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THE NETTER COLLECTION
of Medical Illustrations
2nd Edition
Reproductive System
Endocrine System
Respiratory System
Integumentary System
Urinary System
Musculoskeletal System
Digestive System
Nervous System
Cardiovascular System
VOLUME 8
The Netter Collection
OF MEDICAL ILLUSTRATIONS
Cardiovascular System
2nd Edition
A compilation of paintings prepared by
Frank H. Netter, MD
Edited by
C. Richard Conti, MD, MACC, FESC, FAHA
Emeritus Professor of Medicine
University of Florida College of Medicine
Gainesville, Florida
Additional Illustrations by Carlos A. G. Machado, MD
CONTRIBUTING ILLUSTRATORS
Tiffany S. DaVanzo, MA, CMI
John A. Craig, MD
James A. Perkins, MS, MFA
Anita Impagliazzo, MA, CMI
1600 John F. Kennedy Blvd.
Ste. 1800
Philadelphia, PA 19103-2899
THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS: ISBN: 978-1-4557-4229-5
CARDIOVASCULAR SYSTEM, VOLUME 8, SECOND EDITION
Copyright © 2014 by Saunders, an imprint of Elsevier Inc.
No part of this publication may be reproduced or transmitted in any form or by any means, electronic
or mechanical, including photocopying, recording, or any information storage and retrieval system,
without permission in writing from the publisher. Details on how to seek permission, further
information about the Publisher’s permissions policies and our arrangements with organizations such as
the Copyright Clearance Center and the Copyright Licensing Agency can be found at our website:
www.elsevier.com/permissions.
This book and the individual contributions contained in it are protected under copyright by the
Publisher (other than as may be noted herein).
Permission for Netter Art figures may be sought directly from Elsevier’s Health Science Licensing
Department in Philadelphia, PA: phone 1-800-523-1649, ext. 3276, or (215) 239-3276; or email
[email protected]
Notices
Knowledge and best practice in this field are constantly changing. As new research and experience
broaden our understanding, changes in research methods, professional practices, or medical
treatment may become necessary.
Practitioners and researchers must always rely on their own experience and knowledge in
evaluating and using any information, methods, compounds, or experiments described herein. In
using such information or methods they should be mindful of their own safety and the safety of
others, including parties for whom they have a professional responsibility.
With respect to any drug or pharmaceutical products identified, readers are advised to check the
most current information provided (i) on procedures featured or (ii) by the manufacturer of each
product to be administered, to verify the recommended dose or formula, the method and duration
of administration, and contraindications. It is the responsibility of practitioners, relying on their own
experience and knowledge of their patients, to make diagnoses, to determine dosages and the best
treatment for each individual patient, and to take all appropriate safety precautions.
To the fullest extent of the law, neither the Publisher nor the authors, contributors, or editors,
assume any liability for any injury and/or damage to persons or property as a matter of products
liability, negligence or otherwise, or from any use or operation of any methods, products,
instructions, or ideas contained in the material herein.
ISBN: 978-1-4557-4229-5
Senior Content Strategist: Elyse O’Grady
Content Development Manager: Marybeth Thiel
Publishing Services Manager: Patricia Tannian
Senior Project Manager: John Casey
Senior Design Manager: Lou Forgione
Printed in China
Last digit is the print number: 9 8 7 6 5 4 3 2 1
ABOUT THE SERIES
Dr. Frank Netter at work. Dr. Frank H. Netter exemplified the CUSHING’S SYNDROME IN A PATIENT WITH THE CARNEY COMPLEX
The single-volume “blue book” that paved the way for distinct vocations of doctor, artist,
the multivolume Netter Collection of Medical Illustrations and teacher. Even more important, Carney complex is characterized
series, affectionately known as the “green books.” he unified them. Netter’s illustrations by spotty skin pigmentation.
always began with meticulous research Pigmented lentigines and blue
into the forms of the body, a philosophy nevi can be seen on the face–
that steered his broad and deep medical including the eyelids, vermillion
understanding. He often said: “Clarifi- borders of the lips, the
cation is the goal. No matter how beau- conjunctivae, the sclera–and the
tifully it is painted, a medical illustration labia and scrotum.
has little value if it does not make clear Additional features of the
a medical point.” His greatest challenge Carney complex can include:
and greatest success was charting a
middle course between artistic clarity Myxomas: cardiac atrium,
and instructional complexity. That cutaneous (e.g., eyelid),
success is captured in this series, begin- and mammary
ning in 1948, when the first compre- Testicular large-cell
hensive collection of Netter’s work, a calcifying Sertoli cell tumors
single volume, was published by CIBA Growth-hormone
Pharmaceuticals. It met with such success that over the secereting pituitary adenomas
following 40 years the collection was expanded into an Psammomatous
8-volume series—each devoted to a single body system. melanotic schwannomas
In this second edition of the legendary series, we are
delighted to offer Netter’s timeless work, now arranged PPNAD adrenal glands are usually of normal size and most are
and informed by modern text and radiologic imaging studded with black, brown, or red nodules. Most of the pigmented
contributed by field-leading doctors and teachers from nodules are less than 4 mm in diameter and interspersed in the
world-renowned medical institutions and supplemented adjacent atrophic cortex.
with new illustrations created by artists working in the
Netter tradition. Inside the classic green covers, stu- A brand new illustrated plate painted by Carlos
dents and practitioners will find hundreds of original Machado, MD, for The Endocrine System Volume 2.
works of art—the human body in pictures—paired with
the latest in expert medical knowledge and innovation, Dr. Carlos Machado at work.
and anchored in the sublime style of Frank Netter.
Notable artist-physician, Carlos Machado, MD, the
primary successor responsible for continuing the Netter
tradition, has particular appreciation for the “green
book” series: “The Reproductive System is of special sig-
nificance for those who, like me deeply admire Dr. Netter’s
work. In this volume, he masters the representation of tex-
tures of different surfaces, which I like to call ‘the rhythm of
the brush,’ since it is the dimension, the direction of the
strokes and the interval separating them that create the illu-
sion of given textures: organs have their external surfaces,
the surfaces of their cavities, and texture of their parenchy-
mas realistically represented. It set the style for the subsequent
volumes of Netter’s Collection, each an amazing combination
of painting masterpieces and precise scientific information.”
Though the science and teaching of medicine endures
changes in terminology, practice, and discovery, some
things remain the same. A patient is a patient. A teacher
is a teacher. And the pictures of Dr. Netter—he called
them pictures, never paintings—remain the same blend
of beautiful and instructional resources that have guided
physicians’ hands and nurtured their imaginations for
over half a century.
The original series could not exist without the dedi-
cation of all those who edited, authored, or in other
ways contributed, nor, of course, without the excellence
of Dr. Netter. For this exciting second edition, we also
owe our gratitude to the authors, editors, Advisors, and
artists whose relentless efforts were instrumental in
adapting these timeless works into reliable references
for today’s clinicians in training and in practice. From
all of us with the Netter Publishing Team at Elsevier,
we thank you.
THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS v
ABOUT THE AUTHOR
C. Richard Conti, MD, MACC, held an endowed cardiology training at Johns Hopkins and served on the the Gifted Teacher Award by the American College of
chair entitled “Palm Beach Heart Association cardiology faculty at that institution from 1968 through Cardiology and received the Italian Society of Cardiol-
Eminent Scholar” (Clinical Cardiology) and was Pro- 1974 when, at the age of 39, he became Professor of ogy Distinguished Mentor and Scientist Award. He
fessor of Medicine and Adjunct Professor of Physiology Medicine and Director of the Cardiovascular Division served for 24 years as Editor-in-Chief of the interna-
at the University of Florida College of Medicine. He is at the University of Florida. tional journal, Clinical Cardiology, and served 10 years as
a distinguished 1952 graduate of Central Catholic High Editor-in-Chief of the ACC Audio Journal ACCEL
School in Allentown, Pennsylvania, a 1956 Phi Beta Dr. Conti was President of the American College of from 1999 to 2010. He is currently Emeritus Professor
Kappa graduate of Lehigh University, and a 1960 AOA Cardiology and received an Honorary Fellowship from of Medicine at the University of Florida College of
graduate of Johns Hopkins University School of Medi- the College of Medicine of South Africa. He was elected Medicine.
cine. He received his medical training on the Osler to the Johns Hopkins University Society of Scholars
Medical Service of the Johns Hopkins Hospital and his and received a “Docteur Honoris Causa” from the
University of Marseilles. Dr. Conti was selected for
vi THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS
PREFACE AND DEDICATION
PREFACE Despite this requirement, the original artwork is spec- introduced, for example, transcutaneous aortic valve
Unfortunately I did not have the good fortune to know tacular and remains so. Several medical artists working replacement (TAVR).
Dr. Netter personally, but as I read the introduction with Dr. Netter also contributed illustrations that I
written years ago by his wife, Vera Netter, I got the have included in this new edition. This new edition of Netter’s The Heart, now titled
distinct impression that, as she put it, “He was genius Cardiovascular System, comprises six sections, including
at what he did.” Several important new diagnostic and therapeutic anatomy, physiology and pathophysiology, cardiac
concepts have evolved over the past 40 years since the imaging, cardiac embryology, congenital heart disease,
When I first received my copy of The Heart, by initial 1969 printing was published. For example, and acquired heart disease (Section 6). Section 6 is a
Frank Netter, in the 1960s (first printing, 1969) I was cardiac ultrasound is not mentioned in the early edition large section that includes subsections on acute coro-
greatly impressed by the quality of the illustrations nor are four major imaging methods now used: nary syndromes, new information on treatment of car-
and the accompanying text. From the outset it was computed tomographic imaging, magnetic resonance diopulmonary arrest, syncope, sudden cardiac death in
apparent that this was not a textbook of cardiovascu- imaging, nuclear imaging, and angiography. Thus a young athletes, HIV/AIDS and the heart, sleep apnea,
lar medicine and surgery. If one needed to know the new section has been added on imaging, since imaging endocrine disorder and the heart, and collagen vascular
details to perform a procedure or an operation, books plays a major role in modern diagnosis and therapy of diseases and the heart.
that are dedicated to those subjects must be con- cardiac disease. Several new therapeutic areas have
sulted. This book is an effective companion to text- been added, including the medical therapy of acute I need to express my thanks to Marybeth Thiel and
books of cardiovascular medicine and surgery or myocardial infarction, heart failure, arrhythmias, pacing Elyse O’Grady at Elsevier for their oversight, help, and
electronic resources specific to cardiovascular subjects. strategies including biventricular pacing, and cardiac direction of this work . They helped clarify the meaning
I find the illustrations particularly useful as teaching resynchronization therapy in heart failure patients. of many statements I made in the early drafts of this
aids when trying to get across to medical students work. They were tough on me, but they made the book
and young physicians the principles of cardiovascular Although coronary artery surgery was mentioned in a more readable text.
disease. the first edition, coronary artery bypass graft surgery
with saphenous vein grafts or with internal thoracic C. Richard Conti, MD
In 2012 I accepted the challenge and undertook the artery bypass of stenotic epicardial lesions as we know November 2013
task to update the book at the request of the publisher, it now is new. Valve surgery also has changed. Although
Elsevier. I very quickly came to realize that I was not the initial illustrations of early valve surgery using the DEDICATION
quite as smart as I thought I was about cardiovascular Starr Edwards ball valve prosthesis, Beall valve, and This book is dedicated to all the cardiovascular fellows,
matters. So, on many occasions, I informally consulted Hufnagel valve were important in the evolution of valve faculty, and other colleagues at Johns Hopkins School
with many friends about several old and new topics replacement, these procedures are no longer done. of Medicine and the University of Florida College of
contained in the original version of The Heart. Since the Thus I have added illustrations of currently used Medicine that I have worked with and who have taught
text accompanying the illustrations was written in the valve prostheses for aortic valve disease, mitral valve, me practically everything I know about cardiovascular
1960s, an update was needed because of the many and tricuspid valve problems. In addition, interven- medicine.
changes in cardiovascular disease diagnosis and therapy. tional procedures that affect valve function are also
THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS vii
ABOUT THE ARTIST FROM THE FIRST EDITION
What’s it like to be married to a genius? I can tell essence of the subject and organization his presenta- with colorful plants, but the pride of the terrace is the
you—it’s wonderful! My genius doesn’t act the tion. The immediate relaxation and response is electric. tomatoes that my husband cultivates and nurtures all
way people think a genius is supposed to act. He is a Most fascinating to me, however, is to see the glow of spring and summer and then serves with his barbecued
very simple, warm personality who enjoys the ordinary satisfaction which invariably suffuses the face of the steaks. Frank is an early riser but cannot begin the day
everyday things of life. Indeed, he is so taken up with consultant when he sees his lifework graphically before the newspaper is delivered so he can see how
these matters—with me, with the children, his friends, depicted and clarified by the pencil and brush of my “Dick Tracy” and his other cartoon friends have fared.
the stock market, his golf—that I often wonder how he husband’s. In most instances these associations have led His studio is on the lower floor of our duplex and his
manages to create all the pictures he does. On occasion, to long, sincere friendships. usual day there beings at 8 in the morning and lasts to
when he has completed a large series of pictures, I have 4 in the afternoon, but when he is under pressure he
asked him, “Frank, how did you manage to do all Frank also loves languages—and they come to him may keep going till 6 or later. In his early days he
these?” He has answered me, “You know, darling, the very naturally—but time will never permit him to really would often work until 3 or 4 in the morning and
difficult thing about making medical pictures is not study seriously. Once when we were in Switzerland he sometimes right through the night, but now he abhors
the painting at all but rather the study, the thinking, the was somewhat troubled because he learned that the two such hours and refuses to work at night regardless of
planning, the creation of a picture so that it says some- doctors he had wished to consult that morning at the the pressure. His work attire surprises even me some-
thing. Once I have the picture in my mind it is easy to University spoke no English. That evening I went a times. It consists of a pair of paint-stained slacks and
put it on paper.” I know that he is thinking about his little early to meet him at the hospital, expecting to have bright plaid shirt and, to my horror, he often neglects
pictures in the middle of the night when he tosses about my ear filled with his frustration at communicating, to change when he has an outside appointment and
restlessly in bed, in the midst of a conversation when when, through the door, I was dumbfounded to hear a ventures forth in this attire with simply the addition of
he becomes a little detached, or on the golf course when most familiar voice speaking Italian as though he had a jacket, even though his closets are full of clothes. On
occasionally he makes a poor shot. I know also when he never been out of Italy. He says that if he drinks Chianti one occasion, when one of the many aspiring students
is troubled by a particularly difficult problem; then he he can talk Italian, if the drinks champagne he can talk who come to ask his counsel appeared at the house,
sits very quietly and withdrawn, curling a forelock of French, if he eats knockwurst he can talk German. Frank opened the door in his customary work attire
his hair. But, once the problem is solved he becomes his (They must have served Chianti!) and the young man looked at him and said, “I have an
usual outgoing, friendly self again. appointment with your father, Dr. Netter.” When
In English, Frank is very articulate. He is often Frank told him that he was Dr. Netter, his mouth feel
We travel considerably in quest of the knowledge asked to speak at various medical assemblies because open and he said, “But with all those drawings and
that my husband pictorializes and it is always amazing people seem to want to know about his unusual career. books I though you would be an old man.” Frank got
to me, after having been told of the very great scientist Unfortunately, he cannot accept most of these invita- a real chuckle out of that.
we are to meet, to find the scientist is more impressed tions because of time limitations. When he does agree
in having the opportunity of meeting him. It is this to speak, I become nervous as the day of the address The letters received from all parts of the world in all
humility and unconsciousness of his own great gift that approaches and I see him making no preparation. Just languages, even from behind the “Iron Curtain,” attest
endears him to so many. At these meetings it is also before the meeting he will sit down for 15 minutes to the great utility of these books and give Frank the
very interesting to note the great scientist’s surprise to and plan what he will say! He believes that too much strength and desire to go on to the next one, vowing to
find that this artist can converse with him on his own preparation makes a speech stilted and dull. Then make each better than the last to the end that those who
plane regardless of whether the subject be neurophysi- he gets up on the rostrum and delights his audience use them may have the final word in pictorial medicine
ology, thoracic surgery, anatomy, biochemistry, ortho- with philosophy, narrative, and humor as he speaks as it has been given to him.
paedics, or any other phase of medical science. They extemporaneously.
are always amazed to see how quickly he grasps the Vera Netter
We live in Manhattan in an apartment overlooking
the East River. In the spring I decorate the terrace
viii THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS
INTRODUCTION TO THE FIRST EDITION
With each volume that I have undertaken in The about the circulatory system than in the three hundred progress. And so I herewith express my appreciation to
CIBA Collection of Medical Illustrations, I have and fifty thousand years preceding it. In 1902 William these, my collaborators. Without them, this book
vowed at the outset to execute it with great expedition Einthoven devised the string galvanometer, and shortly would, of course, have been impossible; with them, it
and simplicity. But in every case the task has proved to thereafter it was applied, by Sir James Mackenzie and was a joy and a great adventure. To have met them, to
be much more complex and difficult than I had antici- by Sir Thomas Lewis, to the study of the heartbeat, have come to know them, to have worked with them
pated. As I became involved and absorbed in the subject based on the fundamental studies of the cardiac conduc- was a memorable experience. I thank them all for the
matter, many facets of the various topics came to light tion system of Gaskell. Thus, modern cardiology was time they gave me, for the knowledge they imparted
that demanded pictorialization. Just as when a skin born some sixty-five years ago. But it continued to grow to me, for the material with which they supplied me,
diver plunges beneath the surface of a calm sea, he does and mature, nurtured by many, many men and women and above all, for the friendship which they extended
not realize what a myriad of hidden phenomena are to who are too numerous to mention here. Finally came to me.
come into his view, so have I repeatedly discovered new the advent of cardiac surgery, given tremendous
and marvelous worlds beneath the superficial concepts. impetus, within the past two decades, by the practical One collaborator in particular, however, I must single
But, in the case of this volume on the heart, these application of extracorporeal circulation. And, just out, namely, Dr. L. H. S. Van Mierop, who has become
factors have been even more pronounced. They were before this book went to press, the first cardiac trans- simply “Bob” to me. Here is a man, warm and friendly
amplified by the fact that the sea of knowledge in which plants were performed and we were able to include by nature, forthright and simple in demeanor, yet
I was swimming kept continuously rising and expand- something about them herein. Thus, although our imbued with an insatiable quest for truth and the com-
ing. New facts were being discovered, new concepts knowledge of heart function and heart disease may prehension of fundamentals. And his great talents have
evolved, new methods and technics developed. I had seem slow in the perspective of a man’s lifetime, it has enabled him to follow this latter bent, so that he is at
difficulty in keeping abreast of them with my studies as been extremely rapid and, indeed, geometrically accel- once clinician, anatomist, embryologist, investigator,
well as with my pencil and brush. But the exploration erating in the light of human history. It is significant student, and teacher. Because of his contributions, I
was always stimulating and inspiring—so much so that also that as each new step forward was made, it neces- believe that the sections on embryology and on con-
I might have gone on indefinitely expanding, revising, sitated going back and restudying fundamentals. The genital heart disease are both original and classic.
and adding, with the result that the book might never advent of cardiac surgery necessitated a restudy of heart
have appeared. I therefore had to call a halt, although anatomy; the correction of cardiac anomalies called for I wish to thank also, Dr. Fredrick F. Yonkman, the
I am aware that, even as this book goes to press, the a reappraisal of embryology; the discovery of new drugs Editor, for the care and devotion which he gave to this
pace of progress is accelerating. impelled a deeper analysis of cardiac physiology. work. Dr. Yonkman, Mr. A. W. Custer, and other execu-
tives of the CIBA Pharmaceutical Company have
The rate of this acceleration becomes evident in the But progress has not ceased. On the contrary, it encouraged and helped me in every way possible. But
light of a multitude of accomplishments. Somewhat less moves constantly onward at an ever-increasing pace. In the concept, and indeed the origination of this series of
than three hundred and fifty years ago, William Harvey the preparation of this volume it has been a great plea- volumes, must be credited to the foresight and vision
established the concept of the circulation of the blood, sure as well as a great intellectual stimulation to have of Mr. Paul W. Roder of the CIBA company.
and, since that epochal event, more has been learned collaborated with so many men who are catalyzing this
Frank H. Netter, MD
THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS ix
ADVISORY BOARD
A. John Camm, QHP, MD Anthony DeMaria, MD Bruce T. Liang, MD
Professor of Clinical Cardiology Professor of Medicine Director, The Pat and Jim Calhoun Cardiovascular
Department of Cardiac and Vascular Sciences Judith and Jack White Chair in Cardiology
St. George’s Hospital Medical Center Director, Cardiovascular Center Center
London, UK University of California San Diego Medical Center Ray Neag Distinguished Professor of Cardiovascular
Larry Cochard, PhD Division of Cardiovascular Medicine
Associate Professor San Diego, California Biology and Medicine
Northwestern University Eugenio Gaudio, MD University of Connecticut Health Center
The Feinberg School of Medicine Professor, Dipartimento di Anatomia Umana Farmington, Connecticut
Chicago, Illinois Universitá degli Studi di Roma “la Sapienza” Robert Roberts, MD, MACC
J. Michael Criley, MD Rome, Italy President and CEO
Professor Emeritus Hyo-Soo Kim, MD, PhD University of Ottawa Heart Institute
David Geffen School of Medicine Director of Cardiac Catheterization Laboratory and Professor of Medicine
University of California, Los Angeles Director, Ruddy Canadian Cardiovascular Genetics
Los Angeles, California Coronary Intervention
Director of National Research Laboratory for Centre
Ottawa, Ontario, Canada
Cardiovascular Stem Cells
Professor, Department of Internal Medicine
Seoul National University Hospital
Seoul, Korea
x THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS
CONTENTS
SECTION 1—ANATOMY 2-18 Cardiac Depolarization and 4-5 Formation of the Heart Loop: 10-Somite
1-1 Thorax: Lungs in Situ: Anterior View, 2 Repolarization and Mean Instantaneous and 14-Somite Stages, 76
1-2 Thorax: Heart in Situ, 3 Vectors: End of Depolarization Followed
1-3 Thorax: Mediastinum: Cross Section, 4 by Repolarization, 37 4-6 Formation of the Heart Loop: 20-Somite
1-4 Thorax: Pericardial Sac, 5 Stage, 77
1-5 Exposure of the Heart: Anterior 2-19 Axis Deviation in Normal
Electrocardiogram, 38 4-7 Formation of Cardiac Septa: Development
Exposure, 6 of Ventricles and Atrioventricular
1-6 Exposure of the Heart: Base and 2-20 Atrial Enlargement, 39 Valves, 78
2-21 Ventricular Hypertrophy, 40
Diaphragmatic Surfaces, 7 2-22 Bundle Branch Block, 41 4-8 Formation of Cardiac Septa: 27 and 29
1-7 Atria and Ventricles: Right Atrium and 2-23 Wolff-Parkinson-White Syndrome, 42 Days, 79
2-24 Sinus and Atrial Arrhythmias, 43
Right Ventricle, 8 2-25 Premature Contraction, 44 4-9 Formation of Cardiac Septa: 31 and 33
1-8 Atria and Ventricles: Left Atrium and Left 2-26 Sinus Arrest, Sinus Block, and Days, 80
Ventricle, 9 Atrioventricular Block, 45 4-10 Formation of Cardiac Septa: 37 and 55
1-9 Atria and Ventricles: Atria, Ventricles, and 2-27 Tachycardia, Fibrillation, and Atrial Days, 81
Interventricular Septum, 10 Flutter, 46 4-11 Formation of Cardiac Septa: Heart Tube
1-10 Valves: Cardiac Valves Open and 2-28 Effect of Digitalis and Calcium/ Derivatives, 82
Closed, 11 Potassium Levels on 4-12 Formation of Cardiac Septa: Partitioning
1-11 Valves: Valves and Fibrous Skeleton of Electrocardiogram, 47 of the Heart Tube: Atrial Septation, 83
2-29 Cardiac Pacing: Dual Chamber and
Heart, 12 Biventricular, 48 4-13 Formation of Cardiac Septa: Embryonic
1-12 Specialized Conduction System of Origins, Right and Left Sides, 84
SECTION 3—IMAGING
Heart, 13 3-1 Radiology: Frontal Projection, 50 4-14 Development of Major Blood Vessels: 3,
1-13 Coronary Arteries and Cardiac Veins: 3-2 Radiology: Right Anterior Oblique 4, and 10 mm, 85
Sternocostal and Diaphragmatic Projection, 51 4-15 Development of Major Blood Vessels: 14
Surfaces, 14 3-3 Radiology: Left Anterior Oblique mm, 17 mm, and at Term, 86
1-14 Coronary Arteries and Cardiac Veins:
Arteriovenous Variations, 15 Projection, 52 4-16 Development of Major Blood Vessels: 4,
1-15 Innervation of Heart: Nerves of 3-4 Radiology: Lateral Projection, 53 10, and 14 mm, 87
Heart, 16 3-5 Angiocardiography: Anteroposterior
1-16 Innervation of Heart: Schema of 4-17 Development of Major Blood Vessels: 7
Innervation, 17 Projection of Right-Sided Heart mm, 24 mm, and at Term, 88
Structures, 54
SECTION 2—PHYSIOLOGY 3-6 Angiocardiography: Lateral Projection of 4-18 Fetal Circulation Pattern and Changes at
2-1 Cardiovascular Examination: Events in Right-Sided Heart Structures, 55 Birth, 89
3-7 Angiocardiography: Anteroposterior
the Cardiac Cycle: Left Ventricle, 20 Projection of Left-Sided Heart 4-19 Three Early Vascular Systems, 90
2-2 Cardiovascular Examination: Structures, 56
3-8 Angiocardiography: Lateral Projection of SECTION 5—CONGENITAL HEART
Important Components of Cardiac Left-Sided Heart Structures, 57 DISEASE
Examination, 21 3-9 Catheter-Based Coronary Angiography: 5-1 Physical Examination: Diagnostic
2-3 Cardiovascular Examination: Positions for Right Coronary Artery: Arteriographic
Cardiac Auscultation, 22 Views, 58 Clues to Congenital Heart
2-4 Cardiovascular Examination: Areas of 3-10 Catheter-Based Coronary Angiography: Disease, 92
Cardiac Auscultation, 23 Left Coronary Artery: Arteriographic 5-2 Cardiac Vein Anomalies, 93
2-5 Cardiovascular Examination: Views, 59 5-3 Total Anomalous Pulmonary Venous
Murmurs, 24 3-11 Intravascular Ultrasound, 60 Connection, 94
2-6 Neural and Humoral Regulation of 3-12 Transthoracic Cardiac Ultrasound, 61 5-4 Surgery for Anomalous Pulmonary
Cardiac Function, 25 3-13 Doppler Echocardiography, 62 Venous Return, 95
2-7 Physiologic Changes During 3-14 Transesophageal Echocardiography, 63 5-5 Anomalies of the Atria, 96
Pregnancy, 26 3-15 Exercise and Contrast 5-6 Defects of the Atrial Septum:
2-8 Cardiac Catheterization: Vascular Echocardiography, 64 Anatomy, 97
Access, 27 3-16 Myocardial Perfusion Imaging, 65 5-7 Defects of the Atrial Septum:
2-9 Cardiac Catheterization: Left-Sided Heart 3-17 Ventriculography, 66 Surgery, 98
Catheterization, 28 3-18 Computed Tomographic Angiography: 5-8 Defects of the Atrial Septum: Septal
2-10 Cardiac Catheterization: Normal Cardiac Cycle and Calcium Contrast Occluder Device, 99
Saturations (O2) and Pressure, 29 Studies, 67 5-9 Endocardial Cushion Defects: Anatomy
2-11 Cardiac Catheterization: Examples of O2 3-19 Computed Tomographic Angiography: and Embryology, 100
and Pressure Findings and Pressure Interpretation, 68 5-10 Endocardial Cushion Defects: Surgery for
Tracings in Heart Diseases, 30 3-20 Cardiac Magnetic Resonance Ostium Primum and Cleft Mitral
2-12 Cardiac Catheterization: Normal Cardiac Imaging, 69 Valve, 101
Blood Flow During Inspiration and 3-21 Cardiac Magnetic Resonance Imaging 5-11 Anomalies of Tricuspid Valve: Tricuspid
Expiration, 31 (Continued), 70 Atresia, 102
2-13 Specialized Conduction System: 5-12 Anomalies of Tricuspid Valve: Glenn
Physiology of Specialized Conduction SECTION 4—EMBRYOLOGY Surgery for Tricuspid Atresia, 103
System, 32 4-1 Early Embryonic Development, 72 5-13 Anomalies of Tricuspid Valve: Ebstein’s
2-14 Specialized Conduction System: Electrical 4-2 Early Intraembryonic Vasculogenesis, 73 Anomaly, 104
Activity of the Heart, 33 4-3 Formation of the Heart Tube: One-Somite 5-14 Anomalies of Tricuspid Valve: Types of
2-15 Electrocardiogram, 34 Ebstein’s Anomaly, 105
2-16 Electrocardiographic Leads and Reference and Two-Somite Stages, 74 5-15 Anomalies of the Ventricular
Lines, 35 4-4 Formation of the Heart Tube: Four-Somite Septum, 106
2-17 Cardiac Depolarization and 5-16 Anomalies of the Ventricular Septum
Repolarization and Mean Instantaneous and Seven-Somite Stages, 75 (Continued), 107
Vectors: Progression of 5-17 Anomalies of the Ventricular Septum:
Depolarization, 36 Transatrial Repair of Ventricular Septal
Defect, 108
5-18 Anomalies of Right Ventricular
Outflow Tract: Tetralogy of
Fallot, 109
THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS xi
Contents
5-19 Anomalies of Right Ventricular Outflow 6-15 Chronic Angina Revascularization PROSTHETIC VALVE SURGERY
Tract: Pathophysiology and Blalock- Procedures: Rotational Atherectomy and 6-50 First Generation of Synthetic Prosthetic
Taussig Operation for Tetralogy of Distal Protection Device, 148
Fallot, 110 Valves, 183
ACUTE CORONARY SYNDROMES 6-51 Second Generation of Synthetic Prosthetic
5-20 Anomalies of Right Ventricular Outflow 6-16 Pathophysiology of Acute Coronary
Tract: Corrective Operation for Tetralogy Valves and Biologic Valves, 184
of Fallot, 111 Syndromes, 149 6-52 Mitral Valve Replacement, 185
6-17 Myocardial Infarction: Changes in the 6-53 Aortic Valve Replacement, 186
5-21 Anomalies of Right Ventricular Outflow 6-54 Excision of Aortic Aneurysm and
Tract: Repair of Tetralogy of Fallot, 112 Heart, 150
6-18 Myocardial Infarction: Changes in the Replacement of Aortic Valve for Cystic
5-22 Anomalies of Right Ventricular Outflow Medial Necrosis, 187
Tract: Eisenmenger Complex and Double- Heart (Continued), 151 6-55 Multiple Valve Replacement, 188
Outlet Right Ventricle, 113 6-19 Myocardial Infarction: Changes in the 6-56 Insertion of Trileaflet Aortic Valve, 189
6-57 Aortic Valve Biologic Grafts, 190
5-23 Anomalies of Right Ventricular Outflow Heart (Continued), 152
Tract: Pulmonary Valvular Stenosis and 6-20 Myocardial Infarction: Changes in the TRICUSPID VALVE DISEASE
Atresia, 114 6-58 Tricuspid Stenosis and Regurgitation and
Heart (Continued), 153
5-24 Anomalies of Left Ventricular Outflow 6-21 Manifestations of Myocardial Infarction: Multivalvular Disease, 191
Tract: Aortic Atresia, Bicuspid Aortic 6-59 Tricuspid Stenosis and/or
Valve, and Aortic Valvular Stenosis, 115 First Day to Several Weeks, 154
6-22 Manifestations of Myocardial Infarction: Insufficiency, 192
5-25 Anomalies of Left Ventricular Outflow
Tract: Fibrous and Idiopathic Effects of Myocardial Ischemia, Injury, AMYLOIDOSIS, MYOCARDITIS, AND OTHER
Hypertrophic Subaortic Stenoses, 116 and Infarction on ECG, 155 CARDIOMYOPATHIES
6-23 Recanalization of Occluded Coronary 6-60 Amyloidosis, 193
5-26 Anomalies of Left Ventricular Outflow Artery in Acute Myocardial 6-61 Septic Myocarditis, 194
Tract: Norwood Correction of Hypoplastic Infarction, 156 6-62 Diphtheritic and Viral Myocarditis, 195
Left Heart Syndrome, 117 6-24 Intra-aortic Balloon 6-63 Myocarditis in Sarcoidosis and
Counterpulsation, 157
5-27 Transposition of the Great Vessels, 118 ACUTE RHEUMATIC FEVER AND RHEUMATIC Scleroderma, 196
5-28 Transposition of the Great Vessels: HEART DISEASE 6-64 Idiopathic Myocarditis, 197
6-25 Rheumatic Fever in Sydenham’s Chorea: 6-65 Endomyocardial Fibrosis, 198
Mustard and Blalock-Hanlon Infection, Disease Course, and Heart 6-66 Löffler’s Endocarditis, 199
Operations, 119 Muscle, 158 6-67 Becker’s Disease, 200
5-29 Transposition of the Great Vessels: 6-26 Rheumatic Fever in Sydenham’s Chorea: 6-68 Beriberi, 201
Balloon Atrial Septostomy and Arterial Noncardiac Manifestations, 159 6-69 Cardiomyopathies, 202
Repair of Transposition of the Great 6-27 Rheumatic Heart Disease: Acute 6-70 Acquired Immunodeficiency Syndrome
Arteries, 120 Pericarditis and Myocarditis, 160
5-30 Transposition of the Great Vessels with 6-28 Rheumatic Heart Disease: Acute Valvular and the Heart, 203
Inversion of Ventricles, 121 Involvement, 161 6-71 Substance Abuse and the Heart, 204
5-31 Anomalies of the Truncus Septum, 122 6-29 Rheumatic Heart Disease: Residual
5-32 Anomalous Left Coronary Artery and Changes of Acute Rheumatic PERICARDIAL DISEASE
Aneurysm of Sinus of Valsalva, 123 Carditis, 162 6-72 Presentation and Treatment of
5-33 Anomalous Coronary Arteries Seen in 6-30 Rheumatic Heart Disease: Mitral Stenosis:
Adult Patients, 124 Pathologic Anatomy, 163 Pericarditis, 205
5-34 Anomalies of Aortic Arch System: Patent 6-31 Rheumatic Heart Disease: Mitral Stenosis: 6-73 Etiologies of Pericarditis, 206
Ductus Arteriosus, 125 Pathophysiology and Clinical 6-74 Constrictive Pericarditis, 207
5-35 Anomalies of Aortic Arch System: Aspects, 164
Aberrant Right Subclavian Artery, 126 6-32 Rheumatic Heart Disease: Mitral Stenosis: ACUTE AND CHRONIC COR PULMONALE AND
5-36 Anomalies of Aortic Arch System: Double Secondary Anatomic Effects, 165 PULMONARY EMBOLISM
Aortic Arch and Right Aortic Arch 6-33 Rheumatic Heart Disease: Mitral Stenosis: 6-75 Acute Cor Pulmonale and Pulmonary
Anomalies, 127 Secondary Pulmonary Effects, 166
5-37 Anomalies of Aortic Arch System: 6-34 Rheumatic Heart Disease: Mitral Stenosis: Embolism: Massive Embolization, 208
Anomalous Origins of the Pulmonary Thromboembolic Complications, 167 6-76 Acute Cor Pulmonale and Pulmonary
Artery, 128 6-35 Rheumatic Heart Disease: Mitral Stenosis:
5-38 Anomalies of the Aortic Arch System: Thromboembolic Complications: Principal Embolism: Embolism of Lesser Degree
Anatomic Features of Aortic Coarctation Sites of Embolism from Left Atrial Without Infarction, 209
in Older Children and Neonates, 129 Thrombosis, 168 6-77 Lesions That May Cause Pulmonary
5-39 Anomalies of Aortic Arch System: 6-36 Rheumatic Heart Disease: Mitral Stenosis: Hypertension and Chronic Cor
Coarctation of Aorta, 130 Thromboembolic Complications: Mitral Pulmonale, 210
5-40 Endocardial Fibroelastosis and Glycogen Balloon Valvuloplasty, 169 6-78 Chronic Cor Pulmonale, 211
Storage Disease, 131 6-37 Rheumatic Heart Disease: Mitral 6-79 Deep Vein Thrombosis, 212
Regurgitation, 170
SECTION 6—ACQUIRED HEART DISEASE 6-38 Rheumatic Heart Disease: Mitral INFECTIVE ENDOCARDITIS
ISCHEMIC HEART DISEASE Regurgitation: Pathophysiology and 6-80 Infective Endocarditis: Portals of Entry
6-1 Structure of Coronary Arteries, 134 Clinical Aspects, 171
6-2 Pathogenesis of Atherosclerosis, 135 6-39 Mitral Valve Clip, 172 and Predisposing Lesions, 213
6-3 Risk Factors in Etiology of 6-40 Mitral Valve Repair, 173 6-81 Early Lesions of Infective
6-41 Mitral Valve Prolapse, 174
Atherosclerosis, 136 AORTIC AND VASCULAR DISEASE Endocarditis, 214
6-4 Pathologic Changes in Coronary Artery 6-42 Aortic Stenosis: Rheumatic and 6-82 Advanced Lesions of Infective
Nonrheumatic Causes, 175
Disease, 137 6-43 Aortic Stenosis: Rheumatic and Endocarditis, 215
6-5 End-Organ Damage by Vascular Nonrheumatic Causes (Continued), 176 6-83 Right-Sided Heart Involvement in
6-44 Aortic Regurgitation: Pathology, 177
Disease, 138 6-45 Aortic Regurgitation: Pathology Infective Endocarditis, 216
6-6 Unstable Plaque Formation, 139 (Continued), 178 6-84 Cardiac Sequelae of Infective
6-7 Angiogenesis and Arteriogenesis, 140 6-46 Transcutaneous Aortic Valve
CHRONIC ANGINA Replacement, 179 Endocarditis, 217
6-8 Overview of Myocardial Ischemia, 141 6-47 Cystic Medial Necrosis of Aorta, 180 6-85 Mycotic Aneurysms and Emboli in the
6-9 Angina Pectoris, 142 6-48 Cystic Medial Necrosis of Aorta: Surgical
6-10 Detection of Myocardial Ischemia, 143 Management, 181 Heart, 218
6-11 Degree of Flow-Limiting Stenoses, 144 6-49 Syphilitic Aortic Disease, 182 6-86 Remote Embolic Effects of Infective
6-12 Left-Sided Heart Angiography, 145
6-13 Fractional Flow Reserve, 146 Endocarditis, 219
6-14 Chronic Angina Revascularization 6-87 Nonbacterial Thrombotic (Marantic)
Procedures: Stent Deployment, 147 Endocarditis, 220
CARDIOPULMONARY RESUSCITATION AND
HYPOTHERMIA THERAPY
6-88 External Cardiopulmonary
Resuscitation, 221
6-89 Internal Cardiac Massage, 222
6-90 Defibrillation, 223
xii THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS
Contents
CONNECTIVE TISSUE DISEASE 6-115 Hypertension and Congestive Heart 6-133 Right-Sided and Left-Sided Heart Failure
6-91 Rheumatoid Arthritis, 224 Failure Disease, 248 in Dilated Cardiomyopathy and
6-92 Ankylosing Spondylitis, 225 Pulmonary Congestion, 266
6-93 Polymyositis and Dermatomyositis, 226 6-116 Obstructive Sleep Apnea and
6-94 Scleroderma (Progressive Systemic Hypertension, 249 6-134 Pulmonary Congestion or Edema of
Cardiac and Other Origins, 267
Sclerosis), 227 NEUROMUSCULAR DISORDERS
6-95 Systemic Lupus Erythematosus, 228 6-117 Duchenne Muscular Dystrophy, 250 6-135 Causes and Pathogenesis of Pulmonary
ENDOCRINE DISORDERS AND CARDIAC DISEASE 6-118 Myotonic Dystrophy, 251 Edema, 268
6-96 Acromegaly, 229 6-119 Friedreich’s Ataxia, 252
6-97 Hyperthyroidism: Thyrotoxicosis, 230 6-120 Disorders of Potassium Metabolism, 253 6-136 Cardiac Origins of Peripheral or Systemic
6-98 Hypothyroidism: Myxedema, 231 PENETRATING AND NONPENETRATING HEART TRAUMA Congestion or Edema, 269
6-99 Cushing’s Syndrome, 232 6-121 Cardiac Tamponade in Penetrating Heart
6-100 Primary Hyperaldosteronism: 6-137 Therapy for Pulmonary Edema and
Wounds, 254 Paroxysmal Dyspnea, 270
Mineralocorticoid Hypertension, 233 6-122 Relative Distribution of Penetrating Heart
6-101 Pheochromocytoma, 234 6-138 Biventricular Pacing and Intracardiac
HEART TUMORS Wounds, 255 Defibrillator: Benefit of Biventricular
6-102 Myxoma and Rhabdomyoma, 235 6-123 Variable Course of Penetrating Heart Pacing, 271
6-103 Metastatic Tumors of the Heart, 236
Wounds, 256 6-139 Biventricular Pacing and Implantable
HYPERTENSION 6-124 Thoracotomy and Cardiorrhaphy, 257 Cardiac Defibrillator, 272
6-104 Hypertension Regulation: Interdependent 6-125 Thoracotomy and Cardiorrhaphy
6-140 Diastolic Heart Failure, 273
and Interacting Factors in Blood Pressure (Continued), 258 6-141 Heart Transplantation: Orthotopic Biatrial
Regulation, 237 6-126 Nonpenetrating Heart Wounds:
6-105 Etiology of Hypertension, 238 Cardiac Transplantation, 274
6-106 Hypertension Regulation: Renin- Pathogenesis and Variable Course of 6-142 Heart Transplantation: Bicaval Cardiac
Angiotensin System, 239 Cardiac Contusion, 259
6-107 Hypertension Regulation: Wave 6-127 Nonpenetrating Heart Wounds: Transplantation, 275
Reflection and Isolated Systolic Myocardial Rupture and Valvular 6-143 Heart Transplantation: HeartMate XVE
Hypertension, 240 Injuries, 260
6-108 Causes of Secondary Hypertension 6-128 Nonpenetrating Heart Wounds: and II Left Ventricular Assist
Possibly Amenable to Surgery, 241 Mechanism of Sudden Cardiac Death in Systems, 276
6-109 Retinal Changes in Hypertension, 242 Commotio Cordis, 261
6-110 Occlusive Disease of Main Renal PERCUTANEOUS INTERVENTION PROCEDURES SUDDEN CARDIAC DEATH IN YOUNG ATHLETES
Artery, 243 6-129 Percutaneous Approaches to Reduce 6-144 Sudden Death in Hypertrophic
6-111 Occlusive Disease of Main Renal Artery Cerebral Emboli, 262
(Continued), 244 6-130 Cerebrovascular Emboli Protection Cardiomyopathy, 277
6-112 Kidneys and Hypertension, 245 Device, 263 SYNCOPE
6-113 Heart Disease in Hypertension, 246 6-131 Interventional Approaches to Peripheral 6-145 Management of Syncope, 278
6-114 Heart Disease in Hypertension Arterial Disease, 264
(Continued), 247 PARASITIC DISEASE AND THE HEART
HEART FAILURE 6-146 Trichinosis, 279
6-132 Right-Sided and Left-Sided Heart Failure 6-147 Chagas Disease (Trypanosomiasis), 280
6-148 Amebic Pericarditis, 281
and Systemic Congestion: Physical 6-149 Echinococcus Infection and Hydatid
Examination, 265
Pericarditis, 282
THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS xiii
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SECTION 1
ANATOMY
Plate 1-1 Cardiovascular System
LUNGS IN SITU: ANTERIOR VIEW
Thorax Thyroid gland Trachea and inferior thyroid veins
Omohyoid, sternothyroid, and sternohyoid muscles Common carotid artery
Before describing the anatomy of the heart, it is helpful Internal jugular vein
to review other anatomic features of the thoracic cavity Manubrium of sternum Phrenic nerve
and organs. Sternocleidomastoid muscle Anterior scalene muscle
Thoracic duct
The thorax proper constitutes the upper part of the External jugular vein Brachial plexus
body or trunk, with a shape between a barrel and a Costal part of parietal Subclavian artery and vein
truncated cone that is functionally favorable. Although pleura (cut away) Internal thoracic artery
the intrathoracic pressure is often subatmospheric, the and vein
chest wall is still able to retain its integrity by means of Clavicle Axillary artery and vein
rather thin, lightweight skeletal elements. The thoracic Pectoralis major muscle Cardiac notch
cavity occupies only the upper part of the thoracic cage. Pectoralis of left lung
The abdominal (peritoneal) cavity reaches upward as minor muscle
high as the lower tip of the sternum, affording protec- Intercostal
tion to large, easily injured abdominal organs such as muscles
the liver, spleen, stomach, and kidneys.
Superior lobe, Superior lobe,
The thoracic and abdominal cavities are separated by Middle lobe, Inferior lobe
the dome-shaped diaphragm, a sheet of tissue consisting Inferior lobe of left lung
of a peripheral muscular part and a central tendinous of right lung Costo-
part that closes the thoracic cavity interiorly. Superiorly, mediastinal
the narrow upper thoracic aperture—bounded by the Oblique fissure space
upper part of the sternum, the short stout first ribs, and Oblique fissure
the body of the first thoracic vertebra (T1)—gives Horizontal fissure Diaphragm
access to the root of the neck and is not closed by a of right lung 7th costal cartilage Musculophrenic artery
specific structure. The thorax is bounded posteriorly by Costodia- Xiphoid process Lingula of superior lobe of left lung
the bodies of the 12 thoracic vertebrae and the posterior phragmatic recess Internal thoracic artery
portions of the ribs, anteriorly by the sternum, costal Mediastinal part of parietal pleura
cartilages, and anterior portions of the ribs, and laterally Diaphragmatic part Fibrous pericardium
by the remaining parts of the ribs. The spaces between of parietal pleura
successive ribs are bridged by the intercostal muscles.
Pleural reflections
The sternum (breastbone) lies anterior in the midline
and superficially. The clavicles and the first seven pairs whereas the eighth, ninth, and tenth pairs articulate the superior surface of the first rib, two grooves are
of ribs articulate with it. The sternum consists of three with each other and do not reach the sternum. The 11th divided by a tubercle—the tuberculum scaleni—that
parts: the bony manubrium and corpus sterni and the and 12th pairs are small and poorly developed, ending forms the point of insertion of the anterior scalene
small, cartilaginous xiphoid process. The clavicles articu- in free cartilaginous tips. The ribs are thickest posteri- muscle. The groove in front of the muscle is occupied
late with the manubrium on its upper border, and the orly; they flatten out and widen as they curve forward. by the subclavian vein, whereas the subclavian artery
notch between these joints is the interclavicular (or Along the inferior and inner surface of the posterior follows the groove behind the tubercle. The second rib
suprasternal) notch. Just below the sternoclavicular part of each rib, a groove—the sulcus costae—affords is longer than the first and resembles the other ribs
joints, the cartilages of the first ribs are attached to the protection to the intercostal vessels and nerve. except the small 11th and 12th ribs.
sternum. No joint spaces are present here. The manu-
brium and the body of the sternum are united by fibro- The first two and last two ribs differ somewhat from The spaces between successive ribs are occupied by
cartilage. The junction between the manubrium and the previous description. The first rib (see Plate 1-2) is intercostal muscles (see Plate 1-1). Each external intercos-
the body of the sternum usually forms a prominent very short and relatively heavier than the other ribs. On tal muscle arises from the lower border of the rib above,
ridge, accentuated by the two parts of the sternum
forming a slight angle with each other, the sternal angle
of Louis. This is an important landmark because the
cartilages of the second ribs articulate with the sternum
at this point. The third, smallest part of the sternum is
the xiphoid cartilage, a thin, spoon-shaped process
attached to the lower end of the sternal body.
Most of the bony thorax is formed by the ribs, usually
12 on each side of the trunk. The ribs consist of a series
of thin, curved, rather elastic bones that articulate pos-
teriorly with the thoracic vertebrae and terminate ante-
riorly in the costal cartilages. The first seven pairs of
ribs attach to the sternum by means of their cartilages,
2 THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS
Plate 1-2 Anatomy
HEART IN SITU
Inferior thyroid veins Trachea
Thymus Left brachiocephalic vein
Brachiocephalic trunk Left common carotid artery
Right brachiocephalic vein Vagus nerve (X)
Internal jugular vein
Phrenic nerve Arch of aorta
Anterior scalene muscle Thoracic duct
External jugular vein
Thorax (Continued) Brachial plexus Left recurrent laryngeal nerve
Superior vena cava Internal thoracic artery
runs obliquely downward and medially, and inserts into Subclavian artery and vein Phrenic nerve and
the upper border of the rib below. Each internal inter- pericardiacophrenic
costal muscle arises from the lower border of the rib 1st rib artery and vein
above and runs downward and outward to insert on the Mediastinal
upper border of the rib below. Between these two Phrenic nerve part of
muscle layers lie the intercostal vessels, whereas the and pericar- parietal
intercostal nerves lie between the internal and the diacophrenic pleura
innermost intercostal muscles. artery and vein
Many muscles of the upper extremities originate Right lung
from the chest wall, including the pectoralis major (see
Plate 1-1) and pectoralis minor muscles and the serratus Left lung
anterior muscle, which originate from the anterior and
lateral portions of the chest wall. Pericardium Internal
thoracic
Several neck muscles originate from the upper rim of Diaphragm Line of fusion artery
the thoracic cage. The sternohyoid and sternothyroid (see
Plate 1-1) are thin, straplike muscles that arise from the Mediastinal Parts of of fibrous
superior border and posterior surface of the sternum Diaphragmatic parietal pericardium
and insert into the hyoid bone and the thyroid cartilage, Costal pleura to diaphragm Superior Musculophrenic artery
respectively. The sternocleidomastoid muscle (SCM) arises epigastric
(see Plate 1-1) as a stout sternal head from the upper artery
border of the sternum, adjacent to the sternoclavicular
joint, and as a second clavicular head from the medial and enters the axilla. The subclavian vein runs parallel most superficially and the vagus nerve lies beneath,
third of the clavicle. The interval between the two to the subclavian artery but in front of the anterior between the common carotid artery and internal jugular
heads is usually visible as a slight depression, behind scalene muscle. veins. On the left side the thoracic duct (see Plate 1-1)
which the apex of the lung rises from the thorax into crosses over the subclavian artery and runs anteriorly
the root of the neck. Above this interval the two heads Deep in the lower portion of the neck under the to empty into the proximal subclavian vein.
of the SCM unite to form a single muscular belly that SCM, a narrow space is bordered anteriorly by the
passes obliquely upward, backward, and laterally to omohyoid and strap muscles, posteriorly by the anterior Blood for the chest wall is supplied by the intercostal
insert into the lateral surface of the mastoid process and scalene muscle and prevertebral fascia, and medially by arteries and the internal thoracic (internal mammary)
occipital bone. the pharynx, esophagus, trachea, and thyroid gland (see arteries. After originating from the aorta, the posterior
Plate 1-1). In this space the common carotid artery, intercostal arteries cross the vertebral bodies and enter
Superficial to the SCM, the external jugular vein internal jugular vein, and vagus nerve are enclosed in a their corresponding intercostal spaces, passing along
passes perpendicularly downward from its origin at the common connective-tissue sheath; the jugular vein runs the inferior border of the ribs between the internal and
lower border of the parotid gland, crosses the SCM,
and penetrates the deep fascia of the neck to empty into
the subclavian vein.
Of the deeper neck muscles, the three scalene muscles
originate from the transverse processes of the cervical
vertebrae. The anterior scalene muscle inserts into the
scalene tubercle of the first rib; the medial scalene
muscle also attaches to the upper surface of the first rib,
but more posteriorly. The posterior scalene muscle
inserts on the second rib. The components of the cervi-
cal nerve plexus emerge from the groove between the
anterior and middle scalene muscles. The anterior
scalene muscle is crossed laterally and anteriorly by the
phrenic nerve, which originates from the cervical plexus
and runs downward and behind the subclavian vein to
enter the thoracic cavity. The groove between the ante-
rior and middle scalene muscles widens inferiorly to
form a triangular opening through which emerge the
components of the brachial plexus and the subclavian
artery. After ascending from the thoracic cavity, the
subclavian artery crosses the upper surface of the first
rib, lying in the groove posterior to the scalene muscle,
THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS 3
P late 1-3 Cardiovascular System
MEDIASTINUM: CROSS SECTION
Right ventricle Sternum 5th left costal cartilage
Internal thoracic artery and vein
Tricuspid Septal cusp Transversus thoracis muscle
valve Posterior cusp
Interventricular Anterior cusp Pectoralis major muscle
part, Pleural cavity
Atrioventricular
Thorax (Continued) part of Muscular part of
membranous interventricular
external intercostal muscles. The vessels are well pro- septum septum
tected posteriorly by the subcostal groove. The internal
thoracic arteries originate from the inferior surface of Superior Left ventricle
the subclavian arteries and run downward, lateral to, vena cava
and (for a short distance) with the phrenic nerve, reach- Papillary muscle
ing the posterior surface of the anterior chest wall. The
arteries continue their downward course for approxi- Right atrium Phrenic nerve
mately 14 inch laterally to the edges of the sternum, and pericardia-
dividing just above the diaphragm into their two termi- Pericardial cavity cophrenic
nal branches: the musculophrenic and superior epigastric artery and vein
arteries. Along their course the internal thoracic arteries
give rise to branches to the thymus, mediastinum, and Mediastinal part Anterior Mitral
pericardium posteriorly; to the perforating branches to of parietal pleura cusp valve
the skin and subcutaneous tissues anteriorly; and finally Posterior
to the lateral branches that pass along the rib cartilages Right lung cusp
and anastomose with the posterior intercostal arteries. (middle lobe)
The veins of the thoracic wall correspond in their Phrenic nerve Left atrium
course with the arteries. The 10 lower intercostal veins and pericar-
on the right enter the azygos vein, and the upper two diacophrenic Coronary sinus
intercostal veins enter either the azygos or the brachio- artery and vein
cephalic (innominate) vein. The lower intercostal veins Left lung
on the left side enter the hemiazygos or accessory hemia- Branches of right (superior lobe)
zygos vein. The three left superior intercostal veins enter main bronchus
the left brachiocephalic vein by a common stem, the left
superior intercostal vein. Right inferior Branches of
pulmonary vein left main bronchus
The chest wall receives its nerve supply from the
intercostal nerves, which accompany the intercostal Oblique Left inferior
vessels. pericardial sinus pulmonary vein
Most of the thoracic cavity is occupied by the two Esophagus and 8th rib Thoracic (descending)
lungs, each of which is enclosed by its pleura. Each esophageal plexus aorta
pleura forms a closed sac invaginated by the lung so that
part of it covers (and is adherent to) the inner surface Azygos vein Left sympathetic trunk
of the chest wall, the diaphragm, and the mediastinum, Thoracic duct
known as the costal, the diaphragmatic, and the mediasti- Hemiazygos vein
nal pleura, respectively, and collectively as the parietal T8 vertebra
pleura (see Plate 1-2). That part of the mediastinal
pleura that covers the pericardium is called the pericar- Left greater thoracic splanchnic nerve
dial pleura; the remainder (visceral pleura) covers the
lung. The virtual space between the visceral and parietal pleural cavities almost meet behind the upper sternum, the vestigial transverse thoracic muscle. The superior
pleurae contains a tiny amount of clear fluid. The but the left costomediastinal reflection deviates laterally mediastinum contains the thymus gland (see Plate 1-2),
pleural reflections (see Plate 1-1), between the costal and below the fourth rib cartilage, exposing a small trian- which largely disappears by about age 12 years leaving
diaphragmatic portions of the parietal pleura, lie lower gular portion of the pericardium that is not covered by a small pad of fat and areolar tissue, and the brachioce-
than the corresponding lower edge of the lung. The pleura. At the same level, the anteroinferior portion of phalic veins, which join each other on the right to form
resulting space normally is not completely filled by the the left superior lobe recedes even more, leaving a the superior vena cava (see Plate 1-5). Posterior to the
lung, even on deep inspiration, and is called the recessus portion of the pericardial pleura that is not covered by brachiocephalic veins, the phrenic and vagus nerves
costodiaphragmaticus. lung tissue. descend from the neck. The phrenic nerves, accompa-
nied by the pericardiacophrenic vessels, run laterally, ante-
The right lung consists of three lobes—the superior, The central space between the two pleural cavities is rior to the lung roots and along the pericardium, until
middle, and inferior lobes—and is somewhat larger the mediastinum. The mediastinum is divided arbi- they reach the diaphragm.
than the left lung, which has two—the superior and trarily into superior, anterior, middle, and posterior
inferior lobes (see Plate 1-1). The smaller size of the mediastina. The shallow anterior mediastinum contains The aortic arch ascends from the heart into the supe-
left lung results from the eccentric position of the heart, a portion of the left internal thoracic vessels and rior mediastinum, almost reaches the upper border of
which encroaches on the left pleural cavity. The two
4 THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS
Plate 1-4 Anatomy
PERICARDIAL SAC
Ascending aorta
Superior vena cava Arch of aorta
Pericardium (cut edge)
Left auricle (atrial appendage) Pulmonary trunk
Left ventricle Transverse pericardial
Coronary sinus sinus
Left pulmonary veins
Thorax (Continued) Posterior inter- Oblique vein of left
ventricular sulcus atrium (of Marshall)
the manubrium sterni, courses obliquely backward and Right ventricle Oblique pericardial
to the left over the left main bronchus, and continues as Diaphragmatic part sinus
the descending aorta downward, anteriorly, and slightly of pericardium
to the left of the vertebral column. Originating from Left atrium
the convexity of the arch, from the proximal to the Sternocostal part of Esophageal
distal position, are the brachiocephalic, left common pericardium (cut edge) prominence
carotid, and subclavian arteries. Right pulmonary vein
Heart drawn out of opened pericardial sac: left lateral view Right atrium
The right vagus nerve (see Plate 1-5) passes between Inferior vena cava
the subclavian artery and vein and gives off the right Right phrenic nerve
recurrent nerve, which loops around the subclavian and pericardiaco- Arch of aorta
artery to ascend along the trachea. The left vagus nerve phrenic vessels Ascending aorta
runs between the subclavian vein and the aortic arch, Superior vena cava Mediastinal part of
giving rise to the left recurrent nerve (see Plate 1-5), Transverse parietal pleura (cut edge)
which similarly loops around the arch to ascend along pericardial sinus Left phrenic nerve and
the trachea. Superior vena cava pericardiacophrenic vessels
Right pulmonary veins Pulmonary trunk (bifurcation)
The trachea descends from the neck behind the Mediastinal part
aortic arch and bifurcates into right and left main of parietal pleura Left lung
bronchi at the level of the sternal angle. Behind the (cut edge) Left pulmonary veins
trachea runs the normally collapsed esophagus (see Plate Pericardium
1-4), joined by the vagus nerves just beyond the branch- (cut edge) Pericardium (cut edge)
ing off of the recurrent nerves from the vagi. Behind Inferior vena cava Oblique pericardial sinus
the esophagus, between the azygos vein and the Line of fusion Esophageal prominence
descending aorta, the thoracic duct (see Plate 1-2) of fibrous pericardium
ascends, coursing behind the aortic arch to enter the to diaphragm Diaphragmatic part
neck, where it empties into the left subclavian vein. of pericardium
Against the necks of the ribs, the sympathetic trunks Pericardial sac with heart removed: anterior view
descend from the neck, first giving off the greater tho-
racic splanchnic nerve (major splanchnic nerve) (see Plate sternum, separated only by areolar and fatty tissue and inferior vena cava, called the oblique pericardial sinus.
1-3) at about the level of the sixth rib and then the minor (endothoracic fascia) and the transverse thoracic Small recesses exist between the superior and inferior
or lesser and lowest thoracic splanchnic nerves. muscle. pulmonary veins on each side and behind the fold of the
left vena cava (ligament of Marshall), a small crease of
The posterior mediastinum is a shallow space con- The great vessels enter and leave the pericardial pericardium running from the left aspect of the pulmo-
taining the lower portions of the esophagus, vagus cavity at its base. A curved, transversely running pas- nary trunk to the left atrium, between the neck of the
nerves, descending aorta, azygos and hemiazygos veins, sageway between the arterial and venous poles of the left auricle and the left pulmonary veins. The left vena
thoracic duct, and sympathetic nerve chains. The heart is called the transverse pericardial sinus. Posteriorly, cava fold contains the vestigial remains of the left
remaining and largest part of the mediastinum, the a blind recess of the pericardial cavity is bordered by common cardinal vein.
middle mediastinum, contains the pericardium, heart, the pericardial reflection between the pulmonary veins
lung roots, and phrenic nerves.
The pericardial cavity is the third serous cavity con-
tained in the chest, with the two pleural cavities. The
pericardial cavity is conical in shape, with the base of
the cone lying posteriorly to the right and the apex
anteriorly to the left. It completely invests the heart
and the proximal portions of the great vessels. As with
the pleura, a visceral portion of the pericardium is dis-
tinguished overlying the heart and proximal great
vessels, usually called the epicardium, as is a parietal
portion. The inferior part of the parietal pericardium
is densely adherent to the middle tendinous part of
the diaphragm. Most of the lateral and anterior por-
tions are contiguous but not normally adherent to the
pleura. A small triangular part of the anterior portion
of the parietal pericardium lies directly behind the
THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS 5
Plate 1-5 Cardiovascular System
Exposure of the Heart ANTERIOR EXPOSURE
Pericardium (cut edge) at site Brachiocephalic trunk
of reflection from great vessels Left brachiocephalic vein
Arch of aorta
Right vagus nerve Left common carotid artery
Right recurrent laryngeal nerve Left internal jugular vein
Left vagus nerve (X)
Right brachiocephalic vein Ligamentum arteriosum
Phrenic nerve Left recurrent laryngeal nerve
Pulmonary trunk
Subclavian artery and vein Left pulmonary
Internal thoracic artery
artery and vein Transverse
pericardial
Phrenic nerve and sinus
pericardiacophrenic
artery and vein Hilum
Superior vena cava of left
Right pulmonary lung
artery
Transverse
pericardial sinus
Right superior
pulmonary vein
Hilum of
right lung
Mediastinal
pleura
(cut edge)
STERNOCOSTAL ASPECT Right ventricle
Within the pericardium lies the heart, a hollow, muscu-
lar, four-chambered organ suspended at its base by the Conus arteriosus
great vessels. In situ the heart occupies an asymmetric
position, with its apex pointing anteriorly, inferiorly, Left auricle (atrial appendage) Mediastinal part
and about 60 degrees toward the left. Its four chambers of parietal pleura
are arranged in two functionally similar pairs, separated (cut edge)
from each other by the cardiac septum (see Plate 1-5). Anterior interventricular sulcus Pericardium (cut edge)
Each pair consists of a thin-walled atrium and a thicker- and anterior interventricular
walled ventricle. branch of left coronary artery Left border (obtuse
margin) of heart
The anatomic nomenclature of the heart removes it Coronary sulcus and right coronary artery Apex of heart
from the body and places it on its apex, and thus the Right auricle (atrial appendage)
cardiac septum is in a sagittal plane. This practice has Left ventricle
led to misconceptions and difficulties in orientation Right atrium
among cardiologists and surgeons. On a chest radio- Left superior pulmonary vein
graph, for example, the left cardiac border is formed by Pericardium (cut edge) Inferior border (acute margin) of heart
the left ventricle, but the right border is formed by the
right atrium, not the right ventricle, which lies anterior. The right atrium and right ventricle are separated Superiorly, the pulmonary trunk is seen originating
The major and important part of the left atrium lies by the right atrioventricular (coronary) sulcus, through from the right ventricle and leaving the pericardium
directly posterior and in the midline in front of the which runs the right coronary artery, embedded in a just before it bifurcates into its two main branches: the
spine and esophagus, allowing the pulmonary veins to be variable amount of fat. To the left of the right ventricle, right and left pulmonary arteries. To the right of the
as short as possible. a small segment of the left ventricle is visible, separated pulmonary trunk lies the intrapericardial portion of
from it by the anterior interventricular sulcus (groove). the ascending aorta, the base of which is largely covered
On removing the anterior chest wall and opening the The anterior interventricular (descending) branch of the by the right auricle (right atrial appendage). The base of
pericardium, most of the presenting part of the heart is left coronary artery (see Plate 1-5) lies in this groove, the aorta, including the first part of the right coronary
formed by the right ventricle, with its exposed surface again embedded in fat. artery, is surrounded by lobules of fatty tissue called
triangular in shape. The right atrium lies to the right
of the right ventricle.
The term “auricle” is often improperly used instead
of atrium. The true auricle is then regrettably called
“auricular appendage” instead of atrial appendage,
which is morphologically correct. The term “auricular
fibrillation” is clinically incorrect and should be atrial
fibrillation.
6 THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS
Plate 1-6 Anatomy
BASE AND DIAPHRAGMATIC SURFACES
Right pulmonary artery Arch of aorta
Left pulmonary artery
Left auricle Right auricle (atrial appendage)
(atrial appendage) Superior vena cava
Left superior Right superior
pulmonary vein pulmonary vein
Right atrium
Left atrium
Left inferior Sulcus terminalis
pulmonary vein
Pericardial reflection Right inferior
pulmonary vein
Oblique vein Inferior vena cava
of left atrium Right ventricle
(of Marshall)
Coronary sinus
Left ventricle
Base of heart: posterior view
Exposure of the Heart Left subclavian artery Brachiocephalic trunk
Left common carotid artery Arch of aorta
(Continued) Superior vena cava
Left pulmonary artery Right pulmonary artery
Rindfleisch folds, the largest and uppermost of which is Left superior pulmonary vein Right superior
rather constant. Left auricle (atrial appendage) pulmonary vein
Left inferior pulmonary vein Right inferior
POSTERIOR AND DIAPHRAGMATIC ASPECTS pulmonary vein
After removal of the heart from the pericardium, its Oblique vein
posterior (basilar) and diaphragmatic aspects can be of left atrium Sulcus terminalis
inspected. The superior vena cava (SVC) and inferior (of Marshall)
vena cava (IVC) enter the right atrium, with the long Right atrium
axis of both cavae inclined slightly forward and the IVC
in a more medial position. A pronounced groove, the Left atrium Inferior vena cava
sulcus terminalis, separates the right aspect of the SVC
from the base of the right auricle. As this groove Pericardial reflection Coronary sulcus and
descends along the posterior aspect of the right atrium, Coronary sinus right coronary artery
it becomes less distinct.
Left ventricle Posterior interventricular sulcus
The right pulmonary veins (usually two but occasion- Apex and posterior interventricular
ally three) arise from the right lung and cross the right branch of right coronary artery
atrium posteriorly to enter the right side of the left (posterior descending artery)
atrium. The two left pulmonary veins enter the left side Right ventricle
of the left atrium, sometimes by a large common stem.
The posterior wall of the left atrium forms the anterior Base and diaphragmatic surface: posteroinferior view
wall of the oblique pericardial sinus. Normally, the left
atrium is not in contact with the diaphragm. The coronary sinus lies between the left atrium and The diaphragmatic surfaces of the right ventricle
the left ventricle in the posterior (diaphragmatic) portion and the left ventricle are separated by the posterior
The bifurcation of the pulmonary trunk lies on the of the left atrioventricular groove (coronary sulcus). The interventricular sulcus (groove). This sulcus is continu-
roof of the left atrium. The left pulmonary artery courses cardiac veins enter the coronary sinus, which has the ous with the anterior interventricular groove just to
immediately toward the left lung, and the right pulmo- appearance of a short, wide vein. However, its wall the right of the cardiac apex, which in a normal heart
nary artery runs behind the proximal SVC and above consists of cardiac muscle, and because of its embryonic is formed by the left ventricle. The posterior inter-
the right pulmonary veins to the right lung. origin, the coronary sinus should be considered a true ventricular (descending) artery and middle cardiac
cardiac structure. Its right extremity turns forward and vein lie in the posterior interventricular sulcus,
The aortic arch crosses the pulmonary artery bifurca- upward to enter the right atrium. embedded in fat.
tion after giving off its three main branches: the bra-
chiocephalic (innominate), left common carotid, and left
subclavian arteries. Variations in this pattern occur and
usually are not significant.
THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS 7
Plate 1-7 Cardiovascular System
RIGHT ATRIUM AND RIGHT VENTRICLE
Ascending aorta
Superior vena cava Pulmonary trunk
Right pulmonary artery Right auricle (atrial appendage)
Pericardial reflection Conus arteriosus
Crista terminalis
Right superior Atrioventricular part
pulmonary vein of membranous
Left atrium septum
Right inferior Septal cusp
pulmonary vein of tricuspid valve
Interatrial septum Pectinate muscles
Limbus of fossa ovalis Opening of
coronary sinus
Fossa ovalis
Valve
Inferior vena cava (thebesian)
Valve (eustachian) of coronary
of inferior vena cava sinus
Opened right atrium: right lateral view
Atria and Ventricles
RIGHT ATRIUM Pericardial reflection Pulmonary trunk
The right atrium consists of two parts: (1) a posterior Aorta
smooth-walled part derived from the embryonic sinus Transverse pericardial sinus
venosus, into which enter the superior and inferior Transverse
venae cavae, and (2) a thin-walled trabeculated part that pericardial sinus Anterior semilunar cusp Pulmonary
constitutes the original embryonic right atrium. The valve
two parts of the atrium are separated by a ridge of Superior vena cava Right semilunar cusp
muscle. This ridge, the crista terminalis (see Plate 1-7), Left semilunar cusp
is most prominent superiorly, next to the SVC orifice, Right auricle
then fades out to the right of the IVC ostium. Its posi- (atrial appendage) Conus arteriosus
tion corresponds to that of the sulcus terminalis exter-
nally (see Plate 1-6). Often described as a remnant of Right atrium Supraventricular crest
the embryonic right venous valve. the crista terminalis Membranous part of
actually lies just to the right of the valve. interventricular septum Septal papillary muscle
From the lateral aspect of the crista terminalis, a large Anterior Interventricular septum
number of pectinate muscles run laterally and generally cusp (muscular part)
parallel to each other along the free wall of the atrium. Septal
The atrial wall is paper-thin and translucent between Tricuspid cusp Septomarginal
the pectinate muscles. The triangular-shaped superior valve trabecula
portion of the right atrium—the right auricle—is also Posterior (moderator band)
filled with pectinate muscles. One pectinate muscle cusp
originating from the crista terminalis is usually larger
than the others and is called the taenia sagittalis. Chordae tendineae
The right auricle usually is not well demarcated Posterior papillary muscle
externally from the rest of the atrium. The right auricle
is a convenient, ready-made point of entry for the Anterior papillary muscle
cardiac surgeon and is used extensively. Trabeculae carneae
The anterior border of the IVC ostium is guarded by The posteromedial wall of the right atrium is formed Opened right ventricle: anterior view
a fold of tissue, the inferior vena cava (eustachian) valve, by the interatrial septum, which has a thin, fibrous,
which varies greatly in size and may even be absent. central ovoid portion. The interatrial septum forms a RIGHT VENTRICLE
When large, the IVC valve is usually perforated by shallow depression in the septum called the fossa ovalis. The right ventricular cavity (see Plate 1-7) can be divided
numerous openings, forming a delicate lacelike struc- The remainder of the septum is muscular and usually arbitrarily into a posteroinferior inflow portion, con-
ture known as the network of Chiari. The coronary sinus forms a ridge around the fossa ovalis, the limbus fossae taining the tricuspid valve, and an anterosuperior outflow
enters the right atrium just anterior to the medial ovalis. A probe can be passed under the anterosuperior portion, from which the pulmonary trunk originates.
extremity of the IVC valve. The eustachian valve’s orifice part of the limbus into the left atrium in some cases, These two parts are separated by prominent muscular
may also be guarded by a valvelike fold, the coronary and the foramen (fossa) ovalis is then “probe patent.” bands, including the parietal band, the supraventricular
sinus (thebesian) valve. Both IVC valves and coronary Anteromedially, the tricuspid valve gives access to the crest (crista supraventricularis), the septal band, and
sinus valves are derived from the large, embryonic right right ventricle. the moderator band. These bands form a wide, almost
venous valve. circular orifice with no impediment to flow in the
normal heart.
8 THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS
Plate 1-8 Anatomy
Atria and Ventricles LEFT ATRIUM AND LEFT VENTRICLE
(Continued) Pericardial reflection Arch of aorta
Transverse pericardial sinus Ligamentum
Left auricle (atrial appendage) arteriosum
Oblique vein of left atrium (of Marshall) Left pulmonary
artery
Mitral Posterior cusp Right pulmonary
valve Anterior cusp artery
Left atrium
Anterior papillary muscle
Chordae tendineae Right pulmonary
Posterior veins
papillary muscle
Left pulmonary veins
Coronary sinus
Inferior vena cava
Flap opened in left lateral wall of left ventricle
The wall of the inflow portion is heavily trabeculated, Aortic Left auricle (atrial appendage) Arch of aorta
particularly in its most apical portion. These trabeculae valve
carneae enclose a more or less elongated, ovoid opening. Conus arteriosus Left pulmonary
The outflow portion of the right ventricle, often called Left semilunar cusp artery
the infundibulum, contains only a few trabeculae. The Right pulmonary
subpulmonic area is smooth walled. Right semilunar cusp artery
Posterior semilunar cusp Left superior
A number of papillary muscles anchor the tricuspid pulmonary vein
valve cusps to the right ventricular wall through many Mem- Interventricular part Right pulmonary
slender, fibrous strands called the chordae tendineae. Two branous Atrioventricular veins
papillary muscles, the medial and anterior, are reason- septum part Valve of
ably constant in position but vary in size and shape. The foramen ovale
other papillary muscles are extremely variable in all Muscular part of Left atrium
respects. Approximately where the crista supraventricu- interventricular Inferior vena cava
laris joins the septal band, the small medial papillary septum Coronary sinus
muscle receives chordae tendineae from the anterior and Mitral valve
septal cusps of the tricuspid valve. Often well developed (cut away)
in infants, the medial papillary muscle is almost absent
in adults or is reduced to a tendinous patch. An impor- Section through left atrium and ventricle with mitral valve cut away
tant surgical landmark, the medial papillary muscle is
also of diagnostic value to the cardiac pathologist with LEFT ATRIUM position of the fetal valve of the foramen ovale. A narrow
its interesting embryonic origin. The anterior papillary The left atrium consists mainly of a smooth-walled sac slit may allow a probe to be passed from the right
muscle originates from the moderator band and receives with the transverse axis larger than the vertical and atrium to the left atrium.
chordae from the anterior and posterior cusps of the sagittal axes. On the right, two or occasionally three
tricuspid valve. In variable numbers, the usually small pulmonary veins enter the left atrium; on the left there The left auricle is a continuation of the left
posterior papillary muscle and septal papillary muscle are also two (sometimes one) pulmonary veins. The upper anterior part of the left atrium. The auricle’s
receive chordae from the posterior and medial (septal) wall of the left atrium is distinctly thicker than that of variable shape may be long and kinked in one or more
cusps. The muscles originating from the posteroinfe- the right atrium. The septal surface is usually fairly places. Its lumen contains small pectinate muscles,
rior border of the septal band are important in the smooth, with only an irregular area indicating the and there usually is a distinct waistlike narrowing
analysis of some congenital cardiac anomalies. proximally.
The pulmonary trunk arises superiorly from the right
ventricle and passes backward and slightly upward. It
bifurcates into right and left pulmonary arteries (see
Plate 1-7) just after leaving the pericardial cavity. A
short ligament—the ligamentum arteriosum (see Plate
1-8)—connects the upper aspect of the bifurcation to
the inferior surface of the aortic arch (arch of aorta; see
Plate 1-6). It is a remnant of the fetal ductus arteriosus
(duct of Botallo).
THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS 9
Plate 1-9 Cardiovascular System
ATRIA, VENTRICLES, AND INTERVENTRICULAR SEPTUM
Left atrium Anterior cusp of mitral valve
Left auricle (atrial appendage)
Pulmonary trunk
Left pulmonary veins Openings of coronary arteries
Posterior cusp Ascending aorta
Anterior cusp
Mitral valve Right auricle
(atrial appendage)
Right superior pulmonary vein Left semi- Aortic
Ascending aorta lunar cusp valve
Right semi-
Aortic Left semilunar cusp lunar cusp
valve Posterior
semilunar (non-
coronary) cusp Supraven-
tricular
Superior vena cava crest
Membranous septum Atrio- Outflow
ventric- to pul-
ular monary
part trunk
Inter-
ventric-
ular
part
Atria and Ventricles Right atrium Right anterior
papillary
(Continued) Tricuspid Anterior cusp muscle (cut)
valve (retracted) Septomarginal trabecula
LEFT VENTRICLE Septal cusp (moderator band)
The left ventricle (see Plate 1-8) is egg shaped with the Posterior cusp Right ventricle
blunt end cut off, where the mitral valve and aortic valve Septal (medial) papillary muscle
are located adjacent to each other. The valves are sepa- Right ventricle Left ventricle
rated only by a fibrous band giving off most of the Left anterior papillary muscle
anterior (aortic) cusp of the mitral valve and the adjacent Left posterior papillary muscle
portions of the left and posterior aortic valve cusps. The Left ventricle
average thickness of the left ventricular (LV) wall is Muscular part of interventricular septum
about three times that of the right ventricular (RV) wall. Right posterior papillary muscle
The LV trabeculae carneae are somewhat less coarse,
with some just tendinous cords. As in the right ventri- Right anterior papillary muscle (cut)
cle, the trabeculae are much more numerous and dense
in the apex of the left ventricle. The basilar third of the Four- chamber view
septum is smooth.
Plane of section
Usually there are two stout papillary muscles. The dual
embryonic origin of each is often revealed by their bifid opened right ventricle (see Plate 1-7, bottom), the mem- On sectioning of the septum in an approximately
apices; each receives chordae tendineae from both major branous septum lies deep to the supraventricular crest and transverse plane, the basilar portion of the ventricular
mitral valve cusps. Occasionally a third, small papillary is divided into two parts by the origin of the medial septum, including the membranous septum, is seen to
muscle is present laterally. (septal) cusp of the tricuspid valve. As a result, one portion deviate to the right, so that a plane through the major
of the membranous septum lies between the left ven- portion of the septum bisects the aortic valve. It must
Most of the ventricular septum is muscular. Normally tricle and the right ventricle—the interventricular part— be emphasized that the total cardiac septum shows a
it bulges into the right ventricle, showing that a trans- and the other between the left ventricle and the right complex, longitudinal twist and does not lie in any
verse section of the left ventricle is almost circular. The atrium—the atrioventricular part. single plane.
muscular portion has approximately the same thickness
as the parietal LV wall. The ventricular septum consists
of two layers, a thin layer on the RV side and a thicker
layer on the LV side. The major septal arteries tend to
run between these two layers. In the human heart a
variable but generally small area of the septum imme-
diately below the right and posterior aortic valve cusps is
thin and membranous.
The demarcation between the muscular and the
membranous part of the ventricular septum is distinct
and is called the limbus marginalis. As seen from the
10 THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS
Plate 1-10 Anatomy
CARDIAC VALVES OPEN AND CLOSED
Pulmonary Anterior semilunar cusp Conus arteriosus
valve Left fibrous trigone
Right semilunar cusp Right coronary artery
Left semilunar cusp
Aortic Right (coronary) Atrioventricular part
valve semilunar cusp of membranous septum
Left (coronary)
semilunar cusp Anterior
Posterior cusp
(noncoronary) Septal Tri-
semilunar cusp cusp cuspid
valve
Circumflex branch*
Anterior cusp Posterior
Mitral Commissural cusp
valve cusps
Right fibrous ring
Posterior cusp (of tricuspid valve)
Right fibrous trigone
Left fibrous ring Atrioventricular (AV)
(of mitral valve) nodal branch†
Posterior interventricular branch†
Heart in diastole: viewed from base with atria removed
Pulmonary Anterior semilunar cusp Conus arteriosus
valve Right semilunar cusp Left fibrous trigone
Left semilunar cusp Right coronary artery
Right (coronary) Interventricular
semilunar cusp part
Aortic Left (coronary) Atrio- Membranous
valve semilunar cusp ventricular septum
Posterior part
(noncoronary)
semilunar cusp Anterior
cusp
Valves Circumflex branch* Septal Tricuspid
cusp valve
Each atrioventricular (AV) valve apparatus consists of a Mitral Anterior cusp Posterior
number of cusps, chordae tendineae, and papillary valve Posterior cusp cusp
muscles. The cusps are thin, yellowish white, glistening
trapezoid-shaped membranes with fine, irregular edges. Left fibrous ring (of mitral valve) Right fibrous ring
They originate from the annulus fibrosus, a poorly Posterior interventricular branch† (of tricuspid valve)
defined and unimpressive fibrous ring around each AV Right fibrous trigone
orifice. The amount of fibrous tissue increases only at Atrioventricular (AV) nodal branch†
the right and left fibrous trigones.
Heart in systole: viewed from base with atria removed
The atrial surface of the AV valve is rather smooth
(except near the free edge) and not well demarcated *Of left coronary artery
from the atrial wall. The ventricular surface is irregular †Of right coronary artery
because of the insertion of the chordae tendineae and
is separated from the ventricular wall by a narrow space. The chordae of the first order insert into the extreme the mainstays of the valves and are comparable
edge of the valve by a large number of very fine to the stays of an umbrella.
The extreme edges of the cusps are thin and delicate strands. Their function seems to be merely to The chordae of the third order originate from the
with a sawtooth appearance from the insertion of prevent the opposing borders of the cusps from ventricular wall much nearer the origin of the
equally fine chordae. Away from the edge, the atrial inverting. cusps. These chordae often form bands or foldlike
surface of the cusps is finely nodular, particularly in structures that may contain muscle.
small children. These nodules are called the noduli The chordae of the second order insert on the ven- The first two groups originate from or near the
Albini. On closure of an AV valve, the narrow border tricular surface of the cusps, approximately at the apices of the papillary muscles. They form a few strong,
between the row of Albini nodules and the free edge of level of the Albini nodules, or even higher. These tendinous cords that subdivide into several thinner
each cusp presses against that of the next, resulting in are stronger and less numerous. They function as
a secure, watertight closure. The chordae tendineae
may be divided into the following three groups:
THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS 11
P late 1-11 Cardiovascular System
VALVES AND FIBROUS SKELETON OF HEART
Aortic sinuses (of Valsalva) Ascending aorta Commissure of semilunar
valve cusps
Opening of left coronary artery
Opening of right Nodule of semilunar valve
coronary artery (body of Arantius)
Lunula
Mem- Interven- Left Aortic
branous tricular part semilunar cusp valve
septum Atrio- Posterior
ventricular semilunar cusp
part
Right
semilunar cusp
Muscular Anterior papillary muscle
part of inter- Anterior cusp of mitral valve
ventricular
septum Aortic valve
Opening of inferior vena cava Right atrium Atrioventricular
part
Opening of Interventricular Mem-
coronary sinus part (behind valve) branous
Chordae septum
tendineae
Septal Posterior cusp Tri-
papillary Anterior cusp cuspid
muscle Septal cusp valve
Posterior
papillary Posterior papillary
muscle muscle (sectioned)
(sectioned) Anterior papillary
muscle
Tricuspid (right atrioventricular) valve
Valves (Continued) Left atrium Anterior cusp
Chordae
strands as they approach the valve edges. Occasionally, tendineae Posterior cusp Mitral
particularly on the left side, the chordae of the first two Anterior Commissural valve
orders may be wholly muscular, even in normal hearts, papillary cusps
so that the papillary muscle seems to insert directly into muscle
the cusp. This is not surprising because the papillary (sectioned) Anterior papillary
muscles, the chordae tendineae, and most of the cusps are Posterior muscle (sectioned)
derived from the embryonic ventricular trabeculae and papillary
therefore were all muscular at one time. muscle Fibrous (Albini’s) nodules
The tricuspid valve consists of an anterior, a medial Mitral (left atrioventricular) valve
(septal), and one or two posterior cusps. The depth of
the commissures between the cusps is variable, but the the arteries from which these and the valve cusps arise; Arantii. On each side of the nodules of Arantius, along
commissures never reach the annulus, so the cusps are rather, the arterial wall expands into three dilated the entire free edge of the cusp, there is a thin, half-
only incompletely separated from each other. pouches, the sinuses of Valsalva, whose walls are much moon–shaped area called the lunula that has fine stria-
thinner than those of the aorta or pulmonary artery. tions parallel to the edge. The lunulae are usually
The mitral (bicuspid) valve actually is made up of four The origin of the valve cusps is therefore not straight perforated near the insertion of the cusps on the aortic
cusps: two large ones—the anterior (aortic) and posterior but scalloped. wall. In valve closure, because the areas of adjacent
(mural) cusps—and two small commissural cusps. Here, as lunulae appose each other, such perforations do not
in the tricuspid valve, the commissures are never com- The cusps of the arterial semilunar valve are largely cause insufficiency of the valve and are functionally of
plete, and they should not be so constructed in the smooth and thin. At the center of the free margin of no significance.
surgical treatment of mitral stenosis. each cusp is a small fibrous nodule called the nodulus
The arterial or semilunar valves differ greatly in
structure from the AV valves. Each consists of three
pocketlike cusps of approximately equal size. Although,
functionally the transition between the ventricle and
the artery is abrupt and easily determined, this cannot
be done anatomically in any simple manner. There is
no distinct, circular ring of fibrous tissue at the base of
12 THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS
P late 1-12 Anatomy
Specialized Conduction Ascending aorta
System of Heart
Superior vena cava Atrioventricular part Membranous septum
Sinoatrial (SA) Interventricular part
nodal artery
Sinoatrial Pulmonary valve
(SA) node Atrioventricular (AV) node
Crista terminalis
Atrioventricular (AV)
Right fibrous ring bundle (of His)
(of tricuspid valve)
Right bundle
Inferior vena cava
Purkinje fibers
Septomarginal
trabecula
(moderator band)
Anterior
papillary muscle
Subendocardial
branches
(Purkinje fibers)
Right side
The specialized heart tissues include the sinoatrial (SA) Posterior semilunar cusp Arch of aorta
node, atrioventricular (AV) node, common atrioventricu- Aortic valve Left semilunar cusp
lar bundle or bundle of His, right and left bundle Pulmonary trunk
branches, and peripheral ramifications of these bundle Right semilunar cusp Left auricle
branches, which make up the subendocardial and intra-
myocardial Purkinje network. In addition, other fiber Membranous Interventricular part Right
groups in the atria meet some of the histologic and septum pulmonary
electrophysiologic criteria for specialization. These Atrioventricular part veins
tissues constitute Bachmann’s bundle and the inter- Mitral valve
nodal conducting paths of the right atrium. Left bundle (cut away)
Anterior Muscular part of
The body of the SA node is in the wall of the right papillary interventricular
atrium, at the junction between the atrium proper and muscle septum
the superior vena cava. At the lower end, the nodal fibers Subendocardial Inferior vena cava
change and form the common bundle. The common branches
bundle divides into right and left bundle branches, (Purkinje fibers)
which extend subendocardially along both septal sur- Posterior
faces. The left bundle branch rapidly subdivides, papillary
forming a broad sheet of fascicles sweeping over the left muscle
interventricular septal surface. The right bundle branch
extends for a distance without subdivision; one branch Left side
usually passes through the moderator band, and other
parts extend over the endocardial surface of the ven- described by Wenckebach. The posterior internodal tract The only normal anatomic communication between
tricle. Peripherally, both bundle branches subdivide and extends from the tail of the sinus node along the crista the atria and ventricles of the mammalian heart is the
form the subendocardial network of Purkinje fibers, terminalis, through the eustachian ridge, the right atrioventricular node with the common bundle of His.
which extend a variable distance into the ventricular superior margin of the AV node. A description of the On the atrial side, the AV node communicates with the
walls and are in direct continuity with fibers of the interconnections of internodal tracts with the atrium atrium through the branched and interweaving fibers of
ventricular muscle. and AV node follows. the internodal tracts and perhaps through connections
with ordinary atrial musculature. In addition, in studies
In definitive histologic studies of the human atrium, Physiologic evidence suggests that the spread of the of the canine AV node, fiber tracts appear to bypass the
James demonstrated the existence of three discrete sinus impulse to the left atrium and from the sinus node nodal body and connect with distal portions close to the
internodal paths and the relationship of one of these to to the AV node normally depends primarily on activa- junction of nodal fibers and the common AV bundle.
Bachmann’s bundle. The anterior internodal tract leaves tion of the anterior internodal tract and Bachmann’s Similar “bypass” fibers can be demonstrated in studies
the head of the sinus node and spreads to the left, divid- bundle. The physiologic significance of these tracts is of the human AV node.
ing to form two branches: One extends along the dorsal also described here.
aspect of the interatrial band to ramify over the left
atrium. This subdivision constitutes the specialized
fibers of Bachmann’s bundle. The other branch curves
across the interatrial septum to the region of the AV
node, where it merges with fibers from other nodal
tracts. The middle internodal tract leaves the posterodor-
sal margin of the sinus node and crosses the interatrial
septum to merge at the AV node with other specialized
atrial fibers. This tract corresponds to the bundle
THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS 13
Plate 1-13 Cardiovascular System
STERNOCOSTAL AND DIAPHRAGMATIC SURFACES
Sinoatrial (SA) Left auricle (cut)
nodal branch
Atrial branch of right Left coronary artery
coronary artery Circumflex branch of
Right left coronary artery
coronary artery Great cardiac vein
Anterior Left (obtuse)
cardiac veins marginal artery
Anterior inter-
Small cardiac vein ventricular
Right (acute) branch (left anterior
marginal branch descending) of left
of right coronary artery coronary artery
Diagonal branch
Interventricular septal branches of anterior
Sternocostal surface interventricular
artery
Coronary Arteries and
Cardiac Veins
BLOOD SUPPLY OF THE HEART Oblique vein of left atrium Sinuatrial (SA) nodal branch
The normal heart and the proximal portions of the (of Marshall) Sinuatrial (SA) node
great vessels receive their blood supply from two coro- Great cardiac vein
nary arteries. The left coronary artery (LCA) originates Circumflex branch of Small cardiac vein
from the left sinus of Valsalva near its upper border, at left coronary artery
about the level of the free edge of the valve cusp. The Left marginal branch Right coronary artery
LCA usually has a short (0.5-2 cm) common stem that Coronary sinus Posterior interventricular
bifurcates or trifurcates. One branch, the anterior inter- Posterior left branch (posterior
ventricular (descending) branch, courses downward in the ventricular branch descending) of right
anterior interventricular groove (largely embedded in Posterior vein coronary artery
fat), rounds the acute margin of the heart just to the of left ventricle Right marginal branch
right of the apex, and ascends a short distance up the Middle Diaphragmatic surface
posterior interventricular groove. cardiac vein the anterior RV wall. A usually well-developed and
large branch runs along the acute margin of the
The left anterior descending branch of the LCA gives Interventricular heart. The posterior interventricular (descending) branch
off branches to the adjacent anterior RV wall (which septal branches descends along the posterior interventricular groove,
usually anastomose with branches from the right coro- not quite reaching the apex, and supplies the posterior
nary artery) and septal branches (which supply anterior In cases where the LCA trifurcates, the third branch, third or more of the interventricular septum. The dia-
two thirds and apical portions of septum), as well as a coming off between the anterior interventricular and phragmatic part of the right ventricle is largely supplied
number of branches to the anteroapical portions of the the circumflex branches, is merely an LV branch that by small, parallel branches from the marginal and pos-
left ventricle, including the anterior papillary muscle. originates from the main artery. terior descending arteries, not from the parent vessel
One septal branch originating from the upper third The right coronary artery (RCA) arises from the right
of the anterior interventricular branch is usually larger anterior sinus of Valsalva of the aorta and runs along
than the others and supplies the midseptum, including the right AV sulcus, embedded in fat. The RCA rounds
the bundle of His and bundle branches of the conduc- the acute margin to reach the crux in the majority of
tion system. This branch also may supply the anterior cases, and it gives off a variable number of branches to
papillary muscle of the right ventricle through the mod-
erator band. The second, usually smaller circumflex
branch of the left coronary artery runs in the left AV sulcus
and gives off branches to the upper lateral left ventricu-
lar wall and the left atrium. The circumflex branch
usually terminates at the obtuse margin of the heart,
but it can reach the crux (junction of posterior inter-
ventricular sulcus and posterior AV groove). In this case
the circumflex branch supplies the entire left ventricle
and ventricular septum with blood, with or without the
right coronary artery.
14 THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS
P late 1-14 Anatomy
ARTERIOVENOUS VARIATIONS
Anterior interventricular (left anterior descending) Posterior interventricular (posterior descending)
branch of left coronary artery is very short. Apical branch is derived from circumflex branch of
part of anterior (sternocostal) surface supplied by left coronary artery instead of from right
branches from posterior interventricular (posterior coronary artery.
descending) branch of right coronary artery
Coronary Arteries and curving around apex.
Cardiac Veins (Continued)
itself. The latter generally crosses the crux, giving off Posterior interventricular (posterior descending) Posterior interventricular (posterior descending)
the posterior interventricular branch and a small branch branch is absent. Area supplied chiefly by small branch is absent. Area supplied chiefly by elongated
to the atrioventricular node. It terminates in a number branches from circumflex branch of left coronary anterior interventricular (left anterior descending)
of branches to the LV wall. artery and from right coronary artery. branch curving around apex.
The posterior papillary muscle of the left ventricle Most of the cardiac or coronary veins enter the coro- atrium independently, and the anterior cardiac veins
usually has a dual blood supply from both the left and nary sinus. The three largest veins are the great cardiac always do.
the right coronary artery. vein, middle cardiac vein, and posterior left ventricular vein.
The ostia of these veins may be guarded by fairly well- Small venous systems in the atrial septum (and
Of the right atrial branches of the right coronary artery, developed unicuspid or bicuspid valves. The oblique vein probably in ventricular walls and septum) enter the
one is of great importance. This branch originates from of the left atrium (of Marshall) enters the sinus near the cardiac chambers directly, called the thebesian veins.
the RCA shortly after its takeoff and ascends along the orifice of the great cardiac vein, and its ostium never The existence of so-called arterioluminal and arte
anteromedial wall of the right atrium. It enters the has a valve. The small cardiac vein may enter the right riosinusoidal vessels is debatable and the evidence
upper part of the atrial septum, reappears as the superior inconclusive.
vena cava branch (nodal artery) posterior and to the left
of the SVC ostium, rounds the ostium, and runs close
to (or through) the sinoatrial node (see Plate 1-13),
giving off branches to the crista terminalis and pectinate
muscles.
Variations in the branching pattern are extremely
common in the human heart. In about 67% of cases the
RCA crosses the crux and supplies part of the LV wall
and the ventricular septum. In 15% of cases (as in dogs
and many other mammals) the LCA circumflex branch
crosses the crux, giving off the posterior interventricu-
lar branch and supplying the entire left ventricle, the
ventricular septum, and part of the RV wall. In about
18% of cases, both coronary arteries reach the crux. No
real posterior interventricular branch may exist, but
the posterior septum is penetrated at the posterior
interventricular groove by many branches from the
LCA, RCA, or both. In about 40% of cases the SVC
branch is a continuation of a large anterior atrial branch
of the LCA rather than of the anterior atrial branch of
the RCA.
Also, the first branch of the RCA may originate inde-
pendent of the right sinus of Valsalva rather than from
the parent artery. Rarely, the second or even the third
RCA branch arises independently.
THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS 15
Plate 1-15 Cardiovascular System
NERVES OF HEART
Superior cervical Right vagus nerve (X) Left vagus nerve (X)
sympathetic ganglion
Innervation of Heart Superior cervical
(Conjoined sympathetic sympathetic ganglion
The heart is supplied by sympathetic and parasympa- and vagal) superior
thetic nerves that arise primarily in the cervical region cervical cardiac nerves Superior cervical
because initially the heart develops in the neck. Later Middle cervical (sympathetic) cardiac nerve
the heart migrates downward into the thorax, along sympathetic ganglion Superior cervical
with its nerves. Middle cervical (sym- (vagal) cardiac branch
pathetic) cardiac nerve
The cervical and upper thoracic sympathetic trunk Phrenic nerve Middle cervical
ganglia contribute cardiac branches, all of which pass Inferior cervical sympathetic ganglion
through the cardiac plexus, usually without forming syn- (vagal) cardiac branch
apses. These ganglia are ultimately distributed to the Vertebral ganglion Phrenic nerve
various layers of the heart wall through the coronary Inferior thyroid artery Middle cervical
plexuses. Three pairs of sympathetic cardiac nerves are Vertebral artery (sympathetic)
derived from the cervical ganglia of the sympathetic Cervicothoracic cardiac nerve
trunks, and others arise from the upper thoracic ganglia. (stellate) ganglion Inferior cervical
Ansa subclavia (vagal) cardiac branch
The superior cervical sympathetic cardiac nerve origi- Right recurrent Vertebral ganglion
nates by several rootlets from the corresponding gan- laryngeal nerve Cervicothoracic
glion. It often unites with the superior vagal cardiac (stellate) ganglion
nerve(s), and this conjoined nerve then descends behind Inferior cervical
the carotid sheath, communicating en route through sympathetic
slender rami with the pharyngeal, laryngeal, carotid, cardiac nerves
and thyroid nerves. On the right side, the conjoined
nerve passes posterolateral to the subclavian and bra- Inferior cervical 3rd thoracic
chiocephalic arteries and aortic arch; on the left it (sympathetic) sympathetic
curves downward across the left side of the aortic arch. cardiac nerves ganglion
Thoracic cardiac branch Thoracic
The middle cervical sympathetic cardiac nerve is often of vagus nerve (sympathetic)
the largest of the cervical cardiac nerves. It is formed 4th thoracic cardiac branches
by filaments from the middle and vertebral ganglia of the sympathetic ganglion Thoracic cardiac
sympathetic trunk. This cardiac nerve usually runs Thoracic (sympathetic) branch of
independent of the cardiac plexus but may unite with cardiac branches vagus nerve
other cardiac nerves, and it is interconnected with tra- Left recurrent
cheal, esophageal, and thyroid branches of the sympa- Cardiac plexus laryngeal nerve
thetic trunks.
Phrenic nerve (cut)
The inferior cervical sympathetic cardiac nerves consist
of filaments arising from the stellate (cervicothoracic) The thoracic vagal cardiac nerves are a series of fila- right and left sides of the plexus surround and accom-
ganglion and ansa subclavia. These cardiac nerves often ments arising from the vagus nerve of each side, at or pany the coronary arteries and their branches. The
combine with each other or with other cardiac nerves below the level of the thoracic inlet, and also from both cardiac plexus lies between the concavity of the aortic
before reaching the cardiac plexus, and inconstant com- recurrent laryngeal nerves, with the left contributing arch and the tracheal bifurcation and is sometimes
munications exist between these nerves and the phrenic more filaments than the right. These often unite with described as consisting of superficial and deep parts,
nerves. other cardiac nerves in their passage to the cardiac although their depths vary minimally, and they are inti-
plexus. mately interconnected. However, a superficial tenuous
The thoracic sympathetic cardiac nerves are four or five preaortic plexus exists over the ascending aorta.
slender branches on each side that arise from the cor- CARDIAC PLEXUS
responding upper thoracic sympathetic trunk ganglia. All the vagal and the sympathetic cardiac nerves con- A proportion of the vagal fibers relay in several
These cardiac nerves run forward and medially to the verge on the cardiac plexus, and filaments from the ganglia present in the cardiac plexus. The largest, the
cardiac plexus. Some enter the plexus directly, whereas ganglion of Wrisberg, lies below the aortic arch between
others are united for variable distances with filaments the division of the pulmonary trunk and the tracheal
destined for the lungs, aorta, trachea, and esophagus.
The vagal (parasympathetic) cardiac branches vary in
size, number, and arrangement but can be grouped as
superior and inferior cervical and thoracic vagal cardiac
nerves. The superior cervical vagal cardiac nerve forms
from two or three filaments that leave the vagus in the
upper part of the neck and usually unites with the cor-
responding sympathetic cardiac nerve. This conjoined
nerve then descends to the cardiac plexus (see earlier).
The inferior cervical vagal cardiac nerve(s), one to three
in number, arise in the lower third of the neck and often
join or communicate with the cardiac branches from
the middle cervical sympathetic ganglia and the vertebral
and/or stellate sympathetic ganglia. If they remain
separate, these cardiac nerves lie posterolateral to the
brachiocephalic artery and aortic arch on the right side
and lateral to the left common carotid artery and aortic
arch on the left side.
16 THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS
P late 1-16 Anatomy
SCHEMA OF INNERVATION
Innervation of Superior cervical Posterior (dorsal) nucleus of vagus nerve
Heart (Continued) sympathetic ganglion Nucleus of
Superior cervical solitary tract
(sympathetic)
cardiac nerve Medulla
oblongata
bifurcation. Other, smaller collections of parasympa- Middle cervical Vagus nerves
thetic cells—the intrinsic cardiac ganglia—are located sympathetic ganglion Superior cervical
mainly in the atrial subendocardial tissue, along the AV (vagal) cardiac branches
sulcus and near the roots of the great vessels. Relatively Middle cervical Inferior cervical
few cardiac ganglia are found over the ventricles, but (sympathetic) (vagal) cardiac branches
enough exist to question the view that the ventricular cardiac nerve
innervation is entirely or predominantly sympathetic. Ascending
Vertebral connections
The cardiac sympathetic and parasympathetic nerves ganglion (variation)
carry both afferent and efferent fibers. The afferents T1
transmit impulses to the central nervous system from Ansa subclavia T2
discrete cardiac receptor endings and terminal net- T3
works plentiful in these reflexogenous zones, such as Cervicothoracic T4
the endocardium around openings of the caval and pul- (stellate) ganglion
monary veins, over the interatrial septum, and in the Cardiac
AV valves. The efferents carry impulses that are modi- 1st intercostal nerve plexus
fied reflexively by afferent impulses from the heart and
great vessels. Efferent fibers are under the overall Inferior cervical
control of the higher centers in the brain, the hypo- (sympathetic)
thalamus, and the brainstem. cardiac nerve
Thoracic cardiac
The more important pathways are illustrated in branch of vagus nerve
Plates 1-15 and 1-16. Afferents from the heart and the 2nd thoracic
great vessels are shown traveling to the cord via the sympathetic
sympathetic cardiac nerves, whereas others are carried ganglion
upward to nuclei in the medulla oblongata by the vagus White ramus
nerves. The efferents pursue similar routes but travel in communicans
a centrifugal direction. The cell bodies of the afferent Gray ramus
neurons are situated in the dorsal root ganglia of the communicans
upper four or five thoracic nerves and in the inferior vagal
ganglia. 4th thoracic
sympathetic ganglion
The preganglionic parasympathetic fibers are the axons
of cells in the dorsal vagal nuclei, and these fibers relay Thoracic (sympathetic)
in cardiac plexus or intrinsic cardiac ganglia. The cardiac branches
preganglionic sympathetic fibers are the axons of cells
located in the lateral gray columns of the upper four or Sympathetic preganglionic
five thoracic segments. These fibers enter the corre- Sympathetic postganglionic
sponding spinal nerves and leave them in white rami Parasympathetic preganglionic
communicantes. which pass to adjacent ganglia in the Parasympathetic postganglionic
sympathetic trunks. Some fibers relay in these ganglia, Visceral afferent accompanying
however, and the postganglionic fibers (the axons of sympathetic fibers
ganglionic cells) are conveyed to the heart in the thoracic Visceral afferent accompanying
sympathetic cardiac nerves. Others ascend in the sympa- parasympathetic fibers
thetic trunks to form synapses with cells in the superior,
middle, and vertebral ganglia, and the postganglionic fibers Despite their insignificant size, the thoracic sympa- spinal cord. Because many cardiac pain fibers run
reach the heart via cardiac branches of these ganglia. thetic cardiac nerves carry many efferent accelerator through the preaortic plexus, some advocate excision of
Therefore the parasympathetic relays occur in ganglia and afferent fibers to and from the heart and great this plexus as a simpler, safer alternative to upper tho-
near or in the heart, whereas the sympathetic relays vessels. Other cardiac pain afferents run in the middle racic sympathetic ganglionectomy for relief of angina
are located in ganglia at some distance from the and inferior cervical sympathetic cardiac nerves, but after pectoris.
heart. Consequently, the parasympathetic postgangli- entering the corresponding cervical ganglia, they
onic fibers are relatively short and circumscribed in descend within the sympathetic trunks to the thoracic Afferent fibers from the pericardium are carried
their distribution. region before passing through rami communicantes mainly in the phrenic nerves, although afferents from
into the upper four or five thoracic nerves, then to the the visceral serous pericardium are conveyed in the
Afferent and efferent fibers probably run in all the coronary plexuses.
sympathetic and the parasympathetic cardiac nerves,
although afferents may not be present in the superior
cervical sympathetic cardiac nerves. Many afferent vagal
fibers from the heart and great vessels are involved in
reflexes depressing cardiac activity, and in some animals
these fibers are aggregated in a separate “depressor
nerve” and in humans may run in cardiac branches of
the laryngeal nerves.
THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS 17
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SECTION 2
PHYSIOLOGY
Plate 2-1 Cardiovascular System
EVENTS IN THE CARDIAC CYCLE: LEFT VENTRICLE
Aortic Aortic valve closes
pressure S2
Aortic valve opens
S4S1
Heart sounds
Mitral valve closes Mitral valve opens
LA pressure Systolic
LV pressure ejection
Systolic Diastolic
Normal cardiac cycle
Cardiovascular Examination than 0.9, some peripheral artery disease may be or LV sounds and murmurs. The left side (left decubi-
present. tus) position accentuates the rumbling murmur of
EVENTS IN THE CARDIAC CYCLE: mitral stenosis. The bent-forward position is preferred
LEFT VENTRICLE Jugular venous pulsations seen when the patient is for aortic diastolic murmurs, whereas the supine posi-
The events occurring during the cardiac cycle are lying with the upper body elevated to 30 degrees sug- tion is best for pulmonic and tricuspid murmurs.
driven by the left ventricular (LV) pressure. The mitral gests elevated RA pressure of several causes.
valve closes and results in the first heart sound (S1) when AREAS OF CARDIAC AUSCULTATION
LV pressure rises above left atrial (LA) pressure (see Precordial palpation before auscultation of the heart The conventional designations for areas of auscultation
Plate 2-1). The aortic valve opens when LV pressure can help the examiner make the proper cardiac diagno- have been mitral, tricuspid, aortic, and pulmonary.
rises above aortic diastolic pressure and is the onset of sis. The apical impulse can suggest LV hypertrophy Current understanding divides the thorax into seven
systolic ejection. The aortic valve closes and produces (enlargement) if sustained and slow rising. Palpation areas: left ventricular, right ventricular, left atrial, right
the second heart sound (S2) when LV pressure falls along the left sternal border may reveal a parasternal atrial, aortic, pulmonary, and descending thoracic aortic
below aortic pressure and terminates systolic ejection. lift, which suggests an elevated right ventricular (RV) (see Plate 2-4).
The mitral valve opens when LV pressure falls below pressure of about 40 mm Hg. Plate 2-2 illustrates some Left Ventricular Area
LA pressure. The fourth heart sound (S4) occurs in late examples of carotid pulses and venous pulsations and The apical area (“mitral” area) is the best location for
diastole following atrial contractions. cardiac apical impulses associated with specific cardiac detecting not only the murmur of mitral stenosis or
disease states. insufficiency but also the LV or atrial gallops and the
Cardiac auscultation is not the only way to examine aortic component of the second sound (A component of II).
the cardiovascular system. Peripheral vessels reflect The basic instrument of auscultation is the human The murmurs of aortic stenosis and especially of
what is occurring in the cardiovascular system; for ear. Although the stethoscope has technical advantages, aortic insufficiency also are often heard well at this
example, carotid and femoral artery examination can it often distorts, decreases, or selectively emphasizes location. However, these vibrations are detected over a
reveal peripheral vascular disease. Bruits over these certain vibrations. Frequently, the naked ear is superior larger area formed by the entire left ventricle, center-
vessels may indicate carotid stenosis or aortofemoral to the stethoscope in the detection of low-pitched vibra- ing around the apical beat and extending to the fourth
stenosis. An abdominal bruit may indicate renal artery tions (S3, S4) because the ear is a larger collector of and fifth left interspaces medially and to the anterior
stenosis. A decrease in blood pressure in either arm sound and fuses auditory with palpatory perception. axillary line laterally. In patients with ventricular
suggests subclavian artery stenosis. If the ankle- enlargement, the sound shifts to either the left or the
brachial index (ratio of systolic pressure in arm to sys- POSITIONS FOR CARDIAC AUSCULTATION right.
tolic pressure in ankle using Doppler technique) is less In auscultation, various patient positions can be used
(see Plate 2-3). The patient may be sitting, supine, lying
on the left side, or bent forward to increase the contact
of the apex with the chest wall, as preferred for mitral
20 THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS
P late 2-2 Physiology
IMPORTANT COMPONENTS OF CARDIAC EXAMINATION
Examples of carotid Examples of venous
pulses and the pulses and the entities
entities with which with which they
they are associated are associated
Normal S1 S2 Normal S1 S2
S1 S2
Phono c
Phono Jugular
pulse
Carotid ECG a v h
pulse x y
ECG
Hypertrophic cardiomyopathy Tricuspid regurgitation
(Bisferiens pulse) Phono S1SM S2 S1 SM S2
Jugular a v S3a v S3
S1 S2 pulse
Phono ECG y y
Carotid
pulse
ECG Pulmonary hypertension
Aortic regurgitation secondary to mitral
stenosis
(Corrigan’s pulse) Diastolic Phono SM
murmur Jugular a S1 S2
S1 S2 pulse
cx v y
Phono
Carotid ECG
pulse
ECG
Cardiac apical impulse
(palpation of the precordium)
Cardiovascular Examination
Careful auscultation of the abdomen can reveal S1 S2 S1 S2
(Continued) bruits from vessels such as aorta and renal arteries. Hyperdynamic
impulse
(hypertrophic
Right Ventricular Area Dilatation of the abdominal portion of cardio-
The “tricuspid” area is renamed the right ventricular the aorta can be recognized by palpation. myopathy)
area. In addition to the murmurs of tricuspid stenosis Diminished or absent peripheral pulses Normal
and insufficiency, RV and atrial gallops and the murmurs indicate peripheral vascular disease.
of pulmonary insufficiency and ventricular septal defect S1 S2
can be well heard here. The RV area includes the lower across the aorta or dilatation of the ascending aorta, and
part of the sternum and the fourth and fifth interspaces, abnormalities of the neck arteries, as well as the aortic Diffuse and
2 to 4 cm to the left and 2 cm to the right of the ejection click and aortic component of S2. sustained
sternum. This area may extend also to the point of Pulmonary Area (left ventricular
maximal impulse, in the presence of severe RV enlarge- The pulmonary area should refer to the pulmonary dysfunction)
ment; the “apex” in such patients is formed by the right artery rather than the pulmonary (pulmonic) valve. The
ventricle. murmurs of pulmonary stenosis and insufficiency, second left interspace near the sternal edge and extends
the murmur caused by increased flow or dilatation of upward to the clavicle and downward to the third left
Aortic Area the pulmonary artery, the pulmonary ejection click, the interspace near the sternal margin. However, it may
The aortic component of S2 and the murmurs of aortic pulmonary component of the second sound (P component of also extend posteriorly at the level of the fourth and
valve defects are often heard well at the third left inter- II), and the murmur of patent ductus arteriosus are fifth dorsal vertebrae.
space (Erb’s area). This point is frequently more reveal- heard best here. The pulmonary area is formed by the
ing than the second right interspace, except in patients MOST SIGNIFICANT AUSCULTATORY
with dilatation of the ascending aorta, where the manu- FINDINGS
brium or the second right interspace may be more Heart Sounds
informative. The aortic area should designate both the The first heart sound (S1) is often louder over the LV
aortic root and part of the ascending aorta. The vibra- area (apex and midprecordium), whereas the second heart
tions heard best in this area include the murmurs caused sound (S2) is frequently louder over the aortic and
by aortic stenosis, aortic insufficiency, augmented flow
THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS 21
Plate 2-3 Cardiovascular System
POSITIONS FOR CARDIAC AUSCULTATION
Leaning forward
Cardiovascular Examination
(Continued)
pulmonary areas (base). The first sound is a long noise diastolic overload of the right side of the heart and in Supine
of lower tonality, whereas the second sound is shorter right bundle branch block, because of a delay in the Left decubitus
and sharper. pulmonary component. Patients with left bundle branch
block may present with such a delay in the aortic com- The fourth heart sound (S4) is not heard in the normal
In normal adolescents or young people, S1 may be ponent as to cause paradoxical splitting. heart. S4 is audible over the LV area in hypertension,
split. The best area for hearing this split sound is at during myocardial ischemia, or when the ventricle is
the third left interspace. This splitting is not influenced The third heart sound (S3) may be normal in children, stiff and noncompliant, as in diastolic dysfunction. S4
by respiration. The loudness of S1 is decreased in myo- adolescents, and young athletes but may be audible over can also be heard in patients with ventricular volume
carditis, myocardial infarction (MI), myocardial fibro- the LV or RV area in ventricular overload, myocarditis, overload, myocarditis, tachycardia, atrial flutter, and
sis, hypothyroidism, mitral insufficiency (soft), aortic tachycardia, or heart failure. complete or incomplete atrioventricular (A-V) block or
insufficiency, and pericarditis with effusion. S1 is obstruction. The fourth sound is then called atrial
increased in mitral stenosis, systemic hypertension, gallop. A left atrial gallop is frequently heard in aortic
and hyperthyroidism.
The second sound is frequently split during inspira-
tion and in normal children and young people. The best
area for hearing this splitting is the third left interspace,
close to the sternum (Erb’s point). S2 has an increased
loudness of the aortic component in systemic hyperten-
sion, coarctation of the aorta, and aortitis. Decreased
loudness of S2 characterizes aortic stenosis. The aortic
component may be so delayed as to follow the pulmo-
nary component, a paradoxical splitting. S2 has increased
loudness of the pulmonary component in pulmonary
hypertension, whereas loudness is decreased in pulmo-
nary stenosis. The pulmonary component not only is
smaller but also is delayed, causing a wider splitting. S2
has wider, fixed splitting in conditions presenting a
22 THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS
Plate 2-4 Physiology
Systolic
AREAS OF CADIAC AUSCULTATION
Patent ductus arteriosus: continuous, rumbling
Diastolic
Aortic 1 AO 1 Aortic
insufficiency: RV PA stenosis:
blowing, 2 harsh,
high-pitched 3 2 crescendo-
Mitral 4 3 decrescendo
stenosis: 4 Ventricular
rumbling, 5 septal defect:
low-pitched 6 LV 5 harsh,
7 pansystolic
8 6 Mitral
insufficiency:
7 soft, blowing,
8 pansystolic
Common areas for auscultation in valvular defects and congenital shunts
AO=aortic area (murmurs of aortic stenosis LV=left ventricular area (murmurs of
and aortic insufficiency) mitral stenosis and mitral insufficiency)
PA=pulmonary artery area (murmurs of 3rd left interspace (most murmurs of pulmonary,
pulmonary stenosis and insufficiency) aortic, and tricuspid origin, and of ventricular
Cardiovascular Examination RV=right ventricular area (murmurs of septal defect; splitting of 2nd sound)
tricuspid valve disease) Arrows point to best areas for auscultation
(Continued)
1 1 AS
stenosis or systemic hypertension. A right atrial gallop 2 AO MI
is often heard in pulmonary stenosis or pulmonary 3 PA 2 AO PA
hypertension. A slightly different type is the summation 3 MS AI
gallop, caused by the summation of S3 and S4. This is 4 Usual transmission of “inflow”-
most often seen in patients with tachycardia and grade 5 RV 4 and “outflow”-tract murmurs of
1 A-V block. 6 LV left heart: AS=aortic stenosis;
7 5 RV AI=aortic insufficiency;
A systolic ejection click can be heard over either the Projection of auscultatory LV MS=mitral stenosis;
pulmonary area (pulmonary ejection sound) or the aortic areas in isolated left 6 MI=mitral insufficiency
area (aortic ejection sound). These clicks are caused by ventricular enlargement
“doming” of the aortic or pulmonary valve; the aortic 7
valve may be bicuspid. These ejection sounds occur Projection of auscultatory
with dilatation of the aorta or pulmonary artery or nar- areas in isolated right
rowing of the aortic or pulmonary valve, usually with ventricular enlargement
poststenotic dilatation. The ejection click is a high-
frequency sound due to abrupt halting of the valve Murmurs The murmur of A-V valve stenosis is a typical,
opening. The regurgitant murmur of A-V valve insufficiency is low-pitched rumble which acquires higher pitch and
holosystolic and usually loud (see Plate 2-5). The murmur greater loudness in presystole (presystolic accentuation)
A diastolic opening snap can be heard in the fourth left of mitral insufficiency is maximal over the LV area and if there is sinus rhythm. It is heard best in mitral ste-
interspace, close to the sternum, over the entire LV easily audible at the left axilla, whereas the murmur of nosis in the fourth left intercostal space, halfway
area, or even over the entire precordium, in patients tricuspid insufficiency is maximal over the RV area and between the apex and the sternal border. In tricuspid
with a pliable noncalcified valve. This is the mitral is well heard over the right precordium. Inspiration or stenosis this rumble is heard best over the RV area. This
opening snap most often heard in mitral stenosis. Occa- inspiratory apnea increases the loudness of the tricuspid murmur becomes louder in inspiration because of
sionally it can be heard in diastolic overload of the left murmur but decreases the loudness of the mitral increased flow across the tricuspid valve during
side of the heart (mitral insufficiency, patent ductus). A murmur. inspiration.
tricuspid opening snap is audible over the RV area in
patients with tricuspid stenosis and occasionally can be
heard in diastolic overload of the right ventricle (tricus-
pid insufficiency, atrial septal defect).
THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS 23
Plate 2-5 Cardiovascular System
MURMURS
RR
Electro- TU P
cardiogram QS
QS I
Mitral I Opening Scheme of
insufficiency: SM II snap typical shape
pansystolic of murmurs
murmur (sm); III
high-
frequency I II Opening I
phono- PM snap PM
cardiogram
Mitral A P DM I
stenosis:
large 1st Ejection II I
sound, widely I sound
Cardiovascular Examination split 2nd
sound, SM
(Continued) opening snap,
diastolic (DM) I II
The regurgitant murmur of semilunar valve insuffi- and pre- DM
ciency is a high-pitched, blowing, occasionally musical systolic (PM)
decrescendo. In aortic insufficiency the murmur is murmur;
loudest in the third left interspace (Erb’s area), and can low-frequency
be followed along the left sternal border toward the phono-
apex. If the ascending aorta is dilated, the murmur is cardiogram
louder in the second right interspace and can be fol- Aortic
lowed downward along the right sternal border. In pul- stenosis:
monary insufficiency the murmur is loudest over the “diamond-
second left interspace and can be followed downward shaped”
from the upper left to the lower right part of the systolic
sternum. If the patient has pulmonary hypertension, murmur (SM)
the murmur sounds similar to aortic regurgitation. If high-
the pulmonary artery pressure is normal or low, the frequency
murmur may have a rumbling character. phono-
cardiogram
The stenotic murmur of the semilunar valves is the Aortic
loudest of all murmurs. It is harsh, starts slightly after insufficeincy:
S1 with aortic valve opening, and is often preceded long
by an ejection click, especially if the valve is bicuspid diastolic
and mobile. The murmur often has a crescendo- murmur (DM)
decrescendo quality and ends before or with S2, with slow
depending on the severity of the stenosis. In aortic decrease of
stenosis the murmur is maximal in the third left or amplitude;
second right interspace. It is readily heard over the high-
suprasternal area and the carotid arteries and can be frequency
phono-
cardiogram
heard at the apex. In subvalvular aortic stenosis, it is aortic systolic and diastolic pressures are higher than
maximal over the LV area. In pulmonary stenosis the pulmonary systolic and diastolic pressures. It is best
murmur is best heard over the pulmonary area. It radi- heard over the first and second intercostal spaces.
ates moderately downward and often can be heard in
the back over the lungs. Friction Rubs
Friction rubs can be heard over various areas and
The murmur caused by a ventricular septal defect is resemble the sound made by rubbing new leather.
long, harsh, and pansystolic. It is heard best over the Friction rubs can be heard in atrial systole,
RV area. ventricular systole, and ventricular diastole (i.e., three-
component rub).
The murmur caused by patency of the ductus arterio-
sus is a continuous, machinery-like murmur because
24 THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS
Plate 2-6 Physiology
Emotional stress or anticipation
of exercise may stimulate
sympathetic nerves via
hypothalamus.
Carotid
sinuses
Afferent nerve fibers from baroreceptors in carotid IX
sinuses via glossopharyngeal nerves (IX) and in aorta
via vagus nerves (X) form afferent limbs of reflex arcs
to vagus and sympathetic efferents.
Dorsal nucleus X
of vagus and
cardioregulatory Vagus efferent cardiac fibers go chiefly to SA node
center and A-V node: stimulation causes release of
Descending acetylcholine at nerve endings, slowing heart rate
tract in and conduction; vagal inhibition causes
intermedio- acceleration of heart rate and conduction.
lateral column
of gray mater Sympathetic efferent fiber stimulation accelerates
of spinal cord heart rate, increases force of contraction, and dilates
coronary arteries by releasing norepinephrine at
nerve endings, stimulating β receptors.
Sympathetic trunk Increased pH heightens
catecholamine and lowers
acetylcholine actions.
pH
Output of catecholamines Circulating catecholamines
from suprarenal medulla have same action as sympathetic
promoted by sympathetic efferent nerves on
stimulation coronary arteries.
Neural and Humoral increased filling that occurs when diastolic filling time The nervous mechanisms controlling heart rate
Regulation of Cardiac is increased. include the baroreceptor reflexes, with afferent arms from
Function the carotid sinus, the arch of the aorta, and other pres-
The heart is normally under the restraint of vagal soreceptor zones operating as negative feedback mech-
The efferent innervation of the heart is controlled by inhibition, and thus bilateral vagotomy increases the anisms to regulate pressure in the arteries. These
both the sympathetic nervous system and the parasym- heart rate. Vagal stimulation not only slows the heart but reflexes affect not only heart activity but also the caliber
pathetic nervous system. Afferent fibers accompany the also slows conduction across the A-V node. Sectioning of the resistance vessels in the vascular system.
efferents of both systems. The sympathetic fibers have of the cardiac sympathetics does not lower heart rate
positive chronotropic (rate-increasing) effects and pos- under normal circumstances. The heart is also affected reflexively by afferent
itive inotropic (force-increasing) effects. The parasym- impulses via the autonomic nervous system. The
pathetic fibers have a negative chronotropic effect and The totally denervated heart loses some (but surpris- response may be tachycardia or bradycardia, depend-
may be somewhat negatively inotropic (but small ingly little) of its capacity to respond to changes in its ing on whether the sympathetic or parasympathetic
and masked) in the intact circulatory system by the load. The denervated heart still responds to humoral system is activated more strongly in the individual
influences, more slowly and less fully, but it is remark- patient. Tachycardia is the common response in
able how well the secondary mechanisms, such as the excitement.
suprarenal medullary output of catecholamines, can
substitute for the primary mechanism that controls
heart rate in exercise.
THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS 25
Plate 2-7 Cardiovascular System
Hematologic changes in pregnancy
Estrogen Percent increase in 60
Renin intravascular volumes Plasma volume
Angiotensin II (% increase) 50
Aldosterone Blood volume
Na+/H2O retention
40
30
Erythropoiesis 20
Red cell volume
10
Human chorionic 5 10 15 20 25 30 35 40
somatomammotropin Weeks of gestation
Multifactorial stimulation of fluid retention and erythropoiesis in pregnancy results in a 50% increase in plasma
volume and a 30% increase in red cell mass, creating a relative “physiologic” anemia and an increased blood volume.
Changes in cardiac output
Increased Percent increase in 50 Cardiac output
cardiac output cardiac output 40
(% increase) 30
20
10
5 10 15 20 25 30 35 40
Weeks of gestation
Cardiac output increases 50% in normal pregnancy, predominantly from increased stroke volume in first
and second trimesters and increased pulse rate in third trimester.
Postural changes
Physiologic Changes During Fetus Vena caval Postural changes in systolic 120
Pregnancy Supine compression and diastolic blood pressure 105 Lateral decubitus (Systolic)
During a normal pregnancy, a woman undergoes mul- Compression (mm Hg) 90
tiple cardiovascular physiologic changes to support the relieved Supine
increased metabolic demands of the woman and the
unborn child. The changes are fairly typical in a healthy 75 Lateral decubitus
pregnant woman but may vary in magnitude from 60
patient to patient. Early in the pregnancy, the first tri- 45 (Diastolic)
mester, the changes are usually mild or may not be
evident. The classic changes include the following; 30 Supine
• Blood volume gradually increases from mild in the 15
first trimester to moderate in the second trimester
to marked in the third trimester. These volume Gravid 5 10 15 20 25 30 35 40
changes often are not reflected in ventricular uterus Weeks of gestation
volume changes and systolic function of the left
ventricle usually remains normal, as determined by Left lateral decubitus
cardiac ultrasound. Positional changes have hemodynamically significant effects on pregnant women. Compression of the inferior vena
cava by the gravid uterus in the supine position may cause hypotension and syncope. Condition is relieved by altering
• With the increase in blood volume a concomitant position from supine to lateral decubitus to relieve compression and restore venous return and cardiac output.
increase in cardiac output usually occurs, possibly
from the Starling mechanism. It becomes maximal systemic vascular resistance, especially in the slightly increased to greatly increased in the third
in the second trimester and decreasing to moderate second trimester, which probably influences the trimester.
in the third trimester. marked increase in cardiac output and stroke Anatomic factors related to the enlarged uterus can
volume. also influence physiologic changes, particularly in the
• Stroke volume tends to increase when cardiac • Heart rate gradually increases from normal or third trimester. Inferior vena cava compression can
output increases in the second trimester but usually slightly increased to greatly increased in the third increase femoral venous pressure and can elevate the
normalizes or decreases in the third trimester. trimester. diaphragm, which in turn can shift the axis of the heart
• Along with the changes in heart rate, oxygen con- and alter the axis of the electrocardiogram toward
• Systolic blood pressure tends to decrease or remain sumption gradually increases from normal or the left.
normal throughout pregnancy, whereas pulse pres-
sure widens because of a decrease in diastolic
pressure. This is related to a marked decrease in
26 THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS
Plate 2-8 Physiology
VASCULAR ACCESS Points of
measuring
Right-heart catheterization pressure
Catheter can be introduced
into basilic vein, goes Superior vena cava
via axillary, subclavian, Wedged in small branch
brachiocephalic veins of pulmonary artery
and superior vena cava Pulmonary trunk
to right heart Right ventricle
Right atrium
Catheter may be Inferior vena cava
introduced via
jugular or
saphenous vein
Cardiac Catheterization
VASCULAR ACCESS AND RIGHT-SIDED Left-heart catheter access Guide wire in the left coronary artery
HEART CATHETERIZATION Guide catheter
Femoral artery Brachial artery
Cardiac catheterization, first attempted by Forssmann
on himself in 1928, was developed by Cournand, from the pulmonary artery are used with other data to Radial artery
Richards, and their colleagues and is now a common calculate the pulmonary blood flow with thermodilu-
procedure in both clinical and research laboratories. tion and balloon-tipped catheters. Measurement of Special sensors at the tip of a catheter have been
pressures through the catheter using external pressure designed for the detection and recording of intracardiac
Technique transducers allows determination of the phasic form of ECGs and pressures.
The primary goal of right-sided heart catheterization is the pressure in any location. Pressures recorded as a Complications
to access the conditions existing in the chambers and catheter traverses a valve permit an evaluation of the Brief arrhythmias, vasovagal episodes, and minor phle-
great vessels of the right side of the heart. In these site and degree of valvular stenosis. bitis may be observed in patients undergoing catheter-
procedures a radiopaque flexible catheter of various ization. More serious complications are rare.
designs, including balloon tipped, is introduced into a
vein, usually the femoral or jugular, percutaneously
using local anesthesia. After introduction into the vein,
the catheter is manipulated under fluoroscopic control
and constant electrocardiographic monitoring down-
stream through the venous system to the right atrium,
and eventually into the right ventricle and pulmonary
artery. The catheter is often wedged and is advanced into
the most peripheral branch of the pulmonary artery
that will accept the catheter tip or occlusion by a
balloon-tipped catheter.. A pressure recorded from the
wedge position has essentially the same mean pressure
as the left atrium and the same but delayed phasic fea-
tures. If there is no mitral stenosis, the pulmonary capil-
lary wedge pressure (PCWP) reflects the left ventricular
end-diastolic pressure (LVEDP).
Diagnostic Procedures
The position of the catheter in the fluoroscopic image
may indicate some departure from the intracardiac
course normally taken by a catheter. Examples include
passage into a persistent left superior vena cava through
the coronary sinus from the right atrium, passage
through a patent ductus arteriosus, and traversal of an
interatrial or interventricular septal defect.
Blood can be sampled for oxygen or other analysis,
and pressures can be measured through the catheter
from any point reached. Oxygen samples can be used
to determine the site of entry into the right side of the
heart and the size of a left-to-right intracardiac shunt
at atrial, ventricular, or pulmonary artery levels in
patients with congenital heart disease. Oxygen values
THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS 27
Plate 2-9 Cardiovascular System
LEFT-SIDED HEART CATHETERIZATION
Catheter
introduced Seldinger technique for catheterization of
into brachial femoral artery
or Needle introduced
femoral artery into artery
and passed
retrograde via Guidewire passed
aorta to through needle
left ventricle
Needle withdrawn
Catheter introduced
over wire
Cardiac Catheterization
(Continued)
LEFT-SIDED HEART CATHETERIZATION Diagnostic Procedures catheter withdrawal, although rarely may require
Sampling and pressure measurements for left-sided therapy. Other complications include arterial spasm
Technique heart catheterization do not differ from right-sided and the rare dissection or occlusion of the artery.
The aim of left-sided heart catheterization is the study of procedures. Valvular abnormalities can be estimated Perforations of the walls of an artery or the aorta, a
conditions in the chambers and vessels of the left side using simultaneous pressure measurements on both heart chamber, or a coronary artery also can occur
of the heart. In congenital heart disease the catheter sides of the valve. rarely. Fluid should never be forced through a cath-
may reach the left side of the heart from a right-sided eter from which blood cannot be withdrawn, particu-
heart chamber, passing through an atrial septal defect Complications larly if the catheter is in the ascending aorta; a clot
or a patent ductus arteriosus. Arrhythmias, the most common complication of left- can be expressed and embolize peripherally to the
sided catheterization, usually respond to simple brain.
More often the left side of the heart is approached
by retrograde passage of the catheter from its point of
insertion into a peripheral artery, most commonly by
percutaneous technic. This technique was designed by
Seldinger (see Plate 2-9). The catheter is manipulated
under fluoroscopic control in a retrograde direction
using the Seldinger technique through the artery to the
aorta and frequently across the aortic valve into the left
ventricle. Entry into the left atrium retrograde through
the mitral valve is possible but not typically used.
Approach to the left atrium can also be accomplished
using a transseptal technique by passage of the trans-
septal catheter and transseptal needle from a right
femoral vein to the right atrium and across the atrial
septum at the level of the fossa ovalis. The catheter can
then be advanced into the left ventricle. Direct percu-
taneous needle puncture of the LV apex may be done
to reach the left ventricle in special circumstances, such
as LV pressure measurement in patients with mechani-
cal aortic and mitral valves.
28 THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS
Plate 2-10 Physiology
NORMAL SATURATIONS (O2) AND PRESSURE
Hmgm a v Hmgm a v
10 c
5 Pulmonary wedge: 97% 10 c
mean <12
97%
5
L. atrium: mean <8
Pulmonary artery: 140 L. ventricle:
25 systolic <25 systolic <120
diastolic <10 120 diastolic <8
20 mean <15 100
15
10 L. atrium 80
5 95%
Pulm. 8 60
artery
Aorta 75% L. ventricle 40
95% 20/8 95%
R. atriuam:cmean < 5 120/8 20
v 120/80
5 0
R. atrium
0 xy 75%
5
150 Aorta:
R. ventricle: R. ventricle 140 systolic <120
25 systolic <25 75% 130 diastolic <80
20/5 120
diastolic <5 110
20 100
15 90
80
10 70
60
5 50
Ole Diastole Systole Diastole Normal % oxygen saturation, O2 volume %, and Ole Diastole Systole Diastole
R pressure ranges in heart chambers and great
vessels with pressure tracings in relation to ECG R
ECG
T P TP ECG
T P TP
Cardiac Catheterization NORMAL OXYGEN SATURATIONS NORMAL INTRACARDIAC PRESSURES
AND PRESSURE
(Continued) Atrial and Wedge Pressures
In the venae cavae, right atrium, right ventricle, and The phasic pressures in the right atrium, the left atrium,
CARDIAC OUTPUT: THERMODILUTION pulmonary arteries, oxygen saturation (SO2) is normally and the pulmonary artery wedge position (essentially a
TECHNIQUE close to 75% (see Plate 2-10). Small, phasic variations slightly delayed left atrial pressure) share the same char-
A balloon-tipped pulmonary artery catheter (Swan- in So2 of blood sampled from the right-sided heart acteristics, with small differences in the amplitude and
Ganz catheter) with a thermistor at the tip (introduced chambers can be measured. The variation is maximal in timing of the phasic features. In normal sinus rhythm
in 1970) floats into the pulmonary artery from the right the right atrium, where contributions of blood from the the pressure pulse in these chambers is characterized by
ventricle as an embolus when the balloon is inflated. renal veins (with a relatively high So2), from the hepatic an a wave produced by the atrial contraction that begins
The balloon occludes the distal pulmonary branches, veins (with relatively low So2), from the coronary sinus with completion of the atrial P wave in the electrocar-
and a pressure similar to the PCWP can be measured. (with very low So2), and from the lower inferior vena diogram (ECG). After a brief delay, the P wave is fol-
When deflated, the catheter measures pulmonary artery cava and superior vena cava (with intermediate So2), lowed by the QRS signaling the depolarization of the
pressure, and the thermistor measures a thermodilution meet and start mixing. The mixing is probably com- ventricular myocardium. Immediately after depolariza-
curve after injection of 10 mL of cold saline or glucose plete by the time the blood reaches the pulmonary tion, ventricular contraction begins. The A-V valves
into the right atrium. The cardiac output can be calcu- artery. In the pulmonary wedge position, 97% to 99% close, and the c waves in the atrial pressure curves are
lated from the measured thermodilution curve. When saturated blood can be withdrawn through the wedged produced by changes in the dimensions of the atria and
the cardiac output is low, the temperature change from catheter, approximating the values of pulmonary venous by bulging of the valves into the atria secondary to
right to distal pulmonary artery changes little. When blood. Blood leaving the pulmonary capillary bed is at ventricular contraction. After the c wave, pressure
the cardiac output is high, the temperature change is least 97% saturated. Blood entering the left atrium is decreases to a low value (the x descent) in response to
large. Thus the degree of change in temperature is slightly less saturated because of its admixture with further atrial volume changes during continued ven-
directly proportional to the cardiac output. blood passing through pulmonary arteriovenous and tricular contraction. During the remainder of systole,
other small shunts. continuous venous inflow produces an increase in
THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS 29
P late 2-11 Cardiovascular System
EXAMPLES OF O2 AND PRESSURE FINDINGS AND PRESSURE TRACINGS IN HEART DISEASES
Cardiac Catheterization 80/60 40/20 8
95% 85% 95%
(Continued)
Ventricular 10 5 10
pressure, the v wave). The peaks of the v waves coincide septal 97% 75% 97%
with the opening of the mitral and tricuspid valves. A defect
pressure decrease in the atria (the y descent) accompa- 80/8
nies the transfer of blood from the atria into the 40/5 95% Numerals in RED
ventricles. 85% indicate abnormal
Ventricular Pressures readings;
Except for the peak systolic pressure in the left ventricle dash over numerals
being approximately five times greater than that in the indicates mean pressure
right, the phasic pressures in the left and right ventricles
are similar in contour. The ventricles begin to contract 20 Pulmonary artery
approximately 60 milliseconds after the QRS in the 10
ECG, with the right preceding the left. This action is
associated with closure of the A-V valves, resulting in 95/70 15/6 8 100
elevated ventricular pressures. During the subsequent 80% 70% 95%
period of sequential myocardial contraction, lasting 10
msec and 40 msec for the right and left ventricles, Tetralogy 80 Right ventricle
respectively, there are no volume changes, the period of 60
of isovolumic contraction. Fallot 10 5 10 mm Hg
97% 70% 97%
When the ventricular pressures exceed the end-
diastolic pressures in the pulmonary artery and aorta, the 95/6 40
semilunar valves open and ejection begins. During the 95%
ejection period, the right ventricle and pulmonary
artery and the left ventricle and aorta have the same 95/6 20
phasic pressures until, systole being completed, the 70%
semilunar valves close and the pressures begin to drop
in the ventricles. This is followed by the brief period of 120
isovolumic relaxation.
120/70 70/30 100 Left ventricle
As soon as the ventricular pressures fall below the 95% 75% Left atrium
pressures in the atria, the A-V valves open; and diastole 30 80 Gradient
starts and proceeds with venous filling of the common 95% 60
ventricular and atrial chambers, leading to superposable
pressures in the atria and ventricles. Mitral 30 4 30 mm Hg
Aortic and Pulmonary Artery Pressures stenosis 97% 75% 97%
During ejection the ventricular pressures and the pres-
sures in the aorta or pulmonary artery are identical and 120/8 40
are characterized by a smooth rise to a peak, then a 95%
steady fall to the dicrotic notch, signaling the closure
of the aortic and pulmonary valves. This is followed by 70/4 20
a steady decrease in pressure as a “runoff” of blood from 75%
the arterial system into the venous system occurs
through the capillary beds. This is abruptly terminated 100/70 25/8 200 Left ventricle
by the next ejection. 95% 75% 180
8 160
ABNORMAL OXYGEN AND PRESSURE 95% 140
FINDINGS 120 Gradient
Ventricular Septal Defect 100
In ventricular septal defect a shunt of 95% saturated Aortic 8 4 8 mm Hg Aorta
blood is ejected during systole by the left ventricle stenosis 97% 75% 97% 80
through the defect into the right ventricle, under the 60
influence of the normally occurring pressure difference 200/8 40
between the two ventricles (see Plate 2-11). There the 95% 20
shunted blood contaminates the less-saturated mixed-
venous blood. Thus an increased volume of blood with 25/4
a greater-than-normal So2 (85%) flows into the pulmo- 75%
nary artery. In the majority of cases the volume of blood
shunted depends on the systolic pressure difference pressures in the pulmonary artery and right ventricle Tetralogy of Fallot
between the two ventricles and on size of the defect. are usually elevated because of the increased pulmonary The basic abnormalities in the tetralogy of Fallot are
The increased So2 of the blood in the pulmonary artery vascular resistance, which is secondary to the failure of pulmonary stenosis (valvular or infundibular) interven-
is in direct proportion to the volume of the shunt. The neonatal involution to take place in the normal prenatal tricular septal defect, disproportion in the diameter
medial hypertrophy of the small arteries. The pressures between and usually some displacement of the aorta and
may be greatly elevated by subsequent intimal and pulmonary artery, with secondary RV hypertrophy (see
other pathologic changes. Eventually, after develop- Plate 2-11). Because of the pulmonary stenosis, which
ment of very high RV pressures, the shunt may be significantly increases normal outflow resistance, RV
reversed, and desaturated blood may flow from the hypertension may reach systemic levels. This results in
right to the left ventricle and the systemic arteries. a shunt of unsaturated blood through the defect, with
30 THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS
Plate 2-12 Physiology
Septal shift
NORMAL CARDIAC BLOOD FLOW DURING INSPIRATION AND EXPIRATION
Normal inspiration Normal expiration
Pulmonary volume
RA LA Intrapericardial pressure RA LA
RV LV Intracardiac pressures RV LV
(right heart > left heart)
Blood flow to left heart
(pulmonary vein)
Blood flow to right heart
Intrapleural pressure
Transmural aortic
root pressure
Stroke volume (minimal)
On inspiration, intrapleural pressure drops and abdominal pressure On expiration, intrapleural pressure increases and abdominal
increases with increased blood flow through the right side of heart and pressure decreases with decreased blood flow through the right
slight decrease in flow to left side of heart. Increased aortic root side of heart and increase in flow to left side of heart.
transmural pressure adds a minor amount of LV afterload.
Inspiration Expiration Inspiration Expiration 100
LV
50
RV 0
Simultaneous measurement of RV and LV systolic pressure reveals a concordant decrease in pressure in both chambers during inspiration,
with a similar concordant increase in pressure in both ventricles during expiration. Pressure changes are exaggerated for emphasis.
Cardiac Catheterization proportional to the square of the cross-sectional area of gradient across the valve. Progressive obstruction to LV
the valve orifice and is directly proportional to the outflow magnifies these effects and leads to LV hyper-
(Continued) square of the volume flow. The gradient is greater with trophy and eventually acute or chronic LV systolic and
increases in the degree of stenosis and during exercise. diastolic failure (see Plate 2-11).
a mild reduction in So2 in the left ventricle and a greater The LA hypertension is accompanied by pulmonary
reduction in the aorta and systemic arteries. The latter venous hypertension, which results in pulmonary EFFECTS OF INSPIRATION AND EXPIRATION
causes the cyanosis characteristic of these patients. The hypertension and RV hypertension, increased RV work, ON INTRACARDIAC PRESSURES AND FLOW
greatly reduced pulmonary blood flow reaches full satu- and hypertrophy. Diastolic pressures in the pulmonary During inspiration, systolic blood pressure decreases
ration in the lungs. Systolic pressure in the right ven- artery and left atrium are identical until pulmonary and pulse rate increases slightly, because the intratho-
tricle reaches the level of the aortic pressure. Distal to vascular resistance is increased because of pathologic racic pressure becomes more negative relative to atmo-
the pulmonary stenosis, however, the pressures are changes in the vascular bed, resulting in a gradient spheric pressure. Systemic venous return increases,
lower than normal, and the pressure contour is often between the two pressures. Acute bouts of LA hyper- more blood flows into the right side of the heart, and
distorted. tension lead to pulmonary edema, whereas chronic pul- pulmonary vasculature compliance increases (see Plate
Mitral Stenosis monary artery hypertension may eventually cause RV 2-12). This results in pooling of blood in the lungs and
The resistance to diastolic flow from left atrium to left failure. a decrease in pulmonary venous return, reducing flow
ventricle after narrowing of the mitral valve increases to the left side of the heart. The reduced left-sided heart
left atrial (LA) pressures and eventually reduces LV flow Aortic Stenosis filling leads to a decreased stroke volume and systolic
(see Plate 2-11). A pressure gradient across the mitral In aortic stenosis, obstruction to the ejection of blood blood pressure. The decrease in systolic blood pressure
valve throughout diastole can be demonstrated by from the ventricle into the aorta, caused by subvalvular, leads to a faster heart rate because of the baroreceptor
simultaneous PCWP measurements or direct LA and valvular, or supravalvular stenosis, results in abnormally reflex, which stimulates sympathetic outflow to the
LV pressure measurements. This gradient is inversely high pressure in the left ventricle and abnormally low heart. These changes are reversed with expiration.
pressure in the aorta and thus a systolic pressure
THE NETTER COLLECTION OF MEDICAL ILLUSTRATIONS 31
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