</td><td align="left">84.4</td><td align="left">104.1</td><td align="left">39.4</td><td align="left">84.1</td><td align="left">3313</td></tr> +<tr><td align="left">10:00 a.m.</td><td align="left">118.2</td><td align="left">83.6</td><td align="left">100.9</td><td align="left">34.6</td><td align="left">70.7</td><td align="left">2446</td></tr> +<tr><td align="left">11:00 a.m.</td><td align="left">116.2</td><td align="left">84.8</td><td align="left">100.5</td><td align="left">31.4</td><td align="left">67.7</td><td align="left">2126</td></tr> +<tr><td align="left">12:00 m</td><td align="left">114.4</td><td align="left">83.2</td><td align="left">98.8</td><td align="left">31.2</td><td align="left">66.2</td><td align="left">2065</td><td align="left">Before luncheon</td></tr> +<tr><td align="left">12:30 p.m.</td><td align="left">122.8</td><td align="left">83.2</td><td align="left">103.0</td><td align="left">39.6</td><td align="left">70.9</td><td align="left">2808</td><td align="left">After luncheon</td></tr> +<tr><td align="left">1:00 p.m.</td><td align="left">122.3</td><td align="left">82.0</td><td align="left">102.1</td><td align="left">40.3</td><td align="left">79.7</td><td align="left">3212</td></tr> +<tr><td align="left">2:00 p.m.</td><td align="left">118.4</td><td align="left">81.4</td><td align="left">99.9</td><td align="left">37.0</td><td align="left">77.6</td><td align="left">2871</td></tr> +<tr><td align="left">3:00 p.m.</td><td align="left">118.8</td><td align="left">82.6</td><td align="left">100.7</td><td align="left">36.2</td><td align="left">75.1</td><td align="left">2719</td></tr> +<tr><td align="left">4:00 p.m.</td><td align="left">115.8</td><td align="left">82.0</td><td align="left">98.9</td><td align="left">33.8</td><td align="left">71.9</td><td align="left">2420</td></tr> +<tr><td align="left">5:00 p.m.</td><td align="left">117.2</td><td align="left">83.4</td><td align="left">100.3</td><td align="left">33.8</td><td align="left">69.6</td><td align="left">2352</td></tr> +<tr><td align="left">6:00 p.m.</td><td align="left">117.4</td><td align="left">84.4</td><td align="left">100.9</td><td align="left">33.0</td><td align="left">72.8</td><td align="left">2402</td><td align="left">Before dinner</td></tr> +<tr><td align="left">6:45 p.m.</td><td align="left">124.6</td><td align="left">83.1</td><td align="left">103.8</td><td align="left">41.5</td><td align="left">80.4</td><td align="left">3337</td><td align="left">After dinner</td></tr> +<tr><td align="left">7:00 p.m.</td><td align="left">125.2</td><td align="left">84.2</td><td align="left">104.7</td><td align="left">41.0</td><td align="left">76.1</td><td align="left">3120</td></tr> +<tr><td align="left">7:30 p.m.</td><td align="left">122.0</td><td align="left">84.0</td><td align="left">103.0</td><td align="left">38.0</td><td align="left">73.7</td><td align="left">2801</td></tr> +<tr><td align="left">8:00 p.m.</td><td align="left">119.6</td><td align="left">85.0</td><td align="left">102.3</td><td align="left">34.6</td><td align="left">72.3</td><td align="left">2502</td></tr> +<tr><td align="left">8:30 p.m.</td><td align="left">119.7</td><td align="left">84.0</td><td align="left">101.3</td><td align="left">34.7</td><td align="left">69.0</td><td align="left">2394</td></tr> +<tr><td align="left">9:00 p.m.</td><td align="left">120.0</td><td align="left">86.2</td><td align="left">103.1</td><td align="left">33.8</td><td align="left">68.0</td><td align="left">2298</td></tr> +<tr><td align="left">Average</td><td align="left">120.0</td><td align="left">85.0</td><td align="left">102.5</td><td align="left">35.0</td><td align="left">72.0</td><td align="left">2550</td></tr> +</table> + +<div class="center">(Taken from Weysse and Lutz.)</div> + + +<p>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.</p> + +<p><span class="pagenum"><a name="Page_105" id="Page_105">[105]</a></span>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. <sup>1</sup>⁄<sub>100</sub> (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.</p> + +<p>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.</p> + +<p>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.</p> + +<p>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.)</p> + +<p>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<span class="pagenum"><a name="Page_106" id="Page_106">[106]</a></span> +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.</p> + + +<h4>Hypertension</h4> + +<p>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.</p> + +<p>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<span class="pagenum"><a name="Page_107" id="Page_107">[107]</a></span> +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.</p> + +<p>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<a name="FNanchor_7_7" id="FNanchor_7_7"></a><a href="#Footnote_7_7" class="fnanchor">[7]</a> 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.</p> + +<p>What makes hypertension of significance is not the hypertension +itself, but the fact that it is the expression of<span class="pagenum"><a name="Page_108" id="Page_108">[108]</a></span> +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.</p> + +<p>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.</p> + +<p>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,<a name="FNanchor_8_8" id="FNanchor_8_8"></a><a href="#Footnote_8_8" class="fnanchor">[8]</a> 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, <i>overload</i>, 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.</p> +<p><span class="pagenum"><a name="Page_109" id="Page_109">[109]</a></span></p> +<p>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<a name="FNanchor_9_9" id="FNanchor_9_9"></a><a href="#Footnote_9_9" class="fnanchor">[9]</a> 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).</p> + +<p>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.</p> + +<p>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.</p> + +<p>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<span class="pagenum"><a name="Page_110" id="Page_110">[110]</a></span> +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.</p> + +<p>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<a name="FNanchor_10_10" id="FNanchor_10_10"></a><a href="#Footnote_10_10" class="fnanchor">[10]</a> 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.</p> + +<p>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.</p> + +<p>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<span class="pagenum"><a name="Page_111" id="Page_111">[111]</a></span> +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.</p> + +<p>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.</p> + +<p>Stone<a name="FNanchor_11_11" id="FNanchor_11_11"></a><a href="#Footnote_11_11" class="fnanchor">[11]</a> 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<span class="pagenum"><a name="Page_112" id="Page_112">[112]</a></span> +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 ½ 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.</p> + +<p>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."</p> + +<p>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.</p> + +<p>Group A. Chronic nephritis.</p> + +<p>Group B. Essential hypertension.</p> + +<p>Group C. Arteriosclerotic hypertension.</p> + +<p>Group A. <i>Chronic Nephritis.</i> 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<span class="pagenum"><a name="Page_113" id="Page_113">[113]</a></span> +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.</p> + +<p>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.</p> + +<p>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.</p> + +<p>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,<span class="pagenum"><a name="Page_114" id="Page_114">[114]</a></span> +these cases fall into the group of secondary contracted kidneys, +chronic parenchymatous nephritis.</p> + +<blockquote><p>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<sub>3</sub> 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<sub>2</sub> +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.</p></blockquote> + +<p>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<span class="pagenum"><a name="Page_115" id="Page_115">[115]</a></span> +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.</p> + +<p>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.</p> + +<blockquote><p>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<span class="pagenum"><a name="Page_116" id="Page_116">[116]</a></span> +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.</p></blockquote> + +<p>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.</p> + +<p>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.</p> + +<p>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 <i>cor bovinum</i>, dilated +and hypertrophied. The cavity of the left ventricle is much +dilated. The aorta is dilated and sclerosed.</p> + +<p><span class="pagenum"><a name="Page_117" id="Page_117">[117]</a></span>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.</p> + +<blockquote><p>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 <i>cor bovinum</i>. The kidneys were typical of this condition, possibly +somewhat larger than usual.</p></blockquote> + + +<h4>Hypotension</h4> + +<p>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<span class="pagenum"><a name="Page_118" id="Page_118">[118]</a></span> +most fevers and in a great variety of diseases, including +anemias.</p> + +<p>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.</p> + +<p>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.</p> + +<p>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.</p> + +<p>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.</p> + +<p>In pleurisy with effusion and in pericarditis with effusion +there is hypotension.</p> + +<p>Collapse, whether from poisoning by drugs or as the result +of dysentery, cholera, or profuse vomiting from whatever +cause, reduces the blood pressure.</p> + +<p>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."</p> + +<p>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:</p> + +<p>"Hypotension or subnormal blood pressure is universally<span class="pagenum"><a name="Page_119" id="Page_119">[119]</a></span> +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.</p> + +<p>"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.</p> + +<p>"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.</p> + +<p>"... 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...."</p> + +<p>There are a few drugs which lower the blood pressure,<span class="pagenum"><a name="Page_120" id="Page_120">[120]</a></span> +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.</p> + + +<div class="center">SOME DRUGS WHICH INFLUENCE THE BLOOD PRESSURE</div> + +<p> +<b>Pressure Raisers</b><br /> +<br /> +Adrenalin, when injected directly<br /> +into a vein or deep into the muscles.<br /> +The action is transitory.<br /> +<br /> +Caffeine, preferably in the form<br /> +of caffeine-sodium-benzoate. A good<br /> +drug.<br /> +<br /> +Strychnine, which does not act directly<br /> +but seemingly through the<br /> +higher centers.<br /> +<br /> +Ergot, somewhat uncertain.<br /> +<br /> +Nicotine, not used therapeutically.<br /> +<br /> +Camphor, used in sterile olive oil<br /> +and injected deeply into the muscles.<br /> +<br /> +Digitalis, when the cardiac tone is<br /> +low and decompensation is present.<br /> +Its action is prolonged but slow. Injections<br /> +of the infundibular portion<br /> +of the pituitary body. Not in use<br /> +clinically.<br /> +<br /> +<br /> +<b>Pressure Depressors</b><br /> +<br /> +Nitroglycerine and amyl nitrite,<br /> +action transitory but rapid.<br /> +<br /> +Sodium nitrite and erythrol tetranitrate.<br /> +Action somewhat more prolonged.<br /> +<br /> +Aconite, veratrum viride, chloral,<br /> +etc. These depress the heart.<br /> +<br /> +Purgatives, drastic and hydragogue.<br /> +<br /> +Potassium and sodium iodide may<br /> +lower blood pressure. When they do,<br /> +the action is prolonged.<br /> +<br /> +Diuretin and theocin-sodium-acetate.<br /> +</p> + + +<h4>Venous Pressure</h4> + +<p>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.</p> + +<div class="figcenter" style="width: 330px;"> + +<a name="Venous_blood_pressure_instrument" id="Venous_blood_pressure_instrument"></a> + + +<img src="images/fig_033.png" width="330" height="500" alt="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." title="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." /> +<span class="caption">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.</span> +</div> + +<p>In the apparatus shown in the figure (Fig. 33), Drs. +Hooker and Eyster succeeded in making estimations of the +venous pressure. The box <i>B</i> is held in position by the tapes +<i>A</i>, 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 <i>G</i>, by a rubber tube, +from which a T-tube enters the rubber bulb <i>E</i>. When the +bulb <i>E</i> is compressed between the plates <i>D</i>, by the coarse<span class="pagenum"><a name="Page_121" id="Page_121">[121]</a></span> +thumbscrew <i>C</i>, air is forced into the box <i>B</i>, exerting a pressure +on the vein lying exposed beneath. This pressure is +transmitted directly to the manometer <b>G</b>, 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<span class="pagenum"><a name="Page_122" id="Page_122">[122]</a></span> +these figures to the manometer reading, we obtain the +venous pressure at the heart level.</p> + +<p>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.</p> + +<div class="figcenter bord" style="width: 500px;"> + +<a name="New_venous_pressure_instrument" id="New_venous_pressure_instrument"></a> + + +<img src="images/fig_034.png" width="500" height="424" alt="Fig. 34.—New venous pressure instrument. (After Eyster.)" title="Fig. 34.—New venous pressure instrument. (After Eyster.)" /> +<span class="caption">Fig. 34.—New venous pressure instrument. (After Eyster.)</span> +</div> + +<p>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<span class="pagenum"><a name="Page_123" id="Page_123">[123]</a></span> +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.</p> + +<p>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.</p> + + +<h4>The Pulse</h4> + +<p>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.</p> + + +<h4>The Venous Pulse</h4> + +<p>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<span class="pagenum"><a name="Page_124" id="Page_124">[124]</a></span> +to the fluctuations in the cardiac cycle. To understand +these waves and their values, the accompanying +figure is helpful. (Fig. 35.)</p> + +<div class="figcenter" style="width: 500px;"> + +<a name="Events_in_the_cardiac_cycle" id="Events_in_the_cardiac_cycle"></a> + + +<img src="images/fig_035.png" width="500" height="459" alt="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.)" title="Fig. 35.—Semidiagrammatic representation of the events in the cardiac cycle.... (After Hirschfelder.)" /> +<span class="caption">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.)</span> +</div> + +<p>Bachmann summarizes the normal waves in the venous +pulse tracing as follows:</p> + +<p>"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 (<i>a</i>) 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 (<i>S</i>) is +presystolic in time, and originates in the sudden projection<span class="pagenum"><a name="Page_125" id="Page_125">[125]</a></span> +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 (<i>v</i>) 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.</p> + +<p><span class="pagenum"><a name="Page_126" id="Page_126">[126]</a></span>"The first negative wave (between positive wave <i>a</i> and +<i>S</i>) is due to the relaxing auricle. The second negative +wave (<i>Af</i>) 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 (<i>Vf</i>) 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.)</p> + +<div class="figcenter" style="width: 500px;"> + +<a name="Simultaneous_tracings_of_the_jugular_and_carotid_pulses" id="Simultaneous_tracings_of_the_jugular_and_carotid_pulses"></a> + + +<img src="images/fig_036.png" width="500" height="295" alt="Fig. 36.—Simultaneous tracings of the jugular and carotid pulses showing normal waves +in the venous pulse and relation to carotid pulse. (After Bachmann.)" title="Fig. 36.—Simultaneous tracings of the jugular and carotid pulses showing normal waves +in the venous pulse and relation to carotid pulse. (After Bachmann.)" /> +<span class="caption">Fig. 36.—Simultaneous tracings of the jugular and carotid pulses showing normal waves +in the venous pulse and relation to carotid pulse. (After Bachmann.)</span> +</div> + +<p>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.)</p> + +<div class="figcenter" style="width: 500px;"> + +<a name="Jugular_and_carotid_tracings" id="Jugular_and_carotid_tracings"></a> + + +<img src="images/fig_037.png" width="500" height="169" alt="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.)" title="Fig. 37.—Jugular and carotid tracing from a normal individual with a well-marked +third heart sound.... (After Hirschfelder.)" /> +<span class="caption">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.)</span> +</div> + +<h4>The Electrocardiogram</h4> + +<p>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<span class="pagenum"><a name="Page_127" id="Page_127">[127]</a></span> +is orderly, regular, and normally invariable. (Fig. +38.)</p> + +<div class="figcenter" style="width: 473px;"> + +<a name="Right_side_of_the_heart_showing_distribution_of_the_two_vagus_nerves" id="Right_side_of_the_heart_showing_distribution_of_the_two_vagus_nerves"></a> + + +<img src="images/fig_038.png" width="473" height="500" alt="Fig. 38.—Right side of the heart showing diagrammatically the distribution of the +two vagus nerves to different parts of the viscus....(Hare's Practice of Medicine.)" title="Fig. 38.—Right side of the heart showing diagrammatically the distribution of the +two vagus nerves to different parts of the viscus.... (Hare's Practice of Medicine.)" /> +<span class="caption">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.)</span> +</div> + +<p>The sino-auricular (s-a) node is the most irritable portion +of the heart, it is endowed with the greatest amount<span class="pagenum"><a name="Page_129" id="Page_129">[129]</a></span><span class="pagenum"><a name="Page_128" id="Page_128"></a></span> +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.</p> + +<p>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.</p> + +<p>The record is made in three so-called Leads.</p> + +<div class="center"> +Lead I<br /> +<br /> +The electrodes are attached to right arm and left arm.<br /> +<br /> +Lead II<br /> +<br /> +The electrodes are attached to right arm and left leg.<br /> +<br /> +Lead III<br /> +<br /> +The electrodes are attached to left arm and left leg.<br /> +</div> + +<p>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 <i>P</i>, <i>Q</i>, <i>R</i>, <i>S</i>, <i>T</i>. There is some difference +in the three leads. "The wave <i>P</i> is positive in <i>all +leads</i>. <i>P</i> to <i>R</i> interval varies slightly in the <i>three leads</i>. +All the waves of <i>Lead II</i> are greater than those of <i>Leads I</i> +and <i>III</i>. The wave <i>R</i> is positive in <i>all leads</i>. <i>T</i> is usually +positive in <i>all leads</i>, 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.)</p> + +<div class="figcenter" style="width: 312px;"> + +<a name="Normal_electrocardiogram" id="Normal_electrocardiogram"></a> + + +<img src="images/fig_039.png" width="312" height="500" alt="Fig. 39.—Normal electrocardiogram. (After Hart.)" title="Fig. 39.—Normal electrocardiogram. (After Hart.)" /> +<span class="caption">Fig. 39.—Normal electrocardiogram. (After Hart.)</span> +</div> + +<p>The <i>P</i> wave is admitted to be the wave of auricular contraction. +<i>Q</i>, <i>R</i>, <i>S</i>, is the ventricular complex caused, it is<span class="pagenum"><a name="Page_130" id="Page_130">[130]</a></span> +thought, by the current passing over the ventricles. <i>T</i> +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 <i>T</i> wave is usually increased +in size during exercise.</p> + +<p>The <i>P-R</i> 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.</p> + +<p>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.</p> + +<hr style="width: 65%;" /> +<p><span class="pagenum"><a name="Page_131" id="Page_131">[131]</a></span></p> +<h2><a name="CHAPTER_IV" id="CHAPTER_IV"></a>CHAPTER IV.</h2> + +<h3>IMPORTANT CARDIAC IRREGULARITIES +ASSOCIATED WITH ARTERIOSCLEROSIS</h3> + + +<p>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.</p> + +<p>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.</p> + + +<h4>Auricular Flutter</h4> + +<p>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<span class="pagenum"><a name="Page_132" id="Page_132">[132]</a></span> +of a heart in such a state (Fig. 40) shows the +ventricle beating regularly but at a much slower rate than +the auricle.</p> + +<div class="figcenter" style="width: 459px;"> + +<a name="Auricular_flutter" id="Auricular_flutter"></a> + + +<img src="images/fig_040.png" width="459" height="500" alt="Fig. 40.—(After Hart.)" title="Fig. 40.—(After Hart.)" /> +<span class="caption">Fig. 40.—(After Hart.)</span> +</div> + +<p>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.</p> + +<p><span class="pagenum"><a name="Page_133" id="Page_133">[133]</a></span>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.</p> + + +<h4>Auricular Fibrillation</h4> + +<p>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.</p> + +<div class="figcenter" style="width: 487px;"> + +<a name="Auricular_fibrillation" id="Auricular_fibrillation"></a> + + +<img src="images/fig_041.png" width="487" height="500" alt="Fig. 41.—Electrocardiogram showing auricular fibrillation in Leads I (upper) and II +(middle and lower). (Courtesy of Dr. G. C. Robinson.)" title="Fig. 41.—Electrocardiogram showing auricular fibrillation in Leads I (upper) and II +(middle and lower). (Courtesy of Dr. G. C. Robinson.)" /> +<span class="caption">Fig. 41.—Electrocardiogram showing auricular fibrillation in Leads I (upper) and II +(middle and lower). (Courtesy of Dr. G. C. Robinson.)</span> +</div> + +<div class="figcenter" style="width: 500px;"> + +<a name="Auricular_fibrillations" id="Auricular_fibrillations"></a> + +<img src="images/fig_042.png" width="500" height="218" alt="Fig. 42.—Auricular fibrillation. (After Hart.)" title="Fig. 42.—Auricular fibrillation. (After Hart.)" /> +<span class="caption">Fig. 42.—Auricular fibrillation. (After Hart.)</span> +</div> + +<p>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<span class="pagenum"><a name="Page_135" id="Page_135">[135]</a></span><span class="pagenum"><a name="Page_134" id="Page_134"></a></span> +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.</p> + +<p>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.</p> + +<p>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<span class="pagenum"><a name="Page_136" id="Page_136">[136]</a></span> +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.)</p> + +<div class="figcenter" style="width: 500px;"> + +<a name="Pulse_deficit" id="Pulse_deficit"></a> + + +<img src="images/fig_043.png" width="500" height="243" alt="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.)" title="Fig. 43.—The shaded area represents the pulse deficit..." /> +<span class="caption">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.)</span> +</div> +<p>For example: "B. S., April 29, 1910, Apex 131; radial, 101; deficit, 30.</p> + +<p> +BRACHIAL PRESSURE RADIAL COUNT<br /> +<span style="margin-left: 1.5em;">100 mm. Hg. 0</span><br /> +<span style="margin-left: 2em;">90 mm. 13 13 x 90 = 1170</span><br /> +<span style="margin-left: 2em;">80 mm. 47 - 13 = 34 x 80 = 2720</span><br /> +<span style="margin-left: 2em;">70 mm. 75 - 47 = 28 x 70 = 1960</span><br /> +<span style="margin-left: 2em;">60 mm. 82 - 75 = 7 x 60 = 420</span><br /> +<span style="margin-left: 2em;">50 mm. 101 - 82 = 19 x 50 = 950</span><br /> +<span style="margin-left: 21em;">——</span><br /> +<span style="margin-left: 16em;">Apex = 131) 7220</span><br /> +<span style="margin-left: 21em;">——</span><br /> +<span style="margin-left: 6em;">Average systolic blood-pressure 55 plus</span><br /> +</p> + +<p>B. S., May 11, 1910, Apex 79; radial, 72; deficit 7.</p> + +<p> +BRACHIAL PRESSURE RADIAL COUNT<br /> +<span style="margin-left: 1.5em;">120 mm. Hg. 0</span><br /> +<span style="margin-left: 1.5em;">110 mm. 44 44 x 110 = 4840</span><br /> +<span style="margin-left: 1.5em;">100 mm. 64 - 44 = 20 x 100 = 2000</span><br /> +<span style="margin-left: 2em;">90 mm. 72 - 64 = 8 x 90 = 720</span><br /> +<span style="margin-left: 21.5em;">——</span><br /> +<span style="margin-left: 16.5em;">Apex = 79) 7560</span><br /> +<span style="margin-left: 21.5em;">——</span><br /> +<span style="margin-left: 1.5em;">Average systolic blood-pressure 95 plus"</span><br /> +</p> + +<p>The diastolic pressure in these cases can not be determined +except approximately. This may be done by using +an instrument with a dial and noting the pressure where +the oscillations of the dial hand show the maximum excursion. +The diastolic pressure is not at all important under +such conditions of acute cardiac breakdown. It would +make no difference in treatment whether the case was one<span class="pagenum"><a name="Page_138" id="Page_138">[138]</a></span><span class="pagenum"><a name="Page_137" id="Page_137"></a></span> +of pure cardiac disease or one of the hypertension groups. +After the heart has rallied and the circulation is reestablished, +then a careful determination of the diastolic pressure +can be made and the prognosis will rest on what is +found at the compensated stage.</p> + + +<h4>Ventricular Fibrillation</h4> + +<p>Ventricular fibrillation as its name implies, is fibrillation +of the ventricle analogous to that of the auricle, but the +condition is rarely observed as it is incompatible with life. +It has been shown that hearts at the time of death at times +enter a state of fibrillation of the ventricles and that cases +of sudden death may be due to this condition. Recently +G. Canby Robinson<a name="FNanchor_12_12" id="FNanchor_12_12"></a><a href="#Footnote_12_12" class="fnanchor">[12]</a> has seen and made electrocardiograms +of a case of ventricular fibrillation. (Fig. 44.) The case +was that of a woman forty-five years old, "who had a series +of attacks of prolonged cardiac syncope, closely resembling +Stokes-Adams syndrome, from which she recovered." +During an attack of unconsciousness in which there +was no apex beat for about four minutes, the electrocardiogram +was taken. Following this the tracings showed an +almost regular heart beating at the rate of 85 to 100 per +minute. The patient had three convulsions and died with +edema of lungs about 30 hours after the attack of ventricular +fibrillation.</p> + +<div class="figcenter" style="width: 500px;"> + +<a name="Ventricular_fibrillation" id="Ventricular_fibrillation"></a> + + +<img src="images/fig_044.png" width="500" height="169" alt="Fig. 44.—Upper curve. Record obtained during period of cardiac syncopy at 2:48 p.m., Lead II. Lower curve from dog. +Ventricular fibrillation observed in the exposed heart. Lead from right foreleg and left hind leg. (Courtesy of Dr. G. C. Robinson.)" title="Fig. 44.—Upper curve. Record obtained during period of cardiac syncopy at 2:48 p.m., Lead II. Lower curve from dog. +Ventricular fibrillation observed in the exposed heart. Lead from right foreleg and left hind leg. (Courtesy of Dr. G. C. Robinson.)" /> +<span class="caption">Fig. 44.—Upper curve. Record obtained during period of cardiac syncopy at 2:48 p.m., Lead II. Lower curve from dog. +Ventricular fibrillation observed in the exposed heart. Lead from right foreleg and left hind leg. (Courtesy of Dr. G. C. Robinson.)</span> +</div> + +<p>Autopsy revealed chronic fibrous endocarditis of aortic +and mitral valves, arteriosclerosis, bilateral carcinoma of +the ovaries, and signs of general chronic passive congestion.</p> + +<p>It is possible that the syncopal attacks in this case were +the result of sclerosis of the vessels supplying the heart +muscle although careful microscopical examination did not +throw much light on the ultimate cause.</p> + + +<h4>Extrasystole</h4> + +<p>Whenever there is a dropped beat or an intermittent pulse +one may be sure that it is the result of an extrasystole.<span class="pagenum"><a name="Page_139" id="Page_139">[139]</a></span> +Such extrasystoles are produced in the ventricle at some +point other than the regular path of conduction of impulses. +The extrasystole may have its origin in either the auricle +or the ventricle. If there is auricular extrasystole it can +not usually be recognized except by graphic methods. (Fig. +45.) The ventricular extrasystole on the contrary is commonly +seen and readily recognized. Most of those seen in +the clinic have their origin in some part of the ventricular +wall. Their two characteristics are that they occur too +early and that they are followed by a pause longer than the +normal diastolic pause. (Fig. 46.)</p> + +<div class="figcenter" style="width: 500px;"> + +<a name="Auricular_extrasystoles" id="Auricular_extrasystoles"></a> + + +<img src="images/fig_045.png" width="500" height="259" alt="Fig. 45.—Electrocardiogram showing auricular extrasystoles (P). (Courtesy of Dr. G. C. +Robinson.)" title="Fig. 45.—Electrocardiogram showing auricular extrasystoles (P). (Courtesy of Dr. G. C. +Robinson.)" /> +<span class="caption">Fig. 45.—Electrocardiogram showing auricular extrasystoles (P). (Courtesy of Dr. G. C. +Robinson.)</span> +</div> + +<div class="figcenter" style="width: 500px;"> + +<a name="Ventricular_extrasystole" id="Ventricular_extrasystole"></a> + + +<img src="images/fig_046.png" width="500" height="122" alt="Fig. 46.—Electrocardiogram showing ventricular extrasystole. Heart rate 56-60 +beats per minute. Note that diastolic pause in which extrasystole occurs is practically +equal to two normal diastolic pauses. (Courtesy of Dr. G. C. Robinson.)" title="Fig. 46.—Electrocardiogram showing ventricular extrasystole.... (Courtesy of Dr. G. C. Robinson.)" /> +<span class="caption">Fig. 46.—Electrocardiogram showing ventricular extrasystole. Heart rate 56-60 +beats per minute. Note that diastolic pause in which extrasystole occurs is practically +equal to two normal diastolic pauses. (Courtesy of Dr. G. C. Robinson.)</span> +</div> + +<p>When one listens over the chest to a heart when extrasystoles +are occurring, one suddenly hears a weak beat<span class="pagenum"><a name="Page_140" id="Page_140">[140]</a></span> +which has taken place rather too early after the previous +systole to be strong enough to effect the opening of the +aortic valves. Consequently there is no pulse, the blood +does not move, and that beat is lost to the circulation. +Moreover, when the next regular stimulus comes from the +s-a node it finds the ventricle in a refractory condition, +having just ceased a contraction, and it is not until the next +sinus impulse that the ventricle responds normally. (Fig. +46.)</p> + +<p>Patients who have occasional extrasystoles will say that +all of a sudden the heart turns upside down in the chest. +Sometimes there is slight sharp twinge of pain. Patients +are at times quite alarmed about their condition. Provided +there is no evidence of gross myocardial lesion, the extrasystole +itself is of no great significance.</p> + +<p>While many cases showing pathologic causes for extrasystoles +have more or less marked arteriosclerosis, there +are other states in which no arteriosclerosis is found where +the extrasystole is present.</p> + + +<h4>Heart Block</h4> + +<p>As heart block occurs frequently in cases characterized +by extensive arteriosclerosis, a brief discussion of the essential +features will be given. It is, however, probable that +arteriosclerosis is not the cause of any of the cases of heart +block directly, but it is only a result of the same etiological +conditions which produce the lesion or lesions which result +in heart block. We may define heart block as the condition +in which the auricles and ventricles beat independently +of each other. There may be delayed conduction (Fig. 47), +partial (Fig. 48), or complete heart block (Fig. 49). In +the former there are ventricular silences, during which the +auricles beat two, three, four, five, even up to nine times, +with only one ventricular contraction. It is believed by +most physiologists that the essential factor in the production +of heart block is an interference in the conduction of<span class="pagenum"><a name="Page_141" id="Page_141">[141]</a></span> +impulses from the auricles to the ventricles through the +band of tissue known as the auriculoventricular bundle.</p> + +<div class="figcenter" style="width: 500px;"> + +<a name="Delayed_conduction" id="Delayed_conduction"></a> + + +<img src="images/fig_047.png" width="500" height="86" alt="Fig. 47.—Electrocardiogram showing delayed conduction (lengthening of P-R interval). +These P-R intervals are quite regular. When irregular there is apt to be extrasystole +of ventricle or occasional blocking of impulse going to ventricle. (Courtesy of +Dr. G. C. Robinson.)" title="Fig. 47.—Electrocardiogram showing delayed conduction (lengthening of P-R interval).... (Courtesy of +Dr. G. C. Robinson.)" /> +<span class="caption">Fig. 47.—Electrocardiogram showing delayed conduction (lengthening of P-R interval). +These P-R intervals are quite regular. When irregular there is apt to be extrasystole +of ventricle or occasional blocking of impulse going to ventricle. (Courtesy of +Dr. G. C. Robinson.)</span> +</div> + +<div class="figcenter" style="width: 500px;"> + +<a name="Partial_heart_block" id="Partial_heart_block"></a> + + +<img src="images/fig_048.png" width="500" height="383" alt="Fig. 48.—Electrocardiogram showing partial heart-block in the three leads. Note +the variability of P-R interval calculated in seconds in Lead II. (Courtesy of Dr. +G. C. Robinson.)" title="Fig. 48.—Electrocardiogram showing partial heart-block in the three leads. Note +the variability of P-R interval calculated in seconds in Lead II. (Courtesy of Dr. +G. C. Robinson.)" /> +<span class="caption">Fig. 48.—Electrocardiogram showing partial heart-block in the three leads. Note +the variability of P-R interval calculated in seconds in Lead II. (Courtesy of Dr. +G. C. Robinson.)</span> +</div> + +<div class="figcenter" style="width: 500px;"> + +<a name="Complete_heart_block" id="Complete_heart_block"></a> + + +<img src="images/fig_049.png" width="500" height="377" alt="Fig. 49.—Complete heart block. (Courtesy of Dr. G. C. Robinson.)" title="Fig. 49.—Complete heart block. (Courtesy of Dr. G. C. Robinson.)" /> +<span class="caption">Fig. 49.—Complete heart block. (Courtesy of Dr. G. C. Robinson.)</span> +</div> + +<p>The bundle of muscles described by His in 1905, connecting +the auricles and ventricles, has been definitely +shown to be the path through which impulses having their +origin in the orifices of the great veins pass to the ventricles.<span class="pagenum"><a name="Page_142" id="Page_142">[142]</a></span> +The situation and size of this bundle has been thus +described in man by Retzer:</p> + +<p>"When viewed from the left side, the bundle lies just +above the muscular septum of the ventricles and below the +membranous septum. In some hearts the muscular septum +is so well developed that it envelops the bundle. It is then +difficult to find, but occasionally it can be seen directly +by means of transmitted light. From the left side the bundle +can be followed no farther posteriorly than the right +fibrous trigone, for here the connective tissue becomes so +dense that it is difficult to dissect it away. The impression +is, therefore, received that this mass of connective tissue +forms the insertion of the bundle. The bundle may be followed +anteriorly until it becomes intimately mixed with the +musculature of the ventricles.</p> + +<p><span class="pagenum"><a name="Page_143" id="Page_143">[143]</a></span>"When viewed from the right side of the heart, the +bundle can not be seen, because it is covered by the mesial +leaflet of the tricuspid valve, whose line of attachment +passes obliquely over the membranous septum. Then, if +the endocardium is removed from the posterior part of the +septum of the auricle up to the membranous septum, the +posterior part of the auriculoventricular bundle will be exposed. +If, in addition, the membranous septum be removed, +the bundle may be traced from the point to which it could +be followed when viewed from the left side as it passes +posteriorly over the muscular septum. In the region of the +auriculoventricular junction it loses its compactness, the +fibers divide, and the bundle seems to fork. One branch +passes into the superficial part of the valve musculature +which descends from the auricles, and the other branch +passes directly into the musculature of the auricle.</p> + +<p>"Briefly, the auriculoventricular bundle runs posteriorly +in the septum of the ventricles about 10 mm. below the +posterior leaflet of the aortic semilunar valves; with a gentle +curve it passes posteriorly just over the upper edge of +the muscular septum and sends its fibers into the musculature +of the right auricle and of the auricular valves. In +the heart of the adult the bundle is 18 mm. long, 2.5 mm. +wide, and 1.5 mm. thick." (Erlanger.)</p> + +<p>All normal impulses have their origin in the sino-auricular +node at the junction of the superior vena cava with +the right auricle (Fig. 50). From there the impulse travels +in the wall of the auricle in the interauricular septum to the +node of Tawara or A-V node (Fig. 51), thence through the +bundle of His to be distributed to the fibers of the right and +left ventricles. This sequence is orderly and perfectly +regular.</p> + +<div class="figcenter" style="width: 500px;"> + +<a name="Alternating_periods_of_sinus_rhythm_and_auriculoventricular_rhythm" id="Alternating_periods_of_sinus_rhythm_and_auriculoventricular_rhythm"></a> + + +<img src="images/fig_050.png" width="500" height="95" alt="Fig. 50.—Showing alternating periods of sinus rhythm and auriculoventricular rhythm. +(After Eyster and Evans.)" title="Fig. 50.—Showing alternating periods of sinus rhythm and auriculoventricular rhythm. +(After Eyster and Evans.)" /> +<span class="caption">Fig. 50.—Showing alternating periods of sinus rhythm and auriculoventricular rhythm. +(After Eyster and Evans.)</span> +</div> + +<div class="figcenter" style="width: 500px;"> + +<a name="Auriculoventricular_or_nodal_rhythm" id="Auriculoventricular_or_nodal_rhythm"></a> + + +<img src="images/fig_051.png" width="500" height="264" alt="Fig. 51.—Period of auriculoventricular or "nodal" rhythm following exercise in sitting +posture. (After Eyster and Evans.)" title="Fig. 51.—Period of auriculoventricular or "nodal" rhythm following exercise in sitting +posture. (After Eyster and Evans.)" /> +<span class="caption">Fig. 51.—Period of auriculoventricular or "nodal" rhythm following exercise in sitting +posture. (After Eyster and Evans.)</span> +</div> + +<p>It has also been shown that the independent auricular +and ventricular rates vary somewhat, that of the auricle +being in general faster than that of the ventricle. A strip +of mammalian ventricle placed outside of the body in<span class="pagenum"><a name="Page_144" id="Page_144">[144]</a></span> +proper surroundings will begin to beat automatically at +the rate of about 40 beats a minute. Experimentally various +grades of heart block have been produced in the dog's +heart by more or less compression of the bundle at the A-V +ring. The block may be partial, when two to nine auricular +beats occur to every one of the ventricle, up to absolute<span class="pagenum"><a name="Page_145" id="Page_145">[145]</a></span> +complete block when the auricles and ventricles beat independently +of one another.</p> + +<p>In any stage of partial block, pressure on the vagus nerve<span class="pagenum"><a name="Page_146" id="Page_146">[146]</a></span> +in the neck produces certain specific changes. (Fig. 52.) +Robinson and Draper<a name="FNanchor_13_13" id="FNanchor_13_13"></a><a href="#Footnote_13_13" class="fnanchor">[13]</a> have found qualitative differences +in the two vagi. The right vagus sends most of its fibers to +the s-a node (Fig. 53) and has a more evident influence on +the rate and force of the cardiac contractions. The majority +of fibers from the left vagus are distributed to the A-V +node so that its most evident action is upon the conductivity +of the impulse. Pressure then on the right vagus will +have a tendency to slow the whole heart. Pressure on the +left vagus will have a tendency to prolong the P-R interval +until even complete block occurs. Even when the heart +block is complete, stimulation of the accelerator nerve, as a +rule, increases the rate of both auricles and ventricles.</p> + +<div class="figcenter" style="width: 500px;"> + +<a name="Influence_of_mechanical_pressure_on_the_right_vagus_nerve" id="Influence_of_mechanical_pressure_on_the_right_vagus_nerve"></a> + + +<img src="images/fig_052.png" width="500" height="69" alt="Fig. 52.—Influence of mechanical pressure on the right vagus nerve. (After Eyster +and Evans.)" title="Fig. 52.—Influence of mechanical pressure on the right vagus nerve. (After Eyster +and Evans.)" /> +<span class="caption">Fig. 52.—Influence of mechanical pressure on the right vagus nerve. (After Eyster +and Evans.)</span> +</div> + +<div class="figcenter" style="width: 356px;"> + +<a name="Schematic_distribution_of_right_and_left_vagus" id="Schematic_distribution_of_right_and_left_vagus"></a> + + +<img src="images/fig_053.png" width="356" height="500" alt="Fig. 53.—Schematic distribution of right and left vagus. (After Hart.)" title="Fig. 53.—Schematic distribution of right and left vagus. (After Hart.)" /> +<span class="caption">Fig. 53.—Schematic distribution of right and left vagus. (After Hart.)</span> +</div> + +<p>If the block is functional, depending upon some temporary +overstimulation of the vagus nerve, atropin, which +paralyzes the endings of the vagus, will naturally lift the +block. If the block is due to some actual lesion of the bundle +of His, such as fibrosis, gumma, or other lesion, then +atropin will have no influence to terminate the block. In +this manner we are able to distinguish between functional +and organic heart block.</p> + +<hr style="width: 65%;" /> +<p><span class="pagenum"><a name="Page_147" id="Page_147">[147]</a></span></p> +<h2><a name="CHAPTER_V" id="CHAPTER_V"></a>CHAPTER V.</h2> + +<h3>BLOOD PRESSURE IN ITS CLINICAL APPLICATIONS</h3> + + +<p>It is well to bear constantly in mind the point made over +and over in this work, that blood pressure is only one of +many methods of acquiring information. He who worships +his sphygmomanometer as a thing apart and infallible will +sooner or later come to grief. Judgment must be used in +interpreting changes in blood pressure just as judgment is +essential in properly evaluating any instrumental help in +diagnosis. One must not forget the personal equation +which enters into even accurate instrumental recording in +medicine and surgery.</p> + +<p>In this chapter there will be no attempt to quote largely +from what others have said or thought. Every one has +his own opinion as to the value of certain methods after he +has worked with them for a long time. The ideas here expressed, +except in cases where no opportunity has offered +to make personal studies, are those gathered from personal +experience.</p> + + +<h4>Blood Pressure in Surgery</h4> + +<p>Careful estimation of the blood pressure in surgical cases +has, at times, great value. In all surgical diseases the most +important fact to know is not the systolic pressure, but the +pulse pressure. If the pulse pressure keeps within the +range of normal, does not drop much below 30 mm. in an +adult, then so far as we can tell the circulation is being +carried on. When the systolic pressure is gradually falling +and the diastolic remains the same, the circulation is +failing and unless the pulse pressure can be established +again the patient will die. Again we see the value of the +pulse pressure.</p> + +<p><span class="pagenum"><a name="Page_148" id="Page_148">[148]</a></span>All prolonged febrile diseases tend to produce a lowering +of the blood pressure picture. The diastolic does not fall to +the same extent as the systolic so that there is a pulse pressure +smaller than normal. This is to be expected from what +we know of the general depression of the circulation in +fevers. The blood pressure reading is only a graphic record +of what we have long known, and enables us from day +to day accurately to measure the general circulation.</p> + + +<h4>Head Injuries</h4> + +<p>It was claimed that in fracture of the skull or in concussion +much could be gained by frequent estimations of +the blood pressure. This seemed probable in the light of +experiments on compressing the brains of dogs by the use +of bags inserted through trephine openings (Cushing). In +the clinic, however, it has not been found of any material +value. It has a value in differentiating a simple fracture, +let us say, from a case of uremia which is picked up on the +street with a bump on the head. There the high pressure +usually found would at once direct attention to the kidneys +and the newer methods of blood examination would at once +settle the question. Naturally uremics may also have skull +fracture. There the diagnosis would be complicated. A +decompression done at once would be indicated. If the +skull fracture happened in a uremic, the decompression +would probably do no harm. In fact, there are some who +advise decompression for uremia.</p> + + +<h4>Shock and Hemorrhage</h4> + +<p>In shock the blood pressure picture is low but the pulse +pressure drops to abnormally low figures. It seems to me +that the blood pressure instrument has its greatest value +in surgery in the warning it gives to the operating surgeon +in cases of impending shock.</p> + +<p>It is well known that the first effect of ether, the commonly<span class="pagenum"><a name="Page_151" id="Page_151">[151]</a></span><span class="pagenum"><a name="Page_150" id="Page_150"></a></span><span class="pagenum"><a name="Page_149" id="Page_149"></a></span> +used anesthetic, is to raise the blood pressure and +quicken the pulse rate. The whole blood pressure picture +is at first elevated (Fig. 54). Soon the whole pressure falls +slightly but continues at a higher level than normal. The +diastolic pressure drops back nearly to normal and the increased +pulse pressure is due almost entirely to the slight +rise in the systolic pressure. Now the whole duty of the anesthetist +is to administer the ether so that this ratio of systolic +and diastolic is maintained throughout the operation. +Warning comes to him of impending shock before it comes +to any one in the neighborhood (Fig. 55). Any sudden +change in the pressure is a signal for increased watchfulness. +Should the pressure all at once drop he can immediately +notify the surgeon and institute measures to resuscitate +the patient.</p> + +<div class="figcenter" style="width: 368px;"> + +<a name="Blood_pressure_record_from_a_normal_reaction_to_ether" id="Blood_pressure_record_from_a_normal_reaction_to_ether"></a> + + +<img src="images/fig_054.png" width="368" height="500" alt="Fig. 54.—Blood pressure record from a normal reaction to ether. Note that the +systolic and diastolic rise and fall together. At the end of the anesthetization the pulse +pressure is practically the same as at the beginning. Compare this with the record in +Fig. 55, where the operation had to be discontinued on account of the onset of shock." title="Fig. 54.—Blood pressure record from a normal reaction to ether. " /> +<span class="caption">Fig. 54.—Blood pressure record from a normal reaction to ether. Note that the +systolic and diastolic rise and fall together. At the end of the anesthetization the pulse +pressure is practically the same as at the beginning. Compare this with the record in +Fig. 55, where the operation had to be discontinued on account of the onset of shock.</span> +</div> + +<div class="figcenter" style="width: 440px;"> + +<a name="Chart_showing_the_method_of_recording_blood_pressure_during_an" id="Chart_showing_the_method_of_recording_blood_pressure_during_an"></a> + + +<img src="images/fig_055.png" width="440" height="600" alt="Fig. 55.—Beginning of operative shock. Chart showing the method of recording blood pressure +during operation. + +Note that the pulse and respiration show no remarkable changes, but the blood pressure +steadily fell, the systolic more than the diastolic so that the pulse pressure was gradually reaching +the danger point. Further work on this case was stopped following the warning given by the +blood pressure. The patient was returned to the ward and a week later anesthesia was again +given, the operation was completed, and the patient had a satisfactory convalescence." title="Fig. 55.—Beginning of operative shock. Chart showing the method of recording blood pressure +during operation...." /> +<span class="caption">Fig. 55.—Beginning of operative shock. Chart showing the method of recording blood pressure +during operation. + +Note that the pulse and respiration show no remarkable changes, but the blood pressure +steadily fell, the systolic more than the diastolic so that the pulse pressure was gradually reaching +the danger point. Further work on this case was stopped following the warning given by the +blood pressure. The patient was returned to the ward and a week later anesthesia was again +given, the operation was completed, and the patient had a satisfactory convalescence.</span> +</div> + +<p>A method which is widely used is as follows: The anesthetist +wraps the cuff of one of the dial instruments around +the patient's arm, and arranges the dial so that it can easily<span class="pagenum"><a name="Page_152" id="Page_152">[152]</a></span> +be seen by him at all times. This does not in any way interfere +with the work of the surgeon. Over the brachial artery +below the cuff is the bell of a binaural stethoscope held +in place by the strap attachment now on the market. The +tubes of the stethoscope are long enough to reach conveniently +to the ear pieces. A watch is pinned to the sheet of +the table. He has a chart, as illustrated (Fig. 56) on a +board and makes a dot in every space for five minute intervals. +By joining the lines a curve is obtained which tells +at a glance what the circulation is doing. I feel sure that +more attention and care exercised on the part of the anesthetist +would be the means of conserving many lives lost +from shock following operation.</p> + +<div class="figcenter bord" style="width: 500px;"> + +<a name="Method_of_using_blood_pressure_instrument_during_operation" id="Method_of_using_blood_pressure_instrument_during_operation"></a> + + +<img src="images/fig_056.png" width="500" height="398" alt="Fig. 56.—Showing method of using blood pressure instrument during operation without +interfering with the operator or assistants. Sheet thrown back to show cuff on +arm of patient. Anesthetist has chart on table beside him, dial pinned to pad in full +view, bulb near hand. Extra tubing must be put on the blood pressure instrument." title="Fig. 56.—Showing method of using blood pressure instrument during operation without +interfering with the operator or assistants." /> +<span class="caption">Fig. 56.—Showing method of using blood pressure instrument during operation without +interfering with the operator or assistants. Sheet thrown back to show cuff on +arm of patient. Anesthetist has chart on table beside him, dial pinned to pad in full +view, bulb near hand. Extra tubing must be put on the blood pressure instrument.</span> +</div> + +<p>A sudden drop in the pressure picture may mean a large +hemorrhage. The gradual return of the pressure picture +means that the vasomotor mechanism has acted to keep up +the pulse pressure. Should the diastolic pressure continually +fall, it may mean that the hemorrhage is still taking +place (Wiggers).</p> + + +<h4>Blood Pressure in Obstetrics</h4> + +<p>One might affirm almost without fear of contradiction +that the constant determination of blood pressure during +pregnancy is more important than the examination of the +urine. Within recent years a number of observers having +access to a large material, have given the results of their +findings. There is a striking unanimity of opinion, although +now and then a difference in minor details.</p> + +<p>The blood pressure should be taken frequently during +pregnancy. The usual and highly essential precautions in +taking pressure in general apply most particularly in these +cases. Towards the end of pregnancy the pressure should +if possible be taken daily and oftener if necessary.</p> + +<p>Pressure in women is usually below 120 mm. Many patients +have a temporary rise in blood pressure during pregnancy, +due oftenest to constipation, without developing<span class="pagenum"><a name="Page_153" id="Page_153">[153]</a></span> +other symptoms. This is common to all conditions and has +no significance. Some think that an abnormally low pressure, +that is, a systolic below 90 mm., suggests that the +patient is likely to react unduly to the strain of labor. This +is denied by others. Among 1000 cases (Irving) the pressure +was below 90 in only one case. A gradually rising +pressure precedes albuminuria, as a rule. If there is albumin +without change in pressure the albumin may usually +be disregarded. Some think that a pressure over 130 mm. +systolic should be carefully watched. The danger limit +is set by some at 150 mm. If the blood pressure from the +very first is high, it may mean only that that was the patient's +normal pressure. This calls for increased watchfulness. +It is held by some that high blood pressure favors +hemorrhage and probably explains the hemorrhagic lesions +in the placenta and some viscera in eclampsia and albuminuria.</p> + +<p>All are agreed that the most significant change is the +gradual but sure rise from a low pressure. When this is +combined with albuminuria the danger of toxemia is imminent. +The high blood pressure in those under thirty +years of age seems to be a more certain sign of approaching +toxemia than the same pressure in those older. The +pressure falls within a few days to its normal after delivery +in the toxic cases.</p> + +<p>Although the emesis gravidarum is held to be a sign of +a toxemia of some unknown nature, the blood pressure is +never raised even in the pernicious form.</p> + + +<h4>Infectious Diseases</h4> + +<p>In all infectious diseases the blood pressure tends to be +lower than normal. During chills the systolic may rise to +great height due to the violent muscular contractions.</p> + +<p>We found the blood pressure of great value in giving +information concerning the circulation. Again we repeat<span class="pagenum"><a name="Page_154" id="Page_154">[154]</a></span> +that it is not the systolic alone or the diastolic alone but the +pulse pressure which we wish to keep informed about. In +pneumonia we have tried out Gibson's law only to discard +it. This so-called law is that in pneumonia the systolic +pressure in millimeters should remain above the figure for +the pulse rate. When the figure in mm. of pressure is +equalled by or exceeded by the pulse rate the prognosis is +grave.</p> + +<p>In typhoid fever we have made many estimations at various +stages of the disease. We can only say that the pressure +picture tends to fall during the course. The systolic +falls more than the diastolic so that it is not uncommon +to see pulse pressures of 20 mm. at the beginning of convalescence +in spite of the high caloric feeding practiced. +At the time of perforation the systolic pressure may be +raised. This is only the reflex from the initial pain. Soon +the pressure falls and if peritonitis sets in, the pressure is +exceedingly low and the pulse pressure gradually falls until +the circulation can no longer be carried on. In large +hemorrhage the pressure suddenly falls. If only one hemorrhage +has occurred a gradual rise takes place, but the +general pressure picture remains at a lower level for days, +gradually returning where it was before the hemorrhage.</p> + +<p>In beginning failure of the circulation we found elevation +of the foot of the bed about nine inches to be of such +value that we felt there must be some increase in blood pressure. +Numerous readings were made covering a period of +several months. Although we felt certain that the circulation +was improved, we rarely needed cardiac stimulation, +we never could prove any increase of blood pressure with +the sphygmomanometer.</p> + +<p>In all infectious diseases there is no help offered by blood +pressure estimations in diagnosis. The sole and important +use is that of keeping track of the circulation.</p> +<p><span class="pagenum"><a name="Page_155" id="Page_155">[155]</a></span></p> + +<h4>Valvular Heart Disease</h4> + +<p>No rules can be laid down for blood pressure in valvular +heart disease. Aortic stenosis, the rarest of the valvular +lesions, is practically always accompanied by high pressure +picture. Mitral stenosis on the contrary usually shows a +low pressure picture. Mitral insufficiency may show an +exceedingly low picture or an exceedingly high picture. +Aortic insufficiency also may be accompanied by a high +systolic or by a normal systolic pressure. It depends on the +etiology. Practically all the rheumatic cases have low pressure, +the syphilitic cases have a high pressure. It is characteristic +of all cases of aortic insufficiency that the diastolic +pressure is low, even as low as 30 mm. The pulse +pressure is invariably high. Usually there is no difficulty +in determining the diastolic pressure. The intense third +tone suddenly becomes dull at the point of diastolic pressure +and frequently the dull sound can be distinctly heard +over the artery down to the zero of the scale. If difficulty +is found in reading the diastolic as the pressure is reduced, +the estimation may be reversed and the pressure gradually +increased from zero to the point where the dull tone suddenly +becomes loud and clear. These points always coincide.</p> + + +<h4>Kidney Diseases</h4> + +<p>This has already been discussed somewhat fully in Chapter +III and will receive more consideration later. It might +be remarked in passing that in a case of seeming coma +where albumin is found in the urine but where the blood +pressure is low or normal, I have found at autopsy in several +cases pyonephrosis and not chronic nephritis. The +blood pressure may be useful in differentiating uremic coma +from the coma of pyonephrosis. Also in the cases of coma +with anasarca, either the acute, subacute or chronic form +the blood pressure is not raised as a rule. Other diseases +of the kidney, as tuberculosis, cancer, infection with pyogenic<span class="pagenum"><a name="Page_156" id="Page_156">[156]</a></span> +organisms, are not accompanied with any notable +changes in blood pressure.</p> + + +<h4>Other Diseases, Liver, Spleen, Abdomen, etc.</h4> + +<p>Blood pressure is only of value in the above diseases in +affording information concerning the state of the circulation. +There is nothing characteristic about the pressure +in any of these diseases.</p> + +<hr style="width: 65%;" /> +<p><span class="pagenum"><a name="Page_157" id="Page_157">[157]</a></span></p> +<h2><a name="CHAPTER_VI" id="CHAPTER_VI"></a>CHAPTER VI.</h2> + +<h3>ETIOLOGY</h3> + + +<p>The causes of arteriosclerosis are many and varied. No +two persons have the same resisting power toward poisons +that circulate in the blood. Some go through life exposed +to all the infectious diseases without ever becoming infected, +while others fall easy victims to every disease that +comes, no matter how careful they may be, and it is quite +the same in regard to the resistance of the arterial tissues. +If the tubing is of first class quality and the individual does +not place too much strain on it, he may live to the biblical +three-score years and ten, and possess arteries which have +undergone such slight changes that they are not palpable. +Such a person is, however, the exception. On the other +hand, if the tissue is of poor quality, even the ordinary +wear and tear of life causes early changes in the vessels, +and a person of forty may have hard arteries.</p> + +<p>We have described in a previous chapter the changes +which normally occur in the arteries as age advances. An +artery that is normal for a man of fifty years would be +distinctly abnormal for a boy of fifteen.</p> + +<p>Two broad divisions of arteriosclerosis may be made: +(1) congenital, or the result of inherited tendency; (2) +acquired.</p> + + +<h4>Congenital Form</h4> + +<p>When Dr. O. W. Holmes was asked how to live to the age +of seventy, he replied that a man should begin to pick his +ancestors one hundred years before he was born. Our +parents determine the character of the tissues with which +we start in life, and this determines our general resistance. +We might properly speak of congenital arteriosclerosis<span class="pagenum"><a name="Page_158" id="Page_158">[158]</a></span> +where the affected individual had poor arterial tissue with +which to begin life, for that, in a sense, is a congenital defect, +and arterial tissue that is poor in quality is prone to +disease.</p> + +<p>The author is more and more impressed with the part that +heredity plays in the determination of arterial degeneration. +Especially does syphilis in the parents or grandparents +leave its stigma in the succeeding generations in +the shape of poor arterial tissue which is prone to early +degeneration. Recently W. W. Graves has called attention +to a malformation of the vertebral border of the scapula +which consists in a concavity instead of the normal +convexity of the bone. To this malformation he has given +the name, scaphoid scapula. He considers this to be but +one manifestation of a general lack of development in the +individual. He speaks of this maldevelopment as a blight +and considers that syphilis in the ancestors is responsible +for the condition in the offspring. He finds that even in +children, the subjects of the scaphoid scapula, the arteries +are very definitely thickened. While confirmation of his +observations is lacking, there is no doubt that we must lay +the blame for much of the arteriosclerosis in our patients +to the poor quality of arterial tissue transmitted by ancestors +who have acquired some constitutional disease. It +may have been syphilis, it may have been the degeneration +produced by alcohol or other drug. We can not ignore the +part which heredity plays. The various factors to be considered +in the production of the acquired form of arteriosclerosis +appear to me to be but contributory factors to +a very great extent, the essential and fundamental factor +being the quality of arterial tissue with which the individual +is endowed.</p> + +<p>Arteriosclerosis may occur in infants. Cases have been +reported of calcification of the arteries in infants and children. +The arteriosclerosis may occur without nephritis or +rise of blood pressure. Cerebral hemorrhage in a child<span class="pagenum"><a name="Page_159" id="Page_159">[159]</a></span> +of two years has been seen. Heredity in these cases plays +a most important rôle. In many of the reported cases there +was no question of congenital syphilis. Aneurysms, single +or multiple, have been found in the arteries of children, +and even the pulmonary artery may show sclerotic changes.</p> + + +<h4>Acquired Form</h4> + +<p>As a rule the cases usually seen belong in this group +because it seems as if a connection could be established almost +always between one or more of the etiologic factors +to be described and the disease. While this apparently is +the case, we must never lose sight of the part which the +quality of the tissue plays. When we leave this out of our +calculations we undoubtedly make many false deductions. +When two men of the same age who have been exposed to +the same conditions as far as we can learn, are found to +have quite different arteries, the one normal, the other +thickened, we must postulate congenitally poor tissue on +the part of the latter. Such tissue readily becomes diseased +following conditions which would very likely have +produced no noticeable effect on perfectly normal, healthy +tissue.</p> + + +<h4>Hypertension</h4> + +<p>Hypertension must still be reckoned with in the etiology +of arteriosclerosis although the rôle that it was thought to +play does not seem so important. Changes of blood pressure +alone are not considered by many to be sufficient for +the production of arteriosclerosis. This may play some +part, but there are many other factors mostly unknown +which determine in any case the production of arterial +lesions.</p> + +<p>With every systole of the heart, blood is forced out into +the arterial system against a certain amount of resistance +represented by the tonicity of the capillary area, and the +amount of cohesion between the viscous blood and the walls<span class="pagenum"><a name="Page_160" id="Page_160">[160]</a></span> +of arterioles. When a dilatation of the capillaries over +any large area takes place, the blood pressure falls, provided +there is no compensatory contraction in other areas +to make up for the decreased resistance in the dilated vessels. +The viscosity of the blood, as such, probably has +very little effect on the resistance to the flow. With the +systole of the heart there is a sudden dilatation of the arch +of the aorta, and a wave of expansion follows, which is +transmitted to the periphery and is lost only in the capillaries.</p> + +<p>The blood pressure is constantly changing. Physiologically +there are relatively wide variations in the pressure +in a perfectly normal individual. There are some +persons who have hypotension, a blood pressure much below +the normal. Such persons have usually small hearts, +small aortas, and they seem to have but little resistance +to disease. Many diseases, especially the prolonged fevers, +diminish markedly the blood pressure. Whether the hypertension +is the cause of the structural changes that are found +in the walls of the vessels, or is the result of the diminished +area of the arterial tree through which the same amount +of blood has to be driven as before the vessel walls became +narrowed, is still disputed. As has been stated, experimental +evidence would tend to place the initial blame upon +the poisons circulating in the blood, which first damage the +vessel walls. The subsequent changes then produce thickening +and inelasticity. Some think (Allbutt) that the +hypertension is primary. There are cases seen clinically +that lend support to this view and there is experimental +evidence also (v. Chap. II). Not infrequently individuals +in middle life begin to show increase of arterial blood pressure +without discoverable cause. In such case it may be +that there is slowly progressing chronic nephritis. The +urine if examined only superficially in single specimens may +not reveal any abnormalities. Careful functional examination +by means of the newer tests may reveal functional<span class="pagenum"><a name="Page_161" id="Page_161">[161]</a></span> +deficiency. It must not be supposed that all cases of increasing +hypertension are cases of chronic nephritis. The +opinion has already been expressed (Chap. III) concerning +this point. Experience has convinced me that the opinion +expressed in former editions is not altogether correct.</p> + + +<h4>Age</h4> + +<p>No age is exempt from the lesions of arteriosclerosis if we +consider the two groups. However, the disease is seen for +the most part in persons past middle life. The relative +frequency with which it is found in the different decades +depends on so many factors that it is of no value to tabulate +them. As has been stated, arteriosclerosis of all types is +an involution process that advances with age. Longevity +is a question of the integrity of the arterial tissue, and no +one can tell what sort of "vital rubber" (Osler) any one +of us has. However, many with poor tubing may make +such use of it that it will outlast good tubing that is badly +treated. Unfortunately we have no way of telling early +enough with just what sort of arterial tissue we are starting +life.</p> + + +<h4>Sex</h4> + +<p>There is no doubt that men are far more prone to arterial +disease than women are; all statistics are in accord on this +point. This is explained by the greater exposure of men +to those conditions of life which tend to produce circulatory +strain, and so to produce arteriosclerosis, or vice versa. +Arteriosclerosis in women is not often seen until after the +fiftieth year. Cases of the most extreme grade of pipe +stem arteries are, however, seen in old women, and calcified +arteries are not hard to find among the inmates of an old +woman's home.</p> + + +<h4>Race</h4> + +<p>Some of the most beautiful examples of arteriosclerosis +in this country are seen in the negro. Not only is this<span class="pagenum"><a name="Page_162" id="Page_162">[162]</a></span> +disease more frequent in the black race, but the age of onset +is much earlier than in the Caucasian. The accidents of +arteriosclerosis, viz., aneurysm, cerebral hemorrhage, etc., +are more common among the negro males. The etiologic +factors that are most often found in the history are the +prevalence of syphilis and hard physical labor.</p> + + +<h4>Occupation</h4> + +<p>Certain occupations have a distinct causal relationship to +arteriosclerosis; among such are particularly those entailing +prolonged muscular exercise, especially if much lifting +is necessary. Every one is familiar with the phenomena +accompanying the exertion of lifting. The breath is drawn +in, the glottis is closed, and the muscles of the chest wall +are held rigidly while the exertion lasts. This causes a +great increase in blood pressure, and constant repetition +of this will produce permanent high tension. In hospitals, +the stevedores as a class have marked arteriosclerosis, and, +almost without exception, they are comparatively young +men. Occupations that are accompanied with prolonged +mental strain, such as now occur to the heads of large manufacturing +and financial institutions, also predispose to +early arterial changes. Psychic activity, especially when it +is accompanied by worry, is a potent factor in the production +of the increased blood pressure which is the chief factor +in producing arterial disease. It has been suggested that +sexual continence in high-strung men produces changes in +the nervous system which can conceivably lead to the production +of high tension and further to arteriosclerosis. This, +however, I can not think has any foundation in fact except +in so far as such men are prone to live at high speed and +wear themselves out sooner than the normal person. The +sexual continence <i>per se</i> is not harmful. There are, however, +men who seem not to be harmed by the constant wear +and tear of our modern life. These are the exceptions.</p> + +<p>Workers in factories where paint is made and the ingredients<span class="pagenum"><a name="Page_163" id="Page_163">[163]</a></span> +hand-mixed, are prone to develop arteriosclerosis +early in life. It has been found that the laborers most apt +to be victims of lead intoxication are those who are careless +in their habits of cleanliness, particularly in regard to the +fingernails. The continuous absorption of lead into the +system, brings about a condition of hypertension that has +its inevitable results.</p> + +<p>The fact is that any occupation which entails either the +absorption of toxic substances, or prolonged muscular labor, +will hasten markedly the onset of arterial disease.</p> + + +<h4>Food Poisons</h4> + +<p>The opinion that arteriosclerosis is due in large part to +poisoning by end products or by-products of protein digestion +is now receiving much support. Experiments on +dogs and rabbits have lent some confirmation to chemical +observations. It has been shown that dogs fed for a long +time on putrefied meat developed inflammation and degeneration +of the adventitia and media, with hyperplasia and +calcification of the intima of many arteries. In the pulmonary +and carotid arteries, in the vena cavas and myocardium, +there were extensive necroses and hyaline degeneration. +Moreover, injections of sodium urate and ergot +caused necroses in the muscularis and elastica of the aorta, +pulmonary artery, vena cavas inferior and heart muscle, but +there was no calcification. Guinea pigs which were fed +indol in small doses by the mouth over a long period showed +atheromatous degeneration of the aorta.</p> + + +<h4>Infectious Diseases</h4> + +<p>As more study has been given to the arteries in persons +who have died of the acute infectious diseases, more has +come to light concerning the effects of the toxins of these +diseases on the vessel walls. In the arteries of children +who have died of measles, scarlet fever, diphtheria, cerebrospinal<span class="pagenum"><a name="Page_164" id="Page_164">[164]</a></span> +meningitis, etc., degenerative changes in the arteries +occur, modified only by the length of time that the +toxins have acted.</p> + +<p>Thayer has shown that the arteries of those who have +passed through an attack of moderately severe or severe +typhoid fever are as a rule more readily palpable than are +the vessels of persons of corresponding years who have +never had the disease. Clinically the typhoid toxin appears +to cause the early production of arteriosclerosis. The +changes in the arteries occur for the most part, and always +earlier, in the peripheral arteries, and the media is chiefly +affected. Minute yellowish patches are found on the aorta, +carotids, and coronaries. In persons who have passed +through an attack of one of the fevers, and have later died +from some other cause, regenerative changes are sometimes +found to have taken place in the arteries, consisting of an +ingrowth of elastic fibers from the intact adventitia to the +diseased media.</p> + +<p>That there are some other factors than the infectious disease +which are concerned in the production of arterial +changes seems evident from a study<a name="FNanchor_14_14" id="FNanchor_14_14"></a><a href="#Footnote_14_14" class="fnanchor">[14]</a> made recently among +a group of almshouse inmates ranging in age from 38 to +90 years. The study included 500 persons of both sexes. +Careful histories were taken to determine the presence of +antecedent infectious disease. The radial artery was palpated +to determine the presence of sclerosis. Among the +cases giving a history of one infectious disease the following +table gives the results:</p> + +<div class="center"> +<table border="0" cellpadding="4" cellspacing="0" summary=""> +<tr><td align="left">DISEASE </td><td align="left">NO. </td><td align="left">+ </td><td align="left">++ </td><td align="left">+++ </td><td align="left">POSITIVE </td><td align="left">NEGATIVE</td></tr> +<tr><td align="left">Measles</td><td align="right">47</td><td align="right">10</td><td align="right">6</td><td align="right">12</td><td align="right">28</td><td align="right">19</td></tr> +<tr><td align="left">Infectious arthritis</td><td align="right">38</td><td align="right">9</td><td align="right">6</td><td align="right">4</td><td align="right">19</td><td align="right">19</td></tr> +<tr><td align="left">Pneumonia</td><td align="right">30</td><td align="right">5</td><td align="right">8</td><td align="right">5</td><td align="right">18</td><td align="right">12</td></tr> +<tr><td align="left">Typhoid</td><td align="right">27</td><td align="right">6</td><td align="right">8</td><td align="right">3</td><td align="right">17</td><td align="right">10</td></tr> +<tr><td align="left">Scarlet fever</td><td align="right">10</td><td align="right">0</td><td align="right">0</td><td align="right">4</td><td align="right">4</td><td align="right">6</td></tr> +<tr><td align="left">Smallpox</td><td align="right">14</td><td align="right">1</td><td align="right">4</td><td align="right">0</td><td align="right">5</td><td align="right">9</td></tr> +<tr><td align="left">Miscellaneous</td><td align="right">12</td><td align="right">2</td><td align="right">5</td><td align="right">2</td><td align="right">9</td><td align="right">3</td></tr> +<tr><td align="left"> </td><td align="right">178</td><td align="right">33</td><td align="right">37</td><td align="right">30</td><td align="right">100</td><td align="right">78</td></tr> +</table></div> + + +<p><span class="pagenum"><a name="Page_165" id="Page_165">[165]</a></span></p> +<p>A summary of the cases showed: 252 cases without sclerosis; +248 with sclerosis; 147 cases with infections but no +sclerosis; 180 cases with infections and sclerosis.</p> + +<p>This study failed to throw any positive light on the question. +Infectious diseases undoubtedly play a certain rôle, +particularly those continuing a long time and certain particular +infectious diseases, as measles.</p> + + +<h4>Syphilis</h4> + +<p>Syphilis is one of the most important of the etiologic +factors in the production of arteriosclerosis. It has been +shown that in 85 per cent of cases of aortic insufficiency in +persons, usually males, over forty-five years, who did not +have chronic infective endocarditis, the Wassermann reaction +was positive. Acute aortitis affecting the ascending +and transverse portions of the arch of the aorta is very +commonly seen, and the irregular, scattered, slightly raised, +yellowish-white patches of sclerosis in the arch which are +found years after the syphilitic lesion, are considered by +some to be very characteristic of syphilis. Mesaortitis is +the primary lesion and acts as a <i>locus minoris resistentiæ</i> +where an aneurysm forms.</p> + +<p>Hypertensive cardiovascular cases have been serologically +studied, and a positive Wassermann reaction found +in a large percentage of one series. In fifty cases, 90 per +cent either gave a positive Wassermann reaction or luetin +test, were known to have syphilis, or had children with +hereditary syphilis. This suggests what might be called +"familial cardiovascular syphilis."</p> + +<p>Hypertensive disease is possibly one of the common so-called +"late" manifestations of syphilis. That syphilis is +responsible for the arterial disease in the vessels of the +brain, resulting in apoplexy or sudden cardiac death in middle +life, has long been known. In fact, it is claimed (Osler) +that all aneurysms occurring in persons under thirty years<span class="pagenum"><a name="Page_166" id="Page_166">[166]</a></span> +of age are due to syphilitic aortitis. In the late stages of +syphilis the arterial lesions may be of a diffuse character.</p> + + +<h4>Chronic Drug Intoxications</h4> + +<p>Lead, tobacco, and according to some, tea and coffee, are +to be classed as causal factors in the production of arteriosclerosis. +Certain it is that all these substances have a +tendency to raise the arterial pressure, but whether the +drug itself causes first a degeneration, and later a hypertension +results, or vice versa, is not yet positively known. +We have just mentioned that lead particularly has a marked +effect in producing arterial lesions. Other drugs as adrenalin, +barium chloride, physostigmin, etc., while producing +experimental arteriosclerosis, hardly could produce +the disease in man. <b>Alcohol</b> has been blamed for much, and +as an etiologic factor in the production of arteriosclerosis +formerly was accorded a first place. More recently much +doubt has been thrown on this supposition by the work of +Cabot, who showed that the mere drinking of even large +quantities of spirits had no effect in producing arterial +disease.</p> + +<p>This observation has been recently substantiated by +Hultgen, who carefully studied clinically 460 cases of +chronic alcoholism. He says, "There are no cardiovascular +symptoms which might be termed characteristic of +chronic alcoholism, unless it be the peculiar fetal qualities +of the heart sounds which we know as embryocardia. I +find this very frequent among drinkers, but I can offer only +a tentative explanation for it, namely the following: Embryocardia +can only occur with low tension blood pressure, +and in the absence of renal insufficiency. Hence it +might be considered as a useful condition of no pathologic +significance at all. That alcohol is a sclerogenic pharmakon +and productive of arteriosclerosis with its usual train of +symptoms may be a fact, but its demonstration would be<span class="pagenum"><a name="Page_167" id="Page_167">[167]</a></span> +difficult and is really not shown by my tabulations. There +were cardiovascular changes, such as myocarditis, aortitis, +valvular heart disease and arteriosclerosis in chronic alcoholics +in 54.3 per cent of 461 cases, but this by no means +constitutes a proof of the causal relationship between these +lesions and the abuse of liquors. I believe it, nevertheless, +to be good reasoning to ascribe the bulk of cardiovascular +symptoms to the sclerogenic action of alcohol, while abstaining +from an interpretation of its pathogenesis." Just +what rôle <b>tobacco</b> plays is difficult to say. My own opinion +is, that of itself when used in moderation, it has no ill +effects. However, as tobacco is a drug that may raise the +blood pressure, excessive use must be held responsible for +the production of arteriosclerosis. It is difficult to separate +its effects from those produced by eating and drinking.</p> + + +<h4>Overeating</h4> + +<p>There can be no doubt but that the constant overloading +of the stomach with rich or difficultly digestible food is +responsible for a large number of cases of arteriosclerosis. +Every one must have noted the increase in force and volume +of the heart beat after the ingestion of a large meal. The +constant repetition of such processes conceivably can lead +to damage to the vessel walls through hypertension.</p> + +<p>In the metabolism of food in the intestines there are substances +produced which are poisonous when absorbed directly +into the circulation. Ordinarily these substances +are rendered harmless either before absorption or are detoxicated +in the liver to harmless substances. It is conceivable +that a constant overproduction of such poisons +would eventually damage the defensive mechanism of the +body to such an extent that some of the poisons would +circulate in the blood. An expression of a surplus of one, +at least, of these decomposition products is the appearance +of indican in the urine. It is not believed that indicanuria +has the importance attached to it which some authors would<span class="pagenum"><a name="Page_168" id="Page_168">[168]</a></span> +have us believe. It is found too often and in too many varying +conditions, nevertheless it undoubtedly does reveal the +presence of perverted metabolism.</p> + +<p>In how far the toxins absorbed from the intestinal tract +are responsible for the production of arterial disease, it is +not possible to say. Some observers lay great stress on +this factor as a cause of arteriosclerosis. The author believes +that the rôle played by the absorption of products of +perverted intestinal metabolism is an important one. The +primary change is an increased tension in the arterioles +which later leads to thickening of the coats of the vessels +and to the other consequences of arterial disease. A vicious +circle is thus established which has a tendency to become +progressively worse.</p> + + +<h4>Mental Strain</h4> + +<p>More and more does one become impressed with the fact +that patients with arteriosclerosis are very often those who +take life too seriously and either from ambition or from an +exalted sense of duty lead especially strenuous lives. Not +always are these persons addicted to drug or liquor habit. +Many are rather abstemious in their habits. It is not so +often that we see as a victim of arteriosclerosis, the carefree +person who laughs his way through life without worrying +about the morrow. He is not so prone to arteriosclerosis. +Worry is a far more potent cause of breakdown than +actual manual work. It is the rule to find thickened arteries +among neurasthenics. This may be only part of a generalized +degeneration of all tissue in the body. The blood pressure +in such persons is usually low. So many men of our +better class live under a continuous mental strain in the +business world. The increase in arteriosclerosis cases is +real, not apparent. The intense mental strain seems to cause +a marked increase in blood pressure (for short periods of +mental effort this has been proved) over a period of time<span class="pagenum"><a name="Page_169" id="Page_169">[169]</a></span> +sufficient to cause permanent changes in the vessel walls. +The same sequence of events repeats itself; high tension, +arterial strain, compensatory thickening, hypertrophied +heart, etc.</p> + +<p>Certainly the character of the arterial tissue has much to +do with the determination of degenerative changes which +may result from the action of one or more of the etiologic +factors.</p> + + +<h4>Muscular Overwork</h4> + +<p>Muscular overwork is to be reckoned with as an etiologic +factor. One sees it especially among the laboring class in +both whites and negroes. Possibly other factors, as alcohol +and coarse heavy food, contribute to the early arterial +degeneration. Hypertrophy of the heart occurs in athletes, +and statistics gathered among the oarsmen especially, show +a relatively high mortality at the different decades traceable +to the high tension produced while in training. This +question deserves more consideration than has been accorded +it.</p> + + +<h4>Renal Disease</h4> + +<p>Chronic disease of the kidneys (contracted red kidney) is +one of the most certain producers of hypertension; in fact, +some maintain that high tension, even without demonstrable +kidney lesions, as revealed by careful urine examinations, +is a valuable sign pointing to chronic nephritis. This +is doubted by others, myself among them. Just what causes +the increase in blood pressure sometimes to over 270 mm. +of Hg, is not definitely known. It seems most probable that +it is some poison elaborated by the diseased kidneys and +absorbed into the general circulation. There it acts primarily +on the musculature of the arterioles causing tonic +contraction and an increase of work on the part of the heart +to force the blood through narrowed channels. One fact is +certain. We see patients in coma due to renal disease with<span class="pagenum"><a name="Page_170" id="Page_170">[170]</a></span> +blood pressure much over 200 mm of Hg. As these cases +clear up, the pressure may fall, and should they seemingly +recover, the recovery is accompanied with a marked decrease +in blood pressure, finally reaching the normal for +the individual. Moreover, in the course of a severe acute or +subacute nephritis, hypertension is associated with headache, +partial or total blindness, and drowsiness. When the +pressure is reduced, all these symptoms disappear.</p> + +<p>There is also the chronically shrunken and scarred kidney +known pathologically as the arteriosclerotic kidney. +It is probable that there are two groups of cases which we +may designate: (1) primary; (2) secondary. In the primary +group the kidney disease antedates the sclerosis of +the arteries, and the sclerosis is most probably dependent on +the constant high tension. We know that prolonged hypertension +will produce severe forms of arteriosclerosis. The +arterial disease in this group is caused by the renal disease.</p> + +<p>In the second group the kidney changes are apparently +due to the general arteriosclerosis which, affecting the kidney +vessels, causes changes leading to atrophy and subsequent +fibrous tissue ingrowth of scattered areas. These +cases are not necessarily associated with hypertension; on +the contrary there is more apt to be hypotension. Where +the first group occurs for the most part in young and active +middle-aged people, the second group is the result of involutionary +processes which accompany advanced age.</p> + +<p>However careful a urinalysis may be, there is no assurance +that one can predict the pathologic state of the kidney. +Often so-called normal urine will be secreted by a badly +diseased kidney, whereas a urine which contains considerable +albumin and many casts may be secreted by a kidney +which is only temporarily the seat of inflammation. What +matters after all is not the state of the kidney which the +pathologist describes, but the actual functional response +of the kidney in the body to the various tests now well +known.</p> +<p><span class="pagenum"><a name="Page_171" id="Page_171">[171]</a></span></p> + +<h4>Ductless Glands</h4> + +<p>At the present time the tendency among some writers +is to make the ductless glands the responsible agents in +almost all diseases. Arteriosclerosis is no exception to this +tendency. Sajous, for example, divides the morbid process +producing arteriosclerosis into three types; (1) autolytic, +(2) adrenal, (3) denutrition. In the first type he finds +the pancreas to be the most important gland. It supplies +an internal secretion which "takes a direct part in the protein +metabolism of the tissue cells, and also in the defensive +reactions within these cells, as well as in the phagocytes and +in the blood stream." This being the case exaggeration of +this digestive process has tissue destruction as its result, +arteriosclerosis among them.</p> + +<p>In the adrenal type Sajous argues that adrenalin produces +lesions experimentally, therefore the adrenal gland +has a profound influence by its internal secretion in connection +with the sympathetic system in producing degenerations +leading to arteriosclerosis.</p> + +<p>The denutrition type has as its particular gland the thyroid. +The sclerotic process in the arteries is due to the lack +of thyroid as in cases of myxedema. After a long résumé +of his ideas he concludes "that arteriosclerosis is the result +of excessive or deficient activity of certain ductless glands, +the thyroid and adrenal in particular."</p> + +<p>No one can dogmatically deny the part which the ductless +glands may play in the production of arteriosclerosis, but it +hardly seems that there is enough actual experimental evidence +to show that they take such an important part as Sajous +believes. Until further and more convincing evidence +is offered by competent investigators, I prefer to look with +some skepticism upon the ductless gland theory of the causation +of arteriosclerosis. The field lends itself too easily +to speculation and imagery. Some are already allowing +themselves the mental debauch of this nature.</p> + +<hr style="width: 65%;" /> +<p><span class="pagenum"><a name="Page_172" id="Page_172">[172]</a></span></p> +<h2><a name="CHAPTER_VII" id="CHAPTER_VII"></a>CHAPTER VII.</h2> + +<h3>THE PHYSICAL EXAMINATION OF THE HEART +AND ARTERIES</h3> + + +<h4>Heart Boundaries</h4> + +<p>In order to be able to estimate the departures from normal +in the boundaries of the heart, it is essential that there +be a definite appreciation of the boundaries of the normal +heart in relation to the chest wall.</p> + +<p>It is frequently stated that the right limit of cardiac dullness +is normally, in the adult, just at the right border of +the sternum. This is not strictly accurate. Careful dissections +at the autopsy table and x-ray plates of the chest +made at a distance of two meters from the tube show that +the border of the right auricle is from one to one and a +half and even two centimeters from the edge of the sternum +at the level of the fourth rib, and on the living subject this +can be also demonstrated. The right border of the heart +usually is from 3 to 4 cm. from the midsternal line at the +level of the fourth rib.</p> + +<p>Again there is a term used in defining the apex, known as +the point of maximum impulse. As this does not always +coincide with the apex beat and with the outer lower left +border of the heart, it would be better to use the term apex +beat.</p> + +<p>Normally, then, the cardiac dullness, the so-called relative +cardiac dullness, begins above at the upper border of the +third costal cartilage, as a rule, and taking a somewhat +curved line with the concavity inward, descends to the fifth +interspace or beneath the fifth rib from 9 to 10 cm. from a +line drawn through the center of the sternum parallel to its +length, the midsternal line. This seems to me to be a better +method of recording the size of the heart than by the<span class="pagenum"><a name="Page_173" id="Page_173">[173]</a></span> +lines commonly used; viz., the nipple, or midclavicular, or +parasternal line. Below, the cardiac dullness is merged into +the tympany from the stomach and the dullness from the +liver. At the sixth right costosternal articulation there is +a sharp turn upwards forming at that point with the liver +the cardiohepatic angle. At the fourth right cartilage or +the third interspace, the dullness is from one to two centimeters +from the edge of the sternum. We have then a somewhat +pear-shaped area or triangular area with the apex at +the apex of the heart. The so-called absolute cardiac dullness +does not appear to me to be of any great significance. +In reality it is the limit of lung resonance and may be +greater or less, not so much on account of variations in the +size of the heart, as of variations in size of the lungs and +shape of the chest wall.</p> + +<p>The really crucial question which should always be asked +is, Is the heart enlarged or decreased in size? The position +of the apex beat alone can not determine this, neither can the +limit to the right of the sternum. The distance between +these two points and the depth of the dullness at a distance +of 5 cm. from the midsternal line on the left side, will give +the size of the heart as nearly as can be obtained in the living +subject. A series of measurements in normal adults +average 13 to 14 cm. and 9 to 10 cm. respectively. For +women they are about 1 cm. less in each direction.</p> + +<p>The elaborate mechanism known as the orthodiagraph is +probably the best means of determining the actual limits +of the heart, but few men have such an expensive instrument, +and, moreover, at the bedside such an instrument +could not be used. From comparative measurements I concur +in the belief of those who affirm that careful percussion +will furnish equally as accurate limits.</p> + +<p>The first step in making an examination of the heart is to +expose the patient's chest in a good light, and, sitting at his +right side, carefully inspect the chest. The position of the +apex beat, heaving, bulging, retraction of interspaces, etc.,<span class="pagenum"><a name="Page_174" id="Page_174">[174]</a></span> +can easily be seen if visible. After careful inspection has +given all the data which it is possible to obtain, one next +lays the palm of the hand over the heart and attempts to +palpate the apex beat. The thrust of the apex in a hypertrophied +heart can readily be felt, and one can feel whether +the heart is regular, irregular, intermittent, or has other +change in rhythm. The shock of the closing valves, particularly +the aortic, can be felt, and that and the forcible apical +impulse are very suggestive signs of hypertrophy and +hypertension. Thrills may also be felt and can be timed +in relation to the heart cycle.</p> + + +<h4>Percussion</h4> + +<p>It is to percussion that we next proceed, and for the data +in regard to the size of the heart, it is, for our purpose, the +most valuable of all the physical methods of heart examination.</p> + +<p>First and foremost we wish by percussion to learn the +actual size of the heart, in other words what is ordinarily +called the relative cardiac dullness. With the absolute dullness +we are not concerned. That irregular area represents, +as has been said, actually the <b>limits of lung resonance</b>. The +heart may or may not be covered with lung; there may or +may not be the incisura cardiaca. What I wish to insist +upon is that the size of the area of absolute dullness can +give us no data in regard to the size of the heart. What we +must endeavor to learn is the actual size of the heart as +nearly as our crude means will permit.</p> + +<p>Light, very light, almost inaudible percussion, what Goldscheider +called "Schwellungsperkussion," must be practiced. +Use the middle finger of the right (left) hand as the +hammer and the last joint of the middle finger of the left +(right) hand pressed firmly against the chest, as pleximeter. +I believe it is better to place the pleximeter finger parallel +to the boundary to be limited although some place the finger +perpendicularly, that is, pointing toward the boundary.<span class="pagenum"><a name="Page_175" id="Page_175">[175]</a></span> +Now and then it helps to bend the pleximeter finger at the +second joint, hold it perpendicularly to the chest wall, and +strike the joint directly in line of the finger. This in my +hands has been of great assistance in percussing the limits +of the heart dullness. Pottenger's "light touch palpation" +is a modification of the light palpation and, to my mind, has +no very special advantages. Auscultatory percussion is of +great value at times. The bell of the stethoscope is placed +over the portion of heart uncovered by lung (should such +be the case), and with this point as a center the chest is +lightly and quickly tapped along radii converging toward +the stethoscope. One soon learns to recognize the change +of pitch as the tapping reaches the border of the heart. It +is well to use all methods, especially in difficult cases, and +to compare the results. Personally I have found that by +light percussion I can limit with much accuracy the upper, +right, and left borders of the heart.</p> + +<p>There is much to be gained by using light percussion. +Strong blows set in vibration not only the underlying structures, +but also more or less of the chest wall. We wish to +avoid this source of error, we do not wish to differentiate by +pitch alone. Finally one's pleximeter finger becomes, after +long practice, so sensitive to changes in the resonance of +structures lying below it, that there is actual feeling of impairment +to the slightest degree. This delicate touch is +what we should endeavor to cultivate.</p> + +<p>It is at times of advantage to use immediate percussion. +This is done by bending the fingers of the striking hand, +bringing the tips in a line and striking the chest lightly with +the four fingers as one finger. Some find it easier to percuss +the dullness due to the heart in this way than by mediate +percussion.</p> + +<p>The little hammer and hard rubber, celluloid, bone, or +ivory pleximeter does not seem to me to be nearly as good +as the fingers. Moreover, one always has his hands, but +may forget his hammer and pleximeter.</p> +<p><span class="pagenum"><a name="Page_176" id="Page_176">[176]</a></span></p> + +<h4>Auscultation</h4> + +<p>In auscultating the heart I prefer the binaural stethoscope +of the Ford pattern. The recent substitution of an +aluminum bell for the hard rubber bell is an improvement. +Personally I do not favor the phonendoscope or any of the +new patent non-roaring instruments now for sale by urgent +instrument makers. The phonendoscope has its uses, for +example in auscultating the back when a patient is lying +in bed or in listening to the heart sounds when a patient is +under an anesthetic; but for differentiating the murmurs +and for heart diagnosis, I much prefer the regular bell +stethoscope.</p> + +<p>In arteriosclerosis the two places over which it is important +to listen are the apex and the second right cartilage, +the aortic area. Over the former, one gains data in regard +to the strength of the heart as indicated by the first sound, +over the latter point, one learns of the tension in the aorta +by the character of the sound produced when the aortic +valves close.</p> + +<p>The hypertrophy of the heart in arteriosclerosis is invariably +due to the enlargement and thickening of the left +ventricle. From the nature of the position which the heart +assumes in the thorax, this enlargement is downward and +to the left. The apex beat will therefore be found in the +fifth or sixth interspace, and definitely at an increased distance +from the midsternal line. As stated above, it is +most important that this distance be accurately measured +and put down in the notes of the case for future reference. +No satisfactory prognosis can be given unless this is done, +for the gradual increase or the decrease under treatment in +the size of the heart can thus be definitely known, and, +knowing the other factors, a prognosis may be given which +will be of some value to the patient.</p> +<p><span class="pagenum"><a name="Page_177" id="Page_177">[177]</a></span></p> + +<h4>The Examination of the Arteries</h4> + +<p>It is exceedingly difficult at times to affirm definitely that +an artery, the radial for example, is actually sclerosed. +Much depends on the sensitiveness of the fingers of him +who palpates, and much upon the relation of the palpated +artery to the surrounding, chiefly underlying, structures. +In the examination of arteries it is well to inspect the body +for the pulsations caused by them. Frequently an exceedingly +tortuous artery, such as the brachial, may be seen +throughout its whole extent and yet the radial appear little, +if any, thickened by palpation. Again the artery of a +pulse of high tension which is small in size but full between +the beats, may not be as sclerosed as one which collapses +and feels much softer. It is difficult to obtain accurate data +in regard to the tension in an artery by feeling it with the +fingers of one hand. One should use both hands. With the +middle finger of the right (left) hand the artery is compressed +peripherally, that is, nearest the wrist. The blood +is then pressed out of the artery with the middle finger of +the left (right) hand, so as to obliterate completely the +pulse wave and the two or three inches between the middle +fingers are felt with the index fingers. By holding the finger +firmly on the artery near the wrist so as to block any +wave that may come through the palmar arch by anastomosis +with the ulnar artery and by releasing pressure on the +proximal middle finger, some idea may be had of the degree +of pulse tension. However, no amount of practice can more +than approximate the tension and when one is surest that +he can tell how many millimeters of pressure there are, he +is apt to be farthest wrong when he checks his guess with +the sphygmomanometer.</p> + +<p>Much may be learned from carefully palpating the peripheral +arteries, and, as a rule, the sclerosis of these arteries +means general arteriosclerosis, although there are many +exceptions to this.</p> + +<p><span class="pagenum"><a name="Page_178" id="Page_178">[178]</a></span>A more recent method, and one which in the author's +hands has been found to be valuable, is that proposed by +Wertheim-Salomonson who palpates the artery not with +the ball of the finger but with the fingernail. The finger is +held so that the nail is perpendicular to the surface of the +skin and the artery is felt with the end of the nail. The sensation +is perceived at the root and makes use of all the sensitive +nerve endings there. In this way it is possible to feel<span class="pagenum"><a name="Page_179" id="Page_179">[179]</a></span> +the arterial wall distinctly, and a little practice will enable +one to determine whether or not the vessel wall is thickened. +It is also possible to determine with a considerable degree of +accuracy the diameter of the artery and the size of the wall +when the current is cut off by pressure on the proximal side +of the artery. It is best to have a firm background when +this "fingernail" palpation is used. This may be obtained +by palpating the radial artery against the lower end of the +radius.</p> + +<p>Probably the best method of palpating the arteries, especially +the radial, to determine the degree of sclerosis and +thickening, is to use the tip of the finger and roll it carefully +over the artery. The tip of the finger is exceedingly +sensitive and, moreover, it is a firmer palpating surface +than the ball, thus enabling one to appreciate degrees of +sclerosis which could not be differentiated by palpation +with the soft yielding ball. This finger tip palpation is well +illustrated in the figures here shown. (Figs. 57 and 58.)</p> + +<div class="figcenter bord" style="width: 500px;"> + +<a name="Finger-tip_palpation_of_the_radial_artery" id="Finger-tip_palpation_of_the_radial_artery"></a> + + +<img src="images/fig_057.png" width="500" height="321" alt="Fig. 57.—A method of finger-tip palpation of the radial artery. (Graves.)" title="Fig. 57.—A method of finger-tip palpation of the radial artery. (Graves.)" /> +<span class="caption">Fig. 57.—A method of finger-tip palpation of the radial artery. (Graves.)</span> +</div> + +<div class="figcenter bord" style="width: 500px;"> + +<a name="Finger-tip_palpations_of_the_radial_artery" id="Finger-tip_palpations_of_the_radial_artery"></a> + + +<img src="images/fig_058.png" width="500" height="316" alt="Fig. 58.—Another method of finger-tip palpation of the radial artery. (Graves.)" title="Fig. 58.—Another method of finger-tip palpation of the radial artery. (Graves.)" /> +<span class="caption">Fig. 58.—Another method of finger-tip palpation of the radial artery. (Graves.)</span> +</div> + + +<h4>Estimation of Blood Pressure</h4> + +<p>It must be borne in mind at the outset that arteriosclerosis +and high blood pressure are not always associated. As +a matter of fact in the severest grades of senile arteriosclerosis +the blood pressure is usually below the normal +for the individual's years. However, as high tension is a +frequent factor in the production of arterial thickening, +blood pressure readings are of importance.</p> + +<p>The instrument which one uses is of minor importance +provided it is properly standardized. The most important +feature of the instrument is the cuff. This must be 12 cm. +wide and be long enough to wrap around the arm several +times so that the pressure is evenly distributed over the +whole arm and not over a small portion. One mercury instrument +we had in the hospital was reported to be at great +variance with a dial instrument. This mercury instrument +was provided with a cuff which was short and was tied<span class="pagenum"><a name="Page_180" id="Page_180">[180]</a></span> +around the arm by means of a piece of tape. This caused +a tight constriction over a small area and rendered the estimation +too high. A new, long tailed cuff easily remedied +the apparent defect in the instrument.</p> + +<p>In taking blood pressures the difference from day to day +of 10 or even 15 mm. of systolic pressure has no great significance. +Fluctuations of the systolic pressure alone, it is +insisted upon, have very little meaning. One must take the +whole pressure picture into consideration and determine +how the picture changes in order to draw any conclusion in +regard to the state of the blood pressure. Failure to pay +attention to this evident point has caused much futile work +to be written and published.</p> + +<p>It is well to emphasize again the point that the blood +pressure picture consists of the systolic, the diastolic, the +pulse pressure and the pulse rate.</p> + + +<h4>Palpation</h4> + +<p>Hoover has called attention to the direct palpation of the +femoral artery just below Poupart's ligament as a more accurate +index of the pressure in the aorta than the palpation +of the radial artery. Possibly one can obtain a more accurate +estimate of the blood pressure in this way. This, +however, is open to dispute. To estimate the blood pressure +by palpating the radial artery is most deceptive. In +about 75 per cent of cases one can tell fairly well whether +the pressure is abnormally high or abnormally low. Small +variations are impossible to determine. Unquestionably it +is most advantageous to get into the habit of palpating the +femoral artery and checking the result with the sphygmomanometer +so that the fingers may be trained to appreciate +as accurately as possible changes of pressure.</p> + +<p>It may be that one day when the instrument is needed it +is not at hand. A well-trained touch then becomes a great +asset.</p> +<p><span class="pagenum"><a name="Page_181" id="Page_181">[181]</a></span></p> + +<h4>Precautions When Estimating Blood Pressure</h4> + +<p>There are certain precautions which must be strictly observed +when deductions are drawn from the manometer +readings. The psychic factor must be reckoned with. Any +emotion may cause marked variations in the pressure. Excitement +and anger are especial sources of error. Even the +slight excitement arising from taking the first blood pressure +on a nervous patient especially is apt to give false +values. Usually the readings must be taken many times at +the first sitting and the first few may have to be set aside. +Worry is a potent factor in raising the pressure. A walk +to the physician's office, especially if rapid, has its effect.</p> + +<p>The position of the patient when the blood pressure is +taken is important. Usually in the office the pressure is +taken when the patient sits in a chair. He should assume a +relaxed, comfortable attitude. The readings should be +made at the same time of day and at the same interval between +meals. The pressure in both arms should be +measured and comparisons should be made only between +readings on the same arm. These precautions may seem +useless and even somewhat trivial, and the conditions difficult +to control. But unless they are carefully observed the +readings will be false, no comparisons can be drawn between +the readings on different days, and the instrument +will most probably be blamed. I have known this to happen +so often that I can not emphasize too strongly the importance +of controlling all the essential conditions which +go to make accurate work.</p> + + +<h4>The Value of Blood Pressure</h4> + +<p>In the past few years there has been a veritable avalanche +of blood pressure instrument salesmen who have +covered the country, sold instruments, and have made many +startling claims for the instrument. They have emphasized +its value out of proportion to what the instrument can do<span class="pagenum"><a name="Page_182" id="Page_182">[182]</a></span> +even in the hands of one familiar will all the defects. Consequently +it is not necessary to emphasize the value of blood +pressure. It seems best to utter a few words of caution in +regard to its interpretation.</p> + +<p>The value lies not in the occasional estimation compared +with some other one reading, but in the frequent estimation +and in the visualization of the blood pressure picture. For +the great majority of diseases the blood pressure has no +particular value except to show that the circulation is not +materially disturbed. The limits of normal are rather wide, +so that consideration of the patient's age, sex, build, etc., +will give us some idea of a base line, so to speak, for any one +person. Wide departures from relatively normal figures +are important, but are not diagnostic or, rather, pathognomonic. +I can not help but feel that the diastolic pressure is +<i>the</i> most important part of the blood pressure picture. Persistent +high diastolic pressure means increased work for the +heart, which, if acting for a long time against the high +peripheral resistance, must eventually hypertrophy. The +arteries become thickened, lose their wonderful elasticity, +fibrous tissue is deposited in their walls, and the vicious +circle is established which leads to pathologic hypertension.</p> + +<p>Blood pressure readings must be intimately mixed with +brains in order to be of any great value in diagnosis or +prognosis.</p> + +<hr style="width: 65%;" /> +<p><span class="pagenum"><a name="Page_183" id="Page_183">[183]</a></span></p> +<h2><a name="CHAPTER_VIII" id="CHAPTER_VIII"></a>CHAPTER VIII.</h2> + +<h3>SYMPTOMS AND PHYSICAL SIGNS</h3> + + +<h4>General</h4> + +<p>Well developed arteriosclerosis shows four pathognomonic +signs: (1) hypertrophy of the heart; (2) accentuation +of the aortic second sound; (3) palpable thickening of +the arteries; and (4) heightened blood pressure. However, +it must not be inferred that these signs must be present in +order to diagnose arteriosclerosis. It has already been said +that a very marked degree of thickening, with even calcification +of the palpable arteries, may occur with absolutely +no increase of blood pressure, and at autopsy a small flabby +heart may be found.</p> + +<p>While arteriosclerosis is usually a disease which is of +slow maturation, nevertheless cases are occasionally seen +which develop rather rapidly. The peripheral arteries have +been noticed to become stiff and hard in as relatively brief +a time as two years from the recognized onset of the disease.</p> + +<p>Since involution processes are physiologic, as has been +described (vide infra), arteriosclerosis may assume an +advanced grade and run its course devoid of symptoms +referable to diseased arteries. It is doubtful whether the +sclerosis itself could produce symptoms, except in cases +later to be described, were it not that the organs supplied +by the diseased arteries suffer from an insufficient blood +supply and the symptoms then become a part of the symptom-complex +of any or all the affected organs.</p> + +<p>There are cases, however, in comparatively young persons +where a combination of certain ill-defined symptoms +gives a clue to the underlying pathologic processes. These +symptoms of early arteriosclerosis are the result of slight<span class="pagenum"><a name="Page_184" id="Page_184">[184]</a></span> +and variable disturbances in the circulation of the various +organs. Normally there are frequent changes in the blood +pressure in the organs, but the vasomotor control of normal +elastic vessels is so perfect that no symptoms are noted by +the individual. When the arteries are sclerosed, they are +less elastic and the blood supply is, therefore, less easily +regulated. At times symptoms occur only after effort. The +patient may tire more readily than he should for a given +amount of mental or bodily exercise; he is weary and depressed, +and occasionally there is noted an unusual intolerance +of alcohol or tobacco. Vertigo is common, especially +on rising in the morning or in suddenly changing from a +sitting to a standing position. Some complain of constant +roaring or ringing in the ears. There may be dull headache +that the accurate fitting of glasses does not alleviate. +Unusual irritability or somnolency with a disinclination +to commence a new task may be present. Sometimes the +effort of concentrating the attention is sufficient to increase +the headache. This has been called "the sign of the painful +thought." Numbness and tingling in the hands, feet, +arms, or legs are also complained of, and neuralgias, not +following the course of the nerves but of the arteries, also +occur. It is important to remember that the train of symptoms +resembling neurasthenia in a person over forty-five +years old may be due to incipient arteriosclerosis. This +tardy neurasthenia frequently accompanies cancer, tuberculosis, +diabetes, and incipient general paralysis, as well as +incipient arteriosclerosis.</p> + +<p>Bleeding from the nose, epistaxis, taking place frequently +in a middle-aged person, sometimes is an early symptom. +The bleeding may be profuse, but is rarely so large as to be +positively harmful. In fact, it may do much good in relieving +tension. Slight edema of the ankles and legs is seen. +Dyspnea on slight exertion is not uncommon. Dyspeptic +symptoms are not infrequent, pyrosis (heartburn), a feeling +of fullness after meals with belching or a feeling of<span class="pagenum"><a name="Page_185" id="Page_185">[185]</a></span> +weight in the epigastrium. The dyspeptic symptoms may +be so marked that one might almost speak of a variety of +arteriosclerosis, the dyspeptic type. For quite a while before +any symptoms that would definitely fix the case as one +of undoubted arteriosclerosis, the patient complains that +foods which previously were digested with no difficulty now +give him gastric distress. The examination of the stomach +contents of a patient presenting gastric symptoms reveals +usually a subacidity. The total acidity measured after the +Ewald test meal may be only 20 and the free HCl may be +absent. Attention has been called to an unnatural pallor +of the face in early arteriosclerosis. Progressive emaciation +is sometimes seen in cases of arteriosclerosis and may +be the only symptom of which the patient complains.</p> + + +<h4>Hypertension</h4> + +<p>Not all cases of arteriosclerosis are accompanied by increased +arterial tension. As has been stated in a previous +chapter, the blood pressure in the arterial system depends +chiefly on two factors; viz., the degree of peripheral (capillary) +resistance, and the force of the ventricular contraction. +The highest arterial pressures recorded with the +sphygmomanometer occur not in pure arteriosclerosis but +in cases where there is concomitant chronic interstitial disease +of the kidneys. When this is found there is always +arteriosclerosis more or less marked. In cases where the +arteries are so sclerosed that they feel like pipe stems there +may be an actual decrease in the blood pressure. Hence +the clinical measuring of the pressure in the brachial artery +alone is not sufficient for a diagnosis of arteriosclerosis. A +persistent high blood pressure even with normal urinary +findings is not a sign of arteriosclerosis. The high tension +later may lead to the production of sclerosis of the arteries, +but in these cases the kidney may be primarily at fault.</p> + +<p>The impression must not be gained that hypertension in<span class="pagenum"><a name="Page_186" id="Page_186">[186]</a></span> +itself always constitutes a disease or even a symptom of disease. +Hypertension itself is practically always a compensatory +process. That is to say, it is the attempt on the part +of the body to equalize the distribution of blood in the body +when there is some poison causing constriction of the small +arteries. In this sense hypertension is not only essential, +but actually life-saving. A heart which is so diseased that +it can not respond to the call for increased action by hypertrophy +of its fibers, would shortly wear out. The very fact +that the heart becomes enlarged and the tension in the +arteries becomes high, indicates that in such a heart there +was great reserve power. But while hypertension is largely +an effort at adjustment among the various parts of the circulation, +it nevertheless tends to increase, provided the +cause or causes which produced it act continuously. Moreover, +as has been said (Chap. II), the arterioles do not respond +to increased work on the part of the heart by expanding, +but by contracting. A vicious circle is thus maintained +which eventually must lead to serious consequences.</p> + +<p>Hypertension is then, if anything, only a symptom which +may or may not demand treatment. That hypertension +leads to the production of sclerosis of the arteries has been +repeatedly affirmed here. In certain cases it is good and +should not be experimented with. In other cases it is bad +and some treatment to reduce the tension must be tried. +The main point is to regard hypertension as one regards a +compensated heart lesion.</p> + +<p>Prof. T. Clifford Allbutt divides the causes of arteriosclerosis +clinically into three classes: (1) The toxic class—the +results of poisons of the most part of extrinsic origin, +chiefly those of certain infections. In some of these +diseases, the blood pressures, as for example, in syphilis, +are ordinarily unaffected; in others, as in lead poisoning, +they are raised. (2) The class he calls hyperpietic,<a name="FNanchor_15_15" id="FNanchor_15_15"></a><a href="#Footnote_15_15" class="fnanchor">[15]</a> in<span class="pagenum"><a name="Page_187" id="Page_187">[187]</a></span> +which an arteriosclerosis is the consequence of tensile +strength, of excessive arterial blood pressure persisting for +some years. A considerable example of this class is the +arteriosclerosis of granular kidney, but in many cases kidney +disease is, clinically speaking, absent. (3) The involutionary +class, in which the change depends upon a senile, or +quasisenile degradation. This may be no more than wear +and tear, a disposition of all or of certain tissues to premature +failure—partly atrophic, partly mechanical—under +ordinary stresses; or it also may be toxic, a slow poisoning +by the "faltering rheums of age." In ordinary cases +of this class the blood pressures for the age of the patient +are not excessive. Although the toxins of the specific +fevers, notably typhoid, as stated above, and influenza, have +been shown to produce arteriosclerosis, this, under favorable +circumstances he believes tends to disappear. This +has been shown by Wiesel.</p> + +<p>As the blood pressure is dependent on the resistance +offered by the capillaries and arterioles, there are only two +ways in which increased pressure can be brought about; +either by rendering the blood more viscous, or by the generation +of some poison from the food taken into the body +which, acting on the vasomotor center or directly on the +finer vessels, arteriolar or capillary, sets up a constriction +over any large area, and mainly in the splanchnic area. In +regard to the liability to arteriosclerosis, this area stands +second only to the aortic and coronary areas. He believes +that arteriosclerosis itself has little effect in raising arterial +pressure. Many cases are seen in which with extreme arteriosclerosis +there was no rise in blood pressure, and some +in which pressures have been rising even long before the +appearance of arterial disease. Prof. Allbutt also believes +that in the hyperpietic cases the arteries undergo a transient +thickening, which can be removed if the causes can be +reached and overcome.</p> + +<p>Clinically speaking, then, hyperpietic arteriosclerosis is<span class="pagenum"><a name="Page_188" id="Page_188">[188]</a></span> +not a disease, but a mechanical result of disease. If the narrowing +of the arterioles is brought about by thickening due +to arteriosclerosis, then it would seem <i>a priori</i> that such +obliteration should cause a rise in pressure. Were the +vascular system a mere mechanical set of tubes and a pump, +this would happen, but other factors of great importance +must be taken into consideration besides the mechanical +factors; viz., chemical and biological factors. Thus, whole +parts may be closed and with compensatory dilatation in +other parts there would be little or no change in pressure, +unless there were hyperpiesis. In established hyperpiesis, +we note two conditions in the radial artery: first, a comparatively +straight vessel with a small diameter; secondly, a +larger, more tortuous vessel, "the large leathery artery." +In the cases of the first group, hyperpiesis is often more +marked, although not appearing so to the examining finger, +than in the second class. In view of the difficulty of estimating +by touch alone the amount of hyperpiesis in a contracted +hard artery, it is often overlooked until a ruptured +vessel in the brain startles us to a realization of our mistake. +The "narrow" artery is more dangerous than the +tortuous one, for with every change in pressure the passive +vessels of the brain must receive blood that under normal +conditions would go to other parts of the circulation.</p> + +<p>In involutionary sclerosis there is a gradual thickening +and tortuosity of the vessel, which although it may be +greater than in the hyperpietic cases, yet is never so dangerous +to life. The heart in hyperpiesis hypertrophies and +dilates, but such a heart is the result, not an integral part, +of the arterial disease.</p> + + +<h4>The Heart</h4> + +<p>When the arterial tree becomes narrowed and the resistance +offered to the flow of blood thereby is increased, more +muscular work is required of the left ventricle and according<span class="pagenum"><a name="Page_189" id="Page_189">[189]</a></span> +to the general laws which govern muscles the ventricle +hypertrophies. There is an actual increase in number of +fibers as well as an increase in the size of the individual +fibers. Some of the best examples of simple hypertrophy +of the left ventricle are found under such circumstances. +The chambers as a rule do not dilate until the resistance becomes +greater than the contraction can overcome, when +symptoms of broken compensation of the heart take place. +The hypertrophy of the left ventricle brings more of this +portion of the heart toward the anterior chest wall. The +enlargement is toward the left, also, consequently the apex-beat +is found below and to the left of its usual site, even an +inch or more beyond the nipple line. The impulse is heaving, +pushing the palpating hand forcibly up from the chest +wall. The visible area of pulsation may occupy three interspaces +and the precordium is seen to heave with every systole. +On auscultation the second sound at the aortic cartilage +is ringing, clear, and accentuated. Not infrequently, +too, the first sound is loud and booming, but has a curious +muffled sound that may even be of a murmurish quality. +The leaflets of the mitral valve may be the seat of sclerosis, +the edges are slightly thickened and do not quite approximate, +thus causing a definite murmur with every systole. +This murmur may be transmitted out into the axilla and be +heard at the inferior angle of the left scapula.</p> + + +<h4>Palpable Arteries</h4> + +<p>Not every artery that can be felt is the subject of arteriosclerosis, +and, as has been stated, palpable arteries being +more or less a condition of advancing years, judgment as +to whether the artery is pathologically or physiologically +thickened may be a matter of individual opinion. A radial +artery that lies close to the lower end of the radius and can +actually be seen to pulsate when the hand is held slightly +extended on the back of the wrist, is easily felt, but must<span class="pagenum"><a name="Page_190" id="Page_190">[190]</a></span> +not, therefore, be considered a sclerosed artery. The radial +may be so deeply situated in the wrist of a fat subject that +it is difficultly palpable. Yet the two cases just described +may have arteries of identical structure, there being no +more retrogressive changes in the one than in the other. +"Experience is fallacious and judgment difficult."</p> + +<p>The small, contracted, wiry artery of a chronic nephritic +may feel like a pipe stem, but if properly felt the mistake +will not be made of considering such an artery an unusually +sclerosed one. When the wave is pressed out of such a +high tension artery, it is found that what seemed to be a +firm sclerosed vessel, was in reality an artery tightly +stretched over the column of blood.</p> + + +<h4>Ocular Signs and Symptoms</h4> + +<p>It would not exaggerate too much to say that the examination +of the eye grounds with the ophthalmoscope is the +most important aid in the early diagnosis of arteriosclerosis. +Long before there are any subjective symptoms, +changes can be seen in the blood vessels of the retina which, +while not always diagnostic, at least call attention to a beginning +chronic disease. As I become more proficient in the +use of the ophthalmoscope, I am impressed with the importance +of the ocular signs of arterial disease. I would urge +practitioners to familiarize themselves with this instrument. +The electrically lighted instruments on the market now have +so simplified the technic that any physician should be able +to see the grosser changes which take place in the arteries +and veins of the retina and in the disc. Frequently the +ophthalmologist is the first to recognize early arteriosclerosis. +In the fundus are seen increased tortuosity of the retinal +vessels and their terminal twigs with more or less bending +of the vessels at their crossings. The arteries are terminal +ones, and small patches of retinitis are therefore found. +The changes have been divided into (1) suggestive, (2) +pathognomonic.</p> +<p><span class="pagenum"><a name="Page_191" id="Page_191">[191]</a></span></p> +<p>Under (1) are:</p> + +<p>(a) Uneven caliber of the vessels,</p> + +<p>(b) Undue tortuosity,</p> + +<p>(c) Increased distinctness of the central light streak,</p> + +<p>(d) An unusually light color of the breadth of the +artery.</p> + +<p>Under (2) are:</p> + +<p>(a) Changes in size and breadth of the retinal arteries +so that they look beaded,</p> + +<p>(b) Distinct loss of translucency,</p> + +<p>(c) Alternate contractions and dilatations in the veins,</p> + +<p>(d) Most important of all, the indentation of the veins +by the stiffened arteries.</p> + +<p>There is yet another sign which appears to be pathognomonic. +The arteries are pale, appear rigid and through the +center, parallel to the course, is a rather bright, fine threadlike +line. The appearance is known as the "silverwire" +artery. It is particularly constant in hypertension where +the most beautiful examples are seen.</p> + +<p>Moreover, there is the arcus senilis, the fine translucent +to opaque circle surrounding the outer portion of the iris. +Practically every one with a well-marked arcus senilis has +arteriosclerosis, but vice versa not every one with even +marked arteriosclerosis has an arcus senilis.</p> + +<p>In general, the symptoms are gradual loss of acute vision, +and attacks of transient loss of vision. The explanation +which has been offered for these phenomena is the contraction +in a diseased central artery.</p> + + +<h4>Nervous Symptoms</h4> + +<p>The onset of arteriosclerosis is, in the majority of cases, +so insidious that certain nervous manifestations, due in all +probability to disturbances in blood pressure, are present +long before the actual sclerosis of the arteries can be felt.<span class="pagenum"><a name="Page_192" id="Page_192">[192]</a></span> +These nervous symptoms are at times the sign posts to show +us the way to accurate diagnosis. There may be gradual +increase in irritability of temper, inability to sleep, +vertigo even extending to transient attacks of unconsciousness. +Loss of memory for details frequently is an early +symptom of sclerosis of the cerebral arteries. Nervous indigestion +may be present. Various paresthesias as numbness, +tingling, a sense of coldness or of heat or burning, a +sense of stiffness or even actual stiffness or weakness may +occur in the arms and legs, more frequently in the legs. +The pain complained of may be due to occlusion of an artery, +although evidence for this is lacking. It has been +thought by some that the pain in angina pectoris might be +due to this cause.</p> + +<p>Several curious and interesting diseases which have +been thought by some to have arteriosclerosis as a basis are +accompanied by pain. Such are erythromelalgia, Raynaud's +disease, "dead fingers," and intermittent claudication.</p> + +<p>Erb has reported a large series of intermittent limp +(claudication) from his private practice. He finds that the +large majority of the cases occur in men. The abuse of +tobacco was evidently the main etiologic factor in about +half of the cases. Repeated exposure to cold and the abuse +of alcohol were responsible for most of the other cases. +Curiously enough he finds that a history of syphilis was +present in only a small proportion of his cases. It is his +firm conviction that intermittent limping—which he thinks +should be called angiosclerotic dysbasia—is frequently incorrectly +diagnosed. It is mistaken for other troubles and +treated wrongly. As gangrene may develop this is particularly +dangerous. The affection generally develops gradually, +although he has seen cases where the onset was rather +acute. The partial or complete lack of the pulse in the foot +is the one striking sign, together with the varying behavior +of the pulse, its disappearance when the feet are cold and<span class="pagenum"><a name="Page_193" id="Page_193">[193]</a></span> +its return after a warm foot bath or under other treatment. +Signs of general arteriosclerosis were present in nearly +every case. When there is a tendency to the development +of intermittent limp he finds that a valuable sign is the manner +in which the leg blanches when it is lifted repeatedly +while the patient is recumbent and becomes hyperemic later +when placed horizontally. In health this change occurs +more rapidly.</p> + +<hr style="width: 65%;" /> +<p><span class="pagenum"><a name="Page_194" id="Page_194">[194]</a></span></p> +<h2><a name="CHAPTER_IX" id="CHAPTER_IX"></a>CHAPTER IX.</h2> + +<h3>SYMPTOMS AND PHYSICAL SIGNS</h3> + + +<h4>Special</h4> + +<p>Our conception of arteriosclerosis as a degenerative process +affecting the vascular tree rather than a disease, removes +the possibility of discussing special symptoms. As +a matter of fact, we know of very few organs where even +profound pathologic changes in the vascular system produced +during life any symptoms which could be laid to +these arterial changes. Kind nature has given to us such +an excess of organs of every kind that the destruction of +large portions of any organ seems to affect the function +but little. So only particular groups of organs, which show +symptomatic changes as the result of arteriosclerotic processes, +will be discussed. It is realized that this may not +give Teutonic completeness to the discussion, but it certainly +saves paper and has a distinct practical value to the +long suffering reader.</p> + +<p>Although arteriosclerosis is a disease which affects the +whole arterial system, it nevertheless never reaches the +same grade all over the body. The difference in the structure +and functions of the various organs determines to great +extent the eventual symptomatology. Endarteritis obliterans +of a small sized artery in the liver or leg would lead to +no marked symptoms, as the circulation is so rich that the +anastomoses of the blood vessels would soon establish a +collateral circulation that would be perfectly competent to +sustain the function of the part. Quite different would it +be should one of the small arteries of the brain, the lenticulo-striate, +for example, which supplies the corpus striatum, +become the seat of a thrombosis or embolism caused by +arteriosclerosis. The arteries of the brain are terminal<span class="pagenum"><a name="Page_195" id="Page_195">[195]</a></span> +arteries and the blood supply would be cut off entirely with +a resulting anemic necrosis of the part supplied by the +artery and a loss of function of the part. What would be +of no moment in the leg or arm might prove even fatal in +the brain.</p> + +<p>The further symptomatology, therefore, of arteriosclerosis +depends entirely on the organ or organs most affected +by the interference with the blood supply. The following +groups may be recognized:</p> + +<p> +1. Cardiac.<br /> +<br /> +2. Renal.<br /> +<br /> +3. Abdominal.<br /> +<br /> +4. Cerebral.<br /> +<br /> +5. Spinal.<br /> +<br /> +6. Local vasomotor effects.<br /> +<br /> +7. Pulmonary.<br /> +</p> + + +<h4>Cardiac</h4> + +<p>Most cases of arteriosclerosis sooner or later present +symptoms referable to the heart. When the organ is hypertrophied +and is already working against an enormous +peripheral resistance, a slight excess of work put upon it +may cause a dilatation of the chambers with the resulting +broken compensation. There is dyspnea on slight exertion, +possibly some precordial distress, slight edema of the ankles +and lower legs and possibly scanty urine. With proper +care, a patient with such symptoms may recover, but the +danger of another break in compensation is enhanced. The +next attack is more severe. The edema is greater, there +may be signs of edema of the lungs, effusions into the serous +cavities may occur. The heart shows marked dilatation. +There is gallop or canter rhythm and there are loud murmurs +at the apex. When a patient is first seen in this stage, +it may be quite impossible to state whether or not there is +true valvular disease of the heart. The muscle is usually +diseased in that there is fibroid degeneration of more or<span class="pagenum"><a name="Page_196" id="Page_196">[196]</a></span> +less extensive character. This factor causes the heart to +lose much of its elasticity and increases the tendency to +permanent dilatation. Such cases must be watched before +one can say that true valvular insufficiency is not present. +The fatal termination of such a case is quite like that of +true valvular disease. There is increasing dyspnea, increasing +anasarca, and the patient usually succumbs to +edema of the lungs, drowned in his own secretions.</p> + +<div class="figcenter" style="width: 422px;"> + +<a name="Aneurysm_of_the_heart_wall" id="Aneurysm_of_the_heart_wall"></a> + + +<img src="images/fig_059.png" width="422" height="500" alt="Fig. 59.—Aneurysm of the heart wall. (Milwaukee County Hospital.)" title="Fig. 59.—Aneurysm of the heart wall. (Milwaukee County Hospital.)" /> +<span class="caption">Fig. 59.—Aneurysm of the heart wall. (Milwaukee County Hospital.)</span> +</div> + +<p>A very rare complication of the fibroid degeneration of +the heart muscle is aneurysm of the heart wall. (Fig. 59.)<span class="pagenum"><a name="Page_197" id="Page_197">[197]</a></span> +The apex of the left ventricle is most commonly the site of +the aneurysm and rupture occasionally occurs. Such an accident +is rapidly fatal. In the arteriosclerotic process which +occurs at the root of the aorta, the coronary arteries become +involved both at the openings and along the courses of the +vessels. A branch or branches or even one artery may +become blocked as a result of obliterating endarteritis. +The arteries of the heart are not terminal vessels but as a +rule blocking of a large branch leads to anemic infarct. +These areas become replaced by fibrous tissue which in the +gross specimen appears as streaks of whitish or yellowish +color in the musculature. Anemic infarcts may not occur. +In such cases the anastomosis between branches of the coronary +arteries is unusually free. Through arteriosclerosis +of the coronary vessels extensive fibrous changes may occur +that lead to a myocardial insufficiency with its attending +symptoms—dyspnea, irregular and intermittent heart, +gallop rhythm, edema, etc. One of the most distressing +and dangerous results of sclerosis of the coronary arteries +and of the root of the aorta is angina pectoris. While in +almost every case of angina pectoris there is disease of the +coronary arteries, the contrary does not hold true, for most +extensive disease, even embolism, of the arteries is frequently +found in persons who never suffered any attacks of +pain. This symptom group is more common in males than +in females and as a rule occurs only in adult life. "In men +under thirty-five syphilitic aortitis is an important factor." +(Osler.)</p> + +<p>Since the valuable experiments of Erlanger on heart +block, considerable attention has been paid to lesions of the +Y-shaped bundle of fibers, a bundle arising at the auriculoventricular +node and extending to the two ventricles, +known also as the auriculoventricular bundle of His. +Interference with the transmission of impulses through this +bundle gives rise to the symptom group known as the +Stokes-Adams syndrome, which is characterized by: (a)<span class="pagenum"><a name="Page_198" id="Page_198">[198]</a></span> +slow pulse, (b) cerebral attacks—vertigo, syncope, transient +apoplectiform and epileptiform seizures, (c) visible +auricular impulses in the veins of the neck. Many of the +cases which occur are in elderly people the subjects of +arteriosclerosis.</p> + +<div class="figcenter bord" style="width: 314px;"> + +<a name="Large_aneurysm_of_the_aorta_eroding_the_sternum" id="Large_aneurysm_of_the_aorta_eroding_the_sternum"></a> + + +<img src="images/fig_060.png" width="314" height="500" alt="Fig. 60.—Large aneurysm of the aorta eroding the sternum. Death from rupture through +the skin preceded by frequent small hemorrhages. (Milwaukee County Hospital.)" title="Fig. 60.—Large aneurysm of the aorta eroding the sternum. Death from rupture through +the skin preceded by frequent small hemorrhages. (Milwaukee County Hospital.)" /> +<span class="caption">Fig. 60.—Large aneurysm of the aorta eroding the sternum. Death from rupture through +the skin preceded by frequent small hemorrhages. (Milwaukee County Hospital.)</span> +</div> + +<p>So far as we now know all cases of the Stokes-Adams +syndrome are caused by heart block which is only another +name for disease in the auriculoventricular bundle. Of +interest here is the fact that besides gummata, ulcers, and +other lesions of the bundle, definite arteriosclerotic changes +have been found.</p> + +<p>"The investigation of a typical case of Stokes-Adams disease +has shown that the symptoms of this case are caused +by some lesion in the heart which gives rise to the condition<span class="pagenum"><a name="Page_199" id="Page_199">[199]</a></span> +now generally termed heart block. Practically all degrees +of heart block have been observed, namely, complete +heart block and partial block with 4:1, 3:1, and 2:1 rhythm, +and occasionally ventricular silences. These stages occurred +during recovery.</p> + +<p>"Experiments testing the reaction of the heart to various +extrinsic influences demonstrate that when the block is complete +the ventricles do not respond to influences presumably +of vagus origin, although the auricles still respond normally +to such influences, that effects exerted upon the heart +presumably through the accelerators still influence the rate +of the ventricles as well as that of the auricles.</p> + +<p>"When the block is partial the rate of the ventricular contraction +varies proportionally with the rate of the auricular +contractions but only within certain limits. When these +limits are exceeded the block becomes more complete, i. e., +a 2:1 rhythm may be changed into a 3:1 rhythm, this into +a 4:1 rhythm, and this into complete block, and vice versa.</p> + +<p>"The syncopal attacks are, in all probability, directly dependent +upon a marked reduction of the ventricular rate. +Such reductions of the ventricular rate are always associated +with an increase of the auricular rate, and it is +believed that the latter is the cause of the former." (Erlanger.)</p> + +<p>The epileptiform seizures of the syndrome may be caused +by the anemia of the brain resulting from failure of the +heart to supply a sufficient quantity of blood.</p> + +<p>The apoplectiform attacks are most probably caused by +venous congestion when the slowing of the ventricular contractions +is not sufficient to cause convulsions, but will just +cause complete unconsciousness.</p> + + +<h4>Renal</h4> + +<p>Chronic nephritis, hypertension, arteriosclerosis form a +most important trinity. Some stoutly affirm that in all +cases of high tension there is chronic renal disease. Certainly<span class="pagenum"><a name="Page_200" id="Page_200">[200]</a></span> +the very highest blood pressures which we see occur +in the chronic interstitial forms of kidney disease. The +cause is most probably to be sought in some poison which +is elaborated in the kidney, is absorbed into the circulation +and acts powerfully either on the vasoconstrictor center +as a stimulus, or directly on the musculature of the +small arteries all over the body. Usually hypertension is +progressive but it may be temporary.</p> + +<p>A man, 43 years old, entered the Milwaukee County Hospital +in uremic coma. The systolic blood pressure was +280-290 mm. Hg, the diastolic pressure 220 mm. (Janeway +instrument). Under treatment his blood pressure gradually +became lower, at the same period the albumin and +casts gradually disappeared from the urine. In two weeks +from admission he seemed perfectly well, there were no +albumin or casts found in the urine, and the systolic blood +pressure was 136 mm., not a high figure for a muscular man +of the laboring class. It must be admitted, however, that +such cases are the exception, not the rule.</p> + +<p>Patients suffering from the association of chronic nephritis +with hypertension die slowly, usually. There is gradual +development of anasarca. Headache is frequent and +severe. Pains all over the body may occur. The sight +may suddenly become dim or may even be lost. Dizziness +may be complained of and dyspnea is usually marked. +Cyanosis comes on, the pulse becomes weak, irregular or +intermittent, heart failure sets in, and the patient dies with +edema of the lungs.</p> + +<p>Another class of renal arteriosclerosis is characterized +by a small granular kidney in which fibrous changes of a +patchy character have taken place. These scattered areas +are the result of obliterating endarteritis of renal arteries +here and there with consequent anemia, death of cells, and +replacement by fibrous tissue. It occurs as part of a generalized +arteriosclerosis in which the whole arterial system +is the seat of diffuse (senile) sclerosis. The palpable arteries<span class="pagenum"><a name="Page_201" id="Page_201">[201]</a></span> +are usually beaded or even encircled with calcareous +deposits and the aorta is the seat of an extensive nodular +and ulcerating sclerosis. The heart is usually small, shows +extensive fibrous and fatty changes and possibly the condition +known as "brown atrophy;" the blood pressure is low. +Such cases do not show any special symptoms. They are +anemic, short of breath on exertion, have the appearance +and show the signs of senility.</p> + +<p>In the first group it is, at times, difficult to say whether +the kidney disease or the arterial disease is the most important. +From a clinical standpoint the decision is not +essential as the end results are much the same in both. +However, when actual uremic symptoms dominate the +picture, it becomes evident that the disease of the kidney is +the chief feature in the causation of the symptoms.</p> + + +<h4>Abdominal or Visceral</h4> + +<p>There is an important group of cases to which but little +attention has been paid until quite recently. This is the +abdominal or visceral type of arteriosclerosis. It has been +stated that arteriosclerosis of the splanchnic vessels almost +invariably causes high tension. Among others, Janeway +has shown that general arteriosclerosis without marked +disease of the splanchnic vessels does not cause as a rule +increase of blood pressure.</p> + +<p>There are cases in which the brunt of the lesion falls upon +the abdominal vessels. Such cases have been called +"angina abdominalis." It has been suggested (Harlow +Brooks) that this type of arteriosclerosis may be determined +by constant overloading of the stomach with food, +especially rich and spiced food. This causes overwork of +the special arteries connected with digestion and so leads +to sclerosis of the vessels of the stomach, pancreas, and intestines. +Personal habits probably influence to great extent +the production of this more or less <b>localized</b> condition.</p> + +<p>The organs supplied by the diseased arteries suffer from<span class="pagenum"><a name="Page_202" id="Page_202">[202]</a></span> +changes analogous to those occurring in general or local +malnutrition, such as starvation, old age, or local anemias. +These changes are atrophy with hemachromatosis (brown +atrophy) or fatty infiltration and degeneration. Following +the degenerative changes there result connective tissue +growth and further limitation of the functionating power of +the affected organs.</p> + +<p>Pain is a more or less constant symptom of visceral +sclerosis. In the early stages there may be only a sense +of oppression, of weight, or of actual pressure in the abdomen +or pit of the stomach. There may be only recurring +attacks of violent abdominal pain accompanied by vomiting. +In some cases symptoms of tenderness in the epigastrium, +pains in the stomach after eating, vomiting and backache +may suggest gastric ulcer. There may be dyspnea and a +sense of anguish accompanied with a rapid and feeble pulse. +Hematemesis may make the symptom group even more like +ulcer of the stomach, and only the course of the disease +with the failure of rigid ulcer treatment and the substitution +of treatment directed toward relief of the arterial +spasm with resulting betterment, enables one to make a +diagnosis. The condition may be present for years and the +symptoms only epigastric tenderness with dizziness and +sweating on lying down after dinner, as in one of Perutz's +patients. The attacks are probably due to spasmodic contraction +of the sclerosed intestinal vessels with a resulting +local rise in blood pressure. The pains are most probably +due to the spasm of the intestinal muscles, and some think +they are located in the sympathetic and mesenteric plexuses.</p> + +<p>This result of arteriosclerosis is not so uncommon, and +by keeping this cause of obscure abdominal pain in mind +we are now and then enabled to save a patient from operation.</p> + +<p>An autopsy on a case which for many years had attacks +of abdominal pain and cramp-like attacks, with high blood +pressure and heart hypertrophy, showed extensive sclerosis<span class="pagenum"><a name="Page_203" id="Page_203">[203]</a></span> +of the abdominal aorta, superior mesenteric and iliacs. +These vessels were calcified. Hypertrophy of the left +ventricle was found. The kidneys were microscopically +normal. There were no changes in the ascending aorta but +in the descending portion there were scattered nodules and +small calcified plaques.</p> + +<p>The attacks of pain from which this patient suffered for +many years, the hypertrophy of the left ventricle and the +increased blood pressure were thought to be directly due +to the sclerosis of the abdominal vessels.</p> + + +<h4>Cerebral</h4> + +<p>It has been stated that arteriosclerosis is a general disease, +yet certain systems of vessels may be affected far +more than others, and indeed there may be marked sclerosis +at one part of the body and none demonstrable at another +part.</p> + +<p>In advanced sclerosis there may be one or more of a series +of accidents due to embolism, thrombosis, or rupture of the +vessels. Such conditions as transient hemiplegia, monoplegia +or aphasia may occur. The attacks may come on +suddenly and be over in a few minutes; what Allbutt calls +"Larval apoplexies." They may last from a few hours +up to a day, and are very characteristic. A patient aged +64 years with pipe stem radials and tortuous hard temporals +would be lying quietly in bed when suddenly he would +stiffen, the eyes would become fixed and the breathing +cease. In a few seconds consciousness returned, the patient +would shake himself, pass his hand over his brow and ask, +"Where am I? Oh, yes, that's all right." He had as many +as thirty of these attacks in twenty-four hours, none of +them lasting over one minute. To just what such attacks +are due, it is hard to say. Some have attributed them to +spasm of the smaller blood vessels of the brain, but there +have never been demonstrated in the vessels any constrictor +fibers.</p> + +<p><span class="pagenum"><a name="Page_204" id="Page_204">[204]</a></span>There is a well recognized form of dementia caused by +arteriosclerosis. In general paralysis of the insane and +in senile dementia the blood vessels are always diseased. +Milder grades of psychic disturbances are accompanied by +such symptoms as mental fatigue, persistent headaches, +vertigo, memory weakness and fainting. Aphasia, periods +of excitement and mental confusion occur in some. Later +stages are at times accompanied by inclination to fabulate, +loss of judgment, disorientation, narrowing of the external +interests, episodes of confusion and hallucinatory delirium.</p> + +<p>The hemiplegias, monoplegias and paraplegias may occur +again and again and last for one or two days. Unless +there has been rupture of the vessels, there is complete recovery +as a rule.</p> + +<p>In persons who have arteriosclerosis with high tension +attacks of melancholia are seen. There are at the same +time fits of depression, insomnia, irritability, fretfulness, +and a generally marked change in disposition. When the +tension is reduced by appropriate treatment these symptoms +disappear, to recur when the tension again becomes +high. On the contrary, attacks of mania are accompanied +by low blood pressure. The dizziness and vertigo in cerebral +arteriosclerosis are probably due to the stiffness of the +vessels which prevents them from following closely the variations +of pressure produced by position, and thus, at +times, the brain is deprived of blood and a transient anemia +occurs.</p> + +<p>Arteriosclerosis of the cerebral vessels is always a serious +condition. The greatest danger is from rupture of a +blood vessel. Another of the dangers is gradual occlusion +of the arteries bringing about necrosis with softening of the +brain substance. The latter is more apt to be associated +with psychic changes, dementia, etc.; the former, with +hemiplegia. It is curious that a small branch of the Sylvian +artery, the lenticulo-striate, which supplies the corpus striatum, +should be the one which most frequently ruptures.<span class="pagenum"><a name="Page_205" id="Page_205">[205]</a></span> +Where the motor fibers from the whole cortex are gathered +together in one compact bundle, a very small hemorrhage +may and does cause very serious effects. A comparatively +large hemorrhage in the silent area of the brain may cause +few or no symptoms.</p> + + +<h4>Spinal</h4> + +<p>It is conceivable that arteriosclerosis of the vessels of +the spinal cord might cause symptoms which would be referred +to the areas of the cord where the process was most +advanced. The lesions would be scattered and consequently +the symptoms might be protean in character.</p> + +<p>True epileptic convulsions dependent on arteriosclerotic +changes are also seen and are not so uncommon.</p> + +<p>This is on the whole a rare condition, much less common +than arteriosclerosis of the cerebral vessels. Collins and +Zabriskie report the following typical case:</p> + +<blockquote><p>"H., a fireman, fifty-one years old, was in ordinary good health until toward +the end of 1902. At that time he noticed that his legs were growing +weak and that they tired easily. Later he complained of a jerking sensation +in different parts of the lower extremities and at times of sharp pain, which +might last from several minutes to two or three hours. The legs were the +seat of a heavy, unwieldy sensation, but there was no numbness or other +paresthesia. About the same time he began to have difficulty in holding the +urine, a symptom which steadily increased in severity. These symptoms continued +until March, 1903, i. e., for three months, then he awakened one morning +to find that he was unable to stand or walk, and the sphincters of the +bowels and bladder relaxed. There was no complaint of pain in the back or +legs, no difficulty in moving the arms, in swallowing or in speaking. He says +he was able to tell when his lower extremities were touched and he could +feel the bed and clothes. He was admitted to the City Hospital three weeks +later and the following record was made on April 21, 1903.</p> + +<p>"The patient was a frail, emaciated man of medium height, who had the +appearance of being 55-60 years of age. He was unable to stand or walk. +When he was lying, he could flex the thigh and the legs slowly and feebly. +There was slight atrophy of the anterior and inner muscles, more of the left +than of the right side. The knee jerks and ankle jerks were absent. Irritation +of the soles caused quite a typical Babinski phenomenon. The patient +had fair strength in the upper extremities, but the arms tired very soon, he +said. The grip was moderate and alike in each hand. The motility of the +face, head, and neck was not noticeably impaired. There was no difficulty<span class="pagenum"><a name="Page_206" id="Page_206">[206]</a></span> +in swallowing, and articulation was not defective. Tactile sensibility was +slightly disordered in the lower extremities, although he could feel contact of +the finger, the point of a pin, and the like. Sensibility was not so acute as +normal; there was a quantitative diminution. Sensory perception was not +delayed. There was a distinct zone of slight hyperesthesia about as wide as +the hand above the femoral trochanters. Above that, sensibility was normal. +There was no discernible impairment of thermal sensibility. No part of the +body was particularly tender on pressure. A bedsore existed over the sacrum, +and there was excoriation of the genitals from constant dribbling of urine.</p> + +<p>"Examination of the chest showed shallow respiratory movements. The +heart was regular, weak, there were no murmurs, the second sound was accentuated. +Examination of the abdomen showed that the liver and spleen +were palpable, but were not enlarged. The abdominal reflexes, both upper and +lower, were sluggish. The patient was slow of speech, likewise apparently of +thought. He did not seem to show an adequate interest in his condition, still +he was fully oriented and seemed to have a fair memory. His mental reflex +was slow. There were indications in the peripheral blood vessels and heart of +a moderate degree of general arteriosclerosis. The peripheral vessels +such as the radial, were palpable, the walls thickened, the blood pressure +increased.</p> + +<p>"The patient did not complain of pain while he was in the hospital, a +period of four weeks, nor was there any particular change in the patient's +symptoms, subjective and objective, during this time. His mental state remained +clear until forty-eight hours before death, when he became sleepy, +stuporous, and comatose, dying apparently of cardiac weakness, which had set +in simultaneously with the clouding of consciousness."</p> + +<p>At autopsy, except for a few small hemorrhages in the posterior horns of +the lower dorsal segments on the right side and a similar condition of the left +anterior horns, there was nothing noticed. On microscopic examination, there +was found widespread sclerosis of the vessels of the cord to a marked degree +with only slight thickening of the vessels of the brain. There were secondary +degenerations of ascending and descending type particularly marked at the +ninth dorsal segment. They included portions of all the tracts, the pyramidal +tract as well. The symptoms in brief were: (1) weakness and easily induced +fatigue of the legs; (2) peculiar sensations in the lower extremities, described +as jerky, numbness, heaviness, and occasionally sharp pain; (3) +progressive incontinence of urine; (4) progressive paraplegia.</p></blockquote> + +<p>Since one of the chief manifestations of syphilis is sclerosis +of the arteries, neurologic cases characterized by irregular +symptoms and signs which can not be placed in any of +the definite system disease groups, are possibly due to +irregularly scattered areas of sclerosis throughout the +spinal cord caused by obliterating arteritis. Such cases +are not so very uncommon. Several have come under my<span class="pagenum"><a name="Page_207" id="Page_207">[207]</a></span> +observation. Further studies of the spinal cords of these +cases at autopsy are necessary before a final opinion can +be given as to their dependence on arteriosclerosis of the +spinal vessels.</p> + + +<h4>Local or Peripheral</h4> + +<p>When the arteriosclerosis in the peripheral arteries +reaches a stage where endarteritis obliterans supervenes, +there is usually no chance for a compensatory or collateral +circulation to be established. The area supplied by the vessel +undergoes dry gangrene. A portion of a toe or finger or +a whole foot or hand may shrivel up. It is more common to +see the spontaneous amputation take place in the lower extremities. +The same effect may be produced by the plugging +of a vessel with a thrombus. There may be much pain +connected with the sudden blocking, whereas the gradual +obliteration of the blood supply of a toe or foot is not as a +rule at all painful. The condition is at times revealed more +or less accidentally when a patient injures his toe or foot +and discovers that there is no sensation in the part and that +the wound instead of healing is inclined to grow larger.</p> + +<p>Other interesting vasomotor phenomena are frequently +connected with arteriosclerosis. Such a one is the curious +condition known as Raynaud's disease, a vascular disorder +which is divided into three grades of intensity: (1) local +syncope, (2) local asphyxia, (3) local or symmetrical gangrene. +This is not the place to describe this condition except +to say that the condition called "dead fingers" is the +most characteristic feature of the first stage. Chilblains +represent the mildest grade of the second stage. The parts +are intensely congested and there may be excruciating pain. +Any one who has ever had chilblains knows how painful +they can be. The general health is not impaired as a rule, +although the attacks are apt to come on when the person is +run down. The third stage may vary from a very mild<span class="pagenum"><a name="Page_208" id="Page_208">[208]</a></span> +grade, with only small necrotic areas at the tips of the +fingers, to extensive multiple gangrene.</p> + +<p>Another and very rare condition in which chronic endarteritis +was the only constant finding is the disease described +by S. Weir Mitchell and called by him erythromelalgia (red +neuralgia). This is "A chronic disease in which a part or +parts—usually one or more extremities—suffer with pain, +flushing, and local fever, made far worse if the parts hang +down." (Weir Mitchell.)</p> + +<p>Probably the most frequently seen result of arteriosclerosis +in the leg arteries is the remarkable condition, first described +by Charcot, known as intermittent claudication. +Persons the subject of this disease are able to walk if they +go slowly. If, however, any attempt be made to hurry the +step, there results total disability accompanied at times by +considerable cramp-like pain. The condition is much more +prone to occur in men than in women, and Hebrews seem +more frequently affected. The cause is most probably to +be sought in the anemia which results from the narrowing +of the channels through which the blood reaches the part. +The stiff, much narrowed arteries allow sufficient blood to +pass along for the nutrition of the part at rest or in quiet +motion. Just as soon as more violent exercise is taken, +calling for more blood, an ischemia of the part supervenes, +for the stiff vessels can not accommodate themselves to +changes in the necessary vascularity of the part. A rest +brings about a gradual return of blood and the function of +the part is restored. Pulsation may be totally absent in the +dorsal arteries of the feet and when the legs are allowed to +hang down there is apt to be deep congestion.</p> + +<p>In this connection a curious case reported by Parkes +Weber will not be out of place. The patient, a male, aged +42 years, complained of cramp-like pains in the sole of the +left foot and calf of the leg occurring after walking for a +few minutes and obliging him to rest frequently. When +the legs were allowed to hang over the side of the bed, the<span class="pagenum"><a name="Page_209" id="Page_209">[209]</a></span> +distal portion of the left foot became red and congested +looking. No pulsation could be felt in the dorsal artery of +the left foot or in the posterior tibial artery. There was no +evidence of cardiovascular or other disease. An ulcer on +the little toe had slowly healed, but cramp-like muscular +pains still occurred on walking. The disease had lasted +about five years without the appearance of gangrene.</p> + +<p>Weber calls this case one of arteritis obliterans with intermittent +claudication.</p> + + +<h4>Pulmonary Artery</h4> + +<p>In the symptomatology of sclerosis of the pulmonary +artery the clinical signs and symptoms are mostly referable +to the obliterating endarteritis of the smaller vessels, while +the physical signs are more apt to reveal the involvement of +the main trunk. A history of severe infection in the past +is frequent, especially smallpox, and accompanying aortic +sclerosis with insufficiency of the mitral valve or stenosis of +this valve is the rule. Striking cyanosis is an early symptom, +while there is little if any dyspnea and edema. Intermittent +dyspragia is common. There seems to be no +tendency to clubbed fingers. Repeated hemorrhages from +the lungs without the formation of infarcts may occur. +There is usually an area of dullness at the upper left margin +of the sternum and nearby parts, sensitive to pressure +and to percussion, and the heart dullness extends unusually +far towards the right. The diagnosis of the right ventricular +hypertrophy may be substantiated by a fluoroscopic examination.</p> + +<hr style="width: 65%;" /> +<p><span class="pagenum"><a name="Page_210" id="Page_210">[210]</a></span></p> +<h2><a name="CHAPTER_X" id="CHAPTER_X"></a>CHAPTER X.</h2> + +<h3>DIAGNOSIS</h3> + + +<h4>Early Diagnosis</h4> + +<p>Arteriosclerosis is essentially a disease of middle life +and old age. It is not unusual, however, to find evidences +of the disease in persons in the third decade and +even in the second decade. Hereditary influences play +a most important rôle, syphilis and the abuse of alcohol +in the family history are particularly momentous. The +recognition of the early changes in the arteries among +young persons depends largely upon how carefully these +changes are looked for. The difference in the point of view +of one man who finds many cases in the comparatively +young, and another man who rarely finds such changes early +in life, at times, depends upon the acuity of perception and +observation and not upon the fact that one man has had a +series of unusually young arteriosclerotic subjects. The +diagnosis of arteriosclerosis may be so easily made that the +tyro could not fail to make it. It is, however, the purpose +of this volume to lay stress on the earliest possible diagnosis +and, if possible, to point out how the diagnosis may be arrived +at. It is obviously much to the advantage of the patient +to know that certain changes are beginning in his +arteries, which, if allowed to go on, will inevitably lead to +one or more of the symptom groups described in the preceding +chapters.</p> + +<p>The combination of (1) hypertrophied heart, (2) increased +blood pressure, (3) palpable arteries, and (4) +ringing, accentuated second sound at the aortic cartilage is, +in reality, the picture of advanced arteriosclerosis. If the +individual is in good condition much may be done by judicious<span class="pagenum"><a name="Page_211" id="Page_211">[211]</a></span> +advice and treatment to ward off complications and +prolong life with a considerable degree of comfort. But we +should not wait until such signs are found before making a +diagnosis and instituting treatment. As in all forms of +chronic disease the early diagnosis is all important.</p> + +<p>The history of the case is the first essential. Often a careful +inquiry into the personal habits of a patient, with the +record of all the preceding infectious diseases will give us +valuable information and may be the means of directing the +attention at once to the possible true condition. Particularly +must we inquire into the family history of gout and +rheumatism. An individual who comes of gouty stock is +certainly more prone to arterial degeneration than one who +can show a healthy heredity. Alcoholism in the family also +is of importance because of the fact that the children of +alcoholics start in life with a poor quality of tissue, and +conditions that would not affect a man from healthy stock +might cause early degeneration of arterial tissue in one of +bad ancestry.</p> + +<p>What infectious diseases has the patient had? Even the +exanthemata may cause degenerations in the arteries, but, +as has been shown, such lesions probably heal completely +with no resulting damage to the vessel. Should the patient +have passed through a long siege of typhoid fever the problem +is quite different. Here (vide supra) (Thayer), the +palpable arteries do appear to be sclerosed permanently. +Probably the length of time that the toxin has had a chance +to act determines the permanent damage to the vessel wall. +More potent than all other diseases to cause early arteriosclerosis +is syphilis, and hence very careful inquiry should +be made in regard to the possibility of infection with this +virus. Not only the fact of actual infection but the duration +and thoroughness of treatment are important matters +for the physician to know.</p> + +<p>What is the patient's occupation? Has he been an +athlete, particularly an oarsman? Has he been under any<span class="pagenum"><a name="Page_212" id="Page_212">[212]</a></span> +severe, prolonged, mental strain? Is he a laborer? If so, +in what form of manual labor is he engaged? Such questions +as these should never be overlooked, as they form the +foundation stones of an accurate diagnosis, and early, accurate +diagnosis, we repeat, is essential to successful +therapy.</p> + +<p>We have called attention to the factor of sustained high +pressure in the production of arteriosclerosis. Constant +overstretching of the vessels leads to efforts of the body to +increase the strength of the part or parts. The material +which is used to strengthen the weakened walls has a higher +elastic resistance than muscle and elastic tissue, but a lower +limit of elasticity, and is none other than the familiar connective +tissue. In athletes, laborers, brain workers who are +under constant mental strain, and in those whose calling +brings them into contact with such poisons as lead, there is +every factor necessary for the production of high tension +and consequently of arteriosclerosis.</p> + +<p>Another question in regard to personal habits is how +much tobacco does the patient use and in what form does he +use it? Our experience is that the cigar smoker is more +prone to present the symptoms of arteriosclerosis than the +cigarette smoker, the pipe smoker, or the one who chews the +tobacco. A very irritable heart results not infrequently +from cigarette smoking but such is almost always found in +young men in whom the lesions of arteriosclerosis are exceedingly +rare. The probabilities are that the arteriosclerosis +in cigar smoking results from the slowly acting poison +which causes a rapid heart rate with an increase of pressure.</p> + +<p>Last but not least, and perhaps the most important question +is, has the patient been a heavy eater? This I believe +to be a potent cause of splanchnic arteriosclerosis with the +resulting indigestion, cramp-like attacks, high blood pressure, +etc. In a joking manner we are accustomed to remark, +"Overeating is the curse of the American people." +There is, however, much truth in that sentence. Osler, than<span class="pagenum"><a name="Page_213" id="Page_213">[213]</a></span> +whom there is no keener observer, states that he is more +and more impressed with the fact that overloading the +stomach with rich or heavy or spiced foods is today one of +the first causes of arterial degeneration. It stands to reason +that this is true. We know that organs exposed constantly +to hard work undergo hypertrophy, and that the +blood tension in those organs is high. Blood tension is, +after all, dependent on capillary resistance, and if the capillaries +are distended with blood, the resistance is great. +The digestive organs can be no exception to this rule. Increased +work means an increase of blood. This inevitably +causes distension of the capillaries with stretching of the +arteries and consequent damage to the walls. Once arteriosclerosis +is present a vicious circle is established.</p> + +<p>A man about forty-five consults us and says that he has +noticed recently that he gets out of breath easily; in tying +his shoes he experiences some dizziness. He finds that he +has palpitation of the heart and possibly pain over the +precordial region now and then. He notices also that he is +irritable, that is, his family tell him he is, and he notices +that things that formerly did not annoy him, now are almost +hateful to him. On examination, one finds a palpable radial, +a somewhat hypertrophied heart and slightly accentuated +second aortic sound. The blood pressure may be +high. The urine may or may not reveal any abnormalities. +Not infrequently, although no albumin may be found, there +are hyaline casts. Such a case of arteriosclerosis is evidently +not to be regarded as early. Then the question +arises, How are we to recognize early arteriosclerosis? I +do not believe that the solution of this problem lies entirely +in the hands of the physician. Some men are fortunate +enough to come up for an examination for life insurance +before an observant doctor who recognizes the palpable +artery, makes out the beginning heart hypertrophy and the +slightly accentuated second aortic sound. The patient will +tell you that he never felt better in his life. He gets up at<span class="pagenum"><a name="Page_214" id="Page_214">[214]</a></span> +seven, works all day, plays golf, drinks his three to six +whiskies, and is proud of his physical development. But +the great mass of people are not fortunate from this standpoint. +They do not seek the advice of the physician until +they are stretched out in bed. They boast of the fact that +for twenty years they have never had a doctor. One may +well say that it is a problem how to reach such persons. It +seems to me that there can be but one way to do this. The +people must be taught that the duty of a physician is just +as much to keep them in health as it is to bring them back +to health when they are ill. To that end people should be +taught that at least twice a year they should be carefully +examined. I do not mean that the patient should present +himself to the doctor and, after a few questions the doctor +say cheerfully, "You are all right." The patient should +be systematically examined. That means a removal of the +clothing and examination on the bare skin. Such cooperation +on the part of patient and doctor would save the patient +years of active life and make of the doctor, what his +position entitles him to be, the benefactor to the community. +Too often careless work on the physician's part lulls the +patient into a false sense of security and he wakes up too +late to find that he has wasted months or years of life. +Early diagnosis of arteriosclerosis is only possible in exceptional +cases unless people present themselves to the physician +with the thought in mind that he is the guardian of +health as well as the healer.</p> + +<p>There are patients who go to the ophthalmologist for +failing vision. Physically they feel quite well. They have +been heavy eaters, hard workers, men and women who have +been under great mental strain. On examination of the +fundus of the eye there is found slight tortuosity of the vessels +with possibly areas of degeneration in the retina. A +careful physical examination will usually reveal the signs +of arteriosclerosis elsewhere. We have mentioned frequently +high tension as an early sign. This must be taken<span class="pagenum"><a name="Page_215" id="Page_215">[215]</a></span> +with somewhat of a reservation, for this reason: not infrequently +a persistent high tension is the earliest sign of +chronic nephritis. The arteries may be pipe stem in character +and the heart small and flabby. However, if one +watches for the palpably thickened superficial arteries (always +bearing in mind the normal palpability as age advances) +and the high tension, he can not go far wrong in his +treatment whether the case is one of chronic nephritis or of +arteriosclerosis.</p> + +<p>There is also this to bear in mind. Arteriosclerosis may +be marked in some vessels and so slight in the peripheral +vessels that it can not with certainty be made out. But +when the radials are sclerosed, it is usually the case that +similar changes exist in other parts. Then too, there may +be marked changes at the root of the aorta leading to +sclerosis of the coronary vessels alone, and the first intimation +that the patient or any one else has that there is disease, +may be an attack of angina pectoris. Except for +symptoms on the part of the heart there is no way to make +the diagnosis of sclerosis of the coronary arteries.</p> + + +<h4>Differential Diagnosis</h4> + +<p>In arriving at a diagnosis, when the question is whether +or not arteriosclerosis is the main etiologic factor, the +most important fact to know is the age of the patient. +Other points that have been dwelt on fully must of necessity +also be borne in mind.</p> + +<p>Possibly the chief conditions that may be confused with +some of the results of arteriosclerosis are pseudo angina +pectoris which may be mistaken for true angina pectoris, +and ulcer of the stomach, appendicitis (?) or other inflammatory +abdominal condition which may be mistaken for +angina abdominalis.</p> + +<p>Differential tables are sometimes of value in fixing the +chief points of difference graphically.</p> + + +<p><span class="pagenum"><a name="Page_216" id="Page_216">[216]</a></span></p> +<p> </p> + + +<table border="0" cellpadding="4" cellspacing="0" summary="Angina Pectoris"> + +<tr> +<td><b>Pseudo angina pectoris</b>.</td><td><b>True angina pectoris</b>.</td> +</tr> + +<tr> +<td> </td> +</tr> + + +<tr> +<td>Etiology rather certain; hysteria, +neurasthenia, toxic agents, and reflex +irritations.</td><td>Etiology not certain but almost always +associated with arteriosclerosis +of the coronary arteries and also +aortic regurgitation.</td></tr> + +<tr> +<td> </td> +</tr> + +<tr> +<td>No age is exempt. Usually in +young people, chiefly females.</td> +<td>Age is important factor. Rare before +forty, and males usually affected.</td> +</tr> + +<tr> +<td> </td><td> </td> +</tr> + +<tr> +<td>Paroxysms of pain occur spontaneously, +are periodic and often nocturnal.</td> +<td>Paroxysms brought on by overexertions +or excessive mental emotion. +Rarely periodic. +</td></tr> + +<tr> +<td> </td><td> </td> +</tr> + +<tr> +<td>Pain, while severe, is diffuse and +sensation is of distension of heart. +No sense of real anguish.</td> +<td>Intense pain, radiating down arm; +heart felt as in a vise. Sense of anguish +and impending dissolution.</td></tr> + +<tr> +<td> </td><td> </td> +</tr> + +<tr> +<td>Duration may be an hour or more.</td> +<td>Duration from few seconds to several +minutes.</td></tr> + +<tr> +<td> </td><td> </td> +</tr> + +<tr> +<td>Restlessness and emotional symptoms +of causative conditions are +prominent.</td> +<td>Silent and fixed attitude, rigidity +rather than restlessness.</td> +</tr> + +<tr> +<td> </td><td> </td> +</tr> + +<tr> +<td>Usually no increase in arterial tension.</td> +<td>Arterial tension is as a rule increased.</td> +</tr> + +<tr> +<td> </td><td> </td> +</tr> + +<tr> +<td>Prognosis favorable.</td> +<td>Prognosis most unfavorable.</td> +</tr> + +</table> +<p> </p> + +<p>In differentiating between ulcer of the stomach and +angina abdominalis the following points may be of service:</p> + +<p> </p> + + + +<table border="0" cellpadding="4" cellspacing="0" summary="Ulcer"> +<tr> +<td><b>Ulcer</b>.</td> +<td><b>Angina abdominalis</b>.</td> +</tr> + +<tr> +<td> </td><td> </td> +</tr> + +<tr> +<td>Occurs as a rule in young persons, +more often females.</td> +<td>Only occurs in adults over forty +who have been heavy eaters and +drinkers, mostly males.</td></tr> + +<tr> +<td> </td><td> </td> +</tr> + +<tr><td>Pain of boring character increased +by food and by certain positions with +food in stomach. Felt through to +left of spine.</td> +<td>Pain cramp-like, diffuse, although +more localized in epigastrium. Not +necessarily any connection with food.</td> +</tr> + +<tr> +<td> </td><td> </td> +</tr> + +<tr> +<td>Occult blood found in stools.</td> + +<td> +No occult blood in stools.</td> +</tr> + +<tr> +<td> </td><td> </td> +</tr> + +<tr><td>Considerable anemia apt to be +present.</td> +<td>Anemia more often absent.</td> +</tr> + +<tr> +<td> </td><td> </td> +</tr> + +<tr> +<td>Arterial tension usually low.</td> +<td>Arterial tension high. (Splanchnic +sclerosis.)</td> +</tr> + +</table> + + + + +<h4>Diseases in Which Arteriosclerosis Is Commonly Found</h4> + +<p>There are certain more or less chronic diseases in which +arteriosclerosis is found either as a separate disease or as +a result of the chronic disease itself, or the sclerosis may be +the cause of the disease. As examples of the first class +are diabetes mellitus and cirrhosis of the liver. As examples<span class="pagenum"><a name="Page_217" id="Page_217">[217]</a></span> +of the second class are chronic nephritis, gout, syphilis, +and lead poisoning. Examples of the third class have already +been fully described. Then certain rare diseases +that have been briefly described in this chapter, viz.: Raynaud's +disease and erythromelalgia are frequently associated +with demonstrable arteriosclerosis.</p> + +<hr style="width: 65%;" /> +<p><span class="pagenum"><a name="Page_218" id="Page_218">[218]</a></span></p> +<h2><a name="CHAPTER_XI" id="CHAPTER_XI"></a>CHAPTER XI.</h2> + +<h3>PROGNOSIS</h3> + + +<p>In a disease that presents as many vagaries as arteriosclerosis, +it is not possible to give a certain prognosis. +Unfortunately we do not as a rule see the arteriosclerotic +until the disease is well advanced, or even after some of the +more serious complications have taken place. By that time +the condition is progressive, and while the prognosis is +grave the individual may live a number of years.</p> + +<p>It is fortunate for the arteriosclerotic that mild grades +of the disease are compatible with a fairly active life. The +disease in this stage may become arrested and the patient +may live many years. Not only in the mild grades is this +possible. Even patients with advanced sclerosis may enjoy +good health provided the organs have not been so damaged +as to render them unfit to perform their functions. The +frequency with which we see advanced arteriosclerosis at +the postmortem table as an accidental discovery, attests +the truth of the foregoing statement. Yet how often does +it happen that individuals, apparently in the best of health, +suddenly succumb to an asthmatic or uremic attack, an +apoplexy, cessation of the heart beat, or a rupture of the +heart due to arteriosclerosis!</p> + +<p>In order to arrive at an intelligent opinion in regard to +prognosis certain factors must be taken into consideration, +chief of which are: the seat of the sclerosis; the probable +stage; the existing complications; and, last and most important, +the patient himself. The whole man must be studied +and even then our prognosis must be most guarded.</p> + +<p>It is much more dangerous for the patient when the +process is in the ascending portion of the arch of the aorta +than when it has attacked the peripheral arteries. Here, +at the root of the aorta, are the openings of the coronary<span class="pagenum"><a name="Page_219" id="Page_219">[219]</a></span> +arteries and the arteries supplying the brain are close by. +The coronary arteries here control the situation. When +loud murmurs are heard at the aortic orifice and the heart +is evidently diseased, it is useful to divide the endocarditis +into two types, the arteriosclerotic and the endocarditic. +The etiology of the former is sclerosis and the prognosis is +grave because of the liability, nay the probability, that the +orifices of the coronary arteries will become narrowed. +The etiology of the second type is in most cases rheumatic +fever or some other infectious disease, and the prognosis +is far better than in the first type. True, the two may be +combined. In such a case, the prognosis is entirely dependent +upon the course of the arteriosclerosis.</p> + +<p>The involvement of the arteries in the kidneys is of considerable +importance, for it is usually bilateral and widespread. +As a rule, the disease makes but slow progress +provided that the general condition of the patient is good, +but at any time from a slight indiscretion or for no assignable +cause, symptoms of renal insufficiency may appear and +may rapidly prove fatal.</p> + +<p>It must not be thought that because the localization of +the arteriosclerosis in the peripheral arteries is usually the +most favorable condition that it is therefore devoid of ill +effects. On the contrary, very serious, even fatal, results +may be brought about by interference with the circulation +with resultant extensive gangrene of the part supplied by +the diseased arteries. The amputation of a portion of a +leg, for instance, may relieve, to some extent, an overburdened +heart and prove life-saving to the patient, but the +neuritic pains are not necessarily relieved. The torture +from these pains may be excruciating.</p> + +<p>No stage of the disease is exempt from its particular +danger. In the early stages of the disease before the +artery or arteries have had time to become strengthened by +proliferation of the connective tissue, there is the danger of +aneurysm. Later, the very same protective mechanism +leads to stiffening and narrowing of the arteries and hence<span class="pagenum"><a name="Page_220" id="Page_220">[220]</a></span> +to increased work on the part of the heart with all of its +consequences. Thrombosis is favored, and where atheromatous +ulcers are formed, embolism is to be feared.</p> + +<p>As the complications and results of arteriosclerosis come +to the front every one must be considered by itself and as +if it were the true disease. There may be a slight apoplectic +attack from which the patient fully recovers, but the +prognosis is now of a grave character, as the chances are +that another attack may supervene and carry off the subject. +Yet, after an apoplectic attack, patients have lived for many +years. Probably the most noted illustration of this is the +life of Pasteur. He had at forty-six hemiplegia with gradual +onset. He recovered with a resulting slight limp, did +some of his best work after the stroke, and lived to be +seventy-three years old. Yet the exception but proves the +rule and the prognosis after one apoplectic stroke should +always be guarded.</p> + +<p>The first attack of cardiac asthma is to be looked upon +as the beginning of the end. The end may be postponed +for some time, but it comes nearer with every subsequent +attack. One may recover from what appears to be a fatal +attack of cardiac asthma accompanied by edema of the lungs +and irregular, intermittent, laboring heart, but the recovery +is slow and the chances that the next attack will be the +fatal one are increased.</p> + +<p>The significance of albuminuria is difficult to determine. +The kidneys secrete albumin under so many conditions that +the mere presence of albumin in the urine may have but +little prognostic value. Many cases are seen where there is +no demonstrable albumin, and yet the patient may suddenly +have a cerebral hemorrhage. As a general rule the urine +should be carefully examined, but not too much stress should +be laid on the discovery of albumin and casts. It is not +always possible to determine the extent of the kidney lesion +by the urinary examination, yet at any time a uremic attack +may appear and prove fatal.</p> + +<p><span class="pagenum"><a name="Page_221" id="Page_221">[221]</a></span>After all the most important fact for the patient is not +what the pathologist finds in his kidneys after he is dead, +but what the living functional capacity of the kidneys is. +This can now be determined in a variety of ways as the +result of extensive work carried out in quite recent years. +The simplest method of determining the functional capacity +of the kidneys is by the injection into the muscles of the +back of a solution containing 6 mg. of the drug phenolsulphonephthalein +in one c.c. of fluid. This comes already +prepared in ampules, with full directions for its employment.<a name="FNanchor_16_16" id="FNanchor_16_16"></a><a href="#Footnote_16_16" class="fnanchor">[16]</a> +Some clinicians use indigo-carmine in place of +phthalein. The general consensus of opinion is in favor +of phthalein.</p> + +<p>The nephritic test meal carefully worked out by Mosenthal<a name="FNanchor_17_17" id="FNanchor_17_17"></a><a href="#Footnote_17_17" class="fnanchor">[17]</a> +gives much valuable information. The determination +of the nonprotein nitrogen or the creatinin in the blood also +reveals the functional capacity of the kidneys.<a name="FNanchor_18_18" id="FNanchor_18_18"></a><a href="#Footnote_18_18" class="fnanchor">[18]</a></p> + +<p>One might say that the appearance of albumin in the +urine of an arteriosclerotic where it had not been before, +is a bad sign, and in making a prognosis this must be taken +into consideration.</p> + +<p>Bleeding from the nose is not infrequently seen in those +who have arteriosclerosis. It can hardly be called a dangerous +symptom as it can always be controlled by tampons. +There are times when epistaxis is decidedly beneficial as it +relieves headache, dizziness, and may avert the danger of +a hemorrhage into the brain substance. It is rare to have +nose bleed except in cases of high tension in plethoric +individuals. My experience has been that it has saved me +the trouble of bleeding the patient. It is always of serious +import in that it indicates a high degree of tension, but +there is scarcely ever any immediate danger from the nose +bleed itself.</p> + +<p>Intestinal hemorrhage is always a grave sign. As has<span class="pagenum"><a name="Page_222" id="Page_222">[222]</a></span> +been shown, arteriosclerosis of the splanchnic vessels not +infrequently occurs, and an embolus or thrombus may completely +occlude the superior mesenteric artery. The +chances of the establishment of a collateral circulation are +small, as the arteries of the intestines are end arteries. +Necrosis of the part follows, blood is found in the stools, +and perforation or gangrene, or both, are apt to follow. +There may be blocking of small branches only, leading to +ulceration of the intestine. Under all conditions the prognosis +is serious.</p> + +<p>The general condition of the patient, his build, physical +strength, powers of recuperation, etc., must be taken into +account in giving a prognosis. The more powerful the individual, +the more favorable, as a rule, is the prognosis, with +this reservation always in mind, that the greater the body +development, the greater is the heart hypertrophy, and the +accidents from high tension must not be overlooked. Many +puny individuals with stiff, calcified arteries go about with +more ease than a robust man with thickened arteries only. +The differentiation as pointed out by Allbutt (page 186), +is well to keep in mind in giving a prognosis. It can not be +too strongly emphasized that it is the whole patient that we +must consider and not any one system that at the time happens +to be the seat of greatest trouble, and by its group of +symptoms dominates the picture.</p> + +<p>It is evident from what has been said that an accurate +prognosis in arteriosclerosis is no easy matter. Were +arteriosclerosis a simple disease of an acute character there +might be grounds for giving a more or less definite prognosis. +The most that can be said is that arteriosclerosis +is always a serious disease from the time that symptoms +begin to make themselves known. The gravity depends altogether +on the seat of the greatest arterial changes, and +is necessarily greater when the seat is in the brain than +when it is in the legs or arms.</p> + +<p>The attitude of the patient himself also determines to a<span class="pagenum"><a name="Page_223" id="Page_223">[223]</a></span> +great extent the prognosis. Some men, especially those +who have always enjoyed good health, turn a deaf ear to +warnings and instead of ordering their lives according to +the advice of the physician, persist in going their own way +in the hope that the luck that has always been with them will +continue to stand at their elbows. Neither firmness nor +pleadings avail with some men. The only salve for the conscience +of the physician is that he has done his best to steer +the patient away from the shoals and breakers. In others +who realize their condition and take advantage of the advice +given as to the regulation of their lives, the prognosis is +generally favorable.</p> + +<p>To sum up the chapter in a few words, I should say: +Always remember that the patient is a human being; study +his habits and character and mode of life; look at him as a +whole; take everything into consideration, and give always +a guarded prognosis.</p> + +<hr style="width: 65%;" /> + +<p><span class="pagenum"><a name="Page_224" id="Page_224">[224]</a></span></p> +<h2><a name="CHAPTER_XII" id="CHAPTER_XII"></a>CHAPTER XII.</h2> + +<h3>PROPHYLAXIS</h3> + + +<p>Arteriosclerosis comes to almost every one who lives out +his allotted time of life. As has been noted within, many +diseases and many habits of life are conducive to the early +appearance of arterial degeneration. Decay and degeneration +of the tissues are necessary concomitants of advancing +years and none of us can escape growing old. From +the period of adolescence certain of the tissues are commencing +a retrograde metamorphosis, and hand in hand +with this goes the deposit of fibrous tissue which later may +become calcified. The arterial tissue is no exception to this +rule, and we have already shown that certain changes normally +take place as the individual grows older, changes +which are arteriosclerotic in type and are quite like those +caused in younger people by many of the etiologic factors +of the disease.</p> + +<p>We are absolutely dependent upon the integrity of our +hearts and blood vessels for the maintenance of activity and +span of life. Respiration may cease and be carried on artificially +for many hours while the heart continues to beat. +Even the heart has been massaged and the individual has +been brought back to life after its pulsations have ceased, +but such cases are few in number. We can not live without +the heart beat and the prophylaxis of arteriosclerosis consists +in the adjustment of our lives to our environment, so +that we may get the maximum amount of work accomplished +with the minimum amount of wear and tear on the blood +vessels.</p> + +<p>The struggle for existence is keen. Competition in every +profession or trade is exceedingly acute, so much so that to +rise to the head in any branch of human activity requires<span class="pagenum"><a name="Page_225" id="Page_225">[225]</a></span> +exceptional powers of mind. Among those who are entered +in this keen competition, the fittest only can survive for any +period of time. The weaklings are bound to succumb. A +scion of healthy stock will stand the wear and tear far better +than will the progeny of diseased parentage.</p> + +<p>It is only necessary to call attention to the part that +alcohol, syphilis and insanity play in heredity. These have +been discussed fully in the earlier part of this book.</p> + +<p>We live rapidly, burning the candle at both ends. It is +not strange that so many comparatively young men and +women grow old prematurely. While heredity is a factor +as far as the prophylaxis of arteriosclerosis is concerned, +of far more importance is the mode of life of the individual. +Scarcely any of us lead strictly temperate lives. If +we do not abuse our bodies by excessive eating and drinking +and so wear out our splanchnic vessels and cause general +sclerosis by the high tension thereby induced, we abuse +our bodies by excessive brain work and worry with all their +multitudinous evils. The prophylaxis of arteriosclerosis +might well be labeled, "The plea for a more rational mode +of life." Moderation in all things is the keynote to health, +and to grow old gracefully is an art that admits of cultivation. +Excesses of any kind, be they mental, moral, or +physical, tend to wear out the organism.</p> + +<p>People habitually eat too much; many drink too much. +They throw into the vascular system excessive fluid combined +frequently with toxic products that cause eventually +a condition of high arterial tension. It has been shown how +poisonous substances absorbed from the intestines have +some influence on the blood pressure. Anything that causes +constant increase of pressure should be studiously avoided.</p> + +<p>Mild exercise is an essential feature of prophylaxis. One +may, by judicious exercise and diet, make of himself a +powerful muscular man without, at the same time, raising +his average blood pressure. The man who goes to excess +and continually overburdens his heart, will suffer the consequences,<span class="pagenum"><a name="Page_226" id="Page_226">[226]</a></span> +for the bill with compound interest will be +charged against him. It is a great mistake for any one to +work incessantly with no physical relaxation of any kind, +and yet, after all, it is not so much physical relaxation that +is necessary, as the pursuit of something entirely different, +so that the mind may be carried into channels other than +the accustomed routes. Diversification of interests is as a +rule restful. That is what every man who reaches adult +life should aim at. Hobbies are sometimes the salvation of +men. They may be ridden hard, but even then they are +helpful in bearing one completely away from daily cares +and worries. The man who can keep the balance between +his mental and physical work is the man who will, other +things being equal, live the longest and enjoy the best +health.</p> + +<p>Nowadays the trend of medicine is toward prophylaxis. +We give the state authority to control epidemics so far as +it is possible by modern measures to control them.</p> + +<p>We urge over and over again the value of early diagnosis +in all chronic diseases, for we know that many of them, and +this applies particularly to arteriosclerosis, could be prevented +from advancing by the recognition of the condition +and the institution of proper hygienic and medicinal treatment.</p> + +<p><i>It is the patent duty of every physician to instruct the +members of his clientele in the fundamental rules of health.</i> +Recently the President of the American Medical Association, +in his address before the 1908 meeting, urged the +dissemination of accurate knowledge concerning diseases +among the laity. While this may be done by city and state +boards of health, it seems far better for the modern trained +physician to work among his own people. With concise +information concerning the modes of infection and the dangers +of waiting until a disease has a firm hold before consulting +the health mender, people should be able to protect +themselves from infections and be able to nip chronic processes<span class="pagenum"><a name="Page_227" id="Page_227">[227]</a></span> +in the bud. But it is difficult to turn the average +individual away from the habit of having a drug-clerk prescribe +a dose of medicine for the ailment that troubles him. +It is really unfortunate that most of the pains and aches and +morbid sensations that one has speedily pass away with +little or no treatment. Herein lies the strength of charlatanism +and quackery. Unfortunate, yes, for a man can not +tell whether the trivial complaint from which he suffers is +any different from the one that was so easily conquered six +months ago. But instead of recovering, he grows worse. +Hope that springs eternal in the human breast, leads him +to dilly-dally until he at last seeks medical advice, only to +find that the disease has made such progress that little can +be done.</p> + +<p><i>Instruct the public to consult the doctors twice a year.</i> +The dentists have their patients return to them at stated +intervals only to see if all is well. <i>How much more rational +it would be if men and women past the age of forty had +a physical examination made twice a year to find out if all +is well.</i></p> + +<p>The prophylaxis of arteriosclerosis is moderation in all +the duties and pleasures of life. This in no sense means +that a man has to nurse himself into neurasthenia for fear +that something will happen to him. As one grows in years +exercise should not be as violent as it was when younger, +and food should be taken in smaller quantities. Many forms +of exercise suggest themselves, particularly walking and +golf. Walking is a much neglected form of exercise which, +in these modern days with our thousand and one means of +locomotion, is becoming almost extinct. There is no better +form of exercise than graded walking. To strengthen the +heart selected hill climbing is one of the best therapeutic +methods that we have. The patient is made to exercise his +heart just as he is made to exercise his legs, and as with +exercise of voluntary muscles comes increase in strength, +so by fitting exercise may the heart muscle be increased in<span class="pagenum"><a name="Page_228" id="Page_228">[228]</a></span> +power. A warning should be sounded, however, against +over exercise. This leads naturally to hypertrophy with +all its disastrous possibilities. Men who have been athletes +when young should guard against overeating and lack of +exercise as they grow older. Many of the factors which +favor the development of arteriosclerosis are already there, +and a sedentary, ordinary life, such as office all day, club +in afternoon, a few drinks and much rich food, will inevitably +lead to well-advanced arterial disease.</p> + +<p>Karl Marx in his famous Socialistic platform said: "No +rights without duties; no duties without rights." So we +may paraphrase this and say: "No brain work without +moderate physical exercise in the open air; no physical exercise +without moderate brain work."</p> + +<p>There is yet one other point that is important, the combination +of concentrated brain work and constant whiskey +drinking. This is most often seen in men of forty-five to +fifty-five, heads of large business concerns who habitually +take from six to twelve drinks of whiskey daily, and with +possibly a bottle of wine for dinner. Such men appear +ruddy and in prime health but, almost invariably, careful +examination will reveal unmistakable signs of arterial disease. +There is usually the enlarged heart and pulse of high +tension with or without the trace of albumin in the urine. +The lurking danger of this group of manifestations has so +impressed the medical directors of several of the large insurance +companies that a blood pressure reading must be +made on all applicants over forty years of age. Should high +blood pressure be found, the premium is increased, as the +expectation of life is proportionately shorter in such men +than in normal persons.</p> + +<p>Therefore, let every physician act his part as guardian +of health. Only in this way is the prophylaxis of arteriosclerosis +possible.</p> + +<hr style="width: 65%;" /> +<p><span class="pagenum"><a name="Page_229" id="Page_229">[229]</a></span></p> +<h2><a name="CHAPTER_XIII" id="CHAPTER_XIII"></a>CHAPTER XIII.</h2> + +<h3>TREATMENT</h3> + + +<p>Although it has been rather dogmatically stated (vide +supra) that every one who reaches old age has arteriosclerosis, +it must not be inferred that absolutely no exceptions to +this rule are found. Cases are known where persons of +ninety years even had soft arteries, and we have seen persons +of eighty whose arteries could not be palpated. When +infants and children are seen with considerable sclerosis, +it proves that, after all, it is the quality of the tissue even +more than the wear and tear, that is the determining factor +in the production of arteriosclerosis. It would be well if +those who can not bring healthy progeny into the world +were to leave this duty to those who can.</p> + +<p>In general the treatment of arteriosclerosis is prophylactic +and symptomatic. In the preceding chapter I had something +to say about prophylaxis in general; I must again +refer to it in detail.</p> + +<p>Arteriosclerosis is essentially a chronic progressive disease, +and the secret of success in the management of it is +not to treat the disease or the stage of the disease, but to +treat the patient who has the disease. To infer the stage +of the disease from the feeling of the sclerosed artery, may +lead to serious mistakes. Persons with calcified arteries +may be perfectly comfortable, while those with only moderate +thickening may have many severe symptoms. The +keynote is individualization. It is manifestly absurd to +treat the laboring man with his arteriosclerosis as one +would treat the successful financier. The habits, mode of +life, every detail, should be studied in every patient if we +expect to gain the greatest measure of success in the treatment. +One may treat fifty patients who have typhoid fever<span class="pagenum"><a name="Page_230" id="Page_230">[230]</a></span> +by a routine method and all may recover. Individualizing, +while of great value in the treatment of acute diseases, yet +is not absolutely essential in order that good results may +be obtained. Far different is it when treating a disease +like arteriosclerosis. One who relies on textbook knowledge +will find himself at a loss to know what to do. Textbooks +can only outline, in the briefest manner, the average +case, and no one ever sees the average book case. At the +bedside with the patients is the place to learn therapeutics +as well as diagnosis. All that can be hoped for in outlining +the treatment of arteriosclerosis is to lay down a few principles. +The tact, the intuition, the subtle something that +makes the successful therapeutist, can not be learned from +books. So the man who treats cases by rule of thumb is a +failure from the beginning. There are certain general +principles that will be our sheet anchors at all times and +for all cases. The art of varying the application of these +fundamentals to suit the individual case, is not to be culled +from printed words.</p> + + +<h4>Hygienic Treatment</h4> + +<p>Every man is more or less the arbiter of his own fate. +Granted that he has good tissue to begin life, his own habits +and actions determine his span of comfortable existence. +No one cares to live after his brain begins to fail, and the +failing brain is often due to disease of the cranial arteries. +The hygienic treatment resolves itself into advice in regard +to prophylaxis.</p> + +<p>First and foremost is exercise. It has seemed to us that +the revival of out-of-door sports is one of the best signs of +promise of the preservation of a virile, hardy race. That +women, as well as men, indulge in the lighter forms of out-of-door +exercise should bring it about that the coming +generation will start in life under the most advantageous +conditions of bodily resistance.</p> + +<p>Among all the forms of exercise, golf probably is the best.<span class="pagenum"><a name="Page_231" id="Page_231">[231]</a></span> +It is not too violent for the middle-aged man, yet it gives +the young athlete quite enough exercise to tire him. It is +played in the open. One is compelled to walk up and down +in pleasant company, for golf is essentially a companionable +game, while he reaps the full benefit of the invigorating exercise. +The blood courses through the muscles and lungs +more rapidly; the contraction of the skeletal muscles serves +to compress the veins and so to aid the return of blood to +the heart: the lungs are rendered hyperemic, deeper and +fuller breaths must be taken; oxidation is necessarily more +rapid, and effete products, which if not completely oxidized +would possibly act as vasoconstrictors, are oxidized to +harmless products and eliminated without irritating the +excretory organs.</p> + +<p>Other forms of out-door exercise that can be recommended +are tennis, canoeing, rowing, fishing, horseback riding, +swimming, etc. Tennis is the most violent of all the +sports mentioned and might readily be overdone. Rowing +as practiced by the eights at college is undoubtedly too violent +a form of exercise, and may be productive in later life +of very grave results. Canoeing is a delightful and invigorating +exercise. The muscles of the arms, shoulders, +and trunk are especially used, the leg muscles scarcely at +all. Nevertheless, the deep breathing that necessarily +comes with all chest exercises aerates every portion of the +lungs, and is of great benefit to the whole body.</p> + +<p>Swimming as an exercise has much to recommend it. In +this sport all the muscles take part and at the same time the +chest is broadened and deepened.</p> + +<p>All these methods of using the muscles to keep oneself in +trim, so to speak, are part and parcel of the general hygienic +mode of life that is conducive to a healthy old age. Exercise +can be overdone, as eating can be overdone. Both are +essential and yet both can be the means of hastening an individual +to a premature grave.</p> + +<p>When the arteriosclerosis has advanced so far that it is<span class="pagenum"><a name="Page_232" id="Page_232">[232]</a></span> +easily recognizable, certain forms of exercise should be absolutely +prohibited. Such are tennis, rowing and swimming. +Horseback riding to be allowed must be strictly supervised. +At times this may be an exceedingly violent exercise. As +an out-of-door sport, there is nothing that equals golf. +The physician, knowing the character of the course, and +the length of it, can say to his patient that he may play six, +nine, twelve, or eighteen holes, depending on the patient's +condition.</p> + +<p>For those who are not able to get out, exercise in the +room with the windows open must take the place of out-of-door +sports. Here the use of chest weights is a most +excellent means of keeping up the tone of the muscles. By +adjusting the weights, the exercise may be made light, +medium, or heavy. Every physician should be familiar +with the chest weight exercises. They are not as good as +open air exercise but they undoubtedly have been the means +of saving years of life to many patients with arterial +disease.</p> + +<p>There comes a time when all forms of exercise must be +prohibited on account of the dyspnea, edema, dizziness, etc. +It seems unwise to keep such a patient in bed, even though +the edema be considerable. Once on his back in bed he +becomes weak, and the danger of edema of the lungs or +hypostatic congestion of the bases, with subsequent bronchopneumonia, +is very great.</p> + +<p>Such patients may be allowed to sit up in a comfortable +chair with the legs supported straight out on a stool or +other chair. The half reclining position is not easy to assume +in bed. Considerable ingenuity must often be exercised +by the physician in making the patient comfortable +without increasing the symptoms from which the patient +suffers following the least amount of exercise. Although +such persons can not exercise actively, they should have +passive exercise in the form of massage, carefully given, so +that no injury is done to the rigid vessels. It is possible to<span class="pagenum"><a name="Page_233" id="Page_233">[233]</a></span> +rupture a vessel, the walls of which are encrusted with lime +salts, and full of small aneurysmal dilatations. Every patient +must be watched carefully and measures instituted for +the individual.</p> + + +<h4>Balneotherapy</h4> + +<p>As a tonic and invigorator, the cold or cool bath (shower +or tub), in the morning on arising can be highly recommended. +It promotes skin activity, is a stimulant to the +bowels and kidneys and to the general circulation, besides +being cleansing. We find today that the morning bath has +become such a necessity to the average American that all +new hotels are fitted with private baths, and old hotels, in +order to get patronage, are arranging as many baths connected +with sleeping rooms as is possible. Our generation +assuredly is a ruddy, clean-bodied one. What the actual +results of this out-door life and frequent bathing will be +for the race remains to be seen, but one can not but feel +that it must build up a stronger, more resistant race of +people, who not only enjoy better health than did their forefathers, +but enjoy it longer.</p> + +<p>Not every one can stand a cold bath. It is folly to urge +it on one to whom it is distasteful, or on one who does not +feel the comfortable glow that should naturally result. For +the well, or those with a tendency to arteriosclerosis, or +those in whose families there have been several members +who had early arteriosclerosis, such proceedings as recommended +could not be improved upon. However, for the +person who has well recognized sclerosis, only warm baths +should be advised, and these not daily. The water should +be at a temperature of 90-95° F. Care should be taken +that persons sent to spas be cautioned against hot baths. +It is not inconceivable that the increased force of the heart +beat that accompanies a hot bath might be sufficient to rupture +a small cranial vessel. Hence, Turkish and Russian +baths should be most unqualifiedly condemned. As a matter<span class="pagenum"><a name="Page_234" id="Page_234">[234]</a></span> +of fact, persons vary so in their habits with regard to +bathing that what might suit one person would do another +much harm.</p> + + +<h4>Personal Habits</h4> + +<p>The personal habits of the individual, more than any +other factor, determine whether or not arteriosclerosis sets +in early in his life. The man or woman who is moderate in +eating and drinking, sees that the kidneys are kept in good +condition, and attends strictly to regularity of the bowels, +lays a good basis for the measure of health which is so +essential for happiness. It has been shown that sclerosis +of the splanchnic vessels may be due to constant irritation +of toxic products elaborated in digesting constantly enormous +meals. In obstinate constipation, many poisons, the +nature of which we do not know, are absorbed and circulate +in the blood. We have not sufficient data to prove that +constipation favors the production of arteriosclerosis, but +our impression has been that it does favor it. Constipation +can often be relieved by a glass of water before breakfast, +a regular time to go to stool, and abdominal massage +or exercises. Some maintain that it is a bad habit only, +and can be readily overcome. Whatever is done, avoid +leading the patient into the drug habit, for the last state +of the patient will be worse than the first. Habits of sleep +are not of such great importance. Most persons get enough +sleep except when under severe mental strain. Most adults +need from seven to eight hours' sleep, although some can +do all their work and keep in prime health on five or six +hours' sleep.</p> + +<p>Tobacco has been accused of causing many ills and has +been thereby much maligned. We can not see that the use +of tobacco in any form in moderation is harmful to most +men. Undoubtedly the blood pressure is raised when mild +tobacco poisoning occurs, and individual peculiarities of reaction +to the weed are multitudinous. But to condemn offhand<span class="pagenum"><a name="Page_235" id="Page_235">[235]</a></span> +its use is the height of folly. There is no reason why +the arteriosclerotic who has always used tobacco in moderation, +should not continue to use it, whether he smoke cigarettes, +cigars, or pipe. His supply should be decreased, but +there is no sense in depriving a man of one of the solaces of +life, unless, as is sometimes the case, abstinence is easier +for the patient than moderation.</p> + +<p>As for alcohol, opinions differ widely.<a name="FNanchor_19_19" id="FNanchor_19_19"></a><a href="#Footnote_19_19" class="fnanchor">[19]</a> Some see in alcohol +one of the most frequent causes of arteriosclerosis; +others do not believe that the part played by alcohol is a +serious one, only in conjunction with other poisonous substances +is it dangerous. Probably unreasoning fanaticism +has had much to do with the wholesale condemnation of +alcoholic beverages. The general effect of alcohol is to +lower the blood pressure by causing marked dilatation of +all the vessels of the skin. True, the alcohol circulates in +the blood, and is broken up in the liver, and this organ +would seem to bear the brunt of the harm done. Alcoholic +drinks in moderation, I do not believe have any deleterious +effect on health. On the contrary, I believe that they may +in some cases assist digestion and assimilation. Indiscriminate +indulgence is to be condemned, as is overindulgence +in exercise or eating. What may be moderate for A, might +be excessive for B. Every man is then the arbiter of his +own fortune and within his own limits can indulge moderately +(a relative term after all) without fear of doing himself +harm. In advanced arteriosclerosis it is necessary to +decrease the supply of alcohol just as it is necessary to cut +down the food supply. This must rest entirely on the +judgment of the physician, who must not act arbitrarily, +but must have his reasons for every one of his orders.</p> + +<h4>Dietetic Treatment</h4> + +<p>Most persons eat too much. We not only satisfy our +hunger, but we satisfy our palates, and, instead of putting<span class="pagenum"><a name="Page_236" id="Page_236">[236]</a></span> +substantial foodstuffs into our stomachs, we frequently take +unto ourselves concoctions that defy description.</p> + +<p>Foodstuffs are composed of one or all of three classes: +(1) proteins, (2) fats, (3) carbohydrates. As examples +of the first are beef and white of egg; of the second, the +oils, butter, lard; of the third, sugar, potato, beet, corn, etc.</p> + +<p>The physiologists and chemists have shown us that both +endogenous and exogenous uric acid in excess will cause a +rise of blood pressure, but the bodies most concerned in +the production of elevated blood pressure are the purin +bodies, those organic compounds which are formed from +proteins and represent chemically a step in the oxidation +of part of the protein molecule to uric acid. Red meat +contains more of the substances producing purin bodies +than any other one common foodstuff, and for this reason +the excessive meat eater is, <i>ceteris paribus</i>, more apt to +develop arteriosclerosis comparatively early in life.</p> + +<p>The fats and carbohydrates contain practically no substances +that react on the body of the ordinary individual +in a deleterious manner during their digestion. The extra +work that is put on the heart by the formation of many +new blood vessels in adipose tissue is the only harmful effect +of overindulgence in these foodstuffs.</p> + +<p>It has been found that nitrogen equilibrium can be maintained +at a wide range of levels. Formerly 135-150 gms. +of protein daily were considered necessary for a man doing +light work. Now it is known that half that amount is sufficient +to keep one in nitrogenous equilibrium, and to enable +one to keep his weight. A person at rest requires even less +than that. One who is engaged in hard physical labor burns +up more fuel in the muscles, and so must have a larger +fuel supply.</p> + +<p>Although we habitually eat too much we drink too little +water. For those who have any form of arterial disease +an excess of fluid is harmful, as the vessels become filled +up and a condition of plethora results, which necessarily<span class="pagenum"><a name="Page_237" id="Page_237">[237]</a></span> +reacts injuriously on the heart and circulation. The drinking +of a glass of water during meals is, in the author's +opinion, good practice. The water must be taken mouthful +at a time, and not gulped down. If this is done, there +results sufficient dilution of the solid food to enable the +gastric juices successfully and rapidly to reach all parts +of the meal.</p> + +<p>Some are in favor of a rigid milk diet for those who +have arteriosclerosis. Some men have lived on nothing +but milk for several years and have not only kept in good +health, but have actually gained weight and led at the +same time active lives. It has been held by others that rigid +milk diet is positively harmful on account of the relatively +large quantity of calcium salts that are ingested. This was +thought to favor the deposition of calcareous material in +the walls of the already diseased arteries. While possibly +there may be some danger of increased calcification, the +majority of clinicians are in favor of a milk cure given at +intervals. Thus the patient is made to take three to +four quarts daily for a period of a month. There is then a +gradual return to a general diet, exclusive of meat, for +several weeks, then another rigid milk diet period.</p> + +<p>If we are bold enough to follow Metschnikoff in his theories +of longevity, we might advise resection of the large +intestine, on the ground that it is an enormous culture tube +that produces prodigious amounts of poisonous substances +which are thrown into the general circulation. To combat +such a grave (?) condition as the carrying of several feet +of large intestine, we are recommended to take buttermilk +or milk soured by means of the <i>b. acidus lacticus</i>. Clinical +experience has taught that in arteriosclerosis buttermilk +is of great value, whether it be the natural product, or made +directly from sweet milk by the addition of the bacilli. The +latter is a smoother product and has, to my mind, a delightful +flavor. It may be diluted with Vichy or plain soda +water. Cases that can not take milk or any other food will<span class="pagenum"><a name="Page_238" id="Page_238">[238]</a></span> +often take buttermilk, and do well on this restricted diet. +From two to four quarts daily should be taken. It should +be drunk slowly as should milk.</p> + + +<h4>Medicinal</h4> + +<p>It has long been thought that the iodides have some specific +effect on the advancing arteriosclerosis, checking its +spread, if not really aiding nature to a limited restoration +of the diseased arteries. It is possible that the eulogies +upon the iodides owe their origin to the successful treatment +of syphilitic arteriosclerosis, in which condition these +drugs have a specific action. However that may be, there +is no doubt that the administration of sodium or potassium +iodide is good therapeutics in cases of arteriosclerosis.</p> + +<p>Unfortunately many persons have such irritable stomachs +that they can not take the iodides, even though they be +diluted many times. They may be made less irritating by +giving them with essence of pepsin. Unless the case is +syphilitic, it is doubtful whether it is of value to increase the +dose gradually until a dram or even more is taken three +times daily after meals. Usually a maximum dose of ten +grains seems to be quite sufficient. This may be taken three +times a day, well diluted, for three months. There follows +a month's rest, then the treatment is resumed for another +period of three months, and so on. Either sodium or potassium +iodide in saturated solution may be given. The sodium +salt is possibly less irritating, and contains more free +iodine than the potassium salt, although the latter is more +generally used. The strontium iodide may also be used.</p> + +<p>One sees a patient now and then who can not take the +iodides, however they may be combined. For such patients +one may obtain good results with iodopin, sajodin, or other +of the preparations put up by reputable firms. Personally I +have never yet seen a patient who could not take the ordinary +iodides in some form or other, and I am opposed to +ready made drugging.</p> + +<p><span class="pagenum"><a name="Page_239" id="Page_239">[239]</a></span>The action of the iodides is to lower the blood pressure, +and they are of greatest value when the blood pressure +is high, and when headache and precordial pain are present.</p> + +<p>When the case is moderately advanced, very mild doses, +gr. ½, morning and evening, of the thyroid extract may be +given. It is generally believed that the internal secretion +of the thyroid and the adrenal are antagonistic. That the +thyroid secretion lowers blood pressure in certain forms of +hypertension is certain, possibly on account of its iodine +content. Some combinations of iodine and thyroid such as +the iodothyroidin have been used and have had some measure +of success attributed to them.</p> + +<p>Hypertension does not always demand active measures +for its reduction. Viewed from the physiologic standpoint, +hypertension is but the expression of a compensating +mechanism which is designed to keep the blood moving +through narrowed channels. Heart hypertrophy then is +absolutely essential to the maintenance of life. It has been +said that the highest blood pressures occur in chronic disease +of the kidneys. The poisonous substances produced +in the kidneys must exert their action through absorption +into the general blood stream. This toxin may be completely +eliminated, if we accept as our criterion the reduction +of tension to normal together with the complete return +of the affected individual to health. A concrete example +is as follows: A man aged 44 years was brought to the +Milwaukee County Hospital in coma. His systolic blood +pressure was over 280 mm. Hg, diastolic 170 mm., his urine +contained considerable albumin and many casts. He had +general anasarca. Venesection was done at once and 300 +c.c. blood obtained. Immediately following this operation +the pressure was 210-150, but within twelve hours it was +again above 280-170. He was given no medication to reduce +pressure except that he was freely purged. He was +given a steam sweat bath daily. Frequent blood pressure +readings were taken. Within seven days the pressure was<span class="pagenum"><a name="Page_240" id="Page_240">[240]</a></span> +130-86. He had, in the meantime, completely recovered +from his symptoms. He was kept in the hospital for two +weeks longer assisting in the work on the ward, and he was +discharged with a pressure (systolic) between 130 and 136 +diastolic 80-84. The treatment was rest in bed, free purging, +venesection, and sweat baths, simple but exceedingly +effective.</p> + +<p>Should there be actual indications for reducing the blood +pressure, I must admit that it can not always be done. The +majority of cases will do well on the sodium nitrite or +erythrol tetranitrate. However, these do not always lower +blood pressure and keep it within normal limits. When a +man has very high tension we do not wish to reduce it to +what it should normally be for the age of the patient, as +symptoms of collapse might set in at any time under such +conditions.</p> + +<p>Observations made with the sphygmomanometer<a name="FNanchor_20_20" id="FNanchor_20_20"></a><a href="#Footnote_20_20" class="fnanchor">[20]</a> show +that the effect of nitroglycerin is transient or of no effect +except in doses which are relatively enormous (one drop of +the one per cent solution given every hour). Sodium nitrite +may lower the blood pressure but the effects will have +worn off in two hours. It is the same with erythrol tetranitrate. +Sodium sulphocyanate in doses of from one to three +grains three times a day is highly recommended by some. +My own experience with it does not lead me to believe that it +is of any great value in hypertension. It, however, may be +tried. Benzyl benzoate has been used recently to reduce +the high blood pressure of hypertension. Macht has reported +some success. In the author's hands it has been +efficacious in a few cases. As long as the patient takes the +drug the pressure may be slightly reduced, but upon the +withdrawal of the drug the pressure returns to its former +level. It is well worth a trial and further experimentation<span class="pagenum"><a name="Page_241" id="Page_241">[241]</a></span> +may reveal better methods of administration. The dose is +from 2 to 6 c.c. mixed with water at intervals.</p> + +<p>In the hypertension of the menopause some have had +success with large doses of corpus luteum extract. As +a matter of fact the drug treatment of hypertension, +when it becomes necessary to treat this condition with +drugs, has suffered a notable set-back since more careful +control has been made with the blood pressure instruments. +In giving any of the depressor drugs their action should +be controlled by blood pressure measurements, for only +in this way can we be sure that the drug is exerting its +physiological effect and we may expect results. The individual +reaction to these drugs varies greatly and no rule +for dosage can be dogmatically laid down. The only successful +therapy is rigid individualization. This is the keystone +to treatment in cases of arteriosclerosis and high +tension.</p> + +<p>It must not be inferred from what has been said that the +nitrites are of no value. They are of decided value but +they have their limitations. The most evanescent of these +drugs is amyl nitrite. This is put up in the form of capsules, +or pearls, containing from one to three minims. When +it is desired to dilate the peripheral vessels suddenly, one +or two of these capsules are broken in a cloth held to the +nose. The effect is almost instantaneous. There is flushing +of the face and other peripheral vessels, particularly +near the head, denoting a relaxation and widening of the +bed of the blood stream, and a consequent decrease in pressure +in the arteries. These effects are over in a short +while. It is only used in attacks of cardiac spasm, as in +angina pectoris. Nitroglycerin, the Spiritus Glonoini of +the U. S. P., acts in about the same manner as amyl nitrite +but the effects last usually a trifle longer. One drop +of the one per cent solution may be given every hour until +physiologic effects are produced. It may be given hypodermically. +This may be a means of reducing pronounced<span class="pagenum"><a name="Page_242" id="Page_242">[242]</a></span> +high tension. This drug has been found of benefit especially +in cases where arteriosclerosis combined with chronic +nephritis causes cardiac asthma. The other drug which +may be of service in these conditions, one whose sphere +of action is somewhat broader, because its effects are more +lasting, is sodium nitrite. This is given in water in doses +of one to three or five grains every four hours. Some +have objected to the use of this drug, but my experience +has made me place considerable confidence in its harmlessness, +provided that the patient is carefully watched. This, +however, applies to all of the nitrite compounds. My experience +with erythrol tetranitrate is not large. It may +be used in place of sodium nitrite.</p> + +<p>For a mild case, one often finds that sweet spirits of +niter is sufficient to control the pressure and relieve the +distressing symptoms, and it is undoubtedly the least harmful +of all the nitrites. Drugs that are of great value, but +of which little is noted in textbooks, are aconite and veratrum +viride. Both of these drugs are well known to be +marked circulatory depressors. Veratrum viride in my experience +should be very cautiously used, and never used +unless a trained attendant is constantly at hand. With regard +to aconite I have no such feeling, and a mixture of +tincture of aconite and spiritus etheris nitrosi may be +given for several weeks with no fear of doing any harm. +Personally, of all the drugs mentioned, I prefer the nitrite +of sodium or the combination just given. They may be advantageously +alternated.</p> + +<p>My own feeling is that the most successful means of treatment +of acute high tension is without the use of drugs. +The most important measure is absolute rest in bed. This +often suffices to lower the blood pressure and to arrest the +symptoms produced by high tension. Venesection I believe +is also of value. True the arterioles appear to contract +almost immediately upon the lessened quantity of blood, +or there is immediate interchange of serum from the tissues<span class="pagenum"><a name="Page_243" id="Page_243">[243]</a></span> +which brings the blood volume back to the original amount. +Whatever happens the pressure is not greatly reduced, at +times not reduced at all, but often the symptoms are relieved. +Hot packs or sweat baths assuredly do reduce the +pressure in many cases. This seems to me to be an exceedingly +valuable measure. Finally the diet should be +nourishing, but very light, not too much fluid should be +ingested, and the bowels should be freely opened.</p> + +<p>With the fibrolysin of Merck, I have had no experience. +Some men assert that they have had good results from +its use, but on the whole the evidence is not highly favorable.</p> + +<p>Morphine is invaluable. No drug is of such value in the +nocturnal dyspneic attacks that occur in the late stages of +arteriosclerosis when the heart or the kidneys are failing. +Morphine not only relaxes spasm and quiets the cerebral +centers, but is an actual heart stimulant under such conditions, +and should never be withheld, as the danger of the +patient's becoming addicted to its use is more fanciful than +real. However, morphine, at times, suppresses the secretion +of urine. So that if after trial the urine becomes +scanty and the edema increases, recourse must be had to +other drugs. The various hypnotics may be used with +caution. One which seems to be very useful is adalin.</p> + +<p>As heart stimulants, one may use strychnine, spartein, +caffein, or camphor. In desperate cases, where a rapidly +diffusible stimulant is needed, a hypodermic syringeful of +ether may be given, and repeated in a short while.</p> + +<p>Several years ago a so-called serum was brought out by +Trunecek which was said to have a favorable effect on the +metabolism of the vessel walls. It was given at first hypodermatically +or intravenously but the former method was +painful. It was later stated that given by mouth it acted +just as well. The results with the Trunecek serum have not +come up to the expectations that the early favorable reports +promised. The original serum was composed as follows:<span class="pagenum"><a name="Page_244" id="Page_244">[244]</a></span> +NaCl, 4.92 gm.; Na<sub>2</sub>SO<sub>4</sub>, 0.44 gm.; Na<sub>2</sub>CO<sub>3</sub>, 0.21 gm.; +K<sub>2</sub>SO<sub>4</sub>, 0.40 gm.; aqua destil. q. s. ad. 100.0 c.c. Later +this was modified for internal use to the following prescription:</p> + +<p> +℞<span style="margin-left: 2em;"> Natrii chlor. 10. gm.</span><br /> +<span style="margin-left: 3em;">Natrii sulphat. 1. gm.</span><br /> +<span style="margin-left: 3em;">Natrii carbonat. 0.40 gm.</span><br /> +<span style="margin-left: 3em;">Natrii phosphat. 0.30 gm.</span><br /> +<span style="margin-left: 3em;">Calcii phosphat.</span><br /> +<span style="margin-left: 3em;">Magnesii phosphat. aa. 0.75 gm.</span><br /> +M. Ft. cachets No. XIII. +</p> + +<p>The contents of every cachet corresponds to 15 c.c. of the +fluid serum or to 150 c.c. of blood serum. The preparation +called antisclerosin consists of the salts contained in the +serum. As to its efficacy, I can not judge, as I have never +felt that it was worth while to use it. Reports of cases in +which it has been tried do not speak very highly of it.</p> + +<p>In the general treatment of arteriosclerosis, there is no +one factor of more importance than the regular daily bowel +movement. Attention to this may save the patient much +discomfort and even acute attacks of cardiac embarrassment. +The choice of the purgative is immaterial, with this +reservation only, that the mild ones, such as cascara, rhubarb, +licorice powder and the mineral waters, should be +thoroughly tried before we resort to the more drastic purgatives. +Plenolphthalein in 3 to 5 grain doses acts remarkably +well in some people as a pleasant laxative. Agar-agar +with or without cascara may be useful.</p> + +<p>Liquid paraffin under a variety of names is a most useful +and efficacious laxative. As its action is purely mechanical +it may be taken indefinitely without doing harm to the intestinal +musculature.</p> + +<p>The old Lady Webster dinner pill is an excellent tonic +aperient. When the heart is embarrassed and edema of the +legs and effusion into the serous cavities have taken place, +then it becomes necessary to use the drastic purgatives +that cause a number of watery movements. Epsom salts<span class="pagenum"><a name="Page_245" id="Page_245">[245]</a></span> +given in concentrated form, elaterin gr. 1-12, the compound +cathartic pill, blue mass and scammony, or even croton +oil may be used. Since the observation of a greatly congested +intestine from a patient who had been given croton +oil, I have ceased to use this purgative, and I doubt much +whether its use is ever justifiable in these cases.</p> + +<p>The management of the ordinary case of arteriosclerosis +resolves itself into a careful hygienic and dietetic regime +with the addition of the iodides, aconite, or the nitrites. +A diet consisting of very little meat, alcohol in moderation +or even absolutely prohibited, and not too much fluid should +be prescribed. Condiments and spices should also be used +sparingly. Cold baths, shower baths, cold and hot sheets +alternating, are of great benefit in assisting the heart to do +its best work by making the large capillary area of the skin +more permeable. It is not true that such baths raise the +blood pressure so markedly. Certain acts, as sneezing, violent +coughing, etc., increase the blood pressure much more +than judicious bathing.</p> + + +<h4>Symptomatic Treatment</h4> + +<p>The fact that arteriosclerosis really loses much of its own +identity and, in later stages, becomes merged with the symptomatology +of the diseases of various organs, as the kidney, +brain, heart, compels us, for completeness' sake, to say a +few words about the treatment of these complications.</p> + +<p>One of the results of arteriosclerosis of the coronary +arteries, angina pectoris, demands prompt treatment. In +the acute attack, the chief object is to relieve the spasm and +pain. Pearls of amyl nitrite should be inhaled, and morphine +sulphate with atropine sulphate given hypodermatically +at the very earliest moment. It is senseless to withhold +morphine. The only possible reason for withholding +it would be uncertainty as to the diagnosis. It is probably +better to err on the safe side, and should the case prove to<span class="pagenum"><a name="Page_246" id="Page_246">[246]</a></span> +be one of pseudo angina, in the next attack sterile water +can be given instead of the morphine and atropine.</p> + +<p>When a patient is seen in the condition of broken compensation +with the much dilated heart, anasarca, dyspnea +and suppression of urine, there is no better practice than +venesection. Especially is this valuable when the tension is +still fairly high and the individual is robust. Following the +abstraction of six to eight ounces of blood (300-500 c.c.)<a name="FNanchor_21_21" id="FNanchor_21_21"></a><a href="#Footnote_21_21" class="fnanchor">[21]</a> +the whole picture changes, so that a man who a short while +before was apparently at death's door, notices his surroundings +and takes an interest again in life. This should be followed +up with thorough purgation, and cardiac stimulants +should be ordered. In such cases digitalis is useful, but its +action is never so striking as in cases of this general character +due to uncompensated valvular disease. It must be remembered +that in arteriosclerosis the changes in the myocardium +must be of a considerable grade for the heart to +give away. Therefore, digitalis can not be expected to act +on a diseased muscle as it acts on a comparatively healthy +muscle. It is only in such cases of broken compensation +that digitalis should ever be used.</p> + +<p>Digitalis is not a general vasoconstrictor as used to be +taught. Its action on the kidney is actually a vasodilator +one. And in its action on the heart the digitonin dilates +the coronary arteries, according to Macht, while the digitoxin +acts on the heart muscle. Overdosing with digitalis +has produced partial heart block in many cases. It is absolutely +contraindicated in Stokes-Adams syndrome.</p> + +<p>There are, however, some cases, especially those with +transudations, when digitalis may be carefully tried even +though high tension be present. It is sometimes of advantage +to combine digitalis with the nitrites although they are +said to be physiologically incompatible.</p> + +<p>Still another drug, that is of great value in conditions such +as have been described, is diuretin. This may be given in +capsule or tablets, grs. x. three times daily. There is only<span class="pagenum"><a name="Page_247" id="Page_247">[247]</a></span> +one caution to express in the use of this drug. It should not +be given when the kidneys are the seat of chronic inflammatory +changes; in fact, actual harm may be done by administering +the drug under such conditions.</p> + +<p>The same is true even to a greater extent with theocin. +This is a powerful diuretic. If given by mouth it should be +well diluted as it is most irritating to the stomach. It is +best given intravenously in doses of two and a half to +three grains dissolved in five to six cubic centimeters of +distilled water. One must be reasonably sure that the kidneys +are not the subject of chronic disease and are functionally, +therefore, below par. The intravenous dose should +not be given oftener than once in four days.</p> + +<p>For the pain in aneurysm, nothing (except, of course, +morphine) is so valuable as iodide of potassium. Patients +who are suffering agony, when put to bed and given KI +grs. x. three times a day, soon lose all the distressing symptoms. +This applies particularly to aneurysms of the arch +of the aorta.</p> + +<p>When the sclerosis has affected the cerebral arteries to +such an extent that symptoms result, the case is, as a rule, +exceedingly grave. Not much can be done except to relieve +the headaches and keep down the blood pressure, if this is +high, by means of rest in bed, the iodides, aconite, or the +nitrites. The cases of transient monoplegias or hemiplegias +can be much relieved by careful hygienic measures and judicious +administration of drugs. Much ingenuity is sometimes +required to overcome the idiosyncrasies of patients, +but care and patience will succeed in surmounting all such +difficulties.</p> + +<p>The treatment of intermittent claudication is the treatment +of arteriosclerosis in general. Sometimes the circulation +in the affected leg or legs is much helped by daily warm +foot baths. Light massage might be tried and the galvanic +current may be used once or twice daily.</p> + +<p><span class="pagenum"><a name="Page_248" id="Page_248">[248]</a></span>There are a few distressing symptoms that occur usually +late in the disease, when complications have already occurred, +which frequently baffle the therapeutic skill of the +physician. The chief of these—insomnia, dyspnea, and +headache—may not be late manifestations, but insomnia and +headache are frequently associated with the moderately +advanced stages of arteriosclerosis. At times all the symptoms +seem to be due to the high tension, the relief of which +causes them to disappear. There are, unfortunately, times +when high tension is not responsible for the headache and +insomnia. Under these circumstances such drugs as trional, +veronal, amylene hydrate, ammonol, etc., may be tried until +one is found which produces sleep. For the headaches, +phenacetin, alone or in combination with caffein and bromide +of sodium, may be tried. Acetanilid, cautiously used, +is at times of value. There have been cases of arteriosclerosis +with low blood pressure, accompanied by severe headaches, +that have been relieved by ergot. Codeine should be +used with care, and morphine only as a very last resource.</p> + +<p>Great care must always be exercised in giving drugs that +depress the circulation, for it is easily conceivable that more +harm than good can come from injudicious drugging.</p> + +<hr style="width: 65%;" /> +<p><span class="pagenum"><a name="Page_249" id="Page_249">[249]</a></span></p> + +<h2><a name="CHAPTER_XIV" id="CHAPTER_XIV"></a>CHAPTER XIV.</h2> + +<h3>ARTERIOSCLEROSIS IN ITS RELATION TO LIFE +INSURANCE</h3> + + +<p>The value of the early recognition of cases of arteriosclerosis +and hypertension has been spoken of within, but it +needs to be further emphasized. There is perhaps no class +among physicians to whom is afforded a better opportunity +of seeing early cases than the medical examiners of life +insurance companies.</p> + +<p>The relationship between a patient and the physician +whom he consults, and the applicant for life insurance and +the examiner are diametrically opposite. In the former +the patient desires to conceal nothing and the physician is +called upon to diagnose and treat disease. In the latter the +applicant, a presumably healthy person, may have much to +conceal and the examiner is there to pass upon the state of +health. The question is this—"Is the applicant now in +good health?" It becomes then of vital importance for the +examiner to be able to detect among other abnormal conditions +the incipient signs of arteriosclerosis and of hypertension. +Parenthetically it may be stated that arteriosclerosis +and hypertension are not one and the same disease as has +been so frequently insisted upon within; the former may +occur without the latter but the latter can not from its very +nature be present for long without arterial thickening supervening. +It is necessary in discussing the question here +to group the two conditions together in order to prevent +needless repetition.</p> + +<p>Such a case as the following is common. A successful +business man of forty-four years was brought to me by an +agent in 1905 for examination. The man was six feet tall, +weighed 218 pounds, had a ruddy color and looked to be the<span class="pagenum"><a name="Page_250" id="Page_250">[250]</a></span> +picture of health. He was not strictly intemperate, he +never became intoxicated, but every day he drank three or +four whiskies and often he had a bottle of wine for dinner +in the evening. When he was examined his pulse was of +good quality and owing to the fleshiness of the wrist it was +difficult to say positively whether the radial artery was +sclerosed or not. In the heart no murmurs were heard, and +it was difficult to be sure that the left ventricle was enlarged. +There was, however, a slight but definite accentuation of the +second sound at the aortic cartilage which might readily +have been overlooked had the patient not been stripped and +a careful examination made with the stethoscope. Upon +taking the blood pressure it was found to be from 170-175 +mm. of Hg. The urine specimen examined at the visit was +normal, no casts were found. The applicant was seen at +his home and the blood pressure measured. It was again +the same. He was seen a third time and practically the +same systolic blood pressure was found. Under protests +from all the agency staff the man was declined. Two years +later he died of apoplexy. The man was angry at being +refused. Instead of looking the matter squarely in the face +he thrust aside the idea that there was anything the matter +with him. He had never had one ill day in his life, his forebears +had lived to ripe old age, and he was sure that he knew +more about himself than the examiner.</p> + +<p>Had this applicant showed a sense of reasonableness he +should have been grateful to the doctor for calling his attention +to a condition which surely would sooner or later prove +either fatal itself or lead to some fatal lesion. It was +learned that this man had gone directly to his family physician +who laughed at such nonsense as had been told the +(now) patient by the examiner.</p> + +<p>Another illustration of a slightly different type of case is +afforded in the following history.</p> + +<p>A man of fifty years of age, five feet ten in height and 164 +lbs. in weight, was brought for examination. In his youth<span class="pagenum"><a name="Page_251" id="Page_251">[251]</a></span> +there was a history of a mild attack of scarlet fever. He +was almost a total abstainer, rarely taking liquor in any +form. Physically he appeared to be an excellent risk. +However, on examining the heart it was found that there +was slight hypertrophy with an accentuated second aortic +sound at the base, and the blood pressure was 180 mm. of +Hg. Some sclerosis of the radial arteries was found. One +company had refused him on account of albumin in the +urine. There was none in the first specimen which was +passed while in the office. The specific gravity was 1014. +A morning specimen was obtained and contained a trace of +albumin. Several specimens were then examined. Some +contained albumin, some had no albumin content. The man +was declined; no protests from the agent as albumin had +been found. There was something tangible in that. Had +the applicant been refused on account of his high tension, +sclerosis of the radials, and slightly enlarged heart there +would undoubtedly have been protests. And yet an applicant +revealing such a state of the cardiovascular system +without albumin in the urine should unhesitatingly be declined. +Attention has been called to hypertension as an +early, and some think an invariable, sign of chronic nephritis. +My own experience has confirmed me in the belief +that in hypertension the kidneys are often the seat of +chronic interstitial changes. Careful palpation of the radial +and brachial arteries will in every case reveal more +or less thickening.</p> + +<p>There is yet another group of cases which the examiner +sees as healthy subjects, namely those cases of sclerosis of +the peripheral arteries without sclerosis of the aorta and +without high tension. In such cases the radials, brachials, +temporals and other superficial arteries are readily palpable, +sometimes even revealing irregularities along the +course of a vessel. Such cases are not subjects for insurance. +The recognition of such a condition is of great importance +to the one who has it and he should be urged to go to<span class="pagenum"><a name="Page_252" id="Page_252">[252]</a></span> +his regular physician for thorough examination. Should the +physician ridicule the idea, as has happened to me more +than once when I was actively engaged in insurance work, +the examiner has done his full duty to the company, the +applicant, and himself.</p> + +<p>A life insurance examiner has a difficult position to fill. +He has four people to satisfy; the applicant, the agent, the +medical director and himself. The straight and narrow +path of strict honesty is his only salvation. By being honest +with himself he necessarily gives a square deal to the +other three parties.</p> + +<p>No applicant who has palpable arteries or hypertension +can be considered a first class risk. It can not be denied +that men with arteriosclerosis live to an advanced age and +may even outlive those who have apparently normal arteries, +but the average life expectancy at any age for an +arteriosclerotic is less than that for a normal person. The +apparently healthy applicant who learns for the first time +when examined for life insurance that he has the early or +moderately advanced signs of arterial disease, should thank +the agent and examiner for showing him the danger signals +ahead. The sensible man then orders his life so that he +puts as little strain on his heart, arteries, and kidneys as +possible and may add many years to his life.</p> + +<p>It is on account of this very insidiousness of onset that I +have elsewhere urged as a prophylactic measure the examination +every six months of all persons over forty years of +age. I am more and more convinced that it is of vital importance +to the health of the public.</p> + +<p>As I have remarked, the average man consults his dentist +at least once a year so that no tooth may be so far diseased +that it can not be saved. It is purely a means of preserving +the teeth. Why not do the same with the whole body? Of +what use is it to save the teeth and lose the body? It seems +to me that the great army of life insurance examiners are +in an enviable position in their ability to add years of life<span class="pagenum"><a name="Page_253" id="Page_253">[253]</a></span> +to many men and women. I doubt whether they realize +their importance in the campaign for health. I should urge +life insurance companies not to employ recent graduates +unless they have had at least a year's hospital experience. +For the company as well as for the individuals I believe +that there is a prognostic sense which the examiner should +have and this can only be acquired by experience.</p> + +<p>I believe that arteriosclerosis and hypertension are increasing +for the reasons which have been given in another +chapter. There can be no doubt that when these conditions +are recognized long before symptoms would naturally supervene, +men and women would not only live longer but +also die more comfortably and many very likely would be +carried off by some disease having no relationship whatever +to arteriosclerosis. Slight enlargement of the heart downward +and to the left, accentuation of the second aortic +sound at the base, a full pulse, arteries which are palpably +thickened, increased blood pressure are signs to which attention +must be paid.</p> + +<p>When the peripheral arteries are palpable they are not +always sclerosed. The radial artery, the one usually palpated, +may lie very close to the bone in a thin person. Under +these conditions the artery can be easily felt. It is +better then to palpate for the brachial as it lies beneath the +inner edge of the biceps muscle. Should this artery be felt +then very probably sclerosis is present. Opinion as to +whether or not sclerosis is present, when it is slight, may +differ. It is difficult at times to say definitely. Should +such be the case the applicant should be most carefully +questioned as to his family and past history, the heart +should be carefully outlined by percussion and the blood +pressure should be taken, both the systolic and diastolic +pressures. The urine should be examined with particular +care. I am aware that the average examination for life insurance +is not made with the care which is bestowed upon a +patient. Yet I see no reason why the same attention to detail<span class="pagenum"><a name="Page_254" id="Page_254">[254]</a></span> +should not be given in one as in the other. The examination +of the great majority of applicants can he made in a +short time, as there is no question of latent chronic disease. +When the exception turns up he should be given a searching +examination and a full report should be sent to the Medical +Director. Only in this way will it be possible to weed out +the undesirable risks.</p> + +<p>On the surface it does not seem to require any great diagnostic +acumen to be a life insurance examiner. In the old +days of many of the companies there were no examiners. +The applicant was brought before the president or other +appointed official and he was passed or rejected on his +general appearance. This has changed, and now the medical +department with its scores of examiners in the field is +a well organized department.</p> + +<p>It seems to me that the examiner should be an exceedingly +able diagnostician and prognosticator. There is no telling +when he may be called upon to pass judgment on a borderline +case. From personal experience I know how difficult +it is to make a decision in some cases. These suspicious +cases after a careful examination had better be passed by +the examiner and a supplementary report sent to the +medical director containing unbiased details. But no applicant +with readily palpable arteries, even though the +blood pressure be normal, should be considered a first class +insurance risk.</p> + +<p>The question of the value of the diastolic pressure reading +in examinations for life insurance is not yet settled to +the satisfaction of all medical directors. Certain medical +directors with clinical experience behind them, lay great +stress on the increased diastolic pressure and consider a +persistent diastolic of 100 mm. really more significant as +an indication of hypertension than a systolic pressure of +160 mm. Other directors pay little or no attention to the +diastolic reading. Should an applicant show a systolic +above the average normal on several successive readings,<span class="pagenum"><a name="Page_255" id="Page_255">[255]</a></span> +he is declined. When one takes into consideration the +psychic effect of knowing that he is being examined for +high blood pressure, it seems unfair to refuse insurance on +such grounds as is constantly done.</p> + +<p>Up to the present there are no extensive series of life-expectancy +tables in which hundreds of thousands of cases +are analyzed from the diastolic pressure values. There are +many such tables for the systolic pressures alone. In the +tabulation of such statistics one must not lose sight of the +important fact that the figures are taken by thousands of +men of varying capacity and different degrees of intelligence. +Such studies to be of any real value must be taken +from records made at the home offices by capable men. We +shall await these tables with interest. In the meantime we +must be permitted to have the impression that the diastolic +pressure has been much neglected. This has no doubt been +due to the difficulty of measuring it with any degree of accuracy. +Now with the auscultatory method and the correct +place to read the diastolic pressure the results of blood +pressure estimations should begin to have some value for +statistical data.</p> + +<p>Clinically the diastolic is probably more important than +the systolic. Until proof is brought to the contrary we shall +believe that in life insurance examinations it has the same +importance.</p> + +<hr style="width: 65%;" /> +<p><span class="pagenum"><a name="Page_256" id="Page_256">[256]</a></span></p> +<h2><a name="CHAPTER_XV" id="CHAPTER_XV"></a>CHAPTER XV.</h2> + +<h3>PRACTICAL SUGGESTIONS</h3> + + +<p>The time spent in obtaining a careful history of a case +is time well spent. Often the diagnosis can be made from +the history alone, the physical examination merely adding +confirmation to the data already obtained.</p> + +<p>The younger the patient who has arteriosclerosis, the +more probable is it that syphilis is the etiologic factor. +A denial of infection should have little weight if the history +of possible exposure is present. Miscarriages in a woman +should arouse the suspicion of lues in her husband. The +complement-fixation reaction will often clear up an apparently +obscure diagnosis.</p> + +<p>There are various ways of examining a patient but there +is only one right way; the examination should be made on +the bare skin. However skillful one may be in the art of +physical diagnosis, he can gather few accurate data by examining +over the clothes even if he use a phonendoscope.</p> + +<p>The immoderate eater is laying up for himself a wealth +of trouble at the time when he can least afford to bear it. +The ounce of advice in time is worth more to him than the +pounds of medicine later.</p> + +<p>It is a wise maxim never to drive a horse too far. Apply +that to the human being and the rule holds equally well.</p> + +<p>There may be no symptoms in a case of advanced arteriosclerosis. +Do not on that account neglect to advise a patient +in whom the disease is accidentally discovered.</p> + +<p>Many a man owes a debt of gratitude to the life insurance +examiner. He rarely feels grateful.</p> + +<p>When a competent ophthalmologist refers a case to a general +practitioner with the statement that he believes from +the appearance of the fundus of the eye that arteriosclerotic<span class="pagenum"><a name="Page_257" id="Page_257">[257]</a></span> +changes are present over the body, the case should be most +carefully examined. The earliest diagnoses are not infrequently +made by the ophthalmologist.</p> + +<p>It is the part of wisdom never to have such a firmly preconceived +idea of the diagnosis that facts observed are +perverted in order to fit into the diagnosis. Let the facts +speak for themselves.</p> + +<p>Beware of the snap diagnosis. Even in a case of well-marked +arteriosclerosis when the diagnosis seems to be +written in large letters all over the patient, go through the +routine. Nine times out of ten this may seem needless. +The tenth time it saves your conscience and reputation. +Always consider that you are examining a tenth case.</p> + +<p>Gradual loss of weight in a person over fifty years old +should arouse the suspicion of arteriosclerosis.</p> + +<p>Do not call the nervous symptoms displayed by a middle-aged +man or woman neurasthenia until you have ruled out +all organic causes, particularly arteriosclerosis.</p> + +<p>When palpating the radial artery, always use both hands +according to the method already described. Pay attention +to the superficial or deep situation of the artery.</p> + +<p>The examination of one specimen of urine does not give +much information, especially if it should be found to contain +no abnormal elements. Fairly accurate data may be +gathered from the mixed night and morning urine; most +accurate data from the twenty-four hour specimen. To be +of any real value there should be frequent examinations of +the day's excretion.</p> + +<p>In measuring the day's output a good rule is as follows: +begin to collect urine after the first morning's micturition +and collect all including the first quantity passed the next +morning. It is best to examine the centrifugated urine for +casts even though no albumin be present. It is useless to +look for casts in an alkaline urine.</p> + +<p>Casts are not infrequently found in chemically normal +urine from a middle-aged patient. Other things being normal,<span class="pagenum"><a name="Page_258" id="Page_258">[258]</a></span> +the finding has no significance. The kidneys must be +carefully tested functionally.</p> + +<p>Blood pressure readings should always be taken with the +patient in the same posture at every estimation. At the +first examination it is advisable to take readings from both +brachial arteries. Let the patient sit comfortably and relax +all muscles.</p> + +<p>Differentiate as soon as possible between the uncompensated +heart caused by valvular disease and that caused +by arteriosclerosis. There is a difference in prognosis. +Both give the same symptoms, and are treated similarly until +compensation returns; thereafter the management of the +two forms is different.</p> + +<p>Aortic incompetence that comes on late in life is generally +the result of curling of the free margins of the valves +caused by syphilitic arteriosclerosis. Prognosis is grave +because of the fact that the heart muscle also is the seat of +degenerative changes and compensatory hypertrophy is established +with difficulty.</p> + +<p>When laying down a regime for a patient, consider his +disposition, and individualize the treatment. Remember +that exercise is an essential feature of the hygiene of the +patient's life but do not forget to be explicit about the +amount and character of the permissible exercise.</p> + +<p>In the prophylaxis of arteriosclerosis, a rational mode of +living is the all-important factor. As a rule, the less meat +one eats, the less is the liability of arterial degeneration as +age advances. The exceptions to this rule are many, and +probably depend upon the character of the "vital rubber" +with which the individual begins life.</p> + +<p>The diet in well-marked cases of arteriosclerosis should +be carefully selected with regard to its nutritive and non-irritating +character. Animal proteins should be sparingly +used. Milk should have an important place in the dietary.</p> + +<p>No drug relieves the pain of uncomplicated aneurysm as +surely as iodide of potassium.</p> + +<p><span class="pagenum"><a name="Page_259" id="Page_259">[259]</a></span>Iodides frequently upset the stomach. Be cautious in the +use of them. The irritable stomach may turn the scales +against your patient.</p> + +<p>Use cardiac stimulants with care and judgment. If all +the valuable ammunition is used up at first, the fight will be +lost.</p> + +<p>Use digitalis with especial care. Its chief usefulness is +in steadying the decompensated heart, improving the conduction +of impulses, and increasing the tone of the cardiac +muscle. <i>It should never be given to patients with very slow +pulses, the subjects of Stokes-Adams syndrome.</i> Digitalis +has been found to produce partial to complete heart block +when therapeutically administered.</p> + +<p>Remember that in the uncompensated heart morphine not +only eases the oppressive dyspnea, but also steadies and +stimulates the heart.</p> + +<p>See to it that the patient has a daily movement of the +bowels. In the early stage try the effect of liquid paraffin +or of the mineral waters such as Pluto, or Hunyadi Janos, +or artificial Carlsbad salts (Sprudel salts). These last can +be made as follows: Sodium chloride, ℥I; sodium bicarbonate, +℥II; sodium sulphate, ℥IV. Take two tablespoonsful of +this in a glass of hot water before breakfast. Should these +not succeed, assist the action of the drugs by the use of +enemata. The pill of aloin, strychnine sulphate, and extract +of cascara, with the addition of a small quantity of hyoscyamus, +is a mild tonic purgative. In cases of constipation +with high tension, there is no drug as valuable as calomel or +one of the other mercurials given occasionally.</p> + +<p>Never give Epsom salts unless copious watery stools are +desired to deplete effusion into the serous cavities or into +the subcutaneous tissue.</p> + +<p>Chronic constipation increases the gravity of the prognosis.</p> + +<p>In case of suppression of urine and anasarca, hot air +packs may be of value. The patient may be wrapped in a<span class="pagenum"><a name="Page_260" id="Page_260">[260]</a></span> +hot wet sheet and covered with blankets. I do not believe in +administering pilocarpine to assist the sweating.</p> + +<p>Remember to treat the patient and not the disease. The +careful hygienic and dietetic treatment, combined with the +least amount of drugging, is the best and most rational +method of treatment.</p> + +<hr style="width: 65%;" /> +<p><span class="pagenum"><a name="Page_261" id="Page_261">[261]</a></span></p> +<h2>INDEX</h2> + + + +<div> +A<br /> +<br /> +Abdominal symptoms, <a href="#Page_201">201</a><br /> +<br /> +Aconite in treatment, <a href="#Page_242">242</a><br /> +<br /> +Acquired arteriosclerosis, <a href="#Page_159">159</a><br /> +<br /> +Adami, effect of syphilis in aorta, <a href="#Page_45">45</a><br /> +<br /> +Adventitia, <a href="#Page_28">28</a><br /> +<br /> +Age in arteriosclerosis, <a href="#Page_161">161</a><br /> +<br /> +Albuminuria, <a href="#Page_221">221</a><br /> +<br /> +Albutt's classification of arteriosclerosis, <a href="#Page_186">186</a><br /> +<br /> +Alcohol, <a href="#Page_166">166</a>, <a href="#Page_228">228</a>, <a href="#Page_235">235</a><br /> +<br /> +Anatomy, <a href="#Page_25">25</a><br /> +<br /> +Angina abdominalis, <a href="#Page_201">201</a>, <a href="#Page_216">216</a><br /> +<span style="margin-left: 1em;">pectoris, <a href="#Page_197">197</a>, <a href="#Page_216">216</a></span><br /> +<span style="margin-left: 2em;">pseudo, <a href="#Page_216">216</a></span><br /> +<br /> +Angiosclerosis, <a href="#Page_26">26</a>, <a href="#Page_64">64</a><br /> +<br /> +Aorta, <a href="#Page_27">27</a><br /> +<span style="margin-left: 1em;">anatomical lesions in, <a href="#Page_33">33</a></span><br /> +<span style="margin-left: 1em;">Aschoff on, <a href="#Page_35">35</a></span><br /> +<span style="margin-left: 1em;">normal, <a href="#Page_41">41</a></span><br /> +<span style="margin-left: 1em;">syphilis in, <a href="#Page_44">44</a></span><br /> +<span style="margin-left: 1em;">thoracic, <a href="#Page_29">29</a></span><br /> +<span style="margin-left: 1em;">thoracic and abdominal, arteriosclerosis of, <a href="#Page_39">39</a></span><br /> +<span style="margin-left: 1em;">velocity of blood in, <a href="#Page_66">66</a></span><br /> +<br /> +Aortic incompetence, <a href="#Page_61">61</a>, <a href="#Page_258">258</a><br /> +<span style="margin-left: 1em;">stenosis, <a href="#Page_60">60</a></span><br /> +<br /> +Aortitis, acute, <a href="#Page_165">165</a><br /> +<br /> +Arcus senilis, <a href="#Page_191">191</a><br /> +<br /> +Arrhythmia, tonal, <a href="#Page_92">92</a>, <a href="#Page_102">102</a><br /> +<br /> +Arterial pressure, <a href="#Page_85">85</a><br /> +<span style="margin-left: 1em;">symptoms, <a href="#Page_189">189</a></span><br /> +<br /> +Arteries, <a href="#Page_29">29</a><br /> +<span style="margin-left: 1em;">examination of, <a href="#Page_172">172</a>, <a href="#Page_177">177</a></span><br /> +<span style="margin-left: 1em;">general structure of, <a href="#Page_27">27</a></span><br /> +<span style="margin-left: 1em;">large, <a href="#Page_30">30</a></span><br /> +<span style="margin-left: 2em;">adventitia of, <a href="#Page_30">30</a></span><br /> +<span style="margin-left: 1em;">palpable, <a href="#Page_189">189</a></span><br /> +<span style="margin-left: 1em;">pulmonary, arteriosclerosis of, <a href="#Page_63">63</a></span><br /> +<br /> +Arteriocapillary fibrosis, <a href="#Page_26">26</a><br /> +<br /> +Arteriosclerotic endocarditis, <a href="#Page_60">60</a>, <a href="#Page_219">219</a><br /> +<br /> +Artery, coronary, cross-section of, <a href="#Page_36">36</a><br /> +<span style="margin-left: 1em;">pulmonary, <a href="#Page_209">209</a></span><br /> +<span style="margin-left: 1em;">radial, <a href="#Page_29">29</a></span><br /> +<br /> +Aschoff on aorta, <a href="#Page_35">35</a><br /> +<br /> +Atheroma, simple, <a href="#Page_32">32</a><br /> +<br /> +Atheromatous abscess, <a href="#Page_38">38</a><br /> +<br /> +Auricular fibrillation, <a href="#Page_133">133</a><br /> +<span style="margin-left: 1em;">flutter, <a href="#Page_131">131</a></span><br /> +<br /> +Auscultation, <a href="#Page_176">176</a><br /> +<br /> +Auscultatory blood pressure phenomenon, <a href="#Page_90">90</a><br /> +<span style="margin-left: 1em;">method of taking blood pressure, <a href="#Page_83">83</a></span><br /> +<span style="margin-left: 1em;">percussion, <a href="#Page_175">175</a></span><br /> +<br /> +<br /> +B<br /> +<br /> +Balneotherapy, <a href="#Page_233">233</a><br /> +<br /> +Basch's blood pressure instrument, <a href="#Page_70">70</a><br /> +<br /> +Blood, circulation of, <a href="#Page_65">65</a><br /> +<span style="margin-left: 1em;">velocity of, <a href="#Page_65">65</a></span><br /> +<span style="margin-left: 2em;">in animals, <a href="#Page_66">66</a></span><br /> +<span style="margin-left: 2em;">in aorta, <a href="#Page_66">66</a></span><br /> +<span style="margin-left: 2em;">in capillaries, <a href="#Page_66">66</a></span><br /> +<span style="margin-left: 1em;">viscosity of, <a href="#Page_68">68</a></span><br /> +<br /> +Blood pressure, <a href="#Page_68">68</a><br /> +<span style="margin-left: 1em;">auscultatory method of taking, <a href="#Page_83">83</a></span><br /> +<span style="margin-left: 1em;">clinical applications of, <a href="#Page_147">147</a></span><br /> +<span style="margin-left: 1em;">diurnal variations of, <a href="#Page_102">102</a></span><br /> +<span style="margin-left: 1em;">drugs influencing, <a href="#Page_120">120</a></span><br /> +<span style="margin-left: 1em;">estimation of, <a href="#Page_179">179</a></span><br /> +<span style="margin-left: 1em;">in cancer, <a href="#Page_118">118</a></span><br /> +<span style="margin-left: 1em;">in collapse, <a href="#Page_118">118</a></span><br /> +<span style="margin-left: 1em;">in exercise, <a href="#Page_105">105</a></span><br /> +<span style="margin-left: 1em;">in head injuries, <a href="#Page_148">148</a></span><br /> +<span style="margin-left: 1em;">in hemorrhages, <a href="#Page_105">105</a>, <a href="#Page_118">118</a>, <a href="#Page_148">148</a></span><br /> +<span style="margin-left: 1em;">in infectious diseases, <a href="#Page_153">153</a></span><br /> +<span style="margin-left: 1em;">in kidney diseases, <a href="#Page_155">155</a></span><br /> +<span style="margin-left: 1em;">in meningitis, <a href="#Page_118">118</a></span><br /> +<span style="margin-left: 1em;">in obstetrics, <a href="#Page_152">152</a></span><br /> +<span style="margin-left: 1em;">in pulmonary tuberculosis, <a href="#Page_119">119</a></span><br /> +<span style="margin-left: 1em;">in shock, <a href="#Page_105">105</a>, <a href="#Page_148">148</a></span><br /> +<span style="margin-left: 1em;">in surgery, <a href="#Page_147">147</a></span><br /> +<span style="margin-left: 1em;">in typhoid fever, <a href="#Page_118">118</a>, <a href="#Page_154">154</a></span><br /> +<span style="margin-left: 1em;">in valvular heart disease, <a href="#Page_155">155</a></span><br /> +<span style="margin-left: 1em;">increase of, <a href="#Page_55">55</a></span><br /> +<span style="margin-left: 1em;">instruments, <a href="#Page_70">70</a></span><br /> +<span style="margin-left: 2em;">Brown's, <a href="#Page_74">74</a></span><br /> +<span style="margin-left: 2em;">Cook's, <a href="#Page_71">71</a></span><br /> +<span style="margin-left: 2em;">Erlanger's, <a href="#Page_72">72</a></span><br /> +<span style="margin-left: 2em;">Faught's, <a href="#Page_75">75</a>, <a href="#Page_80">80</a></span><br /> +<span style="margin-left: 2em;">Hill and Barnard's, <a href="#Page_70">70</a></span><br /> +<span style="margin-left: 2em;">Hirschfelder's, <a href="#Page_73">73</a></span><br /> +<span style="margin-left: 2em;">K. Vierordt's, <a href="#Page_70">70</a></span><br /> +<span style="margin-left: 2em;">Marcy's, <a href="#Page_70">70</a></span><br /> +<span style="margin-left: 2em;">Potain's, <a href="#Page_70">70</a></span><br /> +<span style="margin-left: 2em;">Riva Rocci's, <a href="#Page_70">70</a></span><br /> +<span style="margin-left: 2em;">Roger's, <a href="#Page_77">77</a></span><br /> +<span class="pagenum"><a name="Page_262" id="Page_262">[262]</a></span><span style="margin-left: 2em;">Sanborn's, <a href="#Page_80">80</a></span><br /> +<span style="margin-left: 2em;">Stanton's, <a href="#Page_72">72</a></span><br /> +<span style="margin-left: 2em;">technique of, <a href="#Page_80">80</a></span><br /> +<span style="margin-left: 2em;">"Tycos," <a href="#Page_77">77</a></span><br /> +<span style="margin-left: 2em;">v. Basch's, <a href="#Page_70">70</a></span><br /> +<span style="margin-left: 2em;">v. Recklinghausen's, <a href="#Page_76">76</a></span><br /> +<span style="margin-left: 1em;">mechanism of, <a href="#Page_55">55</a></span><br /> +<span style="margin-left: 1em;">normal variations of, <a href="#Page_88">88</a></span><br /> +<span style="margin-left: 1em;">phenomenon, auscultatory, <a href="#Page_90">90</a></span><br /> +<span style="margin-left: 1em;">precautions when estimating, <a href="#Page_181">181</a></span><br /> +<span style="margin-left: 1em;">value of, <a href="#Page_181">181</a></span><br /> +<br /> +Bowman's capsules, sclerosis of, <a href="#Page_62">62</a><br /> +<br /> +Brain, changes in, <a href="#Page_62">62</a><br /> +<br /> +Brown atrophy, <a href="#Page_60">60</a>, <a href="#Page_118">118</a>, <a href="#Page_201">201</a><br /> +<br /> +<br /> +C<br /> +<br /> +Calcification of media, <a href="#Page_43">43</a>, <a href="#Page_59">59</a><br /> +<br /> +Cancer, blood pressure in, <a href="#Page_118">118</a><br /> +<br /> +Capillaries, anatomy of, <a href="#Page_27">27</a>, <a href="#Page_31">31</a><br /> +<br /> +Capillary pulse, <a href="#Page_67">67</a><br /> +<br /> +Cardiac dullness, <a href="#Page_172">172</a><br /> +<span style="margin-left: 1em;">irregularities in arteriosclerosis, <a href="#Page_131">131</a></span><br /> +<span style="margin-left: 1em;">symptoms, <a href="#Page_195">195</a></span><br /> +<br /> +Cerebral symptoms, <a href="#Page_203">203</a><br /> +<br /> +Circulation of blood, <a href="#Page_65">65</a><br /> +<span style="margin-left: 1em;">physiology of, <a href="#Page_65">65</a></span><br /> +<br /> +Cirrhosis of liver, <a href="#Page_64">64</a>, <a href="#Page_216">216</a><br /> +<br /> +Classification of arteriosclerosis, <a href="#Page_32">32</a>, <a href="#Page_37">37</a><br /> +<span style="margin-left: 1em;">Allbutt's, <a href="#Page_186">186</a></span><br /> +<br /> +Collapse, blood pressure in, <a href="#Page_118">118</a><br /> +<br /> +Congenital arteriosclerosis, <a href="#Page_157">157</a><br /> +<br /> +Cook's blood pressure instrument, <a href="#Page_71">71</a><br /> +<br /> +Cor bovinum, <a href="#Page_116">116</a><br /> +<br /> +Coronary artery, cross section of, <a href="#Page_36">36</a><br /> +<br /> +Corpus luteum, <a href="#Page_241">241</a><br /> +<br /> +<br /> +D<br /> +<br /> +Definition of arteriosclerosis, <a href="#Page_26">26</a><br /> +<br /> +Diabetes mellitus, <a href="#Page_216">216</a><br /> +<br /> +Diagnosis, <a href="#Page_210">210</a><br /> +<span style="margin-left: 1em;">differential, <a href="#Page_215">215</a></span><br /> +<span style="margin-left: 1em;">early, <a href="#Page_210">210</a></span><br /> +<span style="margin-left: 1em;">ophthalmic examination in, <a href="#Page_214">214</a></span><br /> +<br /> +Diastolic pressure, <a href="#Page_69">69</a>, <a href="#Page_83">83</a>, <a href="#Page_85">85</a>, <a href="#Page_94">94</a><br /> +<span style="margin-left: 1em;">importance of, <a href="#Page_97">97</a></span><br /> +<br /> +Dicrotic pulse, <a href="#Page_123">123</a><br /> +<br /> +Dietetic treatment, <a href="#Page_235">235</a><br /> +<br /> +Differential diagnosis, <a href="#Page_166">166</a>, <a href="#Page_215">215</a><br /> +<br /> +Diffuse arteriosclerosis, <a href="#Page_32">32</a>, <a href="#Page_37">37</a>, <a href="#Page_38">38</a>, <a href="#Page_57">57</a><br /> +<br /> +Digitalis in treatment, <a href="#Page_246">246</a>, <a href="#Page_259">259</a><br /> +<br /> +Diuretin in treatment, <a href="#Page_246">246</a><br /> +<br /> +Drug intoxications, <a href="#Page_166">166</a><br /> +<br /> +Drugs influencing blood pressure, <a href="#Page_105">105</a>, <a href="#Page_120">120</a><br /> +<br /> +Ductless glands, <a href="#Page_171">171</a><br /> +<br /> +Dullness, cardiac, <a href="#Page_172">172</a><br /> +<br /> +Dyspeptic symptoms, <a href="#Page_184">184</a><br /> +<br /> +Dyspnea, <a href="#Page_184">184</a><br /> +<span style="margin-left: 1em;">treatment of, <a href="#Page_248">248</a></span><br /> +<br /> +<br /> +E<br /> +<br /> +Electrocardiogram, <a href="#Page_126">126</a><br /> +<br /> +Embolism, <a href="#Page_59">59</a><br /> +<br /> +Endarteritis deformans, <a href="#Page_47">47</a><br /> +<span style="margin-left: 1em;">obliterans, <a href="#Page_46">46</a></span><br /> +<br /> +Endocarditis, arteriosclerotic, <a href="#Page_60">60</a>, <a href="#Page_219">219</a><br /> +<br /> +Endothelial lining, <a href="#Page_27">27</a><br /> +<span style="margin-left: 1em;">tubes, <a href="#Page_31">31</a></span><br /> +<br /> +Epistaxis, <a href="#Page_184">184</a>, <a href="#Page_221">221</a><br /> +<br /> +Erlanger's blood pressure instrument, <a href="#Page_72">72</a><br /> +<br /> +Erythromelalgia, <a href="#Page_192">192</a>, <a href="#Page_208">208</a><br /> +<br /> +Estimation of blood pressure, <a href="#Page_179">179</a><br /> +<br /> +Etiology, <a href="#Page_157">157</a><br /> +<br /> +Examination of arteries, <a href="#Page_172">172</a>, <a href="#Page_177">177</a><br /> +<span style="margin-left: 1em;">of heart, <a href="#Page_172">172</a></span><br /> +<span style="margin-left: 1em;">of urine, <a href="#Page_257">257</a></span><br /> +<br /> +Exercise, blood pressure in, <a href="#Page_105">105</a><br /> +<span style="margin-left: 1em;">in prophylaxis, <a href="#Page_225">225</a></span><br /> +<span style="margin-left: 1em;">in treatment, <a href="#Page_230">230</a></span><br /> +<br /> +Experimental arteriosclerosis, <a href="#Page_50">50</a><br /> +<br /> +Extrasystole, <a href="#Page_138">138</a><br /> +<br /> +<br /> +F<br /> +<br /> +Faught's blood pressure instrument, <a href="#Page_75">75</a>, <a href="#Page_80">80</a><br /> +<br /> +Fibrillation, auricular, <a href="#Page_133">133</a><br /> +<span style="margin-left: 1em;">ventricular, <a href="#Page_138">138</a></span><br /> +<br /> +Fibrolysin in treatment, <a href="#Page_243">243</a><br /> +<br /> +Fingernail palpation, <a href="#Page_178">178</a><br /> +<br /> +Finger tip palpation, <a href="#Page_179">179</a><br /> +<br /> +Flutter, auricular, <a href="#Page_131">131</a><br /> +<br /> +Food poisons in arteriosclerosis, <a href="#Page_163">163</a><br /> +<br /> +<br /> +G<br /> +<br /> +Gibson's law, <a href="#Page_154">154</a><br /> +<br /> +<br /> +H<br /> +<br /> +"H" wave, <a href="#Page_126">126</a><br /> +<br /> +Habits, personal, <a href="#Page_234">234</a><br /> +<br /> +Head injuries, blood pressure in, <a href="#Page_148">148</a><br /> +<br /> +Headache, <a href="#Page_184">184</a><br /> +<span style="margin-left: 1em;">treatment of, <a href="#Page_248">248</a></span><br /> +<br /> +Heart block, <a href="#Page_140">140</a><br /> +<span style="margin-left: 1em;">boundaries, <a href="#Page_172">172</a></span><br /> +<span style="margin-left: 1em;">examination of, <a href="#Page_172">172</a></span><br /> +<span style="margin-left: 1em;">hypertrophy of, <a href="#Page_60">60</a></span><br /> +<span style="margin-left: 1em;">physical examination of, <a href="#Page_172">172</a></span><br /> +<span style="margin-left: 1em;">stimulants, <a href="#Page_243">243</a>, <a href="#Page_246">246</a>, <a href="#Page_259">259</a></span><br /> +<span style="margin-left: 1em;">symptoms, <a href="#Page_188">188</a></span><br /> +<span class="pagenum"><a name="Page_263" id="Page_263">[263]</a></span><br /> +Hemorrhages, blood pressure in, <a href="#Page_118">118</a><br /> +<br /> +Henle, membrane of, <a href="#Page_29">29</a><br /> +<br /> +Hill and Barnard's blood pressure instrument, <a href="#Page_70">70</a><br /> +<br /> +Hirschfelder's blood pressure instrument, <a href="#Page_73">73</a><br /> +<br /> +His, bundle of, <a href="#Page_141">141</a>, <a href="#Page_197">197</a><br /> +<br /> +Hygienic treatment, <a href="#Page_230">230</a><br /> +<br /> +Hyperpietic arteriosclerosis, <a href="#Page_186">186</a><br /> +<br /> +Hypertension, <a href="#Page_60">60</a>, <a href="#Page_106">106</a>, <a href="#Page_169">169</a>, <a href="#Page_185">185</a>, <a href="#Page_249">249</a><br /> +<span style="margin-left: 1em;">cause of arteriosclerosis, <a href="#Page_159">159</a></span><br /> +<span style="margin-left: 1em;">classification of cases, <a href="#Page_112">112</a></span><br /> +<br /> +Hypertrophy of left ventricle, <a href="#Page_58">58</a><br /> +<br /> +Hypotension, <a href="#Page_117">117</a><br /> +<br /> +<br /> +I<br /> +<br /> +Incompetence, aortic, <a href="#Page_61">61</a>, <a href="#Page_258">258</a><br /> +<br /> +Indicanuria, <a href="#Page_167">167</a><br /> +<br /> +Infants, arteriosclerosis in, <a href="#Page_158">158</a><br /> +<br /> +Infectious diseases in arteriosclerosis, <a href="#Page_163">163</a><br /> +<span style="margin-left: 1em;">blood pressure in, <a href="#Page_153">153</a></span><br /> +<br /> +Insomnia, treatment of, <a href="#Page_248">248</a><br /> +<br /> +Intermittent claudication, <a href="#Page_192">192</a>, <a href="#Page_208">208</a><br /> +<span style="margin-left: 1em;">treatment of, <a href="#Page_247">247</a></span><br /> +<br /> +Intoxications, chronic drug, <a href="#Page_166">166</a><br /> +<br /> +Intracranial tension, <a href="#Page_105">105</a><br /> +<br /> +Involutionary arteriosclerosis, <a href="#Page_187">187</a><br /> +<br /> +Iodides in treatment, <a href="#Page_238">238</a>, <a href="#Page_247">247</a>, <a href="#Page_259">259</a><br /> +<br /> +<br /> +K<br /> +<br /> +Kidney diseases, blood pressure in, <a href="#Page_155">155</a><br /> +<br /> +Kidneys, sclerosis of, <a href="#Page_61">61</a>, <a href="#Page_170">170</a><br /> +<br /> +<br /> +L<br /> +<br /> +Life insurance, relation to, <a href="#Page_249">249</a><br /> +<br /> +Light percussion, <a href="#Page_174">174</a><br /> +<span style="margin-left: 1em;">touch palpation, <a href="#Page_175">175</a></span><br /> +<br /> +Liver, cirrhosis, <a href="#Page_64">64</a>, <a href="#Page_216">216</a><br /> +<br /> +Local symptoms, <a href="#Page_207">207</a><br /> +<br /> +<br /> +M<br /> +<br /> +Marey's blood pressure instrument, <a href="#Page_70">70</a><br /> +<br /> +Maximum pressure, <a href="#Page_85">85</a>, <a href="#Page_94">94</a><br /> +<br /> +Mean pressure, <a href="#Page_85">85</a><br /> +<br /> +Media, calcification of, <a href="#Page_43">43</a>, <a href="#Page_59">59</a><br /> +<br /> +Medicinal treatment, <a href="#Page_238">238</a><br /> +<br /> +Meningitis, blood pressure in, <a href="#Page_118">118</a><br /> +<br /> +Mental strain, <a href="#Page_168">168</a><br /> +<br /> +Mesaortitis, <a href="#Page_45">45</a>, <a href="#Page_47">47</a>, <a href="#Page_49">49</a>, <a href="#Page_165">165</a><br /> +<br /> +Mesentery, cross-section of small artery in, <a href="#Page_56">56</a><br /> +<br /> +Milk diet, <a href="#Page_237">237</a><br /> +<br /> +Minimum pressure, <a href="#Page_86">86</a>, <a href="#Page_94">94</a><br /> +<br /> +Moenckeberg type of arteriosclerosis, <a href="#Page_43">43</a><br /> +<br /> +Morphine in treatment, <a href="#Page_243">243</a><br /> +<br /> +Mosenthal test meal, <a href="#Page_221">221</a><br /> +<br /> +Muscular overwork, <a href="#Page_169">169</a><br /> +<br /> +<br /> +N<br /> +<br /> +Nervous symptoms, <a href="#Page_191">191</a><br /> +<br /> +Nitrites in treatment, <a href="#Page_240">240</a><br /> +<br /> +Nitroglycerin in treatment, <a href="#Page_241">241</a><br /> +<br /> +Nodular arteriosclerosis, <a href="#Page_32">32</a>, <a href="#Page_37">37</a><br /> +<br /> +Normal blood pressure variation, <a href="#Page_88">88</a><br /> +<br /> +<br /> +O<br /> +<br /> +Obstetrics, blood pressure in, <a href="#Page_152">152</a><br /> +<br /> +Occupation in arteriosclerosis, <a href="#Page_162">162</a><br /> +<br /> +Ocular symptoms, <a href="#Page_190">190</a><br /> +<br /> +Ophthalmic examination, importance in early diagnosis, <a href="#Page_214">214</a>, <a href="#Page_256">256</a><br /> +<br /> +Orthodiagraph, <a href="#Page_173">173</a><br /> +<br /> +Overeating, <a href="#Page_167">167</a>, <a href="#Page_212">212</a>, <a href="#Page_225">225</a>, <a href="#Page_235">235</a><br /> +<br /> +Overwork, muscular, <a href="#Page_169">169</a><br /> +<br /> +<br /> +P<br /> +<br /> +"P" wave, <a href="#Page_129">129</a><br /> +<br /> +"P-R" interval, <a href="#Page_130">130</a><br /> +<br /> +Palpable arteries, <a href="#Page_189">189</a><br /> +<br /> +Palpation, <a href="#Page_174">174</a>, <a href="#Page_180">180</a><br /> +<span style="margin-left: 1em;">fingernail, <a href="#Page_178">178</a></span><br /> +<span style="margin-left: 1em;">finger tip, <a href="#Page_179">179</a></span><br /> +<span style="margin-left: 1em;">light touch, <a href="#Page_175">175</a></span><br /> +<br /> +Pathology, <a href="#Page_32">32</a><br /> +<br /> +Percussion, <a href="#Page_174">174</a><br /> +<span style="margin-left: 1em;">auscultatory, <a href="#Page_175">175</a></span><br /> +<span style="margin-left: 1em;">light, <a href="#Page_174">174</a></span><br /> +<br /> +Peripheral symptoms, <a href="#Page_207">207</a><br /> +<br /> +Personal habits, <a href="#Page_234">234</a><br /> +<br /> +Phlebosclerosis, <a href="#Page_64">64</a><br /> +<br /> +Phthalein test, <a href="#Page_221">221</a><br /> +<br /> +Physical signs, <a href="#Page_183">183</a><br /> +<br /> +Physiology of the circulation, <a href="#Page_65">65</a><br /> +<br /> +Potain's blood pressure instrument, <a href="#Page_70">70</a><br /> +<br /> +Practical suggestions, <a href="#Page_256">256</a><br /> +<br /> +Pressure, arterial, <a href="#Page_85">85</a><br /> +<span style="margin-left: 1em;">ausculatory method of determining, <a href="#Page_83">83</a></span><br /> +<span style="margin-left: 1em;">diastolic, <a href="#Page_83">83</a>, <a href="#Page_94">94</a></span><br /> +<span style="margin-left: 1em;">estimation of, <a href="#Page_179">179</a></span><br /> +<span style="margin-left: 1em;">in surgery, <a href="#Page_147">147</a></span><br /> +<span style="margin-left: 1em;">maximum, <a href="#Page_85">85</a>, <a href="#Page_94">94</a></span><br /> +<span style="margin-left: 1em;">normal variations, <a href="#Page_88">88</a></span><br /> +<span style="margin-left: 1em;">pulse, <a href="#Page_83">83</a>, <a href="#Page_85">85</a>, <a href="#Page_87">87</a>, <a href="#Page_100">100</a></span><br /> +<span style="margin-left: 1em;">systolic, <a href="#Page_82">82</a>, <a href="#Page_85">85</a></span><br /> +<span style="margin-left: 1em;">technique, <a href="#Page_80">80</a></span><br /> +<span style="margin-left: 1em;">venous, <a href="#Page_120">120</a></span><br /> +<span class="pagenum"><a name="Page_264" id="Page_264">[264]</a></span><br /> +Prognosis, <a href="#Page_218">218</a><br /> +<br /> +Prophylaxis, <a href="#Page_224">224</a><br /> +<span style="margin-left: 1em;">exercise in, <a href="#Page_225">225</a></span><br /> +<br /> +Pseudo angina pectoris, <a href="#Page_216">216</a><br /> +<br /> +Pulmonary artery, <a href="#Page_209">209</a><br /> +<span style="margin-left: 1em;">arteriosclerosis of, <a href="#Page_63">63</a></span><br /> +<span style="margin-left: 1em;">tuberculosis, blood pressure in, <a href="#Page_119">119</a></span><br /> +<br /> +Pulse, <a href="#Page_123">123</a><br /> +<span style="margin-left: 1em;">capillary, <a href="#Page_67">67</a></span><br /> +<span style="margin-left: 1em;">deficit, <a href="#Page_135">135</a></span><br /> +<span style="margin-left: 1em;">dicrotic, <a href="#Page_123">123</a></span><br /> +<span style="margin-left: 1em;">in arteriosclerosis, <a href="#Page_123">123</a></span><br /> +<span style="margin-left: 1em;">pressure, <a href="#Page_69">69</a>, <a href="#Page_83">83</a>, <a href="#Page_85">85</a>, <a href="#Page_87">87</a>, <a href="#Page_100">100</a></span><br /> +<span style="margin-left: 1em;">rate, <a href="#Page_69">69</a></span><br /> +<span style="margin-left: 1em;">venous, <a href="#Page_123">123</a></span><br /> +<br /> +Purgatives in treatment, <a href="#Page_244">244</a>, <a href="#Page_259">259</a><br /> +<br /> +Pyrosis, <a href="#Page_184">184</a><br /> +<br /> +<br /> +Q<br /> +<br /> +"Q R S" complex, <a href="#Page_129">129</a><br /> +<br /> +<br /> +R<br /> +<br /> +Rabbits, lesions produced experimentally in, <a href="#Page_50">50</a><br /> +<br /> +Race in arteriosclerosis, <a href="#Page_161">161</a><br /> +<br /> +Radial artery, <a href="#Page_29">29</a><br /> +<br /> +Radials, sclerosis of, <a href="#Page_43">43</a><br /> +<br /> +Raynaud's disease, <a href="#Page_192">192</a>, <a href="#Page_207">207</a><br /> +<br /> +Recklinghausen's blood pressure instrument, <a href="#Page_76">76</a><br /> +<br /> +Renal disease, <a href="#Page_169">169</a><br /> +<span style="margin-left: 1em;">symptoms, <a href="#Page_199">199</a></span><br /> +<br /> +Rest in treatment, <a href="#Page_242">242</a><br /> +<br /> +Riva-Rocci's blood pressure instrument, <a href="#Page_70">70</a><br /> +<br /> +Rogers' blood pressure instrument, <a href="#Page_77">77</a><br /> +<br /> +<br /> +S<br /> +<br /> +Sanborn's blood pressure instrument, <a href="#Page_80">80</a><br /> +<br /> +Scaphoid scapula, <a href="#Page_158">158</a><br /> +<br /> +Schwellungsperkussion, <a href="#Page_174">174</a><br /> +<br /> +Sclerosis of veins, <a href="#Page_64">64</a><br /> +<br /> +Senile arteriosclerosis, <a href="#Page_32">32</a>, <a href="#Page_37">37</a>, <a href="#Page_43">43</a>, <a href="#Page_59">59</a><br /> +<br /> +Sex in arteriosclerosis, <a href="#Page_161">161</a><br /> +<br /> +Shock, blood pressure in, <a href="#Page_105">105</a>, <a href="#Page_148">148</a><br /> +<br /> +Spinal symptoms, <a href="#Page_205">205</a><br /> +<br /> +Spirochaeta pallida, <a href="#Page_45">45</a><br /> +<br /> +Stanton's blood pressure instrument, <a href="#Page_72">72</a><br /> +<br /> +Stenosis, aortic, <a href="#Page_60">60</a><br /> +<br /> +Stokes-Adams syndrome, <a href="#Page_197">197</a><br /> +<br /> +Stomach, ulcer of, <a href="#Page_216">216</a><br /> +<br /> +Strain hypertrophy, <a href="#Page_47">47</a>, <a href="#Page_54">54</a>, <a href="#Page_55">55</a><br /> +<br /> +Surgery, blood pressure in, <a href="#Page_147">147</a><br /> +<br /> +Symptomatic treatment, <a href="#Page_245">245</a><br /> +<br /> +Symptoms, <a href="#Page_183">183</a><br /> +<span style="margin-left: 1em;">abdominal, <a href="#Page_201">201</a></span><br /> +<span style="margin-left: 1em;">arterial, <a href="#Page_189">189</a></span><br /> +<span style="margin-left: 1em;">cardiac, <a href="#Page_195">195</a></span><br /> +<span style="margin-left: 1em;">cerebral, <a href="#Page_203">203</a></span><br /> +<span style="margin-left: 1em;">dyspeptic, <a href="#Page_184">184</a></span><br /> +<span style="margin-left: 1em;">dyspnea, <a href="#Page_184">184</a></span><br /> +<span style="margin-left: 1em;">general, <a href="#Page_183">183</a></span><br /> +<span style="margin-left: 1em;">headache, <a href="#Page_184">184</a></span><br /> +<span style="margin-left: 1em;">heart, <a href="#Page_188">188</a></span><br /> +<span style="margin-left: 1em;">local, <a href="#Page_207">207</a></span><br /> +<span style="margin-left: 1em;">nervous, <a href="#Page_191">191</a></span><br /> +<span style="margin-left: 1em;">ocular, <a href="#Page_190">190</a></span><br /> +<span style="margin-left: 1em;">peripheral, <a href="#Page_207">207</a></span><br /> +<span style="margin-left: 1em;">pyrosis, <a href="#Page_184">184</a></span><br /> +<span style="margin-left: 1em;">renal, <a href="#Page_199">199</a></span><br /> +<span style="margin-left: 1em;">special, <a href="#Page_194">194</a></span><br /> +<span style="margin-left: 1em;">spinal, <a href="#Page_205">205</a></span><br /> +<span style="margin-left: 1em;">vertigo, <a href="#Page_184">184</a></span><br /> +<span style="margin-left: 1em;">visceral, <a href="#Page_201">201</a></span><br /> +<br /> +Syphilis, <a href="#Page_165">165</a><br /> +<span style="margin-left: 1em;">in aorta, <a href="#Page_44">44</a></span><br /> +<br /> +Syphilitic arteriosclerosis, <a href="#Page_37">37</a><br /> +<br /> +Systolic pressure, <a href="#Page_69">69</a>, <a href="#Page_82">82</a>, <a href="#Page_85">85</a>, <a href="#Page_94">94</a><br /> +<span style="margin-left: 1em;">importance of, <a href="#Page_97">97</a></span><br /> +<br /> +<br /> +T<br /> +<br /> +"T" wave, <a href="#Page_130">130</a><br /> +<br /> +Technique of blood pressure instruments, <a href="#Page_80">80</a><br /> +<br /> +Thayer and Fabyan, <a href="#Page_34">34</a><br /> +<br /> +Theocin, <a href="#Page_247">247</a><br /> +<br /> +Thoma on arteriosclerosis, <a href="#Page_33">33</a><br /> +<br /> +Thoracic aorta, <a href="#Page_29">29</a><br /> +<br /> +Thyroid extract in treatment, <a href="#Page_239">239</a><br /> +<br /> +Tobacco, <a href="#Page_167">167</a>, <a href="#Page_212">212</a>, <a href="#Page_234">234</a><br /> +<br /> +Tonal arrhythmia, <a href="#Page_92">92</a>, <a href="#Page_102">102</a><br /> +<br /> +Toxic arteriosclerosis, <a href="#Page_186">186</a><br /> +<br /> +Treatment, <a href="#Page_229">229</a><br /> +<span style="margin-left: 1em;">aconite in, <a href="#Page_242">242</a></span><br /> +<span style="margin-left: 1em;">balneotherapy in, <a href="#Page_233">233</a></span><br /> +<span style="margin-left: 1em;">corpus luteum, <a href="#Page_241">241</a></span><br /> +<span style="margin-left: 1em;">dietetic, <a href="#Page_235">235</a></span><br /> +<span style="margin-left: 1em;">digitalis in, <a href="#Page_246">246</a>, <a href="#Page_259">259</a></span><br /> +<span style="margin-left: 1em;">diuretin in, <a href="#Page_246">246</a></span><br /> +<span style="margin-left: 1em;">exercise in, <a href="#Page_230">230</a></span><br /> +<span style="margin-left: 1em;">fibrolysin in, <a href="#Page_243">243</a></span><br /> +<span style="margin-left: 1em;">heart stimulants in, <a href="#Page_243">243</a></span><br /> +<span style="margin-left: 1em;">hygienic, <a href="#Page_230">230</a></span><br /> +<span style="margin-left: 1em;">iodides in, <a href="#Page_238">238</a>, <a href="#Page_247">247</a>, <a href="#Page_259">259</a></span><br /> +<span style="margin-left: 1em;">medicinal, <a href="#Page_238">238</a></span><br /> +<span style="margin-left: 1em;">morphine in, <a href="#Page_243">243</a></span><br /> +<span style="margin-left: 1em;">nitrites in, <a href="#Page_240">240</a></span><br /> +<span style="margin-left: 1em;">nitroglycerin in, <a href="#Page_241">241</a></span><br /> +<span style="margin-left: 1em;">of dyspnea, <a href="#Page_248">248</a></span><br /> +<span class="pagenum"><a name="Page_265" id="Page_265">[265]</a></span><span style="margin-left: 1em;">of headache, <a href="#Page_248">248</a></span><br /> +<span style="margin-left: 1em;">of insomnia, <a href="#Page_248">248</a></span><br /> +<span style="margin-left: 1em;">of intermittent claudication, <a href="#Page_247">247</a></span><br /> +<span style="margin-left: 1em;">personal habits in, <a href="#Page_234">234</a></span><br /> +<span style="margin-left: 1em;">purgatives in, <a href="#Page_244">244</a>, <a href="#Page_259">259</a></span><br /> +<span style="margin-left: 1em;">rest in, <a href="#Page_242">242</a></span><br /> +<span style="margin-left: 1em;">symptomatic, <a href="#Page_245">245</a></span><br /> +<span style="margin-left: 1em;">theocin in, <a href="#Page_247">247</a></span><br /> +<span style="margin-left: 1em;">thyroid extract in, <a href="#Page_239">239</a></span><br /> +<span style="margin-left: 1em;">Trunecek's serum in, <a href="#Page_243">243</a></span><br /> +<span style="margin-left: 1em;">venesection in, <a href="#Page_242">242</a></span><br /> +<span style="margin-left: 1em;">veratrum viride in, <a href="#Page_242">242</a></span><br /> +<br /> +Trunecek's serum in treatment, <a href="#Page_243">243</a><br /> +<br /> +Tuberculosis, blood pressure in, <a href="#Page_119">119</a><br /> +<br /> +Tunica intima, <a href="#Page_28">28</a><br /> +<span style="margin-left: 1em;">media, <a href="#Page_28">28</a></span><br /> +<br /> +"Tycos" blood pressure instrument, <a href="#Page_77">77</a><br /> +<br /> +Typhoid fever as cause of arteriosclerosis, <a href="#Page_164">164</a><br /> +<span style="margin-left: 1em;">blood pressure in, <a href="#Page_118">118</a></span><br /> +<br /> +<br /> +U<br /> +<br /> +Ulcer of stomach, <a href="#Page_216">216</a><br /> +<br /> +Urine, examination of, <a href="#Page_257">257</a><br /> +<span style="margin-left: 1em;">suppression of, <a href="#Page_259">259</a></span><br /> +<br /> +<br /> +V<br /> +<br /> +Valvular heart disease, blood pressure in, <a href="#Page_155">155</a><br /> +<br /> +Vasa vasorum, <a href="#Page_29">29</a><br /> +<br /> +Veins, anatomy of, <a href="#Page_30">30</a><br /> +<span style="margin-left: 1em;">sclerosis of, <a href="#Page_64">64</a></span><br /> +<br /> +Velocity of blood in animals, <a href="#Page_66">66</a><br /> +<span style="margin-left: 1em;">of blood in aorta, <a href="#Page_66">66</a></span><br /> +<br /> +Venesection in treatment, <a href="#Page_242">242</a><br /> +<br /> +Venous pressure, <a href="#Page_120">120</a><br /> +<span style="margin-left: 1em;">pulse, <a href="#Page_123">123</a></span><br /> +<br /> +Ventricle, left, hypertrophy of, <a href="#Page_58">58</a><br /> +<br /> +Ventricular fibrillation, <a href="#Page_138">138</a><br /> +<br /> +Veratrum viride in treatment, <a href="#Page_242">242</a><br /> +<br /> +Vertigo, <a href="#Page_184">184</a><br /> +</div> + + + + + +<h3>FOOTNOTES:</h3> + +<div class="footnote"><p><a name="Footnote_1_1" id="Footnote_1_1"></a><a href="#FNanchor_1_1"><span class="label">[1]</span></a> 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.</p></div> + +<div class="footnote"><p><a name="Footnote_2_2" id="Footnote_2_2"></a><a href="#FNanchor_2_2"><span class="label">[2]</span></a> Warthin, A. S.: Am. Jour. Syph., 1918, i, 693.</p></div> + +<div class="footnote"><p><a name="Footnote_3_3" id="Footnote_3_3"></a><a href="#FNanchor_3_3"><span class="label">[3]</span></a> A firm makes a stethoscope so that the bell is clamped on the arm leaving both the +operator's hands free.</p></div> + +<div class="footnote"><p><a name="Footnote_4_4" id="Footnote_4_4"></a><a href="#FNanchor_4_4"><span class="label">[4]</span></a> Weyse, A. W., and Lutz, B. R.: Diurnal Variations in Arterial Blood Pressure, +Am. Jour. Physiol., 1915, xxxvii, 330.</p></div> + +<div class="footnote"><p><a name="Footnote_5_5" id="Footnote_5_5"></a><a href="#FNanchor_5_5"><span class="label">[5]</span></a> Erlanger and Hooker: An Experimental Study of Blood Pressure and of Pulse +Pressure in Man, Johns Hopkins Hosp. Rep., 1904, xii, 145.</p></div> + +<div class="footnote"><p><a name="Footnote_6_6" id="Footnote_6_6"></a><a href="#FNanchor_6_6"><span class="label">[6]</span></a> Dawson and Gorham: The Pulse Pressure as an Index of Systolic Output, Jour. +Exper. Med., 1908, x, 484.</p></div> + +<div class="footnote"><p><a name="Footnote_7_7" id="Footnote_7_7"></a><a href="#FNanchor_7_7"><span class="label">[7]</span></a> Isolation of a New Vasoconstrictor Substance from the Blood and the Adrenal Cortex, +Jour. Am. Med. Assn., 1913, lxi, 2136.</p></div> + +<div class="footnote"><p><a name="Footnote_8_8" id="Footnote_8_8"></a><a href="#FNanchor_8_8"><span class="label">[8]</span></a> Stone, W. J.: The Differentiation of Cerebral and Cardiac Types of Hyperarterial +Tension in Vascular Diseases, Arch. Int. Med., November, 1915, p. 775.</p></div> + +<div class="footnote"><p><a name="Footnote_9_9" id="Footnote_9_9"></a><a href="#FNanchor_9_9"><span class="label">[9]</span></a> 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.</p></div> + +<div class="footnote"><p><a name="Footnote_10_10" id="Footnote_10_10"></a><a href="#FNanchor_10_10"><span class="label">[10]</span></a> McCrae, Thomas: Dilatation of the Arch of the Aorta, Am. Jour. Med. Sc., 1910, +cxl, 469.</p></div> + +<div class="footnote"><p><a name="Footnote_11_11" id="Footnote_11_11"></a><a href="#FNanchor_11_11"><span class="label">[11]</span></a> Stone, W. J.: Arch. Int. Med., 1915, xvl, 775.</p></div> + +<div class="footnote"><p><a name="Footnote_12_12" id="Footnote_12_12"></a><a href="#FNanchor_12_12"><span class="label">[12]</span></a> Robinson, G. C., and Bredeck, J. F.: Arch. Int. Med., 1917, xx, 725.</p></div> + +<div class="footnote"><p><a name="Footnote_13_13" id="Footnote_13_13"></a><a href="#FNanchor_13_13"><span class="label">[13]</span></a> Jour. Exper. Med., 1911, xiv, 217.</p></div> + +<div class="footnote"><p><a name="Footnote_14_14" id="Footnote_14_14"></a><a href="#FNanchor_14_14"><span class="label">[14]</span></a> Warfield, L. M.: Jour. Lab. and Clin. Med., November, 1917.</p></div> + +<div class="footnote"><p><a name="Footnote_15_15" id="Footnote_15_15"></a><a href="#FNanchor_15_15"><span class="label">[15]</span></a> From πιεσω to squeeze, oppress or distress. Hyperpiesis, therefore, signifies excessive +pressure.</p></div> + +<div class="footnote"><p><a name="Footnote_16_16" id="Footnote_16_16"></a><a href="#FNanchor_16_16"><span class="label">[16]</span></a> I have found the small colorimeter made by Hynson, Westcott and Dunning, +Baltimore, Mo., costing $5.00, a very practical instrument.</p></div> + +<div class="footnote"><p><a name="Footnote_17_17" id="Footnote_17_17"></a><a href="#FNanchor_17_17"><span class="label">[17]</span></a> Mosenthal, H. O.: Arch. Int. Med., 1915, xvi, 733.</p></div> + +<div class="footnote"><p><a name="Footnote_18_18" id="Footnote_18_18"></a><a href="#FNanchor_18_18"><span class="label">[18]</span></a> Myers and Lough: Arch. Int. Med., 1915, xvi, 536.</p></div> + +<div class="footnote"><p><a name="Footnote_19_19" id="Footnote_19_19"></a><a href="#FNanchor_19_19"><span class="label">[19]</span></a> Discussion of alcohol at present has value only as it relates to the past. The present +is dry. The future is in the lap of the gods.</p></div> + +<div class="footnote"><p><a name="Footnote_20_20" id="Footnote_20_20"></a><a href="#FNanchor_20_20"><span class="label">[20]</span></a> Miller, Jos. L.: Hypertension and the Value of the Various Methods for Its Reduction. +Jour. Am. Med. Assn., 1910, liv, p. 1666.</p></div> + +<div class="footnote"><p><a name="Footnote_21_21" id="Footnote_21_21"></a><a href="#FNanchor_21_21"><span class="label">[21]</span></a> I have taken as much as 1700 c.c. from a large man. He recovered and went back +to work.</p></div> +<hr style="width: 65%;" /> +<div class='tn'><h3>Transcriber's Notes:</h3> +<p>Irregular hyphenation has been preserved, as in +blood pressure and blood-pressure. Both "Hg" and "Hg." appear.</p> + +<p>Minor typographical errors and inconsistencies have been silently +normalized.</p> +<p>The original printed list of illustrations shows the original locations; they have been moved +closer to their discussion area in the text to not interrupt the flow of reading. +</p> + +</div> + + + + + + + +<pre> + + + + + +End of the Project Gutenberg EBook of Arteriosclerosis and Hypertension:, by +Louis Marshall Warfield + +*** END OF THIS PROJECT GUTENBERG EBOOK ARTERIOSCLEROSIS AND HYPERTENSION: *** + +***** This file should be named 37675-h.htm or 37675-h.zip ***** +This and all associated files of various formats will be found in: + http://www.gutenberg.org/3/7/6/7/37675/ + +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.) + + +Updated editions will replace the previous one--the old editions +will be renamed. + +Creating the works from public domain print editions means that no +one owns a United States copyright in these works, so the Foundation +(and you!) can copy and distribute it in the United States without +permission and without paying copyright royalties. Special rules, +set forth in the General Terms of Use part of this license, apply to +copying and distributing Project Gutenberg-tm electronic works to +protect the PROJECT GUTENBERG-tm concept and trademark. Project +Gutenberg is a registered trademark, and may not be used if you +charge for the eBooks, unless you receive specific permission. If you +do not charge anything for copies of this eBook, complying with the +rules is very easy. You may use this eBook for nearly any purpose +such as creation of derivative works, reports, performances and +research. They may be modified and printed and given away--you may do +practically ANYTHING with public domain eBooks. Redistribution is +subject to the trademark license, especially commercial +redistribution. + + + +*** START: FULL LICENSE *** + +THE FULL PROJECT GUTENBERG LICENSE +PLEASE READ THIS BEFORE YOU DISTRIBUTE OR USE THIS WORK + +To protect the Project Gutenberg-tm mission of promoting the free +distribution of electronic works, by using or distributing this work +(or any other work associated in any way with the phrase "Project +Gutenberg"), you agree to comply with all the terms of the Full Project +Gutenberg-tm License (available with this file or online at +http://gutenberg.org/license). + + +Section 1. General Terms of Use and Redistributing Project Gutenberg-tm +electronic works + +1.A. By reading or using any part of this Project Gutenberg-tm +electronic work, you indicate that you have read, understand, agree to +and accept all the terms of this license and intellectual property +(trademark/copyright) agreement. If you do not agree to abide by all +the terms of this agreement, you must cease using and return or destroy +all copies of Project Gutenberg-tm electronic works in your possession. +If you paid a fee for obtaining a copy of or access to a Project +Gutenberg-tm electronic work and you do not agree to be bound by the +terms of this agreement, you may obtain a refund from the person or +entity to whom you paid the fee as set forth in paragraph 1.E.8. + +1.B. "Project Gutenberg" is a registered trademark. It may only be +used on or associated in any way with an electronic work by people who +agree to be bound by the terms of this agreement. There are a few +things that you can do with most Project Gutenberg-tm electronic works +even without complying with the full terms of this agreement. See +paragraph 1.C below. There are a lot of things you can do with Project +Gutenberg-tm electronic works if you follow the terms of this agreement +and help preserve free future access to Project Gutenberg-tm electronic +works. See paragraph 1.E below. + +1.C. The Project Gutenberg Literary Archive Foundation ("the Foundation" +or PGLAF), owns a compilation copyright in the collection of Project +Gutenberg-tm electronic works. Nearly all the individual works in the +collection are in the public domain in the United States. If an +individual work is in the public domain in the United States and you are +located in the United States, we do not claim a right to prevent you from +copying, distributing, performing, displaying or creating derivative +works based on the work as long as all references to Project Gutenberg +are removed. Of course, we hope that you will support the Project +Gutenberg-tm mission of promoting free access to electronic works by +freely sharing Project Gutenberg-tm works in compliance with the terms of +this agreement for keeping the Project Gutenberg-tm name associated with +the work. You can easily comply with the terms of this agreement by +keeping this work in the same format with its attached full Project +Gutenberg-tm License when you share it without charge with others. + +1.D. The copyright laws of the place where you are located also govern +what you can do with this work. Copyright laws in most countries are in +a constant state of change. If you are outside the United States, check +the laws of your country in addition to the terms of this agreement +before downloading, copying, displaying, performing, distributing or +creating derivative works based on this work or any other Project +Gutenberg-tm work. The Foundation makes no representations concerning +the copyright status of any work in any country outside the United +States. + +1.E. Unless you have removed all references to Project Gutenberg: + +1.E.1. The following sentence, with active links to, or other immediate +access to, the full Project Gutenberg-tm License must appear prominently +whenever any copy of a Project Gutenberg-tm work (any work on which the +phrase "Project Gutenberg" appears, or with which the phrase "Project +Gutenberg" is associated) is accessed, displayed, performed, viewed, +copied or distributed: + +This eBook is for the use of anyone anywhere 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 + +1.E.2. If an individual Project Gutenberg-tm electronic work is derived +from the public domain (does not contain a notice indicating that it is +posted with permission of the copyright holder), the work can be copied +and distributed to anyone in the United States without paying any fees +or charges. If you are redistributing or providing access to a work +with the phrase "Project Gutenberg" associated with or appearing on the +work, you must comply either with the requirements of paragraphs 1.E.1 +through 1.E.7 or obtain permission for the use of the work and the +Project Gutenberg-tm trademark as set forth in paragraphs 1.E.8 or +1.E.9. + +1.E.3. If an individual Project Gutenberg-tm electronic work is posted +with the permission of the copyright holder, your use and distribution +must comply with both paragraphs 1.E.1 through 1.E.7 and any additional +terms imposed by the copyright holder. Additional terms will be linked +to the Project Gutenberg-tm License for all works posted with the +permission of the copyright holder found at the beginning of this work. + +1.E.4. Do not unlink or detach or remove the full Project Gutenberg-tm +License terms from this work, or any files containing a part of this +work or any other work associated with Project Gutenberg-tm. + +1.E.5. Do not copy, display, perform, distribute or redistribute this +electronic work, or any part of this electronic work, without +prominently displaying the sentence set forth in paragraph 1.E.1 with +active links or immediate access to the full terms of the Project +Gutenberg-tm License. + +1.E.6. You may convert to and distribute this work in any binary, +compressed, marked up, nonproprietary or proprietary form, including any +word processing or hypertext form. However, if you provide access to or +distribute copies of a Project Gutenberg-tm work in a format other than +"Plain Vanilla ASCII" or other format used in the official version +posted on the official Project Gutenberg-tm web site (www.gutenberg.org), +you must, at no additional cost, fee or expense to the user, provide a +copy, a means of exporting a copy, or a means of obtaining a copy upon +request, of the work in its original "Plain Vanilla ASCII" or other +form. Any alternate format must include the full Project Gutenberg-tm +License as specified in paragraph 1.E.1. + +1.E.7. Do not charge a fee for access to, viewing, displaying, +performing, copying or distributing any Project Gutenberg-tm works +unless you comply with paragraph 1.E.8 or 1.E.9. + +1.E.8. You may charge a reasonable fee for copies of or providing +access to or distributing Project Gutenberg-tm electronic works provided +that + +- You pay a royalty fee of 20% of the gross profits you derive from + the use of Project Gutenberg-tm works calculated using the method + you already use to calculate your applicable taxes. The fee is + owed to the owner of the Project Gutenberg-tm trademark, but he + has agreed to donate royalties under this paragraph to the + Project Gutenberg Literary Archive Foundation. Royalty payments + must be paid within 60 days following each date on which you + prepare (or are legally required to prepare) your periodic tax + returns. Royalty payments should be clearly marked as such and + sent to the Project Gutenberg Literary Archive Foundation at the + address specified in Section 4, "Information about donations to + the Project Gutenberg Literary Archive Foundation." + +- You provide a full refund of any money paid by a user who notifies + you in writing (or by e-mail) within 30 days of receipt that s/he + does not agree to the terms of the full Project Gutenberg-tm + License. You must require such a user to return or + destroy all copies of the works possessed in a physical medium + and discontinue all use of and all access to other copies of + Project Gutenberg-tm works. + +- You provide, in accordance with paragraph 1.F.3, a full refund of any + money paid for a work or a replacement copy, if a defect in the + electronic work is discovered and reported to you within 90 days + of receipt of the work. + +- You comply with all other terms of this agreement for free + distribution of Project Gutenberg-tm works. + +1.E.9. If you wish to charge a fee or distribute a Project Gutenberg-tm +electronic work or group of works on different terms than are set +forth in this agreement, you must obtain permission in writing from +both the Project Gutenberg Literary Archive Foundation and Michael +Hart, the owner of the Project Gutenberg-tm trademark. Contact the +Foundation as set forth in Section 3 below. + +1.F. + +1.F.1. Project Gutenberg volunteers and employees expend considerable +effort to identify, do copyright research on, transcribe and proofread +public domain works in creating the Project Gutenberg-tm +collection. Despite these efforts, Project Gutenberg-tm electronic +works, and the medium on which they may be stored, may contain +"Defects," such as, but not limited to, incomplete, inaccurate or +corrupt data, transcription errors, a copyright or other intellectual +property infringement, a defective or damaged disk or other medium, a +computer virus, or computer codes that damage or cannot be read by +your equipment. + +1.F.2. LIMITED WARRANTY, DISCLAIMER OF DAMAGES - Except for the "Right +of Replacement or Refund" described in paragraph 1.F.3, the Project +Gutenberg Literary Archive Foundation, the owner of the Project +Gutenberg-tm trademark, and any other party distributing a Project +Gutenberg-tm electronic work under this agreement, disclaim all +liability to you for damages, costs and expenses, including legal +fees. YOU AGREE THAT YOU HAVE NO REMEDIES FOR NEGLIGENCE, STRICT +LIABILITY, BREACH OF WARRANTY OR BREACH OF CONTRACT EXCEPT THOSE +PROVIDED IN PARAGRAPH 1.F.3. YOU AGREE THAT THE FOUNDATION, THE +TRADEMARK OWNER, AND ANY DISTRIBUTOR UNDER THIS AGREEMENT WILL NOT BE +LIABLE TO YOU FOR ACTUAL, DIRECT, INDIRECT, CONSEQUENTIAL, PUNITIVE OR +INCIDENTAL DAMAGES EVEN IF YOU GIVE NOTICE OF THE POSSIBILITY OF SUCH +DAMAGE. + +1.F.3. LIMITED RIGHT OF REPLACEMENT OR REFUND - If you discover a +defect in this electronic work within 90 days of receiving it, you can +receive a refund of the money (if any) you paid for it by sending a +written explanation to the person you received the work from. If you +received the work on a physical medium, you must return the medium with +your written explanation. The person or entity that provided you with +the defective work may elect to provide a replacement copy in lieu of a +refund. If you received the work electronically, the person or entity +providing it to you may choose to give you a second opportunity to +receive the work electronically in lieu of a refund. If the second copy +is also defective, you may demand a refund in writing without further +opportunities to fix the problem. + +1.F.4. Except for the limited right of replacement or refund set forth +in paragraph 1.F.3, this work is provided to you 'AS-IS' WITH NO OTHER +WARRANTIES OF ANY KIND, EXPRESS OR IMPLIED, INCLUDING BUT NOT LIMITED TO +WARRANTIES OF MERCHANTIBILITY OR FITNESS FOR ANY PURPOSE. + +1.F.5. Some states do not allow disclaimers of certain implied +warranties or the exclusion or limitation of certain types of damages. +If any disclaimer or limitation set forth in this agreement violates the +law of the state applicable to this agreement, the agreement shall be +interpreted to make the maximum disclaimer or limitation permitted by +the applicable state law. The invalidity or unenforceability of any +provision of this agreement shall not void the remaining provisions. + +1.F.6. INDEMNITY - You agree to indemnify and hold the Foundation, the +trademark owner, any agent or employee of the Foundation, anyone +providing copies of Project Gutenberg-tm electronic works in accordance +with this agreement, and any volunteers associated with the production, +promotion and distribution of Project Gutenberg-tm electronic works, +harmless from all liability, costs and expenses, including legal fees, +that arise directly or indirectly from any of the following which you do +or cause to occur: (a) distribution of this or any Project Gutenberg-tm +work, (b) alteration, modification, or additions or deletions to any +Project Gutenberg-tm work, and (c) any Defect you cause. + + +Section 2. Information about the Mission of Project Gutenberg-tm + +Project Gutenberg-tm is synonymous with the free distribution of +electronic works in formats readable by the widest variety of computers +including obsolete, old, middle-aged and new computers. It exists +because of the efforts of hundreds of volunteers and donations from +people in all walks of life. + +Volunteers and financial support to provide volunteers with the +assistance they need, are critical to reaching Project Gutenberg-tm's +goals and ensuring that the Project Gutenberg-tm collection will +remain freely available for generations to come. In 2001, the Project +Gutenberg Literary Archive Foundation was created to provide a secure +and permanent future for Project Gutenberg-tm and future generations. +To learn more about the Project Gutenberg Literary Archive Foundation +and how your efforts and donations can help, see Sections 3 and 4 +and the Foundation web page at http://www.pglaf.org. + + +Section 3. Information about the Project Gutenberg Literary Archive +Foundation + +The Project Gutenberg Literary Archive Foundation is a non profit +501(c)(3) educational corporation organized under the laws of the +state of Mississippi and granted tax exempt status by the Internal +Revenue Service. The Foundation's EIN or federal tax identification +number is 64-6221541. Its 501(c)(3) letter is posted at +http://pglaf.org/fundraising. Contributions to the Project Gutenberg +Literary Archive Foundation are tax deductible to the full extent +permitted by U.S. federal laws and your state's laws. + +The Foundation's principal office is located at 4557 Melan Dr. S. +Fairbanks, AK, 99712., but its volunteers and employees are scattered +throughout numerous locations. Its business office is located at +809 North 1500 West, Salt Lake City, UT 84116, (801) 596-1887, email +business@pglaf.org. Email contact links and up to date contact +information can be found at the Foundation's web site and official +page at http://pglaf.org + +For additional contact information: + Dr. Gregory B. Newby + Chief Executive and Director + gbnewby@pglaf.org + + +Section 4. Information about Donations to the Project Gutenberg +Literary Archive Foundation + +Project Gutenberg-tm depends upon and cannot survive without wide +spread public support and donations to carry out its mission of +increasing the number of public domain and licensed works that can be +freely distributed in machine readable form accessible by the widest +array of equipment including outdated equipment. Many small donations +($1 to $5,000) are particularly important to maintaining tax exempt +status with the IRS. + +The Foundation is committed to complying with the laws regulating +charities and charitable donations in all 50 states of the United +States. Compliance requirements are not uniform and it takes a +considerable effort, much paperwork and many fees to meet and keep up +with these requirements. We do not solicit donations in locations +where we have not received written confirmation of compliance. To +SEND DONATIONS or determine the status of compliance for any +particular state visit http://pglaf.org + +While we cannot and do not solicit contributions from states where we +have not met the solicitation requirements, we know of no prohibition +against accepting unsolicited donations from donors in such states who +approach us with offers to donate. + +International donations are gratefully accepted, but we cannot make +any statements concerning tax treatment of donations received from +outside the United States. U.S. laws alone swamp our small staff. + +Please check the Project Gutenberg Web pages for current donation +methods and addresses. Donations are accepted in a number of other +ways including checks, online payments and credit card donations. +To donate, please visit: http://pglaf.org/donate + + +Section 5. General Information About Project Gutenberg-tm electronic +works. + +Professor Michael S. Hart is the originator of the Project Gutenberg-tm +concept of a library of electronic works that could be freely shared +with anyone. For thirty years, he produced and distributed Project +Gutenberg-tm eBooks with only a loose network of volunteer support. + + +Project Gutenberg-tm eBooks are often created from several printed +editions, all of which are confirmed as Public Domain in the U.S. +unless a copyright notice is included. Thus, we do not necessarily +keep eBooks in compliance with any particular paper edition. + + +Most people start at our Web site which has the main PG search facility: + + http://www.gutenberg.org + +This Web site includes information about Project Gutenberg-tm, +including how to make donations to the Project Gutenberg Literary +Archive Foundation, how to help produce our new eBooks, and how to +subscribe to our email newsletter to hear about new eBooks. + + +</pre> + +</body> +</html> diff --git a/37675-h/images/fig_001.png b/37675-h/images/fig_001.png Binary files differnew file mode 100644 index 0000000..6c9485b --- /dev/null +++ b/37675-h/images/fig_001.png diff --git a/37675-h/images/fig_002.png b/37675-h/images/fig_002.png Binary files differnew file mode 100644 index 0000000..5a8fc19 --- /dev/null +++ b/37675-h/images/fig_002.png diff --git a/37675-h/images/fig_003.png b/37675-h/images/fig_003.png Binary files differnew file mode 100644 index 0000000..50e8c3d --- /dev/null +++ b/37675-h/images/fig_003.png diff --git a/37675-h/images/fig_004.png b/37675-h/images/fig_004.png Binary files differnew file mode 100644 index 0000000..124167f --- /dev/null +++ b/37675-h/images/fig_004.png diff --git a/37675-h/images/fig_005.png b/37675-h/images/fig_005.png Binary files differnew file mode 100644 index 0000000..2e66316 --- /dev/null +++ b/37675-h/images/fig_005.png diff --git a/37675-h/images/fig_006.png b/37675-h/images/fig_006.png Binary files differnew file mode 100644 index 0000000..108d965 --- /dev/null +++ b/37675-h/images/fig_006.png diff --git a/37675-h/images/fig_007.png b/37675-h/images/fig_007.png Binary files differnew file mode 100644 index 0000000..e039055 --- /dev/null +++ b/37675-h/images/fig_007.png diff --git a/37675-h/images/fig_008.png b/37675-h/images/fig_008.png Binary files differnew file mode 100644 index 0000000..c32cc31 --- /dev/null +++ b/37675-h/images/fig_008.png diff --git a/37675-h/images/fig_009.png b/37675-h/images/fig_009.png Binary files differnew file mode 100644 index 0000000..1a9c39e --- /dev/null +++ b/37675-h/images/fig_009.png diff --git a/37675-h/images/fig_010.png b/37675-h/images/fig_010.png Binary files differnew file mode 100644 index 0000000..219d1a9 --- /dev/null +++ b/37675-h/images/fig_010.png diff --git a/37675-h/images/fig_011.png b/37675-h/images/fig_011.png Binary files differnew file mode 100644 index 0000000..012d51f --- /dev/null +++ b/37675-h/images/fig_011.png diff --git a/37675-h/images/fig_012.png b/37675-h/images/fig_012.png Binary files differnew file mode 100644 index 0000000..8aa4f2f --- /dev/null +++ b/37675-h/images/fig_012.png diff --git a/37675-h/images/fig_013.png b/37675-h/images/fig_013.png Binary files differnew file mode 100644 index 0000000..ba2ebfc --- /dev/null +++ b/37675-h/images/fig_013.png diff --git a/37675-h/images/fig_014.png b/37675-h/images/fig_014.png Binary files differnew file mode 100644 index 0000000..0268129 --- /dev/null +++ b/37675-h/images/fig_014.png diff --git a/37675-h/images/fig_015.png b/37675-h/images/fig_015.png Binary files differnew file mode 100644 index 0000000..3a0032a --- /dev/null +++ b/37675-h/images/fig_015.png diff --git a/37675-h/images/fig_016.png b/37675-h/images/fig_016.png Binary files differnew file mode 100644 index 0000000..f0d388e --- /dev/null +++ b/37675-h/images/fig_016.png diff --git a/37675-h/images/fig_017.png b/37675-h/images/fig_017.png Binary files differnew file mode 100644 index 0000000..15019e5 --- /dev/null +++ b/37675-h/images/fig_017.png diff --git a/37675-h/images/fig_018.png b/37675-h/images/fig_018.png Binary files differnew file mode 100644 index 0000000..056b536 --- /dev/null +++ b/37675-h/images/fig_018.png diff --git a/37675-h/images/fig_019.png b/37675-h/images/fig_019.png Binary files differnew file mode 100644 index 0000000..a75d124 --- /dev/null +++ b/37675-h/images/fig_019.png diff --git a/37675-h/images/fig_020.png b/37675-h/images/fig_020.png Binary files differnew file mode 100644 index 0000000..fd5fba0 --- /dev/null +++ b/37675-h/images/fig_020.png diff --git a/37675-h/images/fig_021.png b/37675-h/images/fig_021.png Binary files differnew file mode 100644 index 0000000..4734f87 --- /dev/null +++ b/37675-h/images/fig_021.png diff --git a/37675-h/images/fig_022.png b/37675-h/images/fig_022.png Binary files differnew file mode 100644 index 0000000..3364027 --- /dev/null +++ b/37675-h/images/fig_022.png diff --git a/37675-h/images/fig_023.png b/37675-h/images/fig_023.png Binary files differnew file mode 100644 index 0000000..283ae98 --- /dev/null +++ b/37675-h/images/fig_023.png diff --git a/37675-h/images/fig_024.png b/37675-h/images/fig_024.png Binary files differnew file mode 100644 index 0000000..6c428ff --- /dev/null +++ b/37675-h/images/fig_024.png diff --git a/37675-h/images/fig_025.png b/37675-h/images/fig_025.png Binary files differnew file mode 100644 index 0000000..06a5f6e --- /dev/null +++ b/37675-h/images/fig_025.png diff --git a/37675-h/images/fig_026.png b/37675-h/images/fig_026.png Binary files differnew file mode 100644 index 0000000..630f023 --- /dev/null +++ b/37675-h/images/fig_026.png diff --git a/37675-h/images/fig_027.png b/37675-h/images/fig_027.png Binary files differnew file mode 100644 index 0000000..6aeeecd --- /dev/null +++ b/37675-h/images/fig_027.png diff --git a/37675-h/images/fig_028.png b/37675-h/images/fig_028.png Binary files differnew file mode 100644 index 0000000..84758ce --- /dev/null +++ b/37675-h/images/fig_028.png diff --git a/37675-h/images/fig_029.png b/37675-h/images/fig_029.png Binary files differnew file mode 100644 index 0000000..5ee54e3 --- /dev/null +++ b/37675-h/images/fig_029.png diff --git a/37675-h/images/fig_030.png b/37675-h/images/fig_030.png Binary files differnew file mode 100644 index 0000000..96d7ac1 --- /dev/null +++ b/37675-h/images/fig_030.png diff --git a/37675-h/images/fig_031.png b/37675-h/images/fig_031.png Binary files differnew file mode 100644 index 0000000..838156d --- /dev/null +++ b/37675-h/images/fig_031.png diff --git a/37675-h/images/fig_032.png b/37675-h/images/fig_032.png Binary files differnew file mode 100644 index 0000000..b987edf --- /dev/null +++ b/37675-h/images/fig_032.png diff --git a/37675-h/images/fig_033.png b/37675-h/images/fig_033.png Binary files differnew file mode 100644 index 0000000..8cf1300 --- /dev/null +++ b/37675-h/images/fig_033.png diff --git a/37675-h/images/fig_034.png b/37675-h/images/fig_034.png Binary files differnew file mode 100644 index 0000000..14882eb --- /dev/null +++ b/37675-h/images/fig_034.png diff --git a/37675-h/images/fig_035.png b/37675-h/images/fig_035.png Binary files differnew file mode 100644 index 0000000..352152c --- /dev/null +++ b/37675-h/images/fig_035.png diff --git a/37675-h/images/fig_036.png b/37675-h/images/fig_036.png Binary files differnew file mode 100644 index 0000000..a0f47ac --- /dev/null +++ b/37675-h/images/fig_036.png diff --git a/37675-h/images/fig_037.png b/37675-h/images/fig_037.png Binary files differnew file mode 100644 index 0000000..b1f5dca --- /dev/null +++ b/37675-h/images/fig_037.png diff --git a/37675-h/images/fig_038.png b/37675-h/images/fig_038.png Binary files differnew file mode 100644 index 0000000..38f4696 --- /dev/null +++ b/37675-h/images/fig_038.png diff --git a/37675-h/images/fig_039.png b/37675-h/images/fig_039.png Binary files differnew file mode 100644 index 0000000..4be8300 --- /dev/null +++ b/37675-h/images/fig_039.png diff --git a/37675-h/images/fig_040.png b/37675-h/images/fig_040.png Binary files differnew file mode 100644 index 0000000..69724c5 --- /dev/null +++ b/37675-h/images/fig_040.png diff --git a/37675-h/images/fig_041.png b/37675-h/images/fig_041.png Binary files differnew file mode 100644 index 0000000..e447ebe --- /dev/null +++ b/37675-h/images/fig_041.png diff --git a/37675-h/images/fig_042.png b/37675-h/images/fig_042.png Binary files differnew file mode 100644 index 0000000..42b9c28 --- /dev/null +++ b/37675-h/images/fig_042.png diff --git a/37675-h/images/fig_043.png b/37675-h/images/fig_043.png Binary files differnew file mode 100644 index 0000000..3e5f4fe --- /dev/null +++ b/37675-h/images/fig_043.png diff --git a/37675-h/images/fig_044.png b/37675-h/images/fig_044.png Binary files differnew file mode 100644 index 0000000..6090769 --- /dev/null +++ b/37675-h/images/fig_044.png diff --git a/37675-h/images/fig_045.png b/37675-h/images/fig_045.png Binary files differnew file mode 100644 index 0000000..7d7bd95 --- /dev/null +++ b/37675-h/images/fig_045.png diff --git a/37675-h/images/fig_046.png b/37675-h/images/fig_046.png Binary files differnew file mode 100644 index 0000000..5b2d0d6 --- /dev/null +++ b/37675-h/images/fig_046.png diff --git a/37675-h/images/fig_047.png b/37675-h/images/fig_047.png Binary files differnew file mode 100644 index 0000000..c386125 --- /dev/null +++ b/37675-h/images/fig_047.png diff --git a/37675-h/images/fig_048.png b/37675-h/images/fig_048.png Binary files differnew file mode 100644 index 0000000..339a616 --- /dev/null +++ b/37675-h/images/fig_048.png diff --git a/37675-h/images/fig_049.png b/37675-h/images/fig_049.png Binary files differnew file mode 100644 index 0000000..4cdb445 --- /dev/null +++ b/37675-h/images/fig_049.png diff --git a/37675-h/images/fig_050.png b/37675-h/images/fig_050.png Binary files differnew file mode 100644 index 0000000..4dbf3f7 --- /dev/null +++ b/37675-h/images/fig_050.png diff --git a/37675-h/images/fig_051.png b/37675-h/images/fig_051.png Binary files differnew file mode 100644 index 0000000..04710ba --- /dev/null +++ b/37675-h/images/fig_051.png diff --git a/37675-h/images/fig_052.png b/37675-h/images/fig_052.png Binary files differnew file mode 100644 index 0000000..7531580 --- /dev/null +++ b/37675-h/images/fig_052.png diff --git a/37675-h/images/fig_053.png b/37675-h/images/fig_053.png Binary files differnew file mode 100644 index 0000000..f102bf7 --- /dev/null +++ b/37675-h/images/fig_053.png diff --git a/37675-h/images/fig_054.png b/37675-h/images/fig_054.png Binary files differnew file mode 100644 index 0000000..ca42e2a --- /dev/null +++ b/37675-h/images/fig_054.png diff --git a/37675-h/images/fig_055.png b/37675-h/images/fig_055.png Binary files differnew file mode 100644 index 0000000..937fb8a --- /dev/null +++ b/37675-h/images/fig_055.png diff --git a/37675-h/images/fig_056.png b/37675-h/images/fig_056.png Binary files differnew file mode 100644 index 0000000..c8b8902 --- /dev/null +++ b/37675-h/images/fig_056.png diff --git a/37675-h/images/fig_057.png b/37675-h/images/fig_057.png Binary files differnew file mode 100644 index 0000000..1c2e1c9 --- /dev/null +++ b/37675-h/images/fig_057.png diff --git a/37675-h/images/fig_058.png b/37675-h/images/fig_058.png Binary files differnew file mode 100644 index 0000000..f47c9b3 --- /dev/null +++ b/37675-h/images/fig_058.png diff --git a/37675-h/images/fig_059.png b/37675-h/images/fig_059.png Binary files differnew file mode 100644 index 0000000..060f5c5 --- /dev/null +++ b/37675-h/images/fig_059.png diff --git a/37675-h/images/fig_060.png b/37675-h/images/fig_060.png Binary files differnew file mode 100644 index 0000000..3939b74 --- /dev/null +++ b/37675-h/images/fig_060.png |
