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Introduction to
Vascular
Ultrasonography
This page intentionally left blank
Introduction to
Vascular
Ultrasonography
John S. Pellerito, MD, FACR, FSRU, FAIUM
Professor of Radiology
Department of Radiology
Zucker School of Medicine at Hofstra/Northwell
Hempstead, New York
Vice Chairman
Northwell Health System
Manhasset, New York
Joseph F. Polak, MD, MPH, FACR, FAIUM

Tufts University School of Medicine
Director
Ultrasound Reading Center
Boston, Massachusetts
Chief of Radiology
Lemuel Shattuck Hospital
Jamaica Plain, Massachusetts
7TH EDITION
Elsevier
1600 John F. Kennedy Blvd.
Ste 1800
Philadelphia, PA 19103-2899
INTRODUCTION TO VASCULAR ULTRASONOGRAPHY, SEVENTH EDITION ISBN: 978-0-323-42882-8

Copyright © 2020 by Elsevier, Inc. All rights reserved.
No part of this publication may be reproduced or transmitted in any form or by any means, electronic or
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This book and the individual contributions contained in it are protected under copyright by the Publisher
(other than as may be noted herein).
Notice
Practitioners and researchers must always rely on their own experience and knowledge in evaluating and
using any information, methods, compounds or experiments described herein. Because of rapid
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or ideas contained in the material herein.
Previous editions copyrighted 2012, 2005, 2000, 1992, 1986, and 1983.
Library of Congress Control Number: 2019949237
Content Strategist: Russell Gabbedy

Senior Content Development Specialist: Joanie Milnes
Publishing Services Manager: Catherine Jackson
Senior Project Manager: Claire Kramer
Design Direction: Amy Buxton
Printed in Canada
Last digit is the print number: 9 8 7 6 5 4 3 2 1

To Elizabeth, John, Alana, and Daniel for their patience and support.
To my sonographers, vascular technologists, and colleagues for
always giving their best to our patients.
J. S. P.
To Alex and Jo-Anne.

To my colleague sonographers and vascular technologists.
Your work is truly amazing.
J. F. P.
ACKNOWLEDGMENT
I gratefully acknowledge the following individuals After thanking John, my co-editor, I cannot resist
who made this edition possible. My co-editor, giving credit to those individuals whose names
Joseph Polak, my partner in vascular imaging, for are not listed on any of the chapter headings of
always challenging the status quo and his steadfast this, the seventh edition of Introduction to Vascular
dedication to improve patient diagnosis. Ultrasonography. Although the title states “Introduc-
All the authors for their excellent contributions tion,” John and I have tried to communicate the
to this edition. fact that this edition covers a broad range of
My administrative assistant Debbie Kaur, for experiences and levels of knowledge. The beginner
making a tough job look easy and fun. You’re the will find the essence of vascular ultrasound, while
best! the advanced will undoubtedly discover pearls.
My chairs, Jason Naidich and Jesse Chusid, This edition was built on a foundation of
for allowing me the space to develop a world experiences and inputs from those of you who
class vascular laboratory with an excellent team gave feedback, through e-mail, verbally, or in
to support it. performing a book review. All of your comments
My colleagues in the Vascular Lab, James were listened to, and every effort was made to
Naidich, MD, Catherine D’Agostino, MD, and address them in this current edition.
Brian Burke, MD, for maintaining our high-quality As always, I thank my wife, Jo-Anne, for her
standards. patience. I also thank my daughter, Alexandra,
My vascular technologists, Danielle Berne, RN, for understanding that my long hours of work
RVT; Jane Joo Ah Kim, RVT, RDCS; Bindu Rame- often rolled into work at home. This was motivated
shan, RVT; Glenn Prucha, RVT; Maria Sisawang, by my desire to summarize and explain what it
RVT; Christine Dauber, RVT, RDCS; Athanasios took me so many years to understand.
Tziovas, RDMS, RVT; Briana Kresback, RVT; Daniel I give credit to the following sonographers for
Hernandez, RDMS, RVT, RDCS; and Floyd Fed- helping me by providing the high-quality materials
erbush, RVT, for their commitment, diligence, and that ended up in the chapters I authored and
patience with our research, quality assurance often supplemented materials in other chapters.
projects, and new technologies. Foremost, Ms. Jean M. Alessi-Chinetti, RDMS, RVT,
My sonographers, Jessica Moon, RDMS; Nanaz for not hesitating to point out questionable inter-
Maghool, RDMS; Radha Persaud, RDMS, RDCS; pretations and always submitting studies worthy
Grazyna Bober, RDMS; Dennis Burgos, RDMS, of publication. I also have to especially thank
RVT, RDCS; Kathrin Sakni, RDMS, RDCS; Karen Gregory Y. Curto, RDMS, with whom I have now
Dundara, RDMS; Diana Navi, RDMS, RDCS; worked for years and who was tolerant enough
Erzsebet Borbely, RDMS; Tyler Caiati, RDMS; to let me scan even when the schedule was tight.
Myrlise Joachim-Calixte, RDMS; Rekha Lall, RDMS; I thank Richard J. Porter, RVT, for asking simple
Nicole Osmers, RVT; Roxana Palacios, RVT, for questions that were so difficult to answer. I have to
giving 100% to our patients. recognize Nicole Wake, RVT who, despite being a
I would like to thank Adina Haramati, MD, great sonographer, decided to invest her career in
for her excellent illustrations. The folks at Elsevier magnetic resonance imaging. I also thank Andrea L.
and Joanie Milnes, in particular, for their support Ford, RVT, Peter F. Wolstenholme, RVT, Noorjehan
and encouragement. And of course, my family, M. Tambra, CVS, and, more recently, Julio Perez,
Elizabeth, John, Alana, Daniel, Peter, and Marie RVT, for their questions and feedback.
for always being there for me. In this long road, I thank my friend Irwin. The
John S. Pellerito, MD, FACR, FSRU, FAUM last few years have been cruel, but participating in
“Current Practice of Vascular Ultrasound” taught
me much, motivated me, and often helped me
keep my sanity.
Joseph F. Polak, MD, MPH, FACR, FAIUM
vii
About the Editors ix
A BOUT THE EDITORS
John S. Pellerito, MD, FACR, FSRU, FAIUM, is on vascular imaging. His current interests focus on new
Professor of Radiology at Donald and Barbara Zucker imaging techniques in cardiovascular and gynecologic
School of Medicine at Hofstra/Northwell. He is Vice diseases. He is an in-demand lecturer and continues
Chairman of Education for the Imaging Service Line to contribute to national and international continu-
for Northwell Health, as well as the Program Director ing medical education programs. Dr. Pellerito holds
for the Radiology Residency Program and Program multiple editorial appointments and contributes to many
Director for the Body Imaging Fellowship at North educational programs. He is currently on the Board of
Shore University/Long Island Jewish Hospitals. He the Intersocietal Accreditation Commission for Vascular
continues to serve as the Director of the Peripheral Testing and serves on the Board of Governors for the
Vascular Laboratory at North Shore University Hospital. American Institute of Ultrasound in Medicine. He is a
He is also the Medical Director for the Molloy College fellow of the American College of Radiology, American
Cardiovascular Technology Program in Rockville Centre, Institute of Ultrasound in Medicine, and Society of
New York. He is the author of many original articles Radiologists in Ultrasound. He and his wife, Elizabeth,
and book chapters, web lectures, and DVD programs have three children, John, Alana, and Daniel.
ix
x About the Editors
Joseph F. Polak, MD, MPH, FACR, FAIUM, is Professor Vascular Laboratories, has served on the Board of the
of Radiology at Tufts University School of Medicine and American Institute in Ultrasound in Medicine, and is
Chief of Radiology at the Lemuel Shattuck Hospital currently serving on the Board of the Society of Vascular
in Boston. A graduate of McGill University School of Medicine and Intersocietal Accreditation Commission
Medicine and of the Harvard School of Public Health, (vascular testing). He has been co-investigator and
his major clinical interests are in the use of ultrasound director of the Ultrasound Reading Center that was
imaging to detect and follow atherosclerosis. He has funded by the NIH and evaluated many ultrasound
co-authored more than 310 peer-reviewed papers and markers of atherosclerosis such as carotid artery intima-
100 non–peer-reviewed articles and chapters. He has media thickness, carotid artery plaque, carotid artery
served on the Editorial Board of Radiology and cur- distensibility, brachial artery reactivity, and, currently,
rently serves on the Editorial Boards of the Journal of brachial artery intima-media thickness. He is working
Neuroimaging, the Journal of Vascular Ultrasound, and the on developing a calibrated methodology that can be
Journal of Ultrasound in Medicine. He is past-president of used for cardiovascular risk assessment.
the Intersocietal Commission for the Accreditation of
P R E FAC E
The seventh edition of Introduction to Vascular credentialing, accreditation, and quality in the
Ultrasonography is a significant update to our previ- vascular laboratory. We also are excited to have
ous editions. My co-editor, Joseph F. Polak, and several world-renowned experts provide us the
I have pulled together the topics and authors we state of the art in ultrasound contrast applications
thought represented the best of vascular ultrasound for vascular imaging. Of course, we brought back
imaging. Having collaborated together for more many of our favorite authors who received positive
than two decades with our vascular course and the reviews from our previous edition.
sixth edition of this book, we feel that this edition In addition to multiple new figures and illustra-
has met our goal to present the definitive text in tions, a major enhancement to this version of
vascular ultrasound. Jo and I have contributed Introduction to Vascular Ultrasonography is the
to 22 of the 35 chapters. Not only have all the integration of Practical Tips sections throughout
chapters in this edition been revised to deliver all the chapters. These Tips are intended to focus
the newest techniques, protocols, and topics the reader on major teaching points and pearls
in vascular ultrasound, we also invited several for the successful performance and interpretation
new experts to provide their perspectives and of vascular studies.
experience in significant areas. For example, the We are extremely proud to present the seventh
physics section has been completely revamped edition of Introduction to Vascular Ultrasonography.
by Dr. Fred Kremkau, the favored speaker and We hope that this book will provide guidance to
authority in ultrasound physics. We welcome students, technologists, sonographers, and all
Heather Gornik, MD, the current president of practitioners of vascular ultrasound to improve
IAC vascular testing, for her contribution on patient diagnosis and management.
John S. Pellerito, MD, FACR, FSRU, FAIUM
xi
Contributors xiii
C ONTRIBUTORS
Dennis F. Bandyk, MD Heather L. Gornik, MD, RVT, RPVI

Section Chief President, IAC-Vascular Testing Division
Division of Vascular and Endovascular Surgery Co-Director, Vascular Center
University of California San Diego Harrington Heart and Vascular Institute
San Diego, California University Hospitals
Associate Professor of Medicine
Phillip J. Bendick, PhD Case Western Reserve University School of
Technical Director Medicine
Peripheral Vascular Diagnostic Center Cleveland, Ohio
Beaumont Health System
Royal Oak, Michigan Edward G. Grant, MD
Carol B. Benson, MD University of Southern California
Professor of Radiology Keck School of Medicine
Harvard Medical School Los Angeles, California
Director of Ultrasound and Co-Director of
High Risk Obstetrical Ultrasound Ulrike M. Hamper, MD, MBA
Department of Radiology Professor of Radiology, Urology, and Pathology
Brigham and Women’s Hospital Russell H. Morgan Department of Radiology
Boston, Massachusetts and Radiological Science
The Johns Hopkins University School of
George L. Berdejo, BA, RVT, FSVU Medicine
Director, Outpatient Vascular Ultrasound Baltimore, Maryland
Services
Division of Vascular Surgery Jonathan D. Kirsch, MD
White Plains Hospital Associate Professor of Radiology and
White Plains, New York Biomedical Imaging and Internal Medicine
Section Chief, Ultrasound
Brian J. Burke, MD, RVT, FACR, FAIUM Department of Radiology and Biomedical
Assistant Professor Imaging
Department of Radiology Yale University School of Medicine
Hofstra-Northwell School of Medicine New Haven, Connecticut
Uniondale, New York
Attending Radiologist Frederick W. Kremkau, PhD
Department of Radiology Professor of Radiologic Sciences
North Shore University Hospital Center for Experiential and Applied Learning
Manhasset, New York Wake Forest University School of Medicine
Winston-Salem, North Carolina
Corinne Deurdulian, MD
Department of Radiology Mark E. Lockhart, MD, MPH
University of Southern California Chief, Body Imaging Radiology
Keck School of Medicine University of Alabama at Birmingham
Los Angeles, California Birmingham, Alabama
xiii
xiv Contributors
Mahan Mathur, MD Joseph F. Polak, MD, MPH, FACR, FAIUM

Associate Professor of Radiology Professor of Radiology
Director, Medical Student Education Department of Radiology
Associate Director, Diagnostic Radiology Tufts University School of Medicine
Residency Program Director
Department of Radiology and Biomedical Ultrasound Reading Center
Imaging Boston, Massachusetts
Yale School of Medicine Chief of Radiology
New Haven, Connecticut Department of Radiology
Lemuel Shattuck Hospital
William D. Middleton, MD Jamaica Plain, Massachusetts
Mallinckrodt Institute of Radiology Vasileios Rafailidis, MD, MSc, PhD, EDiR
Washington University School of Medicine Department of Radiology
St. Louis, Missouri AHEPA University General Hospital of
Thessaloniki
Darius G. Nabavi, MD Thessaloniki, Greece
Chair, Department of Neurology
Vivantes Klinikum Neukölln Margarita V. Revzin, MD, MS, FSRU
Berlin, Germany Assistant Professor of Diagnostic Radiology
Department of Radiology and Biomedical
Marsha M. Neumyer, BS, RVT, FSVU, Imaging
FSDMS, FAIUM Yale School of Medicine
International Director New Haven, Connecticut
Vascular Diagnostic Educational Services
Harrisburg, Pennsylvania E. Bernd Ringelstein, MD
Medical Faculty
Daniel C. Oppenheimer, MD Department of Neurology
Assistant Professor University Hospital Münster
Department of Imaging Sciences Münster, Germany
University of Rochester Medical Center
Rochester, New York Martin A. Ritter, MD
Consultant Neurologist
John S. Pellerito, MD, FACR, FSRU, Chair, Department of Stroke Medicine
FAIUM Clemenshospital Münster
Professor of Radiology Münster, Germany
Zucker School of Medicine at Michelle L. Robbin, MD, MS
Hofstra/Northwell Professor of Radiology and Biomedical
Hempstead, New York Engineering
Vice Chairman Chief of Ultrasound
Department of Radiology Department of Radiology
Northwell Health System University of Alabama at Birmingham
Manhasset, New York Birmingham, Alabama
Contributors xv
Kathryn A. Robinson, MD Steven R. Talbot, RVT, FSVU

Senior Associate Consultant, Diagnostic Co-Editor, Journal for Vascular Ultrasound
Radiology Research Associate
Assistant Professor of Radiology Division of Vascular Surgery
Mayo Clinic Technical Director, Vascular Laboratory
Rochester, Minnesota Cardiovascular Services
University of Utah Medical Center
Deborah J. Rubens, MD Salt Lake City, Utah
Professor of Imaging Sciences, Oncology, and
Biomedical Engineering R. Eugene Zierler, MD, RPVI, FACS
Associate Chair for Academic Affairs Medical Director
Department of Imaging Sciences D. E. Strandness Jr. Vascular Laboratory
University of Rochester Medical Center University of Washington Medical Center and
Rochester, New York Harborview Medical Center
Professor
Leslie M. Scoutt, MD Department of Surgery
Professor of Radiology, Surgery, and Cardiology University of Washington School of Medicine
Vice Chair for Education Seattle, Washington
Medical Director, Non-Invasive Vascular
Laboratory
Yale University School of Medicine
New Haven, Connecticut
Paul Sidhu, BSc, MBBS, MRCP, FRCR,

DTM&H
Professor of Imaging Sciences
King’s College Hospital
London, Great Britain
Contents xvii
C ONTENTS
SECTION 1 9 ULTRASOUND ASSESSMENT OF THE VERTEBRAL

ARTERIES 183
Basics JOSEPH F. POLAK, MD, MPH
1 THE HEMODYNAMICS OF VASCULAR DISEASE 2 10 ULTRASOUND ASSESSMENT OF THE INTRACRANIAL

JOSEPH F. POLAK, MD, MPH, AND ARTERIES 203
JOHN S. PELLERITO, MD, FACR, FSRU, FAIUM
DARIUS G. NABAVI, MD, MARTIN A. RITTER, MD, AND
E. BERND RINGELSTEIN, MD
2 PRINCIPLES AND INSTRUMENTS OF
ULTRASONOGRAPHY 23
FREDERICK W. KREMKAU, PhD
SECTION 3
Extremity Arteries
3 DOPPLER FLOW IMAGING AND SPECTRAL
ANALYSIS 56
JOHN S. PELLERITO, MD, FACR, FSRU, FAIUM, AND
11 ANATOMY OF THE UPPER AND LOWER EXTREMITY
ARTERIES 236
JOSEPH F. POLAK, MD, MPH
SECTION 2
12 PHYSIOLOGIC TESTING OF LOWER EXTREMITY
Cerebral Vessels ARTERIAL DISEASE 250
MARSHA M. NEUMYER, BS, RVT, FSVU, FSDMS, FAIUM
4 ANATOMY OF THE CEREBRAL STRUCTURE 84
JOSEPH F. POLAK, MD, MPH, AND
13 ASSESSMENT OF UPPER EXTREMITY ARTERIAL
DISEASE 274
5 CAROTID SONOGRAPHY: PROTOCOL AND TECHNICAL
STEVEN R. TALBOT, RVT, FSVU
CONSIDERATIONS 96
14 ULTRASOUND EVALUATION BEFORE AND AFTER
HEMODIALYSIS ACCESS 305
6 EVALUATING CAROTID PLAQUE AND CAROTID MICHELLE L. ROBBIN, MD, MS, AND
MARK E. LOCKHART, MD, MPH
INTIMA-MEDIA THICKNESS 110
JOSEPH F. POLAK, MD, MPH 15 ULTRASOUND ASSESSMENT OF LOWER EXTREMITY
ARTERIES 322
7 ULTRASOUND ASSESSMENT OF CAROTID R. EUGENE ZIERLER, MD, RPVI, FACS, AND
STENOSIS 139 JOHN S. PELLERITO, MD, FACR, FSRU, FAIUM
CORINNE DEURDULIAN, MD, AND EDWARD G. GRANT, MD

16 ULTRASOUND ASSESSMENT DURING AND AFTER
8 HOW TO ASSESS DIFFICULT AND UNCOMMON CAROTID AND PERIPHERAL INTERVENTIONS 345
CAROTID CASES 162 JOSEPH F. POLAK, MD, MPH, AND DENNIS F. BANDYK, MD

xvii
xviii Contents
17 ULTRASOUND IN THE ASSESSMENT AND 26 DOPPLER ULTRASOUND OF THE MESENTERIC

MANAGEMENT OF ARTERIAL EMERGENCIES 370 VASCULATURE 547
BRIAN J. BURKE, MD, RVT, FACR, FAIUM MARGARITA V. REVZIN, MD, MS, FSRU, AND
SECTION 4 27 ULTRASOUND ASSESSMENT OF THE HEPATIC

VASCULATURE 582
Extremity Veins WILLIAM D. MIDDLETON, MD, AND
KATHRYN A. ROBINSON, MD
18 EXTREMITY VENOUS ANATOMY AND TECHNIQUE FOR
ULTRASOUND EXAMINATION 390 28 DUPLEX ULTRASOUND OF NATIVE RENAL
JOHN S. PELLERITO, MD, FACR, FSRU, FAIUM, AND VASCULATURE 615
STEVEN R. TALBOT, RVT, FSVU
MARGARITA V. REVZIN, MD, MS, FSRU, AND
19 ULTRASOUND DIAGNOSIS OF LOWER EXTREMITY
VENOUS THROMBOSIS 418 29 DUPLEX ULTRASOUND EVALUATION OF THE UTERUS
JONATHAN D. KIRSCH, MD, ULRIKE M. HAMPER, MD, MBA, AND OVARIES 654
AND LESLIE M. SCOUTT, MD
20 RISK FACTORS AND THE ROLE OF ULTRASOUND IN

30 DUPLEX ULTRASOUND EVALUATION OF THE MALE
THE MANAGEMENT OF EXTREMITY VENOUS
GENITALIA 678
DISEASE 442
CAROL B. BENSON, MD
31 EVALUATION OF ORGAN TRANSPLANTS 705
21 ULTRASOUND DIAGNOSIS OF VENOUS MAHAN MATHUR, MD, DANIEL C. OPPENHEIMER, MD,
DEBORAH J. RUBENS, MD, AND LESLIE M. SCOUTT, MD
INSUFFICIENCY 461
MARSHA M. NEUMYER, BS, RVT, FSVU, FSDMS, FAIUM
SECTION 6
22 NONVASCULAR FINDINGS ENCOUNTERED DURING
VENOUS SONOGRAPHY 483 Trends in Ultrasound Vascular Imaging
32 CREDENTIALING, ACCREDITATION, AND QUALITY IN
THE VASCULAR LABORATORY 748
SECTION 5 HEATHER L. GORNIK, MD, RVT, RPVI
Abdomen and Pelvis 33 ULTRASOUND SCREENING FOR VASCULAR

DISEASE 758
23 ANATOMY AND NORMAL DOPPLER SIGNATURES OF
ABDOMINAL VESSELS 496
34 CORRELATIVE IMAGING 779
24 ULTRASOUND ASSESSMENT OF THE ABDOMINAL
AORTA 509
JOSEPH F. POLAK, MD, MPH 35 ULTRASOUND CONTRAST AGENTS IN VASCULAR
DISEASE 804
25 ULTRASOUND ASSESSMENT FOLLOWING VASILEIOS RAFAILIDIS, MD, MSc, PhD, EDiR,
ENDOVASCULAR AORTIC ANEURYSM REPAIR 529 PHILLIP J. BENDICK, PhD, AND
JOSEPH F. POLAK, MD, MPH, AND PAUL SIDHU, BSc, MBBS, MRCP, FRCR, DTM&H
GEORGE L. BERDEJO, BA, RVT, FSVU
Introduction to
Vascular
Ultrasonography
SECTION 1
BASICS
1 THE HEMODYNAMICS OF
VASCULAR DISEASE
Joseph F. Polak, MD, MPH, and John S. Pellerito, MD, FACR, FSRU, FAIUM
Overview arterial reservoir and a large venous pool with low

pressure and low kinetic energy. These reservoirs
The human circulatory system is extremely are connected by a system of distributing branch
complex. Blood flow is influenced by many factors: arteries and the microcirculation, which consist
1. The heart influences the strength and amount of arterioles and capillaries (Fig. 1.1).
of ejected blood. As blood flows through the circulatory system,
2. The elastic arteries store energy during systole energy is continuously lost because of the friction
and maintain blood flow during diastole. between the layers of flowing blood. Both pressure
3. The muscular arteries maintain tone. and kinetic energy levels decrease as the red cells
4. The arterioles, capillaries, and the venules supply transit from the arterial to the venous system. The
blood to the different organs. energy necessary for blood flow is continuously
5. The veins ensure adequate return of blood to restored by the pumping action of the heart during
the heart. systole, stored in the elastic wall of the aorta
and large arteries, and released during diastole.
Introduction The generated arterial pressure forces blood to
move from the arterial system into the venous
At each level, anatomy and physiology contribute system and maintains the arterial pressure and
to a steady supply of oxygen by maintaining blood the energy difference needed for blood to keep
flow. Some of the factors responsible for this flowing.
coordinated action can be measured and described The arterial system has high energy levels as a
in reasonably simple terms, but many others are result of the large volume of rapidly flowing blood
complex and difficult to grasp. and the high pressure in the arterial reservoir. The
Keeping these limitations in mind, this chapter pumping action of the heart and the mechanical
presents a basic review of the dynamics of blood characteristics of arteries work synergistically to
flow through the circulation, some of the factors maintain adequate volume, flow, and pressure in
that influence blood flow, and the hemodynamic the arteries. This is in part achieved by maintaining
consequences of arterial and venous occlusive a balance between the amount of blood that enters
disease. These considerations are helpful in and leaves the arterial reservoir. The amount that
understanding the normal physiology of blood enters the arteries during a cardiac cycle is the
circulation and the abnormalities that can occur stroke volume. The amount that leaves depends
in the presence of vascular obstruction. on the arterial pressure and on the total peripheral
resistance, which is controlled, in turn, by the
amount of vasoconstriction in the microcircula-
Physiologic Factors Governing tion. Both can change from beat to beat.
Blood Flow and Its Characteristics Under normal conditions, blood flow to all the
body tissues is adjusted according to the tissues’
Arterial and venous compartments particular needs at a given time. This adjustment
For blood flow to occur between any two points is accomplished by local alterations in the level of
in the circulatory system, there must be an energy arteriolar vasoconstriction within a given organ.
difference between these two points. Usually, this Maintenance of normal volume and pressure in
difference in energy levels is due to a blood pres- the arteries thus ensures the distribution of blood
sure difference. The circulatory system generally flow, and therefore oxygen delivery, to all parts
consists of a high-pressure, high kinetic energy of the body and helps regulate cardiac output.
2
1 The Hemodynamics of Vascular Disease 3
Aorta Vena cava

Arteries Veins
Capillaries
Arterioles Venules
Systolic
Pressure
Diastolic
Area
Resistance
FIG. 1.1 This diagram is a simplified representation of the relative differences in pressure, effective
resistance, and overall vessel cross-luminal area at the different levels of the circulation. The
curves on the bottom correspond to the respective levels of the circulation shown above. For
example, the effective area of the circulation is greatest at the capillary level, whereas the
resistance peaks in the small arteries and arterioles.
pressure) energy is constant. The equation that

Potential and kinetic energy summarizes this relationship is Bernoulli’s equa-
The physical factors that govern how blood tion (Fig. 1.2). If the artery lumen increases, kinetic
once ejected from the heart dissipates energy as energy is converted back into pressure (potential
it transits through the circulation are related to energy) as velocity decreases. Conversely, if the
friction, resistance, and the influences of laminar artery lumen narrows, the potential energy is
and turbulent flow. The basic relationships between converted into kinetic energy. Therefore within
flow, pressure, and resistance as summarized by certain limits, important increases in kinetic energy
Bernoulli’s equation, Poiseuille’s law, and Poi- occur in the systemic circulation when blood flow
seuille’s equation are discussed. The connecting is high (e.g., during exercise) and in mildly stenotic
vascular channels have intrinsic resistances that lesions where luminal narrowing leads to increases
connect either in parallel or in series. These inter- in blood flood velocities. The effects of gravity
connections modulate how blood flows through due to differences in height of the blood vessel
the circulation. (the term ρgz in the equation) are normally
The main form of energy stored in flowing neglected over short arterial segments especially
blood is the potential energy due to the pressure if they are oriented along the horizontal plane.
distending the vessels. This is created by the
pumping action of the heart. However, some of Energy differences related to differences
the energy stored in blood is kinetic and a direct in the levels of body parts
function of its velocity. Usually, the kinetic energy There is a large variation in the potential energy of
component is small compared with the pressure blood due to differences in posture. For example,
energy, and under normal resting conditions, it in the standing position the pressure in the feet
is equivalent to only a few millimeters of mercury is increased by an amount that is proportional
or less. The kinetic energy of blood is proportional to the height of the column of blood resting on
to its density (which is stable in normal circum- the blood in the legs. This hydrostatic pressure
stances) and to the square of its velocity. In essence, increases the transmural pressure and the disten-
over relatively straight arterial segments, the sum tion of the vessels. Gravitational potential energy
of kinetic (blood flow) and potential (blood (potential for doing work related to the effect of
4 SECTION 1 Basics
Stenosis
A B
FIG. 1.3 Blood flow velocity profiles across an arterial
lumen. (A) This parabolic profile is typical of normal
Pressure
laminar flow. The velocity is maximal in the center of the

artery and lowest near the artery wall and decreases
toward the artery wall according to Eq. 1.1. (B) Flattened
profile with a central core of relatively uniform velocity
encountered at the site of a maximal stenosis. This flow
profile is also maintained in the velocity jet before it
dissipates. It is an idealized representation of blood flow
because viscous forces will always impair the motion of
red blood cells so that they are not moving at the same
velocity.
Velocity
Energy differences due to laminar flow

As a hemodynamic approximation, blood flow is
Distance
said to be laminar because blood flows in con-
IDEALIZED STENOSIS centric layers or laminae. Each infinitesimal layer
Energy of flowing blood is constant.
flows with a different velocity. In theory, a thin
Bernoulli’s equation: layer of blood is held stationary next to the vessel
–
P + ½ ρV2 + ρgz = constant wall at zero velocity because of an adhesive force
P = Pressure
between the blood and the inner surface of the
ρ = Density of blood vessel. The next layer flows with low velocity, but
g = Acceleration due to gravity its movement is delayed by the stationary layer
z = Relative height of column of blood
–
V = Average blood flow velocity
because of friction between the layers, generated
by the viscous properties of the fluid. The second
FIG. 1.2 This diagram represents the complementary
layer, in turn, delays the next layer, which flows
changes in potential and kinetic energy taking place at at a greater velocity. The layers in the middle of
an idealized stenosis. Bernoulli’s equation indicates that the vessel flow with the highest velocity and the
as velocity increases the potential energy (pressure) of basic physics underlying this effect are such that
blood decreases. This idealized representation is not to the mean velocity averaged across the vessel is
scale and neglects viscous and inertial forces.
half of the maximal velocity measured in the
center. Because the rate of change of velocity is
greatest near the walls and decreases toward the
gravity on a free-falling body), however, is reduced center of the vessel, a velocity profile in the shape
in the dependent parts of the body by the same of a parabola exists along the vessel diameter, and
amount as the increase resulting from hydrostatic this type of blood flow is typically referred to as
pressure. Therefore differences in the level of the laminar flow (Fig. 1.3A).
body parts do not usually lead to changes in the Loss of energy during blood flow occurs because
driving pressure along the vascular tree unless of friction, and the amount of friction and energy
the column of blood is interrupted, as may be the loss is largely determined by the dimensions of
case when the venous valves close. Changes in the vessels. In a small diameter vessel, especially
energy and pressure associated with differences in in the microcirculation, even the layers in the
height are noticeable with changes in posture or middle of the lumen are relatively close to the
with activation of the calf pump muscles during wall and are thus delayed considerably, resulting
walking. in a significant opposition or resistance to flow
in that vessel segment. In contrast, the central difference, ΔP, and the volume blood flow, Q,
core of blood is far from the walls in large arteries, can be measured, and the resistance can thus be
and the frictional energy losses are less important. calculated as a systemic vascular resistance. Because
As indicated later, friction and energy losses resistance is equal to the pressure difference divided
increase if laminar flow is disturbed. by the volume flow (the pressure difference per
In a cylinder tube model of radius, R, the linear unit flow), it can be thought of as the pressure
velocity, v, of blood flow in a given lamina located difference needed to produce one unit of flow
at a given radial distance, r, from the center is and therefore can be considered as an index of
directly proportional to the pressure difference, the difficulty in forcing blood through vessels.
ΔP, between the ends of the tube and the square
of the radius and is inversely proportional to the Vessel Branching and Energy Dissipation. Poiseuille’s
length of the tube and the viscosity of the fluid. law applies to constant laminar flow of a simple
This is summarized by Poiseuille’s equation for Newtonian fluid (such as water) in a rigid tube
velocity: of uniform diameter. In the blood circulation,
these conditions are not fully met because blood
 ∆P  2 is a nonnewtonian fluid and most vessels do not
v(r ) =  (R − r 2 ) (Eq. 1.1)
 4ηL  stay straight without branching. Instead, the resis-
tance is influenced by the presence of numerous
For volume flow, the equation can be integrated branch vessels with a combined effect similar to
showing that volume flow, Q, is proportional to that observed in electrical circuits. In the case of
the fourth power of the vessel radius: vessels in series, the overall resistance is equal
to the sum of the resistances of the individual
 π∆P  4 vessels, whereas in the case of parallel vessels, the
Q= (r ) (Eq. 1.2)
 8ηL  reciprocal of the total resistance equals the sum of
the reciprocals of the individual vessel resistances.
where Q is the volume flow; ΔP is the pressure Thus, the contribution of any single vessel to the total
difference between the proximal and distal ends resistance of a vascular bed, or the effect of a change
of the tube; r and L are the radius and length of in the dimension of a vessel, depends on the presence
the tube, respectively; and η is the viscosity of the and relative size of the other vessels linked in series
fluid. or in parallel.
Because volume flow is proportional to the In addition, deviations from the conditions to
fourth power of the radius, even small changes which Poiseuille’s law applies also occur in relation
in radius can result in large changes in volume to changes in blood viscosity, which in turn is
flow. For example, a decrease in radius of 10% affected by hematocrit, temperature, vessel diam-
would decrease volume flow in a tube model by eter, and rate of blood flow.
about 35% and a decrease of 50% would lead
to a 95% decrease in volume flow. Because the Loss of Laminar Flow Patterns. Various degrees of
length of the vessels and the viscosity of blood do not deviation from orderly laminar flow occur in the
change much in the cardiovascular system, altera- human circulation. Minor factors responsible for
tions in volume blood flow occur mainly as a result these deviations include changes in blood flow
of changes in the radius of the vessels and in the velocity during the cardiac cycle as a result of
difference in the pressure energy level available for acceleration during early systole and deceleration
blood flow. in late systole and diastole and alterations of the
Poiseuille’s equation can be rewritten as follows: lines of flow due to small changes in the diameter
of the vessel. Alterations in the blood flow profiles
∆P occur at curves (Fig. 1.4), at bifurcations (Fig. 1.5),
R= (Eq. 1.3)
Q at any branch point, and at stenotic lesions. Once
altered, the laminar (parabolic) velocity profile
The resistance term, R, depends on the viscous is often not reestablished for a considerable
properties of the blood and on the dimensions distance. Instead, the velocity distributions can
of the vessels. Although these parameters cannot remain flattened within and just distal to stenotic
be measured in a complex system, the pressure lesions as plug flow (Fig. 1.3B), be skewed after
6 SECTION 1 Basics
Outside carotid bifurcation, the blood flow profile in the

of curve
distal common carotid artery tends to migrate
toward the internal carotid artery while a zone of
Inside boundary layer separation evolves in the proximal
curve internal carotid artery (Fig. 1.5) opposite to the
flow divider. This zone of flow separation can also
occur on the opposite side, near the origin of the
FIG. 1.4 Alterations in the velocity distribution of red external carotid artery.
cells in a curving arterial segment. The velocity distribution Laminar flow may be altered, become disturbed
becomes asymmetric as red cells enter a curve. A laminar or fully turbulent, even in a uniform tube. Tur-
pattern is reestablished downstream over a distance that bulence occurs when the velocity of blood flow
is mostly dependent on the velocity of blood and the
reaches a certain velocity within a tube of a given
diameter of the artery.
diameter. This transition point is expressed by the
dimensionless Reynolds number (Re):
ICA 2rvρ
Re = (Eq. 1.4)
η
where r is the radius of the tube, v is the velocity,

Boundary ρ is the density of the fluid, and η is the viscosity
ECA
layer of the fluid. Because the density (ρ) and viscos-
separation ity (η) of blood are relatively constant at 1.04
Flow
divider to 1.05 g/cm3 and 0.03 to 0.05 poise (g/cm⋅s),
respectively, the development of turbulence depends
mainly on the diameter of the vessel and on the blood
CCA flow velocity. In a tube model, laminar flow tends
to be present if the Reynolds number is less than
2000, is considered in transition between 2000 and
FIG. 1.5 This representation of the carotid artery bifurca- 4000, and is replaced by turbulent flow at values
tion displays the principal alterations that take place in
above 4000. However, in the circulatory system,
a normal bifurcation. The flow profile in the distal common
carotid artery (CCA) starts to deviate from a laminar disturbances and various degrees of turbulence are
pattern to one favoring the internal carotid artery (ICA). likely to occur at lower values because of body
As the red cells enter the carotid sinus, a zone of boundary movements, the pulsatile nature of blood flow,
layer separation (where the effective velocity is zero) changes in vessel dimensions, roughness of the
appears. On one side of the zone of boundary separation,
endothelial surface, and other factors. Turbulence
blood flow is reversed, whereas blood continues forward
on the other side. Blood flow reestablishes a laminar develops more readily in large vessels under condi-
pattern more distally in the ICA. For purposes of illustrations of high flow and can be detected clinically by
tion, the actual effects of the external carotid artery (ECA) the finding of bruits or thrills. This would typically
on blood flow are neglected. be seen in dialysis access fistulae (Fig. 1.6). Bruits
may sometimes be heard over the ascending aorta
during systolic acceleration in normal individuals
curves and branches (Fig. 1.4), or create a jet at at rest and are frequently heard in states of high
stenotic lesions. cardiac output and blood flow, even in more distal
In certain circumstances, laminar flow can arteries, such as the femoral artery.1 Distortion
evolve into a blood flow pattern that is mixed: a of the laminar flow velocity profiles as seen on
flow profile that has both forward and backward Doppler waveforms is the “bread and butter”
flow velocity components across the diameter of of vascular ultrasound. For example, in arteries
the artery. The transition zone where the lamina with severe stenosis, pronounced turbulence is
has zero velocity is then referred to as the site of a diagnostic feature observed in the poststenotic
boundary layer separation. This phenomenon can zone and is typically associated with a bruit (Fig.
occur at branch points and is classically described 1.7) that corresponds to soft tissue vibrations in
at the carotid artery bifurcation (Fig. 1.5). At the the range of 100 to 300 Hz.2
Turbulence occurs because a jet of blood with

PRACTICAL TIPS
high velocity and high kinetic energy suddenly
encounters a normal diameter lumen or a lumen • According to Bernoulli’s principle, when
of increased diameter (because of poststenotic blood flow velocity increases, the pressure
dilatation), where both the velocity and energy of the moving blood decreases.
level are lower than in the stenotic region. • Laminar blood flow is normally described
During turbulent flow, the loss of pressure energy by a parabolic distribution of moving red
between two points in a vessel is greater than cells where the highest velocity is in the
that which would be expected from the factors in middle of the artery and the slowest is
Poiseuille’s and Bernoulli’s equations (Fig. 1.2), near the wall (Poiseuille’s equation).
and the parabolic velocity profile is flattened • Resistance to blood flow increases as the
(Fig. 1.3B). radius of the artery decreases (to the
fourth power).
• Boundary layer separation refers to the
loss of laminar flow at a branch point such
as the carotid bifurcation. It is typically
associated with the formation of eddies
and reversed blood flow on one side and
normal direction of blood flow on the
other. It can also occur at the margin of
the stenotic jet.
• Turbulence occurs distal to a stenosis in a
region where blood flow velocities are still
elevated enough so that the product of
velocity and effective diameter is greater
than the Reynolds number.
FIG. 1.6 The portion of this dialysis access just after the
arterial anastomosis (ANA) has a relatively large diameter Pulsatile pressure and flow changes
and moderately increased velocity. The combination of in the arterial system
an elevated velocity in a larger diameter conduit increases
the Reynolds number to be high enough for blood flow With each heartbeat, a stroke volume of blood is
to transition into turbulence (shaggy and irregular contour ejected into the arterial system, resulting in a pres-
of the Doppler waveform). sure wave that travels throughout the arterial tree.
A
B
FIG. 1.7 (A) This color Doppler image is taken at the distal anastomosis of an iliofemoral graft.
The color Doppler signals propagated into the soft tissues (white arrows) represent soft tissue
vibrations, described as a color bruit artifact. (B) The Doppler gate has been moved over the soft
tissues and the Doppler tracings show low frequency signals that are bidirectional, correspond
to the soft tissue vibrations, and are representative of a bruit.
8 SECTION 1 Basics
The speed of propagation, amplitude (strength),

and shape of the pressure wave change as it
traverses the arterial system. The velocity of the
pulse wave is strongly influenced by the varying
characteristics of the vessel wall it traverses, and the
shape is affected by reflected waves. The velocity Heart
and, in some parts of the circulation, the direction
of flow also vary with each heartbeat. Elastic arteries
Correct interpretation of noninvasive physi-
ologic tests based on recordings of arterial pres- Conduit Transition zone /
sure and velocity, as well as pressure and velocity veins site(s) of major
waveforms, requires knowledge of the factors that reflection
influence these variables. This section considers Muscular
these factors as they occur in various portions of arteries (tone)
the circulatory system.
Pressure changes from cardiac activity

The pumping action of the heart ejects a volume Venules Arteries
of blood into the aorta. The pressure and volume Capillaries
waves propagate to the periphery and maintain FIG. 1.8 This simple representation shows the principal
a pressure differential between the arterial and elements of the circulatory system. Wave reflection can
venous beds. Because of the intermittent pumping take place within the muscular arteries as well as in the
action of the heart, pressure and flow vary in a larger elastic arteries. The effective location of the principal
reflection sites varies with age, migrating more centrally
pulsatile manner. During the rapid phase of ven-
with aging.
tricular ejection, the volume of blood in the arterial
compartment of the circulation increases, raising
the pressure to a systolic peak. During the latter
part of systole, when cardiac ejection decreases, the ejection, the peripheral resistance, and the stiffness
outflow through the peripheral resistance vessels of the arterial walls.
exceeds the volume being ejected by the heart, In general, an increase in any of these factors
and the pressure begins to decline. This decline results in an increase in the pulse amplitude (i.e.,
continues throughout diastole as blood continues pulse pressure, difference between systolic, and
to flow from the arteries into the microcircula- diastolic pressures) and frequently with a con-
tion. During each cardiac cycle, part of the energy comitant increase in systolic pressure. For example,
delivered during systole maintains forward flow, increased stiffness of the arteries with age tends
but a large proportion of this energy forces the to increase both the systolic and pulse pressures
arteries to distend and effectively serve as reservoirs through an increase in the magnitude of reflected
for storing the blood volume and the energy sup- pressure waves from natural branch points in the
plied to the system (Fig. 1.8). This combination, arterial system.
the ejected blood with its kinetic energy and The arterial pressure wave is propagated from
the elastic energy stored in the distended artery the heart distally along the arterial tree. The speed
walls, helps maintain tissue perfusion during of propagation, or pulse wave velocity, increases
diastole. with stiffness of the arterial walls (the elastic
modulus of the artery wall) and with the ratio of
Arterial pressure wave the wall thickness to diameter. In the mammalian
The pulsatile variations in blood volume and circulation, arteries become progressively stiffer
energy occurring with each cardiac cycle are from the aorta toward the periphery. Therefore
manifested as a pressure wave that can be detected the speed of propagation of the wave increases as
throughout the arterial system. The amplitude and it moves peripherally. Also, the gradual increase
shape of the arterial pressure wave depend on a in stiffness tends to increase wave reflection (dis-
complex interplay of factors, which include the cussed later) and in young people has a protective
stroke volume and time course of ventricular effect by decreasing central aortic pressures. With
aging, the degree of stiffening increases to such There is almost a complete disappearance of
a degree that the reflected waves return earlier pressure amplification in the dorsalis pedis artery
and have a detrimental effect by increasing in response to vasodilatation induced by body
the pulse and systolic pressures in the aorta.3–5 heating.10 Similar changes in the distal pressure
The pressure against which the heart ejects the waves result from other factors that alter peripheral
stroke volume and the associated cardiac work resistance, for example, reactive hyperemia and
accordingly increase with age. exercise. By decreasing resistance in the working
muscle, exercise would be expected to decrease
Pressure changes throughout reflection in the exercising extremity. Because
the circulation of vasoconstriction in other parts of the body
The changes in pressure from large arteries through during exercise (the result of cardiovascular
the resistance vessels to the veins are shown in Fig. reflexes that regulate blood pressure and circula-
1.1. Because there is little loss of pressure energy tion), however, the reflection may be increased
from friction in large and distributing elastic arter- and lead to a high degree of amplification. For
ies, they offer relatively little resistance to flow, and example, it has been shown that during walking,
the mean pressure decreases only slightly between the pulse pressure in the radial arteries can exceed
the aorta and the small arteries of the limbs, such that in the aorta by perhaps 100%.11 Differences
as the radial or the dorsalis pedis.6 The diastolic between peripheral amplification of the pulse
pressure also shows only minor changes. The pressure and central augmentation of blood
amplitude of the pressure wave and the systolic pressure due to reflected waves likely explain
pressure actually increase, however, as the wave some of the physiologic differences seen between
travels distally (systolic amplification) because young and older individuals and those with
of the increased stiffness of the peripheral artery atherosclerosis.12,13
branches, the preferential forward transmission
of high frequency components of the pressure Diagnostic implications in peripheral
wave, and the presence of reflected waves.3 These arterial disease
waves arise where the vessels change diameter and The issues discussed earlier are important for
stiffness, divide, or branch and are superimposed correct interpretation of pressure measurements
onto the oncoming primary pulse wave.6 The in patients with peripheral arterial disease.
reflected waves originating from the extremities • The brachial systolic pressure corresponds
are amplified by increases in peripheral resistance.6 closely to aortic or femoral systolic pressures.
Direct measurements of pressure in small arteries It is therefore used as the denominator in
in experimental studies in animals and humans ankle-brachial pressure measurements. It is also
and indirect measurements of systolic pressure in used for calibrating transcutaneous tonometers
human digits have shown that the pulse amplitude used to measure distensibility of the peripheral
and systolic pressure decrease in smaller vessels, arteries and the carotids.
such as in the hands.7–9 However, some pulsatile • The systolic pressure at the ankle usually exceeds
changes in pressure and flow may persist even brachial pressure in normal subjects. Although
in minute arteries and capillaries, at least under an ankle-brachial index of less than 0.9 is a
conditions of peripheral vasodilatation, and can robust cut point for the presence of obstruc-
be recorded by various methods, including plethys- tive disease in the lower extremity, an ankle
mography. The effect of peripheral vasoconstriction systolic pressure that is equal to brachial systolic
on pulsatility in the microcirculation is opposite pressure, or ankle-brachial index of 1.0, may
to that seen in the proximal small or medium indicate the presence of a proximal stenotic
arteries of the extremities. The pulsatile nature of lesion.
the pressure waveform increases with vasoconstriction • The systolic pressure of digital arteries is usually
because of increased wave reflection and decreases lower than the systolic pressure proximal in
with vasodilatation in the small and medium arteries the forearm or the ankle. Measurements of
of the limbs. The reverse occurs in the very small digital systolic pressures such as toe-brachial
arteries, arterioles, and capillaries: vasoconstriction index should therefore be expected to be 1.0 or
reduces pulsatility while vasodilatation enhances lower in normals. An appropriate toe-brachial
pulsatility. index cutoff of 0.75 or 0.8 should be considered
10 SECTION 1 Basics
for the presence of obstructive arterial disease The presence of reversed flow during diastole
as compared with 0.9 for the ankle-brachial can also be understood if one imagines a major
index.14,15 arterial segment, with a certain diastolic pressure,
that has several branch vessels leading to areas
Pulsatile flow patterns with different levels of resistance. If one of the
Pulsatile changes in pressure are associated with proximal branches leads to an area with low
corresponding acceleration of blood flow with peripheral resistance, flow during diastole in the
systole and deceleration in diastole. Although the main vessel will occur toward this branch, and
energy stored in the arterial walls maintains a posi- flow will reverse in the distal portion of the main
tive pressure gradient and overall forward blood vessel if distal branches supply areas with higher
flow in the large arteries and microcirculation peripheral resistance. Such situations of transient
during diastole, temporary cessation of forward flow reversal may exist in the limb during cooling
flow or even diastolic reversal occurs frequently and depend on the distance between arterial seg-
in portions of the human arterial system. ments and their relative compliance. With heating
How these phenomena occur may be clarified or exercise, the peripheral resistance in the distal
by considering pulsatile pressure changes at two cutaneous circulation is significantly decreased
points along the arterial tree like the femoral so that reversal of blood flow is either decreased
and dorsalis pedis arteries (Fig. 1.9). The pres- or simply abolished (Fig. 1.10A). Diastolic flow
sure gradient between these two arteries varies reversal is generally present in arteries that supply
during the cardiac cycle because of differences in vascular beds with high peripheral resistance. It
the shape and magnitude of the original pressure tends to be absent in low-resistance vascular
waves but also because the pressure wave arrives beds or when peripheral resistance is reduced by
later at the dorsalis pedis. The pressure gradient peripheral dilatation, such as that which occurs
is greatest during the first half of systole, at which in the skin with body heating or in the working
time the peak of the wave arrives at the femoral muscle during exercise or reactive hyperemia
artery. The gradient then decreases and by the (Fig. 1.10B). These principles are important in
time the peak arrives at the dorsalis pedis, the assessing blood flow in arteries that supply various
height of the femoral pressure waveform has fallen regions, including the intracranial circulation. For
and a negative pressure gradient appears. Such example, flow reversal can be observed in the
negative gradients, related to different arrival times external carotid because extracranial resistance
of the pressure wave at various sites in the arterial is relatively high, but it is absent in the internal
system, are commonly observed and can reverse the carotid because the cerebrovascular resistance
direction of blood flow. However, the direction of is low.
blood flow may not reverse even in the presence Another way of explaining these changes is to
of a negative pressure gradient when there is a decompose the pressure and velocity waves into
large forward mean blood flow component (i.e., forward and backward components.3,16,17 Pres-
momentum). sure and blood flow waveforms can be viewed
as the sum of the forward pressure waveform
generated by the heart and of the reverse or
160 backward component due to reflection at the
F 1s site of distal resistance (impedance). Although
Pressure (mm Hg)
140 DP
the reflected blood pressure wave is additive to
120 the overall pressure wave (Fig. 1.11), the reflected
100 blood flow waveform is subtractive (Fig. 1.12).
80
The combination of these forward and backward
blood flow waves can lead to negative velocities.
60 With heating, the backward wave decreases, and
Body cooling Body heating
the forward wave maintains blood flow during
FIG. 1.9 Representative pressure waves from the femoral diastole. With cooling, the reflected wave increases
(F) and dorsalis pedis (DP) arteries during heating and
cooling. Note that the pulse pressure of the dorsalis pedis
thereby increasing the extent of blood flow reversal.
artery is greater with vasoconstriction (body cooling) and Low resistance beds do not generate prominent
falls dramatically with vasodilatation (body heating). backward waves.
Pressure difference (mm Hg) 60

1s
40
20
−20
−40
Body cooling Body heating
A
FIG. 1.10 (A) Pressure differences between the femoral

and dorsalis pedis arteries obtained from the waves
shown in Fig. 1.9. With vasodilatation (body heating;
shown on the right) most of the negative pressure
differential between dorsalis pedis and femoral artery
decreases. (B) The effect of exercise is to decrease
peripheral arterial resistance, decreasing the effect of
wave reflection and increasing blood flow velocity. B
Forward
Forward velocity wave
pressure wave
A + A
+
Reflected
pressure wave Reflected
B velocity wave
B
Resultant
Resultant
velocity wave
pressure wave
C C
FIG. 1.11 The effect of reflected pressure and blood flow FIG. 1.12 The effect of a reflected velocity wave on the
waveforms on the final pulse pressure waveform is sum- final velocity wave is summarized here. The reflected
marized here. The forward component of the pressure velocity wave (B) is added to the forward velocity wave
wave (A) is added to the reflected pressure wave (B) to (A) to form the final velocity wave (C). The final shape
form the final pressure wave (C). The final shape depends depends on the location of the artery and the effective
on the location of the artery and the effective distance distance to the major reflecting point(s).
to the major reflecting point(s).
12 SECTION 1 Basics
PRACTICAL TIPS
A1 A2 A3
• Low resistance arterial beds favor
continued forward blood flow during
diastole. –
V1
–
V2
–
V3
• Increased resistance caused by cooling can
alter the normal pattern of forward blood
flow and cause flow reversal in the more CONSERVATION OF MASS
proximal artery conduit. Volume of blood flowing through a vessel
without branches is constant.
• Decreased resistance due to heating or
Average velocity × Area = Constant
exercise decreases the presence of blood – – –
flow reversal. V1 × A21 = V2 × A22 = V3 × A23
• These alterations can be best explained by FIG. 1.13 This diagram is an idealized representation of
viewing the final pressure and velocity the principle of conservation of mass as applied to a
waveforms at a given position in the straight arterial conduit. Basically, the amount of flowing
blood remains constant. On the basis of this principle
arterial bed as the effect of a forward
and assuming the same driving blood pressure, a very
component and of a backward (reflected) tight stenosis that decreases blood flow at the stenosis
component. will decrease blood flow through the whole conduit. What
is not shown here are the collaterals that normally divert
blood flow when arterial segment narrowing worsens.
Effects of Arterial Obstruction

equation (Fig. 1.2). Under ideal conditions and
Arterial obstruction can decrease blood pressure neglecting losses due to friction (viscous forces)
and blood flow distal to the site of blockage, but or to acceleration/deceleration changes (inertial
the effects on pressure and blood flow are greatly forces), conservation of energy will translate
influenced by a number of factors proximal and potential energy (blood pressure) against kinetic
especially distal to the lesion. One must be familiar energy (square of the blood flow velocity).
with these factors when interpreting noninvasive However, this ideal scenario is not seen in real
studies because they affect the pressure and velocity life. As indicated by Poiseuille’s equation, friction
waveforms observed both proximal and distal to (due to viscosity of blood) causes a progressive
the obstructive lesion. In this section of the chapter, loss of energy of the column of flowing blood.
the concept of the critical stenosis is considered, These changes are exacerbated at more severe
as well as the pressure, velocity, and blood flow stenotic lesions. In addition, instability in the
manifestations of arterial obstructive disease. blood flow profiles due to turbulence can cause
additional energy losses distal to the stenosis
Arterial narrowing (Fig. 1.14).
Blood flow through a narrowed segment of the
arterial or venous system is governed by the Critical stenosis
principle of conservation of mass: what goes in Encroachment on the lumen of an artery by an
must come out. Therefore the product of the arteriosclerotic plaque can result in diminished
average blood flow velocity by the cross-sectional pressure and decreased blood flow distal to the
area of the artery should be constant (Fig. 1.13). lesion, but this encroachment on the lumen has
Although this global effect holds for blood flow to be very severe before hemodynamic changes are
through a vessel without branches, it does not manifested. Studies in humans and animals have
take into consideration the loss of blood flow indicated that about 90% of the cross-sectional
velocity or kinetic energy that can take place at area (approximately 69% diameter narrowing) of
the level of a severe arterial narrowing. the aorta must be encroached on before there is
As discussed earlier, the energy of flowing blood a change in the distal pressure and blood flow,
is a combination of the potential energy of blood whereas in smaller vessels, such as the iliac,
(gravity and blood pressure) and the kinetic energy carotid, renal, and femoral arteries, the critical
of blood. This is normally described as Bernoulli’s stenosis level varies from 70% to 90% reduction
Stenosis throat
Boundary layer separation
Flow reversal/
vortex formation Additional
losses due
Centerline pressure
Pressure to turbulence
recovery
Inertial >>
Viscous viscous forces
forces
Inertial (turbulence)
forces
Inertial and
FIG. 1.14 The effects of a stenosis that has
viscous forces
generated a velocity jet are summarized in this
Distance diagram. The transition from large diameter to
small diameter and the reverse transition are
dominated by inertial forces. Viscous forces cause
resistance in the stenosis proper. The poststenotic
Peak centerline velocity
region is a complex interplay of all of these forces.

The velocity jet expands and the associated bound-
ary separation decreases with distance from the
stenosis. The development of turbulence occurs
when the area of increased velocity delineated
by the boundary zone becomes large enough to
become unstable. This occurs over a short distance
Additional because viscous forces are also acting to decrease
losses due blood flow velocity with distance. Turbulence
to turbulence results in a nonrecoverable loss of energy, as do
Distance
the viscous forces at the stenosis proper.
in cross-sectional area (approximately 45% to 69% segment to that of the normal vessel; (5) the rate
diameter narrowing).18,19 of blood flow; (6) the peripheral resistance beyond
Measurements of area reduction are preferred the stenosis; and (7) the pressure gradient between
when looking at overall hemodynamic effects the arterial bed and the venous bed.
of a stenosis, whereas the clinical assessment of The concept of a critical stenosis (i.e., a stenosis
stenosis severity is based in the lumen diameter that causes a reduction in blood flow and pressure)
reduction. The difference between percentage has been treated extensively in the literature.19–21
decrease in cross-sectional area and diameter This concept has been accepted because there is
might seem confusing. A typical stenosis causing generally little or no change in hemodynamics
a 50% reduction in diameter corresponds to a when an artery is first narrowed by disease, but
75% decrease in cross-sectional area, whereas a a relatively rapid decrease in pressure and blood
diameter narrowing of 70% is roughly equivalent flow occurs with greater degrees of narrowing.19 The
to a 90% area reduction. critical stenosis concept is of practical significance
Whether a hemodynamic abnormality results because lesser degrees of narrowing of human
from a stenosis and how severe it may be depend arteries often do not produce significant changes
on several factors, including (1) the length and in hemodynamics or clinical manifestations. It
diameter of the narrowed segment; (2) the rough- must be recognized, however, that the concept of
ness of the endothelial surface; (3) the degree of critical stenosis is a gross simplification of a very
irregularity of the narrowing and its shape (i.e., complex interplay of numerous circulatory factors.
whether the narrowing is abrupt or gradual); (4) In particular, a relative decrease in peripheral
the ratio of the cross-sectional area of the narrowed resistance accompanied by an increase in blood
14 SECTION 1 Basics
150
100 ms
Pressure (mm Hg)
Pressure drop due to stenosis

100
275
50 476
Stenosis
0 O
Arteries Arterioles Veins
and 252
capillaries
N
FIG. 1.15 Decrease in pulse amplitude and systolic and
mean pressures distal to a stenosis. In a minimal stenosis, 170
alterations in pulse pressure such as this may be evident
only during high-volume flow induced by exercise or FIG. 1.16 Dorsalis pedis pulse waves from a normal limb
hyperemia. The diastolic pressure tends not to be affected. (N) and a limb with a proximal occlusion (O). The wave
from the limb with occlusion shows a prolonged time to
peak (252 ms) and increased width at half of the amplitude
flow velocity that occurs with exercise or with (476 ms). (From Carter SA. Investigation and treatment
reactive hyperemia may profoundly alter the effect of arterial occlusive disease of the extremities. Clin Med.
1972;79[5]:13–24 [Part I]; Clin Med. 1972;79[6]:15–22
of a given arterial stenosis.22,23 These factors suggest [Part II].)
that the hemodynamic and clinical significance
of a solitary or multiple arterial stenoses should
be assessed not only at rest but also during physi- These abnormal features of the pulse wave
ologic challenges such as exercise. correlate well with the results of measurement
In evaluating the hemodynamic effect of a of systolic pressure and can be demonstrated by
stenosis, it is also important to recognize that two noninvasive techniques using pulse waveforms
or more stenotic lesions in series have a more recorded with various types of plethysmography
pronounced effect on distal pressure and blood (Fig. 1.16). In the case of very mild stenotic lesions,
flow than does a single lesion of equal total however, little or no pressure or pulse abnormal-
length.24 This difference is a result of large losses ity may be evident distal to the lesion when the
of energy at the entrance, and particularly at the patient is at rest. The presence of such lesions may
exit, of the lesion resulting from grossly disturbed be demonstrated when blood flow increases with
flow patterns, including jet effects, turbulence, and exercise or through the induction of hyperemia.
eddy formation. Thus, the energy losses in tandem Enhanced blood flow through the stenosis results
lesions can exceed those that result from frictional in increased loss of energy because energy loss
resistance in a solitary stenosis, as represented in due to frictional (viscous) forces is proportional
Poiseuille’s equation. to velocity and leads to a detectable decrease in
pressure distal to the lesion.23
Pressure changes
Experiments with graded stenoses in animals have Blood flow changes
indicated that, whereas the diastolic pressure does At rest, the total blood flow to an extremity may
not fall until the stenosis is severe, a decrease in be normal in the presence of a severe arterial ste-
systolic pressure is a sensitive index of reduction nosis or even a complete obstruction of the main
in both the mean pressure and the amplitude artery because of the development of collateral
of the pressure wave distal to a relatively minor circulation, as well as a compensatory decrease in
stenosis (Fig. 1.15).25 Damping of the pressure the peripheral resistance. In such circumstances,
waveform, increased time to peak, and greater measurement of systolic pressure, as discussed
width of the pressure wave at half-amplitude earlier, is a better method of assessing the presence
can be detected distal to an arterial stenosis or and severity of the occlusive or stenotic process
occlusion.26 than measurement of volume blood flow.23 Resting
volume blood flow is reduced only when the recordings by calculating various indices of pul-
occlusion is acute and the collateral circulation satility and damping.28 In the normal peripheral
has not had a chance to develop or, in the case of arteries, blood flow velocity can reverse direc-
a chronic arterial obstruction, when the occlusive tion once or twice. The first blood flow reversal
process is extensive and consists of two or more (below the baseline) corresponds to the dicrotic
lesions in series. Although single lesions might notch seen on pressure waveforms. The second
not be associated with symptoms or significant reversal (toward positive values) favors forward
changes in global blood flow at rest, such lesions blood flow during diastole. Whether the Doppler
can significantly affect the blood supply when waveforms are biphasic or triphasic is probably
need is increased during exercise. In such cases, not of practical clinical significance and may be
the sum of the resistances of the obstructions related to a complex interplay of several factors.
(stenosis, collateral resistance, or both) and of These factors include the basal heart rate and the
the peripheral resistance may prevent a normal shape of the pressure and blood flow waves but
increase in overall blood flow, and symptoms of are most likely related to high peripheral resistance
intermittent claudication may develop. that dampens diastolic flow and therefore depend
Arterial obstruction can lead to changes in the on the degree of peripheral vasoconstriction and
distribution of the available blood flow to neigh- elastic properties of the more proximal arteries.
boring regions or vascular beds, depending on the The presence of the dicrotic notch is the primary
relative resistance and anatomic arrangement of finding that suggests that any proximal lesion, if
these areas. For example, blood flow during exercise present, is not critical.
can increase in the skeletal muscle of the extremity Distal to an arterial stenosis, the pressure wave
distal to an arterial obstruction, but because the is dampened because of a decrease in blood pres-
distal pressure is reduced during exercise, the sure (Fig. 1.15). In addition, blood flow reversal
muscle “steals” blood from the skin, and the blood associated with the dicrotic notch is likely to
supply to the skin of the foot is diminished. Such disappear distal to a significant arterial stenosis.
reduction in blood flow to the skin may manifest The calculated wave indices are thus altered, and
clinically as numbness of the foot, a common the Doppler waveforms have a single component
symptom in patients with claudication. In lower (monophasic) rather than double or triple compo-
extremities with extensive large vessel occlusion nents.11 The disappearance of reversed flow distal
and additional obstruction in small distal branches, to a stenosis probably results from a combination
vasodilator drugs or sympathectomy may divert of several factors, including (1) the maintenance of
flow from the critically ischemic distal areas by forward flow throughout the cardiac cycle (because
decreasing resistance in less ischemic regions.27 of the pressure gradient across the stenosis); (2)
Obstruction of the subclavian artery is known to resistance to reverse flow created by the stenotic
cause cerebral symptoms in some patients because lesion; (3) a decrease in peripheral resistance as
of reversal of flow in the vertebral arteries (the a result of relative ischemia; (4) damping of the
subclavian steal syndrome); similarly, obstructive pressure wave by the lesion; and (5) a decrease
lesions of the internal carotid artery may lead to in mean pressure. All these factors attenuate pres-
reversal of flow in the ophthalmic vessels, which sure pulses thereby decreasing the reflections and
communicate with external carotid branches on amplification that normally contribute to diastolic
the face and scalp. flow reversal. The latter would explain the presence
of monophasic signals that extend only during
Effect of stenosis on pressure and systole (high resistance) rather than throughout
Doppler waveforms the cardiac cycle (low resistance).
In normal peripheral arteries, blood flow velocity Assessment of blood flow velocities at and distal
increases rapidly to a peak during early systole and to arterial obstructions is useful in evaluating the
decreases during early diastole, when flow reversal significance of the occlusive processes. Doppler
can occur. The shape of the resulting pulse velocity spectrum analysis allows the accurate detection
wave resembles the pressure gradient shown in Fig. and quantification of blood flow abnormalities
1.10A. The character of this velocity profile can resulting from stenotic lesions. This subject is con-
be subjectively observed on the Doppler spectral sidered in further detail in Chapter 3, but it is of
waveform or quantified from Doppler waveform interest to comment on the physiologic principles
16 SECTION 1 Basics
illustrated by the Doppler frequency spectra in

PRACTICAL TIPS
normal and abnormal vessels. As noted previously,
the velocity pattern across a stenosis is flattened • The appearance of the Doppler waveform
and has a more constant velocity distribution before, at, and distal to a stenotic lesion
across the diameter of the artery resembling plug depends on the severity of the lesion, as
flow (Fig. 1.3B). As a result, the flow of particles well as the state of the inflowing blood
in the central core of normal arteries is relatively and the arterial resistance distal to the
uniform and has high velocity during systole. stenosis.
The zone where this occurs is referred to as the • Clinical grading of stenosis severity is
“throat” of the stenosis. Typically, this is the site made using lumen diameter reduction
of maximal stenosis and, as expected with plug although area measurement is favored in
flow, shows a very narrow distribution of velocities, hemodynamics.
causing a narrow Doppler spectrum. In addition, • A critical stenosis is recognized by an
a high-grade stenosis is associated with a jet or incremental decrease in volume blood flow
jet flow. The effective diameter of this jet can be and the transition occurs somewhere
narrower than at the throat, and the velocity is between 45% and 69% diameter
therefore slightly higher just downstream to the narrowing depending on artery size and
stenosis throat. This occurs where the effective overall blood flow.
cross-sectional area of flowing blood is the nar- • A stenotic lesion can be unmasked by
rowest or the vena contracta. The stenotic jet can increases in blood flow caused by exercise,
be directly visualized on color Doppler imaging reactive hyperemia, and heating.
and confirmed by sampling the Doppler spectral • The appearance of a velocity jet is a
waveforms. The jet will show a narrow band reliable marker of a significant stenosis.
of velocities at the site of maximum velocity.29 • The velocity jet is not necessarily parallel to
Stenotic lesions result in marked disturbance of the axis of the artery.
blood flow patterns: (1) flow convergence into the • Because the shape of the stenotic lesion
stenosis, (2) plug flow at the physically narrowest can vary, the site of maximum velocity
part of the stenosis, (3) highest velocity at the may be at the site of maximal physical
vena contracta, (4) an exiting velocity jet, and (5) narrowing or slightly distal to this. It is
an area of boundary layer separation and eddy therefore prudent to walk the Doppler
formation around the diverging jet (Fig. 1.14). gate through the lesion and distal to it.
The proper grading of a stenosis requires that the
sonographer move the Doppler gate with small
increments through a suspected stenotic lesion
and distal to it. In essence, the operator walks offer little resistance to flow and blood moves
the Doppler gate through the stenosis. The axis readily from the veins to the heart, where the
of the velocity jet may be off-center with respect pressure is close to atmospheric pressure. Although
to the axis of the vessel. This can affect the accurate the effects of arterial pressure and flow waves are
determination of the Doppler velocities and the rarely transmitted to the systemic veins, phasic
interpretation of the Doppler shifts. Additional changes in venous pressure and blood flow reflect
changes seen with arterial stenosis include widen- changes in right atrial pressures in response to
ing or dispersal of the band of systolic velocity cardiac activity and because of alterations of
(spectral broadening), seen as complete filling in intrathoracic pressure with respiration. Knowledge
of the spectral tracing, and reversal of blood flow of these changes is necessary for correct assessment
due to eddies, as discussed in Chapter 3. of peripheral venous flow with noninvasive labora-
tory studies.
Venous Hemodynamics The final section of this chapter discusses
changes in pressure and blood flow in various
In the supine position, the residual venous pressure portions of the venous system that are associated
after the blood has traversed the arterioles and with cardiac and respiratory cycles. Also considered
capillaries is low (Fig. 1.1). Because of their rela- are alterations in venous hemodynamics that
tively large diameters, medium and large veins occur with changes in posture, the important
consequences of competence or incompetence right atrial volume. The upstroke of the v wave
of venous valves, and the effects of venous results from a passive rise in atrial pressure during
obstruction. late ventricular systole when the tricuspid valve
is closed and the atrium fills with blood from
Flow and pressure changes during the peripheral veins. The v wave downstroke is
the cardiac cycle caused by the fall in pressure that occurs when
There are typical changes in pressure and blood the blood leaves the atria rapidly and fills the
flow during the cardiac cycle in large veins such ventricles, soon after the opening of the tricuspid
as the vena cava (Fig. 1.17). Such oscillations in valve, early in ventricular diastole, the so-called
pressure and flow may, at times, be transmitted to y descent. Early ventricular filling starts at the y
more peripheral vessels. There are three positive descent.
pressure waves (a, c, v) in the central veins cor- These venous pressure waves are associated with
responding to changes in pressure changes in the changes in blood flow. There are two periods of
atria. The a wave is caused by atrial contraction at increased venous flow during each cardiac cycle
end diastole. The upstroke of the c wave is related (Fig. 1.18). The first occurs during ventricular
to the increase in pressure when the tricuspid valve systole, when shortening of the ventricular muscle
is closed and bulges during isovolumetric ven- pulls the tricuspid valve ring toward the apex of
tricular contraction. The subsequent downstroke the heart. This movement of the valve ring tends to
(x descent) results from the fall in pressure during increase atrial volume and decrease atrial pressure,
atrial relaxation caused by pulling the tricuspid thus increasing flow from the extracardiac veins
valve ring toward the apex of the heart during into the atrium. The second phase of increased
ventricular contraction, thus tending to increase venous flow occurs after the tricuspid valve opens
and blood rushes into the ventricles from the atria.
Venous flow is reduced in the intervening periods
of the cardiac cycle as the atrial pressure rises
during and soon after atrial contraction and in the
later part of the ventricular systole. Because there
mm Hg
A
V
D
cm/s
S
FIG. 1.18 The Doppler spectrum obtained from the
subclavian vein shows a typical blood flow pattern associ-
ated with venous blood flow near to the right atrium. A
similar pattern is seen in the hepatic veins. The A-wave
FIG. 1.17 This three-part diagram shows the normal indicates reversed blood flow during right atrial contrac-
changes in pressure and flow in the central veins as tion. The S wave occurs near the end of atrial filling. The
associated with the cardiac cycle. The a wave corresponds V wave marks the end of atrial filling. The D wave indicates
to atrial contraction, the c wave occurs during left ven- the opening of the tricuspid valve and continued ante-
tricular isovolumetric contraction and the v wave bridges grade blood flow through the right atrium into the right
the filling of the atrium (pressure upstroke) and atrial ventricle. The arrow corresponds to the typical location
filling after the tricuspid valve opens (pressure down- of the c wave (Fig. 1.17). RT SCV DIST, Right subclavian
stroke). a, a wave; c, c wave; v, v wave. vein distal.
18 SECTION 1 Basics
cm/s
cm/s
FIG. 1.20 This waveform is typical of tricuspid regurgita-

tion. The common femoral vein (CFV) is typically very
distended and the pattern of blood flow alternates from
antegrade to retrograde flow during each cardiac cycle.
RT, Right.
FIG. 1.19 This figure shows similarities between volume Venous effects of respiration
blood flow in the vena cava and the Doppler tracing
obtained in a subclavian vein. The various waves are
Respiration has profound effects on venous
described in Fig. 1.18. pressure and blood flow. During inspiration, the
volume in the veins of the thorax increases and
the pressure decreases in response to reduced
intrathoracic pressure. Expiration leads to the
are no valves at the junction of the right atrium opposite effect, with decreased venous volume
and vena cava, blood flow transiently reverses in and increased pressure. The venous response to
the large thoracic veins during atrial contraction. respiration is reversed in the abdomen, where the
The changes in pressure and blood flow in the pressure increases during inspiration because of
large central veins that are associated with the the descent of the diaphragm and decreases during
events of the cardiac cycle are not usually evident expiration as the diaphragm ascends. Increased
in the peripheral veins of the extremities. This is abdominal pressure during inspiration decreases
probably the result of damping related to the high pressure gradients between peripheral veins in the
distensibility (compliance) of the veins, as well lower extremities and the abdomen, thus reduc-
as compression of the veins by intra-abdominal ing blood flow in the peripheral vessels. During
pressure and mechanical compression in the expiration, when intra-abdominal pressure is
thoracic inlet. Because the effects of right-sided reduced, the pressure gradient from the lower
heart contractions are more readily transmitted limbs to the abdomen is increased and blood flow
to the large veins of the arms, the pulsatile changes from the peripheral veins rises correspondingly.
in venous blood flow velocity associated with the These phasic changes are seen on corresponding
events of the cardiac cycle tend to be more obvious venous Doppler waveforms (Fig. 1.21).
in the upper extremities than in the veins of the In the veins of the upper limbs, the changes
legs (Fig. 1.19). in blood flow with respiration are opposite to
In abnormal conditions, such as congestive those in the lower extremities. Because of reduced
heart failure or tricuspid insufficiency, venous intrathoracic pressure during inspiration, the
pressure is increased. This elevation of venous pressure gradient from the veins of the upper
pressure may lead to increased transmission of limbs to the right atrium increases and blood
cardiac phasic changes in pressure and blood flow flow increases. During expiration, blood flow
to the peripheral veins of the upper and lower decreases because of the resulting increase in
limbs. Such phasic changes may occasionally be intrathoracic pressure and the corresponding
found in healthy, well-hydrated individuals, prob- rise of the right atrial pressure. The respiratory
ably because a large blood volume distends the changes in blood flow in the upper limbs may be
venous system (Fig. 1.20). influenced by changes in posture. With the upper
FIG. 1.22 The effect of the Valsalva maneuver (VALS)

is to stop blood flow completely and even to reverse
FIG. 1.21 This waveform obtained at the level of the it transiently (arrow). Prolonged reversal of blood flow
common femoral vein (CFV) shows the typical phasicity is associated with venous reflux. RT GSV O, Right great
associated with respiration. The lowest blood flow velocity saphenous vein origin.
occurs at inspiration. The increased intra-abdominal pres-
sure during inspiration slows and may temporarily stop
the flow of returning blood. The presence of respiratory
phasicity indicated a patent venous system in the pelvis (e.g., secondary to infection or inflammation),
and abdomen. LT, Left. the flow tends to be more continuous, and the
respiratory changes in flow are less evident. When
there is increased vasoconstriction in the extremi-
parts of the body elevated, venous flow tends to ties (e.g., when there is a need to conserve body
stop at the height of inspiration and resumes with heat and blood flow through the skin is decreased),
expiration, probably because of the compression venous flow is also markedly decreased, and there
of the subclavian vein at the level of the first rib may be decreased Doppler flow signals over a
during contraction of the accessory muscles of peripheral vein, such as the posterior tibial vein.
respiration. Also, severe arterial obstruction may decrease
The respiratory effects are usually associated overall blood flow and velocity in the vessels of
with clear phasic changes in venous blood flow the extremities and lead to decreased velocity
in the extremities. The respiratory changes in signals over the venous channels.
venous velocity may be exaggerated by respiratory
maneuvers such as the Valsalva maneuver, which Effect of posture
increases intrathoracic and abdominal pressures In the upright position, the hydrostatic pressure
and decreases, abolishes, or even reverses flow in is greatly increased in the dependent part of the
some peripheral veins (Fig. 1.22). Also, the respira- body, particularly in the lower portions of the
tory effects on venous flow may be diminished lower extremities. This increase in hydrostatic
in the lower limbs in individuals who are chest pressure, as indicated earlier, is associated with
or shallow breathers and whose diaphragm may high transmural pressures in the blood vessels
not descend sufficiently to elevate intra-abdominal and, in turn, leads to greater vascular distention.
pressure. Venous flow then tends to be more In the veins, which have low pressure to start
continuous. with and are distensible, considerable pooling of
the blood occurs in the lower parts of the legs.
Venous blood flow and The resulting decrease in venous return to the
peripheral resistance right atrium is associated with diminished cardiac
Blood flow and blood flow velocity in the periph- output. When the normal compensatory reflexes
eral veins, particularly in the extremities, are that increase peripheral resistance are impaired,
profoundly influenced by local factors, which are decreased cardiac output can lead to hypoten-
in turn largely determined by the peripheral sion and fainting. This is the basis for the tilt
resistance or the state of vasoconstriction or test that is occasionally used to confirm that the
vasodilatation. When limb blood flow is markedly sympathetic reflexes have somehow been blunted
increased as a result of peripheral vasodilatation or compromised.30,31
20 SECTION 1 Basics
The movement of the skeletal muscles of the may be impaired and characteristic trophic changes
legs while walking leads to decreased venous in the skin and venous stasis ulcers may result
pressure because of the presence of one-way valves (see Chapter 21).
in the peripheral veins. Contraction of the vol- Peripheral venous Doppler signals can be easily
untary muscles squeezes the veins and propels distinguished from arterial flow signals because of
the blood toward the heart. Muscular contraction (1) direction and (2) absence of cardiac pulsatility.
not only increases venous return and cardiac As indicated earlier, venous Doppler signals may
output but also interrupts the hydrostatic column be absent in low-flow states, especially when the
of venous blood from the heart and thus temporar- limb is cold and auscultation is carried out over
ily decreases pressure in the peripheral veins (e.g., small peripheral veins. Squeezing the limb distal
in the veins at the ankle). This physiologic action to the site of examination should temporarily
is referred to as the calf pump. Interestingly, increase blood flow (augmentation) and produce
individuals with flat pedal arches (flat feet) cannot increased Doppler signals if the vein is patent.
efficiently activate their calf pump thereby increas- Spontaneous venous blood flow signals normally
ing their risk of varicose veins.32 Activity of the possess clear respiratory phasicity. However, an
skeletal muscles of the legs in the presence of obstruction between the heart and the site of
competent venous valves therefore results in the Doppler interrogation will blunt any respira-
intermittent lowering of venous pressure, decreases tory changes in venous blood flow and might
venous pooling, decreases capillary pressure, completely suppress them. Over larger peripheral
reduces filtration of fluid into the extracellular veins, such as the popliteal vein, the absence of
space, and increases blood flow because of an Doppler signals indicates a very high likelihood
increased arteriovenous pressure gradient. of an obstructed proximal vein.
The presence of venous obstruction can be
Effect of external compression shown by the absence of an increase in blood
Applied pressure on the veins of the extremities, flow caused by squeezing the limb distally or by
whether caused by an active muscular contraction activating the calf muscles by asking the patient
or external manual compression, increases venous to flex their foot. Both maneuvers should increase
blood flow and velocity toward the heart and either venous blood flow (augmentation). Absence of
stops blood flow distal to the site of the compres- increased blood flow signals or attenuation of the
sion if the venous valves are competent or causes expected increase in blood flow signals is indicative
venous reflux if the valves are incompetent. The of vein obstruction.
response to a sudden pressure increase is modu- Alternatively, an increase in blood flow is also
lated by the presence of venous obstruction and elicited after releasing a manual compression of
damage to the venous valves. The detection of the proximal limb. If the proximal veins at or
such changes is important when assessing patients near the point of compression are occluded, the
for the presence of acute and chronic venous augmentation of blood flow after release of the
disease and venous insufficiency. (This is discussed compression is attenuated or absent.
further in Chapter 21.)
Venous incompetence
Venous obstruction Blood flow from the peripheral veins is directed
Venous obstruction can be acute or chronic. Acute toward the heart. The venous valves prevent
venous thrombosis may lead to potentially fatal blood from flowing back toward the hands and
pulmonary embolism due to embolization of the feet. However, blood flow may be temporarily
leg vein thrombi and subsequent obstruction of diminished or stopped in the upright posture, at
the pulmonary arteries. The clinical diagnosis of the height of inspiration, or during the Valsalva
acute deep vein thrombosis is unreliable and maneuver. The peripheral veins normally fill
noninvasive venous ultrasound is the primary from the capillaries, and the rate at which they
means of making this diagnosis (see Chapter 19). fill depends on the peripheral resistance and
In the case of severe chronic vein obstruction, arterial blood flow, as determined by the degree
edema might occur because of poor exchange of of peripheral vasoconstriction. This refill time
oxygenated blood in the peripheral soft tissues. increases with age and can be as long as 40 seconds
Also, the nutrition of the skin in the affected region in young adults.33 When there are incompetent
veins proximally, there may be retrograde filling 2. Miller A, Lees RS, Kistler JP, Abbott WM. Effects of sur-
rounding tissue on the sound spectrum of arterial bruits
of the peripheral veins, such as those in the ankle
in vivo. Stroke: A Journal of Cerebral Circulation. 1980;11:
region, from the more proximal veins, in addition 394–398.
to normal filling from the capillary beds. In the 3. Latham RD, Westerhof N, Sipkema P, Rubal BJ, Reuderink
upright position, this retrograde filling causes P, Murgo JP. Regional wave travel and reflections along
persistent levels of elevated hydrostatic pressure the human aorta: a study with six simultaneous micro-
manometric pressures. Circulation. 1985;72:1257–1269.
in the legs and feet and promotes the filtration
4. Munir S, Guilcher A, Kamalesh T, Clapp B, Redwood S,
of fluid into the extravascular spaces. Marber M, et al. Peripheral augmentation index defines
The presence or absence of retrograde blood the relationship between central and peripheral pulse
flow may be detected by examining the Doppler pressure. Hypertension. 2008;51:112–118.
spectral waveforms obtained after the limb is 5. Murgo JP, Westerhof N, Giolma JP, Altobelli SA. Effects of
exercise on aortic input impedance and pressure wave forms
squeezed distally (see Chapter 21). Various ple-
in normal humans. Circulation Research. 1981;48:334–343.
thysmographic methods can detect the rate of 6. Carter SA. Effect of age, cardiovascular disease, and vasomo-
venous filling by measuring changes in venous tor changes on transmission of arterial pressure waves
volume during muscular action such as flexion- through the lower extremities. Angiology. 1978;29:601–606.
extension of the ankle in the upright position. 7. Gaskell P, Krisman AM. The brachial to digital blood
pressure gradient in normal subjects and in patients with
After such exercise, the venous volume and pressure
high blood pressure. Canadian Journal of Biochemistry and
increase more rapidly when the valves are incom- Physiology. 1958;36:889–893.
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rograde blood flow from the more proximal parts of man with special reference to the toes. Canadian Journal
of the limbs. The application of a tourniquet or of Physiology and Pharmacology. 1970;48:469–474.
9. Nielsen PE, Barras JP, Holstein P. Systolic pressure amplifica-
pressure cuff can help localize the site of venous
tion in the arteries of normal subjects. Scandinavian Journal
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10. Carter SA, Tate RB. The effect of body heating and cooling
on the ankle and toe systolic pressures in arterial disease.
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11. Rowell LB, Brengelmann GL, Blackmon JR, Bruce RA,
• Venous waveforms show cardiac pulsatility Murray JA. Disparities between aortic and peripheral
changes the closer the vein is to the heart. pulse pressures induced by upright exercise and vasomotor
These changes are more pronounced in changes in man. Circulation. 1968;37:954–964.
the arms than in the legs. 12. Sharman JE, McEniery CM, Dhakam ZR, Coombes JS,
• Changes in venous blood flow (phasicity) Wilkinson IB, Cockcroft JR. Pulse pressure amplification
during exercise is significantly reduced with age and hyper-
are caused during normal respiration and cholesterolemia. Journal of Hypertension. 2007;25:1249–
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or the performance of the Valsalva 13. Nijdam M-E, Plantinga Y, Hulsen HT, Bos WJW, Grobbee
maneuver. DE, van der Schouw YT, et al. Pulse pressure amplification
• Venous emptying can be compromised by and risk of cardiovascular disease. American Journal of
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Forward and backward waves in the arterial system.
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Journal of Medicine. 1972;287:578–582. many protocols for one condition or specific protocols
24. Li Z-Y, Taviani V, Tang T, Sutcliffe MPF, Gillard JH. The for different situations? European Heart Journal. 2009;
hemodynamic effects of in-tandem carotid artery stenosis: 30:2174–2176.
implications for carotid endarterectomy. Journal of Stroke 32. Criqui MH, Denenberg JO, Bergan J, Langer RD, Fronek
and Cerebrovascular Diseases: The Official Journal of National A. Risk factors for chronic venous disease: the San Diego
Stroke Association. 2010;19:138–145. population study. Journal of Vascular Surgery. 2007;46:
25. Widmer LK, Staub H. Blood pressure in stenosed arteries. 331–337.
Zeitschrift fur Kreislaufforschung. 1962;51:975–979. 33. Stucker M, Reich S, Robak-Pawelczyk B, Moll C, Rudolph
26. Carter SA. Indirect systolic pressures and pulse waves T, Altmeyer PJ, et al. Changes in venous refilling time
in arterial occlusive diseases of the lower extremities. from childhood to adulthood in subjects with apparently
Circulation. 1968;37:624–637. normal veins. Journal of Vascular Surgery. 2005;41:296–302.
27. Uhrenholdt A, Dam WH, Larsen OA, Lassen NA. Para-
doxical effect on peripheral blood flow after sympathetic
PRINCIPLES AND INSTRUMENTS OF
ULTRASONOGRAPHY 2
Frederick W. Kremkau, PhD
Introduction significantly on the frequency or the wave ampli-

tude (strength). As a general rule, gases, including
This chapter serves as an introduction to the air, exhibit the lowest propagation velocities,
physical and technical aspects of vascular sonog- liquids have an intermediate range of velocities,
raphy, including the following: (1) ultrasound and solids have the highest sound transmission
principles, (2) transducers, (3) instruments, (4) velocities. For soft tissues, the average speed of
advanced features, and (5) Doppler principles. sound is 1.54 mm/µs (1540 m/s). Variations exist
These subjects are discussed in greater detail in in the speed of sound from one tissue to another,
various textbooks.1–3 but, as Table 2.1 indicates, the speed of sound in
various soft tissues deviates only slightly from the
Ultrasound Principles assumed average. On average, the speed of sound
transmission in fat is lower than that in muscle.
Sound waves are produced by vibrating sources,
which cause particles in the medium to oscillate Frequency and wavelength
back and forth, setting up the propagating pressure The number of oscillations (cycles) per second of
wave. A wave is a traveling variation in something, the vibrating elements in the transducer is the fre-
such as pressure in the case of sound. As sound quency of the sound wave. Frequency is expressed
propagates, it is attenuated (weakened), scattered in cycles per second, or hertz (Hz). Audible sounds
(spread out), and reflected (bounced back), are in the range of 20 Hz to 20 kHz. Ultrasound
producing echoes from anatomic structures. In refers to sound whose frequency is above the
medical ultrasonography, the transducer serves as audible range (the prefix ultra means “beyond”).
the source and receiver of sound waves. Transduc- Diagnostic ultrasound applications use frequencies
ers are designed such that the sound waves they in the 2 to 15 MHz (megahertz, i.e., 2 million to
generate travel in a narrow beam with a well- 15 million Hz) frequency range. Because higher
defined direction. The reception of reflected and frequencies are associated with improved spatial
scattered echo signals by the transducer not only detail (i.e., better detail resolution), sonographers
produces ultrasound images but also allows the use the highest frequency that still allows adequate
detection and measurement of motion using the depth to visualize tissue in a given scanning situ-
Doppler effect. This section discusses factors that ation. Some applications that require very little
are important in the transmission and reflection penetration use frequencies as high as 50 MHz.
of ultrasound in tissue. Fig. 2.1 shows a sound wave frozen in time. It
illustrates accompanying compressions and rarefac-
Speed of sound tions (expansions) in the medium that result from
Most ultrasound applications involve transmitting the pressure and particle oscillations. The wave-
short bursts, or pulses, of sound (typically two or length λ is the spatial length of a cycle. It is
three cycles long) into the body and receiving described by the equation:
echoes from tissue interfaces. The time between
c
transmitting a pulse and receiving an echo is used λ= (Eq. 2.1)
to determine the depth of the interface. The speed f
of sound in tissue must be known in order to where c is the speed of sound and f is the fre-
calculate this depth. quency. Table 2.2 presents values of wavelengths
The velocity of sound waves mostly depends on in soft tissue for several frequencies. For soft tissues,
the properties of the transmitting medium and not the wavelength λt = 1.54 mm/f, where f is the
23
24 SECTION 1 Basics
TABLE 2.1 Sound Speeds in an object is more easily understood if given relative
Biologic Tissues. to the ultrasonic wavelength for the frequency of
the sound beam. Similarly, the width of the
Speed of Percentage
Sound Change From
ultrasound beam from a transducer depends in
Tissue (mm/µs) Average part on the wavelength. Higher frequency beams
have shorter wavelengths and can be focused more
Fat 1.45 −5.8
tightly than lower frequency beams.
Vitreous humor 1.52 −1.3
Liver 1.55 +0.6
Blood 1.57 +1.9
Muscle 1.58 +2.6
PRACTICAL TIPS
Lens of eye 1.62 +5.2 • The reception of reflected and scattered
Soft tissue average 1.54 echo signals by the transducer not only
produces ultrasound images but also
allows the detection and measurement of
motion using the Doppler effect.
TABLE 2.2 Wavelengths for Various
• Because higher frequencies are associated
Ultrasound Frequencies.
with improved spatial detail, sonographers
Wavelength (mm)
use the highest frequency that still allows
Frequency (MHz) Assuming 1.54 mm/µs
adequate depth to visualize tissue in a
2 0.77 given scanning situation.
5 0.31
10 0.15
15 0.10
Amplitude, intensity, and power
20 0.08
A sound wave is a propagating pressure variation.
The pressure profile that occurs for the wave in
Fig. 2.1 appears in the lower part of the figure.
Compression Rarefaction The pressure amplitude is the maximal increase
(or decrease) in the pressure, relevant to normal
pressure, caused by the sound wave. The unit for
pressure is the pascal (Pa). Ultrasound instruments
Wavelength
can produce peak pressure amplitudes of millions
(λ) of pascals in water when power controls on the
Pressure
0 instrument are set at maximum. As a benchmark for

comparison, atmospheric pressure is approximately
Distance
0.1 MPa, so it is clear that ultrasound beams from
medical devices significantly exceed this value.
FIG. 2.1 Sound waves produced by an ultrasound trans-
ducer. Vibrations of the transducer are coupled into the The high-pressure amplitudes of ultrasound pulses
medium, producing local fluctuations in pressure. The can burst contrast agent bubbles (see later and
fluctuations propagate through the medium in waves. Chapter 35) that are sometimes injected into the
The pressure amplitude is the maximum pressure variation, bloodstream to enhance echo signals. Diagnostic
positive or negative. The diagram schematically illustrates
levels, however, are not believed to create biologic
compressions and rarefactions at an instant of time. The
symbol λ is the acoustic wavelength. effects in tissues if such gas bodies are not present.
The intensity (I) of a sound wave at a point in
the medium is estimated by squaring the pressure
frequency expressed in megahertz. For example, amplitude (P) and using I = P2/(2ρc), where ρ is
if the frequency is 5 MHz, the wavelength in soft the density of the medium and c is the speed of
tissue is approximately 0.3 mm. Higher frequencies sound in it. Units for ultrasound intensity are watts
have shorter wavelengths leading to shorter pulses per meter squared (W/m2) or multiples thereof,
and improved detail resolution. such as mW/cm2. In water, a 2 MPa amplitude
Wavelength has relevance when describing during the pulse corresponds to a pulse average
dimensions of anatomic structures. The size of intensity of 133 W/cm2! This is a high intensity,
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—Dat vragen wij ons zelf ook af. Scotland Yard doet al grondig
onderzoek en wij zullen al spoedig iets naders vernemen.
Op dit oogenblik kwam er een hulpverpleegster aan, die eenige

woorden met de opzichteres wisselde.
Deze wendde zich tot het kleine groepje en zeide:
—Ik word daar juist door hoofdinspecteur Baxter aan de telefoon

geroepen, nog een paar minuten, miss, dan zal ik u en mijnheer uw
vader moeten wegzenden!
Zij knikte de bezoekers vriendelijk toe en volgde de hulpverpleegster

naar een der telefooncellen van het groote gebouw.
Raffles en Beaupré hadden een eigenaardigen blik met elkander

gewisseld, en nu sprak de laatste:
—Op iets dergelijks zult ge wel niet gerekend hebben.
—Ik vraag verschooning—ik wist natuurlijk integendeel zeer goed wat

het gevolg zou zijn! Het moest natuurlijk uitkomen, dat de twee
zoogenaamde detectives hunne gevangenen nooit hadden afgeleverd.
Raffles was reeds opgestaan en zeide nu tot zijn metgezellin:
—Wij moeten gaan, madame! Wij mogen uw vriend de zoo hoog

noodige rust niet onthouden.
—Zult gij goed voor haar zorgen? vroeg Beaupré, terwijl hij Raffles
nogmaals de hand toestak. Bedenk, dat zij alles voor mij is, en dat ik
niets anders op de wereld heb om lief te hebben!
—Ik beloof u, dat ik zooveel als in mijn vermogen is, voor haar zal
waken!
Marthe Debussy boog zich over den gewonde en drukte hem een kus
op het voorhoofd. De twee geliefden wisselden fluisterend eenige innige
woorden, en daarop richtten de beide bezoekers zich naar de deur,
nadat Marthe beloofd had zoo spoedig, mogelijk te zullen terug komen,
en hem het adres had toegefluisterd, waar hij zou kunnen schrijven of
telefoneeren.
Eenige oogenblikken later hadden Raffles en de vrouw, die op zulk een

eigenaardige wijze tot zijn tijdelijke beschermelinge was geworden, het
gasthuis verlaten.
Als zij slechts eenige minuten langer waren gebleven, hadden zij
getuige kunnen zijn van een merkwaardig voorval.
De hoofdverpleegster trad weder binnen, liep met snelle stappen, en

een trek van ongerustheid op het gelaat, naar het bed, waar zooeven de
nieuwe patiënt was neergelegd, en bekeek hem nauwkeurig.
Toen sloeg zij de handen van verbazing ineen en riep:
—Het is zoo! Het gelaat van dien man kwam mij al aanstonds zoo
bekend voor! Het is een van de twee mannen, die hier gisternacht zijn
geweest, om Dubois te bezoeken!
Onwillekeurig had de hoofdverpleegster de woorden zoo luid

uitgesproken, dat Beaupré ze duidelijk had verstaan.
Hij wendde het hoofd met een ruk naar de zijde van het bed, waar de
nieuwe patiënt lag, en trachtte zijn gelaatstrekken te zien.
Juist trad de verpleegster even ter zijde.
Beaupré had moeite, een kreet te weerhouden—daar lag, met wijdopen

oogen, maar blijkbaar volkomen bewusteloos, een lid van de Bende der
Raven, die weder een onderdeel vormde van het gevaarlijke
Genootschap van den Gouden Sleutel, waartoe ook de Fransche
markies behoorde!
Het was een van de beide bandieten, die hem gisteravond onder een
valsch voorgeven hadden bezocht, teneinde hem te bewegen, de
geheimen zijner eigen bende te verraden, in ruil voor het leven zijner
minnares, en te zweren, dat hij nimmer weder als mededinger van Dr.
Fox zou optreden!
Maar hoe kwam die man hier?
Raffles had hem toch zooeven medegedeeld, dat hij die twee kerels, na
hen zoogenaamd te hebben gearresteerd, bewusteloos had gemaakt,
en hij zou toch wel zoo verstandig geweest zijn, dit niet op den
openbaren weg te doen?
Hoe was het mogelijk, dat die man nog altijd bewusteloos was, en dat
geen der doctoren nog naar hem was komen zien?
Hij zou spoediger antwoord op die vraag krijgen dan hij wel vermoedde,
en wel uit den mond van de hoofdverpleegster zelve, een praatgrage
dame, die volstrekt niet kon denken, dat Beaupré deel uitmaakte van
een dievenbende, en meende, dat hij inderdaad het slachtoffer [7]van
een laaghartige poging tot afzetterij was geweest—hetgeen in zekeren
zin ook de waarheid was!
Zij had het bed van den bewustelooze verlaten en trad nu snel op dat
van Beaupré toe.
Toen zij zag, dat hij klaar wakker en blijkbaar volkomen bij zijn
positieven was, begon zij:
—Nu moet ik u toch iets heel bijzonders mededeelen, mijnheer Dubois!

Gij weet, dat ik zooeven aan de telefoon werd geroepen. Wie denkt gij
wel, dat er aan het andere einde van de lijn was?
Beaupré meende wel ongeveer te kunnen zeggen, wie dat was, maar hij
wachtte er zich wel voor, zijn vermoedens te uiten.
Hij haalde de schouders op en zeide glimlachend, wat hem moeilijk

genoeg viel, daar hij begon te begrijpen, dat hij zich in groot gevaar zou
bevinden, zoodra de man daarginds uit zijn bewusteloosheid zou
ontwaken, en zou inzien dat zijn loopbaan der misdaad beëindigd was,
zoodat er geen reden meer was, den Franschen bendechef, die reeds
lang door de Parijsche politie gezocht werd, nog langer te ontzien en
hem dus stellig zou verraden:
—Hoe kan ik dat weten, miss?
—De politie!
Beaupré had dit antwoord verwacht, maar toch liep er een zenuwachtige
rilling over zijn bleek gelaat, welke hij niet geheel en al had kunnen
bedwingen.
—De politie? vroeg hij. Zeker in verband met het bezoek dier beide
kerels, die mij geld wilden afdreigen?
—Juist! Gij zult er van opzien, wat er met hen geschied is! Ik moet u
zeggen, dat ik er niets van begrijp—maar de detective, dien wij hier
verwachten zal wel licht in de duisternis brengen! Hij kan over een
kwartier hier zijn!
Dat was een alles behalve aangename mededeeling voor den

Franschman!
Wel hoopte hij, dat zijn gelaat, zooals het nu was, niet meer zou
overeenkomen met het signalement, dat ongeveer drie jaar geleden
door de Parijsche politie was gezonden aan alle groote politiebureaux
over de geheele wereld, vooral omdat hij zijn fraaien, blonden baard uit
dien tijd had afgeschoren, maar hij was daar verre van zeker van.
Hij wist zich echter te beheerschen en vroeg vrij kalm, alsof de zaak
hem eigenlijk niet al te veel belang inboezemde:
—Wat is er dan eigenlijk gebeurd, miss?
—Dat zal ik u zeggen! Het staat nu wel vast, dat de twee rechercheurs,
die hier gisteren de twee schavuiten in de vestibule van dit gebouw
hebben gearresteerd, in het geheel niet tot de politie behoorden, en ook
geen particuliere detectives waren!
—Dat is niet te gelooven! riep Beaupré met goed gespeelde

verwondering.
—En toch is het de waarheid, riep de hoofdverpleegster zegevierend uit,

alsof zij zelve een rol in dit geheimzinnige drama had vervuld. Die
zoogenaamde detectives waren bedriegers, en zij hebben de twee
mannen, die u hier zijn komen lastig vallen, ontvoerd!
—Maar met welk doel? riep Beaupré uit, die eens wilde zien wat de
politie wel, en wat zij niet wist.
—Ja, het doel—dat is juist het ongehoorde! antwoordde de

hoofdverpleegster. Dat begrijpt niemand! Maar het staat vast, dat hier
een misdrijf gepleegd is, dat niet geheel kon worden volvoerd. Ik zal u
nu zeggen, hoe de politie dit alles weet!
De praatzieke dame was op haar gemak gaan zitten en vervolgde,

terwijl Beaupré als het ware aan haar lippen hing:
—De vier mannen zijn hier voor de deur in een huurauto gestapt en wij
meenden natuurlijk niets anders of de gewaande detectives zouden
hunne arrestanten rechtstreeksch naar Scotland Yard brengen. Er
geschiedde echter iets geheel anders met de twee mannen die hier zijn
geweest! De beide bedriegers hadden hen op de een of andere wijze—
hoe, dat weten de geneesheeren nog niet—bewusteloos gemaakt, en
toen de auto stil stond, hebben zij hen naar een onbewoond huis aan de
Bishop Street gebracht, en daar opgesloten. Maar nu komt het mooie!
De chauffeur, die hen gereden had, was nieuwsgierig uitgevallen! Hij
had een buitengewoon hooge fooi gekregen, om zoo snel mogelijk te
rijden, en dat droeg er niet toe bij, hem te kalmeeren, dat begrijpt gij wel!
—Ik begrijp het volkomen, miss! antwoordde de Fransche Markies, die

brandde van ongeduld om de rest van het verhaal te hooren.
—Hij had duidelijk gezien, dat de twee mannen die hem besteld hadden
de beide anderen onder den arm [8]hadden moeten nemen, en dat die er
al heel gek uitzagen met hun wijd geopende oogen, die echter niets
schenen te zien, en hun automatische bewegingen! Hij kon niet
begrijpen, wat die mannen in dat huis gingen uitvoeren, en omdat hij,
zooals gezegd, heel nieuwsgierig was—zoo reed hij niet weg, maar
plaatste zijn auto om een hoek van een dwarsstraat en stelde zich
verdekt op in een donker portiek!
—En.…..? vroeg Beaupré ademloos.
—Na een half uur kwamen er twee mannen uit het huis—en dat waren
de lieden, die geboeid waren binnengeleid! Maar van boeien was niets
te bekennen en zij liepen ook volkomen recht en natuurlijk! Zij schenen
groote haast te hebben en riepen een auto aan, die juist voorbij reed. En
de chauffeur was zoo overbluft, dat de wagen al uit het gezicht was,
voor hij er aan dacht hen met zijn eigen auto te volgen!
—Merkwaardig! mompelde Beaupré, om iets te zeggen, maar hij was

zeer verschrikt door dezen loop der zaken, waarvan Raffles nog niet het
minste vermoeden scheen te hebben!
—Daar de chauffeur de twee mannen toch niet meer kon achterhalen,

besloot hij de politie te waarschuwen, en die op de hoogte te brengen
van het zonderlinge voorval, waarvan hij zooeven getuige was geweest.
Het duurde eenigen tijd voor er een aantal agenten onder bevel van een
inspecteur ter plaatse waren en de dag begon al aan te breken toen
men eindelijk de buitendeur openbrak, daar er op het herhaaldelijk
schellen niet werd opengedaan en de chauffeur pertinent volhield, dat er
zich nog twee personen in het huis moesten bevinden. En wat denkt gij
wel, dat de agenten vonden?
—De twee rechercheurs? vroeg Beaupré onnoozel.
—Wel neen! antwoordde de hoofdverpleegster ongeduldig. Die waren al

lang weg! Zij vonden daar de twee mannen die hier waren geweest,
geboeid en wel, bewusteloos op een groot bed liggen!
—Dat is kras! bromde de Franschman.
—Niet waar? riep de verhaalster uit. Men deed alles, om de beide

mannen uit hun zonderlinge bewusteloosheid te doen ontwaken, maar
vruchteloos! Toen werd er een dokter bijgehaald—en toen nog een,
maar met hen beiden slaagden zij al evenmin! Zij moesten verklaren
hier voor een raadsel te staan! Zij beproefden alle bekende opwekkende
middelen, maar zij hadden dit evengoed met poppen kunnen doen!
Daarop werd besloten de twee mannen naar een gasthuis te doen
overbrengen! Een hunner ligt daar drie bedden van u af!
—Daar staat mijn verstand bij stil! riep Beaupré uit, ofschoon hij de
geheele zaak volkomen begreep. En waar is de andere?
—In de groote operatiezaal. De geneesheeren zijn op dit oogenblik

bezig allerlei middelen te beproeven om hem tot bewustzijn te brengen.
—En.….. lukt het? vroeg Beaupré snel, terwijl hij de verpleegster met
zijn groote, zwarte oogen vorschend aankeek.
—Neen! Hij ligt daar nog even stil en schijnbaar levenloos, ofschoon het
lichaam warm is, als toen hij hier werd binnen gebracht.
Beiden zwegen en eindelijk vroeg de hoofdverpleegster:
—Kunt gij u in het geheel niet voorstellen wat dit alles te beteekenen
heeft en in welke verhouding die twee zoogenaamde detectives met de
mannen stonden, die u hier gisterenavond zijn komen bezoeken?
—Neen, zeide Beaupré onvervaard, ofschoon hij het zich maar al te

goed kon voorstellen!
—Maar die twee bezoekers van gisteren—die kent gij toch wel?
—Slechts vluchtig, miss!
De hoofdverpleegster wilde nog iets zeggen, toen de deur geopend

werd en er een man met een krachtigen lichaamsbouw, ofschoon niet
zeer groot, met een vierkant, schrander gelaat, waarin twee
donkergrijze, energieke oogen schitterden, de ziekenzaal binnentrad.
Die man was James Sullivan, een der bekwaamste detectives van
Scotland Yard, die reeds eenige malen had deelgenomen aan de jacht
op den Grooten Onbekende, en tot zijn felste vijanden gerekend mocht
worden.
Hij bleef eenige oogenblikken op den drempel staan en trok de dichte,

zwarte wenkbrauwen samen, toen hij de hoofdverpleegster zoo druk in
gesprek zag met den gewonde. [9]
Toen trad hij snel op het bed toe en zeide tamelijk kortaf:
—Vergun mij een oogenblik, zuster.….. Dit is zeker de man, die hier
gisterenavond door messteken zwaar gewond werd binnen gebracht?
—Ja, mijnheer! antwoordde de hoofdverpleegster.
Sullivan trok haar een weinig terzijde en vroeg op zachten toon, zoodat
de zieke hem niet zou kunnen verstaan:
—Hebt gij dien man alles medegedeeld, wat u zooeven per telefoon is
gezegd?
—Ja, mijnheer! antwoordde de zuster aarzelend, en een weinig
schuldbewust, toen zij de ernstige, grijze oogen zoo strak op zich
gevestigd zag.
—Dat doet mij leed! hernam Sullivan en hij klemde de lippen opeen.
—Ik wist niet, dat ik er verkeerd aan deed, stamelde de

hoofdverpleegster. Wie is die man dan?
—Dat weet ik niet, maar hij speelt toch in dit alles een vrij dubbelzinnige
rol en het ware beter geweest, als gij hem onkundig hadt gehouden van
wat wij zoo pas ontdekt hebben! Nu, er is niets meer aan te doen—en ik
zou u nu wel gaarne verzoeken mij den man eenige vragen te laten
stellen. Hij schijnt sterk genoeg te zijn, om een kort verhoor te kunnen
ondergaan!
—Een verhoor! herhaalde de hoofdverpleegster verschrikt. Maar wat

vermoedt gij dan eigenlijk, mijnheer?
—Dat kan ik nu nog niet zeggen, miss! antwoordde Sullivan kortaf. Gij
kunt er trouwens bij tegenwoordig zijn, en goed opletten, of de man zich
zelf wellicht tegenspreekt!
De detective trad nu op het bed toe, zag den gewonde strak aan en
begon:
—Ik ben detective van Scotland Yard en aan mij is de taak opgedragen
onderzoek te doen, naar het geheimzinnig voorval, dat zich deels in dit
ziekenhuis, deels … ergens anders heeft afgespeeld en waarin gij
eveneens een rol hebt gespeeld, misschien ondanks uzelf! Hoe is uw
naam?
Het was een moeilijk oogenblik voor den Franschen Markies.
Hij kende den detective van aangezicht zeer goed en wist wie hij was—
een der beste speurneuzen van de politie der Engelsche hoofdstad.
Maar Sullivan herkende hem niet—dat was duidelijk—en dat was in
ieder geval een goede troef!
De bandiet dwong zich dus tot zoo groot mogelijke kalmte en

antwoordde:
—Mijn naam is Dubois—Pierre Dubois! Ik ben Franschman, als

Engelschman genaturaliseerd.
—Woont gij hier dan al lang?
—Sedert een aantal jaren!
—Men zou naar uw adressen kunnen informeeren?
Dat was een vraag waarop de Franschman niet gerekend had! Want
inderdaad was hij pas drie jaren in Engeland, en daarvan had hij nog
eenige maanden in de Fransche hoofdstad doorgebracht, als chef eener
bende!
Toch antwoordde hij onverschrokken:
—Dat spreekt vanzelf—ofschoon ik mij al die adressen niet al te goed

meer herinner! Ik heb in dozijnen pensions gewoond!
—Ja—dat kan ik mij begrijpen! antwoordde Sullivan droogjes. Men heeft

mij medegedeeld, mijnheer Dubois, dat gij hier zijt binnengebracht,
zwaar gewond door messteken. Zoudt gij mij willen zeggen hoe gij aan
die wonden gekomen zijt?
—Heel eenvoudig—ik ben op straat aangerand!
—Kunt gij het dan verklaren, hoe het komt, dat men u niets ontstolen
heeft? Uw beurs, horloge, uw zilveren sigarettenkoker zijn allen op uw
persoon gevonden!
Een ander zou door die vraag misschien in verwarring zijn gebracht,
maar niet aldus Beaupré!
Hij had zich nu hersteld en was vastbesloten zijn incognito tot het
uiterste te verdedigen.
En zoo antwoordde hij rustig:
—Ik vermoed, dat de straatroovers, die mij hebben overvallen, door de

nadering van agenten op de vlucht zijn gedreven voor zij gevolg hadden
kunnen geven aan hun voornemen mij te berooven.
—Maar gij zijt niet door agenten gevonden!
—Dan hebben zij het zich eenvoudig verbeeld en waren het burgers die
naderden en die mij gevonden hebben! Gij moet mij de opmerking ten
goede houden, mijnheer, maar dit begint veel te gelijken op een verhoor!
Mag ik weten, wat gij eigenlijk denkt of vermoedt? [10]
Sullivan beet zich op de lippen en scheen een oogenblik met zijn

houding verlegen.
Hij wantrouwde dezen man, dat was zeker, maar redenen, deugdelijke
redenen zou hij daarvoor niet kunnen opgeven.
En zoo zeide hij met een lichte buiging:
—Ik denk er niet aan u een verhoor af te nemen, mijnheer Dubois! Ik

wilde slechts eenige inlichtingen uit uw mond vernemen, die mij wellicht
van nut kunnen zijn, bij mijn verdere naspeuringen in deze duistere
zaak! Daarbij wilt gij mij toch zeker wel helpen?
—Ongetwijfeld! Als dit slechts in mijn vermogen is! Vraag vrij uit!
—Als gij mij dit toestaat dan zou ik u willen vragen: wie waren de twee
mannen, die u gisteravond kwamen bezoeken en wat wilden zij van u?
—Het zijn twee schurken, die iets uit mijn verleden weten, waarvan de
openbaarmaking mij groot nadeel zou kunnen berokkenen en daaruit
willen zij munt slaan! antwoordde Beaupré brutaal, ofschoon hij zijn hart
voelde kloppen bij het stellen van deze gevaarlijke vraag. Hun namen
wensch ik om begrijpelijke redenen niet te noemen.
—Maar dan hebben die mannen zich aan een strafbare zaak schuldig
gemaakt! riep Sullivan uit. En als gij een aanklacht in dient, kunnen wij
hen vervolgen wegens poging tot afpersing! Dat kunnen wij slechts dan
doen, als het slachtoffer zelf een klacht bij het parket indient!
—Misschien zal ik dat later ook wel doen, mijnheer! antwoordde

Beaupré. Als ik maar eerst dit ziekenhuis verlaten heb!
Sullivan haalde de schouders op.
—Uw stilzwijgen maakt onze taak niet gemakkelijker! zeide hij. Er heeft
hier een geheimzinnige gebeurtenis plaats gehad, waarin die twee
mannen een gewichtige rol vervullen. En het onderzoek naar de
identiteit van de beide gewaande detectives, die hen zijn komen
arresteeren—met een doel, dat ons volkomen onverklaarbaar is—zou
ons heel wat lichter worden gemaakt, als wij wisten, wie zij zijn!
—Wacht, tot zij uit hun bewusteloosheid ontwaakt zijn, kwam Beaupré
kortaf. Dan zullen zij wel spreken!
Hij had het stoutmoedig gezegd—maar bij zich zelf overwoog hij, dat het
voor hem wel eens zeer onaangename gevolgen zou kunnen hebben,
als de schurken inderdaad begonnen te spreken!
—Dat is ook juist een der meest verrassende zijden van deze gansche
geschiedenis! riep Sullivan uit. Geen der geneesheeren weet te zeggen,
welke eigenaardige verdooving de twee mannen heeft aangegrepen!
Beaupré bromde iets onverstaanbaars in zich zelf, maar hij antwoordde

niet.
Sullivan wierp nogmaals een verstolen, onderzoekenden blik op den
gewonde, en hernam toen:
—Ik wil u thans niet langer lastig vallen, want gij zult wel rust behoeven.
Later echter hoop ik u nogmaals eenige vragen te mogen stellen.
Hij knikte Beaupré toe en stapte vervolgens op het bed toe waar de
bewustelooze ter neder lag.
Eenigen tijd keek hij onafgebroken naar het witte gelaat met de wijd
geopende oogen en toen schudde hij het hoofd en haalde de schouders
op.
—Ik begrijp er niets van! mompelde hij. Het lichaam is blijkbaar warm en
volstrekt niet stijf—het heeft niet weinig van schijndood!
Juist op dit oogenblik ging de deur open en traden twee geneesheeren

binnen. [11]
[Inhoud]
HOOFDSTUK III.
Een raadselachtig geval.
De beide doktoren waren in een druk gesprek met elkander verdiept en

begaven zich dadelijk naar het bed van den bewusteloozen man.
Sullivan maakte dadelijk bescheiden plaats voor hen en bleef een

weinig op een afstand staan.
Wat Beaupré betreft—hij voelde zijn hart in zijn keel kloppen, want als
deze geneesheeren er werkelijk eens in slaagden om den man weder
tot bewustzijn te brengen, dan liep zijn vrijheid groot gevaar!
Want de man daarginds zou zeker wel vastgehouden worden—het zou

spoedig uitkomen wie hij werkelijk was—en dan zou hij den Markies
zeker in het ongeluk willen meeslepen, en diens waren identiteit
verraden.
Een der geneesheeren trad naast het hoofdeinde van het bed en trok
een der oogleden omlaag.
Even bleef het lid in dien zelfden toestand, maar toen schoof het uit zich
zelf langzaam weder naar boven.
De geneesheer lichtte een arm op en liet hem weder vallen, tastte den
pols, opende den mond, niet zonder moeite, en legde een thermometer
onder de tong van den bewustelooze.
Na eenigen tijd trok hij het instrument weder terug en raadpleegde het.
Hij schudde het hoofd, maakte een wanhopig gebaar en zeide op

zachten toon tot zijn collega:
—Normale bloedwarmte—iets meer dan zeven en dertig graden—de

pols een weinig langzaam—maar toch zoo goed als normaal! Geene
reflexbeweging—en een geringe verlamming van de oogspieren—die
blijkbaar slechts van tijdelijken aard is! Volkomen dezelfde
verschijnselen als bij den anderen man. Ik herken het volmondig—ik sta
hier voor een raadsel!
—Hebt gij reeds van alles geprobeerd? vroeg de andere geneesheer.
—Van alles! Onderhuidsche injecties, met een zoutoplossing, morphine

inspuiting, insnijdingen in de voetzool—waarbij ik er op wil wijzen, dat er
geen druppel bloed te voorschijn kwam—electrische bestraling, cocaïne,
cognac, het hielp alles niets! Ik zou zeggen dat wij hier te doen hebben
met atropie van de gevoelszenuwen, een tijdelijke stilstand van het
zintuigelijk waarnemingsvermogen, maar waardoor dat teweeg is
gebracht, en hoe wij het kunnen doen eindigen, dat is mij een raadsel!
—Hoelang zouden lieden zich reeds in dezen toestand bevinden?
—Op dit oogenblik bijna een half etmaal!
Nu trad Sullivan naderbij, stelde zich voor en zeide:
—Ik zou het bijzonder op prijs stellen, als ik u een vraag zou mogen
doen!
—Vraag slechts mijnheer—maar ik vrees, dat ik u wel niet zal kunnen

antwoorden, antwoordde de geneesheer die zooeven den patiënt
onderzocht had.
—Acht gij het mogelijk dat deze man zich uit zich zelf bewogen heeft?
De wenkbrauwen van den geneesheer gingen de hoogte in en als een

antwoord daarop antwoordde hij glimlachend met een kwalijk verborgen
medelijden van den vakman voor den leek:
—Dat is volkomen buiten gesloten!

—Maar hoe verklaart gij het dan, dat deze twee lieden zelf uit een auto
zijn gestapt en een huis zijn binnen gegaan?
—Dat verklaar ik niet, mijnheer—dat ontken ik—antwoordde de

geneesheer kortaf. Dat is onmogelijk! Als er getuigen zijn die verklaren
dat zij dit gedaan hebben, dan kunnen zij niet in de auto bewusteloos
zijn gemaakt, maar dan moet dit in dat huis geschied zijn!
—Ik dank u voor uwe bereidwilligheid om mij te antwoorden, maar ik

ben niet voldaan, antwoordde Sullivan. [12]
—Waarom niet? als ik vragen mag, hernam de geneesheer een weinig

uit de hoogte.
—Omdat ik mij niet kan voorstellen hoe die beide mannen zonder
eenigen tegenstand te bieden, of tenminste hun verbazing te uiten, dat
donkere, onbewoonde huis in de Bishop Street binnen gingen! Zij
moesten immers verwacht hebben naar Scotland Yard of naar een Huis
van Bewaring te worden overgebracht?
De geneesheer gaf niet aanstonds antwoord, maar stond met gefronst

voorhoofd stil, terwijl hij zenuwachtig met de vingers op zijn rug
friemelde.
Toen antwoordde hij een weinig gemelijk:
—Ik kan u op die vraag geen antwoord geven, mijnheer—dat zijn

politiezaken. Wel kan ik u echter zeggen dat er geen sprake van is dat
deze man of zijn metgezel zich zouden hebben kunnen bewegen.
Sullivan haalde vluchtig de schouders op en zeide:
—Als dat uw vaste overtuiging is—dan moet ik mij daar natuurlijk wel bij
neerleggen. Maar het maakt voor mij de zaak des te raadselachtiger.
Beaupré had het geheele gesprek, ofschoon het op tamelijk zachten

toon gevoerd was, gehoord, en hij was door zijn hoop en vrees heen en
weer geschommeld.
Nu waren zijn twee doodsvijanden nog bewusteloos, maar wie weet hoe
lang dat zou duren?
Zij konden weder ieder oogenblik tot het leven terugkeeren—met al de

gevolgen daarvan.
De Franschman zag nu hoe de beide geneesheeren zich verwijderden,

na nogmaals een blik op den bewustelooze geworpen te hebben en het
volgende oogenblik waren zij weg, door Sullivan op den voet gevolgd.
—Ik moet Marthe waarschuwen! mompelde Beaupré zacht. Zij moet

John Raffles op de hoogte brengen. Hij is de eenige die mij kan helpen!
Als die man daarginds spreekt ben ik verloren—en Raffles was de man
die hem bewusteloos heeft gemaakt en hij is dus waarschijnlijk de
eenige die hem weder tot het bewustzijn kan terugroepen. Hij moet hen
hier trachten weg te voeren, voor het te laat is.
En nu begonnen de hersens van den Franschen markies met

koortsachtige haast te werken.
Hij overwoog alle mogelijkheden, en ten slotte meende hij de

eenvoudigste oplossing te hebben gevonden. Hij zou zich houden alsof
zijn toestand plotseling zeer verergerde, en dan zou men zeker niet
weigeren Marthe aanstonds bij hem te laten komen.
Beaupré gaf aanstonds gevolg aan zijn voornemen!
Hij begon te kreunen, wentelde het hoofd van links naar rechts over zijn
kussen en het duurde niet lang of een der verpleegsters kwam
toeloopen, boog zich over hem heen, en vroeg:
—Hebt gij erge pijn?
—Vreeselijk, zuster! antwoordde Beaupré. Ik geloof dat het met mij ten
einde loopt.
—Maar uw toestand was van morgen redelijk, riep de zuster verschrikt
uit. Ik zal aanstonds de hoofdverpleegster roepen.
Deze werd gehaald en kwam haastig op het bed van den gewonde
toeloopen.
Nu was deze inderdaad een weinig uitgeput, door het langdurig en

opwindend gesprek, gevolgd door het verhoor van Sullivan en de vrees
voor zijn vrijheid had het zweet met fijne druppeltjes op zijn slapen doen
parelen.
Hij stak een bevende hand naar de hoofdverpleegster uit en zeide op

heeschen toon:
—Ik geloof dat het met mij mis loopt! Ik smeek u aanstonds mijn vriendin
te laten halen!
—Gij ziet werkelijk heel bleek, zeide de verpleegster verschrikt.
Zij legde den zieke den thermometer aan en bemerkte dat hij hooge
koorts had.
Een oogenblik stond zij in beraad, en toen nam zij een besluit en zeide:
—Geef mij het adres van uw vriendin—ik zal haar laten halen, maar gij
moogt volstrekt niet langer dan vijf minuten met haar spreken.
—Dat beloof ik u, Miss—vijf minuten zijn voldoende om afscheid van

haar te nemen,—kwam de Fransche Markies op dramatischen toon.
Hij noemde een afgelegen straat in een der Noordelijkste wijken van
Londen, een oogenblik later was er een telegram aan het adres van
Marthe Debussy gezonden.
Met koortsachtig ongeduld wachtte Beaupré de komst af van zijn

minnares en zijn vrees en ongerustheid deden hem veel zieker schijnen
dan hij inderdaad was.
Onophoudelijk wendde hij zijn blik naar den bewustelooze, vreezend
hem eensklaps te zien ontwaken. [13]
Het zou niet veel helpen, als hij zich onder de dekens verborg, want „Big
Billy”, zoo was de naam van den bewustelooze, wist zeer goed wie er in
dat bed lag!
Er verliepen twee bange uren—en toen werd de deur opengeworpen en

trad Marthe Debussy doodelijk verschrikt binnen.
Het telegram had haar zeer ontsteld en zij meende niet anders of zij zou
haar minnaar stervende vinden.
Zij snelde op het bed van Beaupré toe, maar deze stelde haar
onmiddellijk met eenige gefluisterde woorden gerust, en hernam daarop
iets luider opdat de verpleegster hem zou kunnen verstaan:
—Ik meende zooeven mijn einde te voelen naderen—en ik wilde je nog

eens zien voor ik stierf! Wij hebben slechts vijf minuten!
De verpleegster verwijderde zich bescheiden, en nu volgde Beaupré

zachtjes:
—„Big Billy” is in deze zelfde zaal gebracht—hij ligt drie bedden van mij
af—kijk aanstonds eens voorzichtig!
Marthe Debussy kon met moeite een kreet van schrik weerhouden, want
ook zij had aanstonds het gevaar begrepen!
Zij kende Big Billy maar al te goed en zij wist dat hij geen medelijden
zou kennen, als hij zelf gearresteerd werd—hij zou trouwens overtuigd
zijn, zijn vriend Dr. Fox een grooten dienst te bewijzen als hij den
Franschen markies, diens mededinger, in het verderf stortte!
Zij keek even schichtig in de aangeduide richting en zeide toen

fluisterend:

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Introduction to Vascular

Ultrasonography 7th Edition John

Stanfield’s Introduction to Health Professions 7th

Introduction to Critical Care Nursing 7th Edition

Introduction to Toxicology 4th Edition John Timbrell

Introduction to the Counseling Profession 7th Edition,

Introduction to law 7th Edition Edition University Of

Introduction to Show Networking John Huntington

Introduction to Radiologic and Imaging Sciences Patient

Introduction to Forensic and Criminal Psychology 7th

Joseph F. Polak, MD, MPH, FACR, FAIUM

INTRODUCTION TO VASCULAR ULTRASONOGRAPHY, SEVENTH EDITION ISBN: 978-0-323-42882-8

Library of Congress Control Number: 2019949237

Content Strategist: Russell Gabbedy

Last digit is the print number: 9 8 7 6 5 4 3 2 1

To Alex and Jo-Anne.

A BOUT THE EDITORS

John S. Pellerito, MD, FACR, FSRU, FAIUM

Dennis F. Bandyk, MD Heather L. Gornik, MD, RVT, RPVI

Mahan Mathur, MD Joseph F. Polak, MD, MPH, FACR, FAIUM

Kathryn A. Robinson, MD Steven R. Talbot, RVT, FSVU

Paul Sidhu, BSc, MBBS, MRCP, FRCR,

SECTION 1 9 ULTRASOUND ASSESSMENT OF THE VERTEBRAL

1 THE HEMODYNAMICS OF VASCULAR DISEASE 2 10 ULTRASOUND ASSESSMENT OF THE INTRACRANIAL

CORINNE DEURDULIAN, MD, AND EDWARD G. GRANT, MD

JOHN S. PELLERITO, MD, FACR, FSRU, FAIUM, AND

17 ULTRASOUND IN THE ASSESSMENT AND 26 DOPPLER ULTRASOUND OF THE MESENTERIC

SECTION 4 27 ULTRASOUND ASSESSMENT OF THE HEPATIC

20 RISK FACTORS AND THE ROLE OF ULTRASOUND IN

Abdomen and Pelvis 33 ULTRASOUND SCREENING FOR VASCULAR

Overview arterial reservoir and a large venous pool with low

Aorta Vena cava

pressure) energy is constant. The equation that

laminar flow. The velocity is maximal in the center of the

Energy differences due to laminar flow

Outside carotid bifurcation, the blood flow profile in the

where r is the radius of the tube, v is the velocity,

Turbulence occurs because a jet of blood with

The speed of propagation, amplitude (strength),

Pressure changes from cardiac activity

Pressure difference (mm Hg) 60

FIG. 1.10 (A) Pressure differences between the femoral

Effects of Arterial Obstruction

region is a complex interplay of all of these forces.

Pressure drop due to stenosis

illustrated by the Doppler frequency spectra in

FIG. 1.20 This waveform is typical of tricuspid regurgita-

FIG. 1.22 The effect of the Valsalva maneuver (VALS)

Introduction significantly on the frequency or the wave ampli-

0 instrument are set at maximum. As a benchmark for

Op dit oogenblik kwam er een hulpverpleegster aan, die eenige

Deze wendde zich tot het kleine groepje en zeide:

—Ik word daar juist door hoofdinspecteur Baxter aan de telefoon

Zij knikte de bezoekers vriendelijk toe en volgde de hulpverpleegster

Raffles en Beaupré hadden een eigenaardigen blik met elkander

—Op iets dergelijks zult ge wel niet gerekend hebben.

—Ik vraag verschooning—ik wist natuurlijk integendeel zeer goed wat

Raffles was reeds opgestaan en zeide nu tot zijn metgezellin:

—Wij moeten gaan, madame! Wij mogen uw vriend de zoo hoog

Eenige oogenblikken later hadden Raffles en de vrouw, die op zulk een

De hoofdverpleegster trad weder binnen, liep met snelle stappen, en

Toen sloeg zij de handen van verbazing ineen en riep:

Onwillekeurig had de hoofdverpleegster de woorden zoo luid