@anesthesia Books 2013 Board Stiff

https://t.
me/Anesthesia_Books
Board Stiff TEE
https://t.me/Anesthesia_Books
Content Strategist: William Schmitt
Content Development Specialist: Rachael Harrison/Nani Clansey
Content Coordinator: Lee Hood
Project Manager: Sukanthi Sukumar
Designer: Steven Stave
Illustration Manager: Lesley Frazier
Illustrator: Dartmouth Publishing
Marketing Manager (UK/USA): Abby Swartz
Board Stiff TEE
Transesophageal Echocardiography
Second Edition
Christopher J. Gallagher, MD
Professor and Residency Director
Stony Brook Department of Anesthesia
Stony Brook University
Stony Brook, NY, USA
John C. Sciarra, MD
Assistant Professor
Cardiovascular and Thoracic Anesthesiology
Fellowship
Program Director
University of Miami
Miami, FL, USA
Steven Ginsberg, MD
Associate Professor of Anesthesiology
Program Director of Cardiothoracic Anesthesia Fellowship
UMDNJ-Robert Wood Johnson Medical School
New Brunswick, NJ, USA
For additional online content visit

www.expertconsult.com
London, New York, Oxford, St Louis, Sydney, Toronto 2013

SAUNDERS an imprint of Elsevier Inc.
© 2013 Elsevier Inc. All rights reserved.
First edition 2004
No part of this publication may be reproduced or transmitted in any form or by any

means, electronic or mechanical, including photocopying, recording, or any information
storage and retrieval system, without permission in writing from the publisher. Details
on how to seek permission, further information about the Publisher’s permissions
policies and our arrangements with organizations such as the Copyright
Clearance Center and the Copyright Licensing Agency, can be found at our
website: www.elsevier.com/permissions.
This book and the individual contributions contained in it are protected under copyright
by the Publisher (other than as may be noted herein).
Notices
Knowledge and best practice in this field are constantly changing. As new research and
experience broaden our understanding, changes in research methods, professional
practices, or medical treatment may become necessary.
Practitioners and researchers must always rely on their own experience and
knowledge in evaluating and using any information, methods, compounds, or
experiments described herein. In using such information or methods they should be
mindful of their own safety and the safety of others, including parties for whom they have
a professional responsibility.
With respect to any drug or pharmaceutical products identified, readers are advised to
check the most current information provided (i) on procedures featured or (ii) by the
manufacturer of each product to be administered, to verify the recommended dose or
formula, the method and duration of administration, and contraindications. It is the
responsibility of practitioners, relying on their own experience and knowledge of their
patients, to make diagnoses, to determine dosages and the best treatment for each
individual patient, and to take all appropriate safety precautions.
To the fullest extent of the law, neither the Publisher nor the authors, contributors, or
editors, assume any liability for any injury and/or damage to persons or property as a
matter of products liability, negligence or otherwise, or from any use or operation of any
methods, products, instructions, or ideas contained in the material herein.
ISBN: 978-1-4557-3805-2
ebook ISBN: 978-1-4557-3759-8
Printed in United States of America
Last digit is the print number: 9 8 7 6 5 4 3 2 1

Contents
Preface to the First Edition vii

Preface to the Second Edition ix
List of Contributors xi
Introduction: Neither Rain nor Snow xv
CHAPTER 1 The Yellow Brick Road 1

Christopher J. Gallagher
CHAPTER 2 Principles of Ultrasound 3

Christopher J. Gallagher and John C. Sciarra
CHAPTER 3 Transducers and Instrumentation 9

CHAPTER 4 Equipment, Infection Control, and Safety 19

Steven Ginsberg and Jonathan Kraidin
CHAPTER 5 Principles of Doppler Ultrasound 25

Jonathan Kraidin, Steven Ginsberg, William Jian and Kevin A. Jian
CHAPTER 6 Quantitative M-mode and Two-dimensional

Echocardiography 39
Varun Dixit, John C. Sciarra and Christopher J. Gallagher
CHAPTER 7 Quantitative Doppler 47

Christopher J. Gallagher, Christina Matadial and Jadelis Giquel
CHAPTER 8 Doppler Profiles and Assessment of Diastolic Function 55

CHAPTER 9 Cardiac Anatomy 67

CHAPTER 10 Pericardium and Extra-Cardiac Structures: Anatomy and

Pathology 77
Enrique Pantin and F. Luke Aldo
CHAPTER 11 Pathology of the Cardiac Valves 97

F. Luke Aldo and Enrique Pantin
CHAPTER 12 Intra-cardiac Masses and Devices 115

Al Solina, F. Luke Aldo and Salvatore Zisa
CHAPTER 13 Left Ventricular Systolic Function 123

Eric W. Nelson
CHAPTER 14 Segmental Left Ventricular Systolic Function 131

John C. Sciarra and Christopher J. Gallagher
vi Contents
CHAPTER 15 The 17 Segment Model 139

John C. Sciarra
CHAPTER 16 Assessment of Perioperative Events and Problems 147

Ricardo Martinez-Ruiz and Christopher J. Gallagher
CHAPTER 17 Congenital Heart Disease 163

Liliana Cohen and Daniel M. Shindler
CHAPTER 18 Artifacts and Pitfalls 173

Christopher J. Gallagher and Gian Paparcuri
CHAPTER 19 Related Diagnostic Modalities 191

Steven Gill, John C. Sciarra and Christopher J. Gallagher
CHAPTER 20 Intraoperative 3-D Echocardiography 195

Gian Paparcuri
CHAPTER 21 The Structured TEE Examination 203

John C. Sciarra
CHAPTER 22
Sonographic Formulas 209
John C. Sciarra
CHAPTER 23
Hemo-dynamo Doc 211
CHAPTER 24
Test Questions 249
William R. Grubb and Andrew T. Burr
Epilogue: Smooth Sailing 273
Index 275
Preface to the First Edition
If you are doing cardiac anesthesia, cardiac surgery, or intensive care

work, and you don’t know Transesophageal Echocardiography, you are
yesterday’s newspaper. You are a repairman for 8-track cassette players.
You are selling slide rules.
You need to know TEE.
Board Stiff TEE is just the ticket. I wrote this book to give you a complete
introduction to the subject, from the physics of ultrasound to the images
you need to recognize to the hemodynamic calculations you can make
with TEE. The whole nine yards. Plus, I direct you to those places where
you can deepen your understanding of TEE.
Board Stiff TEE is the perfect launch pad.
Board Stiff TEE is for the medical student, the anesthesiologist, the sur-
geon, the intensivist, who asks, “Just where do I start?”
The book details

n Why you need to know TEE
n Which books and meetings will help the most
n Everything you need to know if you take the PTEeXAM
n How to work through the quantitative aspects of TEE
Board Stiff TEE is jam-packed with simplified drawings to illustrate all
the points you need to know. No need to decipher a small photograph
of a TEE image; everything here is laid out with the student in mind.
Especially when you start out, it’s hard to tell what’s what in a photo-
graph of a TEE image. These drawings will lay it out for you. Best of all,
learning TEE does not have to be a replay of your root canal. Board Stiff
TEE has a dollop of humor here and there to keep your eyes open and
your airway from obstructing.
Several people helped in this affair. Alicia Borus gave expert secretarial
help; my editor Natasha Andjelkovic reined in my more outlandish prose;
Elsevier’s illustrators redid all the drawings, improving on my “magic
marker in a Crayola pad” work; and J.C. Duffy did the cover and the car-
toons. Through it all, my wife endured my manic ravings.
And final thanks to my daughter Rachel, who is a blast.
This page intentionally left blank
Preface to the Second Edition
A long time ago in a galaxy far, far away…AND SO FORTH.
John C. Sciarra, MD
University of Miami
List of Contributors
Andrew T. Burr, DO
Anesthesia Resident, UMDNJ-Robert Wood Johnson
Medical School, New Brunswick, NJ, USA
Liliana Cohen, MD
Assistant Professor of Cardiology, UMDNJ-Robert
Wood Johnson Medical School, New Brunswick,
NJ, USA
Varun Dixit
Fellow Cardio-Thoracic Anesthesiology, University of
Miami, Miami, FL, USA
Professor and Residency Director, Stony Brook
Department of Anesthesia, Stony Brook University,
Stony Brook, NY, USA
Steven Gill, MD
Cardiothoracic Anesthesiology Fellow, University
of Miami Miller School of Medicine, Jackson
Memorial Hospital, Department of Anesthesiology,
Miami, FL, USA
Steven Ginsberg, MD
Associate Professor of Anesthesiology, Program
Director of Cardiothoracic Anesthesia Fellowship,
UMDNJ-Robert Wood Johnson Medical School,
New Brunswick, NJ, USA
Jadelis Giquel, MD
Assistant Professor, Clinical Anesthesiology,
Department of Anesthesiology/Division of Cardiac
Anesthesia, University of Miami Miller School of
Medicine, Miami, FL, USA
William R. Grubb, MD
Associate Professor of Anesthesiology, UMDNJ-
Robert Wood Johnson Medical School, New
Brunswick, NJ, USA
Kevin A. Jian
Student Illustrator
xii List of Contributors
William Jian
Student Assistant in Research
Jonathan Kraidin, MD
Brunswick, NJ, USA
F. Luke Aldo, DO
Cardiothoracic Anesthesia Fellow, UMDNJ-Robert
NJ, USA
Ricardo Martinez-Ruiz, MD
Associate Professor of Anesthesiology and Surgery,
Chief, Surgical ICU, VA Medical Center; Attending
Physician, Cardiothoracic Anesthesia Division,
Jackson Memorial Hospital, Miller School of
Medicine, University of Miami, Miami, FL, USA
Christina Matadial, MD
Associate Professor of Clinical Anesthesiology,
University of Miami Miller School of Medicine,
Chief of Anesthesiology, Bruce W. Carter VA
Medical Center, Miami, FL, USA
Eric W. Nelson, DO
Assistant Professor, Anesthesia and Perioperative
Medicine, Medical University of South Carolina,
Charleston, SC, USA
Gian Paparcuri, MD
Assistant Professor of Anesthesiology, University
of Miami Leonard M. Miller School of Medicine,
Department of Anesthesiology, Perioperative
Medicine and Pain Management, Miami, FL, USA
Enrique Pantin, MD
Brunswick, NJ, USA
John C. Sciarra, MD
Assistant Professor, Cardiovascular and Thoracic
Anesthesiology Fellowship Program Director,
University of Miami, Miami, FL, USA
Daniel M. Shindler, MD FACC

Professor of Medicine Director, Echocardiography
Laboratory UMDNJ-Robert Wood Johnson
Medical School, New Brunswick, NJ, USA
List of Contributors xiii
Al Solina, MD
Professor and Vice Chairman of Anesthesia, Chief,
Division of Cardiac Anesthesia, UMDNJ-Robert
NJ, USA
Salvatore Zisa, MD
Section Head of Thoracic Anesthesia, UMDNJ-
Brunswick, NJ, USA
Introduction: Neither Rain nor Snow
The policeman tapped his baton on the bare foot sticking out of the
refrigerator box. Behind the policeman, a mailman stood with his left
hand on his leather satchel and his right hand holding a letter from the
National Board of Echocardiography.
“Hey, rise and shine,” the policeman said. “We have something for you,
Dr. Gallagher.”
Gray hair popped out of the other end of the refrigerator box. Gray hair
disappearing in the middle, promising a “tonsured monk” look in another
few years.
Eyes, rimmed red with hard living, hard anesthetizing, and bad investing,
blinked in the sunshine just now peeking under the bridge.
“Officer!” the refrigerator box man said. “Why” he looked around at the
discarded MD 20/20 bottles wrapped in brown paper, the McDonald’s
bags, the metallic doo-dads that fell off passing cars. “Officer. Uh,
excuse me while I freshen up.”
The graying man pulled a Tony Roma’s pre-moistened towelette packet

out of his pocket, shook out a towelette, and rubbed some of the grime
off his face.
“There,” he wiggled out of the box, “now I’m presentable.”
He stood up and brushed crumbs and critters off his green scrubs.
On the front and back, large black lettering warned, “Property of East
Bumblebee Memorial Hospital. Rented, never sold.”
The man looked down, then gave the policeman a sheepish grin.
“I’m renting.”
“Uh-huh.”
The mailman wrinkled his brow at that explanation, then lifted the enve-
lope up to his face. “Says here, ‘Dr. Chris Gallagher,’ and for address it
says, ‘Under a bridge somewhere’.” He looked up at the bridge, then
down at the man in the scrubs. “Am I in the right place with the right
person?”
“Why yes. Yes you are,” the man in scrubs said. “I am, in point of fact,
the very addressee you seek. It warms the cockles of my heart to see
that, once again, ‘Neither rain, nor snow, nor sleet, nor hail, nor heat of
xvi Introduction: Neither Rain nor Snow
day, nor gloom of night, nor vagueness of address’ have stayed you from
the swift completion of your appointed rounds, my good mailperson.”
Both policeman and mailman said, “Uh-huh.”
Opening the letter, the man said, “Oh joy, rapture! I have passed the
examination for special competence in the perioperative use of trans-
esophageal echocardiography! Can you believe my good fortune?”
Policeman and mailman both shook their heads, apparently unable to

believe the man’s good fortune. Overhead, a big rig went “Thump!” and
“Thump!” again as it roared over the expansion joints in the bridge.
The man in scrubs held his letter to his chest, right against the “Property
of East Bumblebee Memorial Hospital” letters.
“Say,” the man gave the policeman and mailman a conspiratorial look,
“you don’t suppose”—he looked behind lest someone surprise them,
then turned back and stood on tiptoe to look over the shoulders of his
two new friends—“you don’t suppose I might parlay this little triumph
into another book, do you?”
The policeman and mailman looked at each other.
“Another book?”
“Why yes,” the man said. “A book about transesophageal echocardio-

graphy!”
“Who would want such a thing?” the policeman asked. He had served in
the Miami Police Department for years. Talking with a babbling maniac
was nothing new to him. At least this maniac wasn’t shooting at anybody.
The policeman preferred spending time with unarmed street people.
“Oh, anyone who might want to save a patient in hemodynamic trouble:

n Medical students
n ICU nurses
n Echocardiography technology students
n Anesthesiologists
n Anesthetists
n Intensivists of all flavors

n Cardiac surgeons
n ER and trauma center staff
n Anyone considering taking the Examination of Special Competence
in Perioperative Transesophageal Echocardiography (PTEeXAM).”
“Thump! Thump!” “Thump! Thump!” Two more trucks passed overhead.

Introduction: Neither Rain nor Snow xvii
The mailman leaned on his left hip and shifted his leather satchel around.
He had a few more letters to deliver, but didn’t seem in a big rush.
The man in scrubs went on, “Transesophageal echocardiography is

making its way into ICUs from sea to shining sea. It is THE way to diag-
nose hemodynamic instability in a hurry. A crystal ball looking into the
near future shows TEEs appearing wherever and whenever a patient is
crashing.”
“And patients can crash anywhere!”
As if on cue, a driver on the bridge jammed on the brakes and a sicken-

ing squeal filled the air. All three men hunched their shoulders, squinted
their eyes, and tensed for the “crash!”
But nothing happened. The policeman, mailman, and bescrubbed man

all looked up, as if their eyes could pierce the concrete and figure out
what happened.
Above, a string of obscenities in Spanish crackled in the air, then an

engine roared to life and the car drove off.
“See what I mean?” the man said. “A crash can occur anywhere,
anytime.”
The policeman and mailman looked at each other and nodded. This nut-
case was on to something here.
Reaching into the refrigerator box, the man in green scrubs pulled out a
stack of papers, a sketch pad, and a magic marker.
“I’ll throw together a little study guide from these notes I took. I’ll include:
1. A guide to the books, meetings, and study material that will help
you learn TEE.
2. A brief review for the Examination of Special Competence in
Perioperative Transesophageal Echocardiography (PTEeXAM).
3. Detailed problem solving for the quantitative aspects of TEE, such
as gradients, valve areas, and chamber pressures.”
“For those of us who are visual learners,” the mailman said, “do you feel
that some simplified drawings may help out? Not that I anticipate much
transesophageal echocardiography work at the Post Office, but you
never know. Second careers and all that.”
The man held up his magic marker. “Simplified drawings to aid the visual
learner, coming right up.”
CHAPTER
The Yellow Brick Road
1 Christopher J. Gallagher
“Follow the yellow brick road.”

—The Mayor of Munchkinland, The Wizard of Oz
(This chapter is included as a kind of time-capsule of how we thought

9 years ago. I make reference to “buying tapes” which is laughably ancient.)
Dorothy received unambiguous directions to get where she needed to
go. Here is your yellow brick road:
1. Go ye to the “Comprehensive Review of Intraoperative Echocardiography”
meeting. It’s held each year in February. For the next 5 years or so it will
be held in San Diego. There are other echo meetings, including a quite
similar review held in Atlanta in September every year. (The talks and
speakers are similar at the meetings.) Both meetings are a little pricey
but they are worth it! If you are considering taking the PTEeXAM, it’s
worth remembering that the same people who make up the exam give
the lectures at the meeting. So figure it out, Sherlock. Need info? Go to
the Society of Cardiovascular Anesthesiology website (www.scahq.org).
2. Do as much hands-on echo as you can at your hospital. Go to the
echo lab. Ask if you can see some old tapes and go over them with
a cardiologist. The more you DO, the more you LEARN. This has
not changed in 9 years.
3. Look at the content outline of the PTEeXAM and see if you know
the subjects listed. That list is waiting for you at www.echoboards.
org/pte/pfoutline.html.
4. Buy the complete set of tapes from the 2002 “Comprehensive
Review” meeting. It’s pricey (over a thousand smackers), and lengthy
(25 tapes, each about 2 hours long), but it’s all there. Maybe get your
department to buy a set of the tapes? Anyway, they are invaluable,
full of great lectures, and all the TEE movies are reproduced clearly
on the tapes. All in all, a good investment. Order them through
CME Unlimited (phone: 800-776-5454 or 760-773-4498;
fax: 760-773-9671; website: www.CMEunlimited.org).
Note: There are much more current reviews online now. And like so
much else, a lot of these reviews are FREE. It is impossible to
keep current, so google away and see what is out there.
5. If your pockets aren’t that deep, buy the syllabuses from the meeting.
There are two, one from days one through three of the meeting, and
one from days four through six of the meeting. You can order them
($35 for one, $60 for the pair) from the Society of Cardiovascular
Anesthesiology (phone: 804-282-0084; fax: 804-282-0090; E-mail:
[email protected]; website: www.scahq.org). Tons of material from 1
my studying and for this book came straight from those syllabuses.
2 Board Stiff TEE
6. Get a hold of the book most people use to study for the TEE exam,
Textbook of Clinical Echocardiography, by Catherine M. Otto.
(W. B. Saunders, 2000; ISBN 0-7216-7669-3). When I talked to
a sales representative at the TEE meeting in 2003, he confirmed
what others told me—Otto has it all. (Between Otto and those
syllabuses, you’ll have all the “book reading” you could possibly
need). Since then, a million more books have come out. Look for
books by Savage and Perrino, among others.
7. Get the 2-CD set TEE: An Interactive Board Review on
CD-ROM, edited by David S. Morse and C. David Collard
(Lippincott Williams & Wilkins, 2002; ISBN 0-7817-3375-8). This
has a series of TEE movies with attached tests. The tests are
multiple choice (like the PTEeXAM). Once you’ve taken the test,
you can check your answers. Best of all, each answer comes with
a complete explanation along with references.
8. Another good CD is TEE on CD: An Interactive Resource,
edited by Steven N. Konstadt and Navin C. Nanda (Lippincott
Williams & Wilkins, 2001; ISBN 0-7817-2629-8). This CD does
have a lot more text than the Morse and Collard CDs, and it is
tough to scroll text for a long time on a computer.
9. More CDs? You bet. Since echo is a moving image, it makes sense
to get CDs that show TEE images moving. Look on amazon.com;
at last count, there are 30-something books on transesophageal
echocardiography, lots with accompanying CDs. Robert Savage
himself (a Big Kahuna in echo circles and organizer of the big TEE
meeting) will have a big book coming out soon, so snap it up!
10. A great book fresh off the press and specifically made for
transesophageal echocardiography is A Practical Approach to
Transesophageal Echocardiography, edited by A. C. Perrino and S. T.
Reeves (Lippincott Williams & Wilkins, 2003; ISBN 0-7817-3638-2).
The second editor of this book is a fellow who talked at the big TEE
conference in San Diego, Dr. Scott T. Reeves. Great speaker! Funny
stories! Knows how to get his point across crystal clear and that’s just
what he and his co-editors did in this book. (If you’re short on dough,
buy their book, put mine back on the shelf, and use the money you
saved to buy a gyro. Then eat the gyro while you’re reading Perrino
and Reeves’ book—but don’t spill the cucumber sauce all over the
pictures). And yes, they have updated versions since then.
What now?
You have a long path ahead of you. No lions and tigers and bears, but
plenty of stuff to learn.
So do like Dorothy. Put one foot ahead of the other, keep those ruby slip-
pers on tight, and follow the yellow brick road.
Of course, these recommendations from the first edition are ancient
history by now. ANYTHING you want to view now can be done online.
Google “Aortic Dissection: TEE” and you will get a lot of videos.
Guess what, (2) is still most important—get as MUCH hands on TEE
work as you can.
CHAPTER
Principles of Ultrasound
2 Christopher J. Gallagher and John C. Sciarra
NATURE OF ULTRASOUND: COMPRESSION

AND RAREFACTION
Ultrasound is sound waves propagated through a medium at a frequency

above that which we can hear. Imaging depends on displaying the time
required for an ultrasound pulse to go to a cardiac structure and return.
We acoustically challenged humans only hear from 20 cycles/second to
20 000 cycles/second, or 20 kilohertz (named after the famous physicist
and car-rental magnate).
Ultrasound starts at 20 kilohertz (20 kHz). For our medical imaging, the

frequency used is between 1 and 20 megahertz (1 and 20 MHz). Take a
look at our probe, and you’ll see something like 5 or 7 MHz.
Keep in mind that sound, or ultrasound, must get propagated through a

medium.
Jimi Hendrix blasted his guitar through the AIR at Woodstock. You
blast your ultrasound through the TISSUE and FLUID with your TEE.
Remember the ads when Alien came out? “In space, no one can hear
you scream.” That’s right, there’s nothing to propagate in a vacuum.
There’s no air for you to compress and rarefy.
Ultrasound does not propagate in air; this will be a recurring problem.

Ultrasound only propagates through tissue and fluids.
FREQUENCY, WAVELENGTH, AND TISSUE

PROPAGATION VELOCITY
Note that frequency is the number of complete cycles per second,

and wavelength is the distance from one corresponding area to the
next (usually peak to peak). Propagation velocity is the wavelength ∞
frequency.
3
4 Board Stiff TEE
FREQUENCY AND WAVELENGTH
Ping!
Short λ
High frequency
1 Second
Long λ
BONG! Low frequency
1 Second
How does that relate to us? The propagation velocity of sound waves
in human tissues is 1540 meters/second. So, since the velocity is pretty
constant, that means the time it takes to go “out and back” correlates
with distance. Time vs distance is the basis of all “bounce technology”
(sonar in a ship, locating enemy submarines; Doppler radar letting us
know about a coming rainstorm; TEE telling us where the aortic dissec-
tion started).
Wavelength is important because resolution (the ability to tell two things

apart) is no better than 1 or 2 wavelengths. So if you have a long, long
wavelength, you won’t be able to tell things apart very well. If you have
a short, short wavelength, you will be able to tell tiny things apart. This
comes into play when you are adjusting the wavelength for near and far
objects.
A frequent consideration that occurs frequently with frequency is this:

the higher the frequency, the better the resolution but the shallower the
penetration.
The flip side, or the wavelength paradigm, is also true: the longer the wave-
length, the deeper the penetration but the worse the resolution. The take-
home message for budding TEE’ogists? To see an object close up, go to
a higher frequency, and you’ll see it in more detail. For a distant object—
say, the pulmonic valve, which lies far from the TEE probe—use a longer
wavelength (or, in other words, a lower frequency). This makes sense if you
remember that frequency and wavelength are inversely related:
Up close: high frequency (or short wavelength)
Far away: low frequency (or long wavelength)

Chapter 2 Principles of Ultrasound 5
PROPERTIES OF ULTRASOUND WAVES
Ultrasound propagates poorly in a gas. That is the main property that

concerns us, since, as you pull the probe higher and higher, you encoun-
ter the trachea or the left main bronchus getting between the probe and
the heart. The gas in these structures forms an impenetrable (for ultra-
sound purposes) wall that obscures our vision, so we can’t see parts of
the aortic arch and the pulmonary arteries (we see the right for a while
and a little of the left, but the left pulmonary artery, especially, gets
“amputated” by the left mainstem bronchus).
This “air dilemma” also causes a problem with off-pump cases, in which
the surgeon may hike the heart up and obscure your vision. (You need to
retreat up the esophagus a little to get a view.)
ULTRASOUND–TISSUE INTERACTIONS
Here’s a little commonsense tip for ultrasound and tissue. Ultrasound

in its usual diagnostic form doesn’t hurt tissue. A zillion kids have been
bombarded with ultrasound waves in utero, and, except for a fondness
for Call of Duty: Black Ops, bare midriffs, and pierced cartilage, there
seems to have been no lasting damage. (Of course, cranked to the
max, sound can crack stones, as we see in the ESWL suite every day.)
But keep in mind that the probe is a machine that converts some of its
energy to heat. So don’t leave the probe running forever, lest you cause
a burn to the esophagus. Turn the TEE off after you’ve done your study
and let it cool.
Reflection
Ultrasound is based on reflection of the signal from internal structures.

Ultrasound is reflected at tissue boundaries, and that is what allows us
to see where, for example, the ventricle ends and the blood begins. The
ultrasound beam goes through tissue of one impedance, hits tissue of
a second impedance, then reflects back to the transducer. Impedance
depends on tissue density and on propagation velocity through the tis-
sue. For our purposes, tissue density is the most important. Heart mus-
cle has higher impedance than blood (it’s thicker, after all).
“Blood is thicker than water,” most people know by rote. Few know
that the second half of that folk saying is: “…but the tissue impedance
of ventricular, atrial, and valve structures is higher than blood tissue
impedance.”
Since reflection is the key to the kingdom, and you prefer a “straight
on” bounce coming back to your transducer, it makes sense that your
best view is straight on, at 180 degrees to the transducer. At any angle
other than 90 degrees, some of the signal will bounce “away” from the
transducer.
6 Board Stiff TEE

STRAIGHT-ON VIEW CLEAREST
Best definition Less definition off to sides
Refraction
Think of the “bent straw” sitting in a glass of water. Same thing happens
with ultrasound waves. Some refract, rather than bounce back, and are lost.

REFRACTION
You want reflection. You get this.
Transducer Transducer
Signal
“bounced back”
Scatter
Some of the signal hits teeny structures and blasts the ultrasound signal
all over the place. This scatter from blood cells allows Doppler measure-
ments of moving blood. That allows us to do color Doppler studies (giv-
ing us a color signal of blood flow), continuous-wave Doppler studies (to
measure blood velocity along an entire length of view), and pulsed-wave
Doppler studies (to measure blood velocity at a specific point). So scatter
comes in most righteously handy.
Attenuation
Some of the ultrasound energy gets used up as heat. This does not
produce a useful signal (unlike scattering, which comes in handy). This
makes the signal get weaker and weaker the farther the ultrasound signal
goes into the body.
TISSUE CHARACTERIZATION
The meaty tissues are denser, absorb more ultrasound, and look gray.
Blood is less dense, and looks black. (Adjust the gain until you get gray
Chapter 2 Principles of Ultrasound 7
for the tissue, black for the blood.) Calcified areas eat up all the ultra-
sound waves and look white. If dense enough, they don’t allow ultra-
sound to go any further and thus throw a shadow distal to them, leading
to artifacts. Calcified things can also cause reflections that “fake out” the
transducer and produce artifacts.
QUESTIONS
1. Frequencies within the range of human hearing are about:

A. 2000 Hz
B. 5000 Hz
C. 10 000 Hz
D. 20 000 Hz
E. All the above
F. Within earshot
2. Ultrasonic frequencies are:

A. 1 million cycles per second
B. Two to 10 million Hz
C. 20 million cycles per second
D. 22 million Hz
E. Hertz rent-a-car
3. The average propagation speed in soft tissues is about:

A. 1540 meter per second
B. 1.54 mm/microsecond
C. faster in bone
D. Similar in blood
E. All the above
F. Zero to 60 in 5.4 seconds
ANSWERS
1. E. Frequencies within the range of human hearing are about

20–20 000 Hz.
2. B. Ultrasonic frequencies are 2–10 million cycles per second (Hz).
3. E. The first two are the same. Bone speeds up propagation since it is
denser than tissue. Blood is like tissue.
CHAPTER Transducers and
3 Instrumentation
PIEZOELECTRIC EFFECT
Understanding the piezoelectric effect takes the mystery out of “Just

what the hell is that little gizmo at the end of my probe, anyway?”
To make a sound wave, you need to wiggle something.
Bang-a-gong, the metal vibrates, and the sound waves go forth. Now
let’s just tie a little creature to the end of a gastroscope, and have him
bang-a-gong fast enough to create 7 million cycles/second for 20 minutes
straight.
No go. We need a better way to get so much wiggling. The guy banging
the gong just won’t do.
Millions of times per second? Better go to electricity, that’s the only thing
that can give you that many wiggles per second. But how to get electric-
ity to wiggle something? Electrify a gong?
9
10 Board Stiff TEE
Piezoelectric crystals to the rescue! These are quartz or ceramic things

that have a magical property. When a current is applied to them, the
polarized particles align perpendicular to the face of the crystal. When
the current goes off, the particles no longer align. This alternating align-
ing and nonaligning results in the face of the crystal bowing out, then
coming back, in effect wobbling just like the gong.
(Who the hell figures this stuff out the very first time, I want to know.)
OK, groovy, so this electrical thing makes a mechanical wave. How does
a piezoelectric crystal “hear”?
Well, according to the Principle of Electromechanical Turn-It-Around-

ness, when a wave comes into and hits the piezoelectric crystal, it
causes a mechanical deformation that then makes a current change. So,
Electricity makes a mechanical wave.
A mechanical wave makes electricity.
Then, through some kind of voodoo known only to electrical engineers

and people with pocket protectors, the TEE sorts all this out and gives
you an image.
CRYSTAL THICKNESS AND RESONANCE
A thin crystal resonates at a high frequency (think of a thin wine glass

that goes “TING!” when you tap it). A thick crystal (think glass beer stein;
better yet, get one and fill it to the top if you’re slogging through this
physics junk) resonates at a low frequency. No big shocker there.
Chapter 3 Transducers and Instrumentation 11
DAMPING
When the signal comes back to the crystal, you don’t want the crystal to
wiggle too wildly. Hence, behind the piezoelectric crystal, damping mate-
rial is in place. The damping material allows a short pulse length, hence
improved resolution. Go back to the concept of the ringing gong. After our
hero has hit the gong, he doesn’t want it ringing and ringing. He grabs the
gong; that allows it to become still, and then he can hit the gong again.
SOUND BEAM FORMATION
Electricity in a short burst (typically 1 to 6 microseconds) hits the crystal

and produces the short blast of ultrasound by means of the piezoelec-
tric effect. The damping material keeps the crystal from “wiggling” too
long, as mentioned above. These short bursts allow better axial (along
the direction of the beam) resolution.
(As you can see, the Content Outline of the PTEeXAM chops up the indi-
vidual items you need to know. In reality, this stuff all flows together in
one smooth explanation in the TEE review course syllabus and in Otto’s
textbook.)
FOCUSING
A sound beam tends to spread apart, like ripples in a pond. (I can almost
envision a “TEE Haiku” coming out of this.) TEE needs a tight beam to be
able to make some split-second measurements of small places, so the
transducer focuses the sound beam. A mechanical lens does this.

LENS AND HAIKU
Transducer Unfocused waves
Transducer Focused waves
Lens
TEE Haiku
Waves rippling, rippling.

Waves make the echo image.
Then bill Medicare.
AXIAL AND LATERAL RESOLUTION
(Here again, we’re chopping up stuff that should run together.)

12 Board Stiff TEE
Axial Resolution
Short bursts—that is, high frequency—give you better axial (along the line)
resolution. Why? You will have a lot of information bouncing back to you,
so you’ll be able to tell, “Aha! This reflected signal tells me something is
just right there, and this other signal tells me that something is just a little
further along the line.” If this, admittedly weak, explanation doesn’t con-
vince you, then try this line of reasoning: Imagine very infrequent signals
going out. How could you tell things are close together then?
Lateral Resolution
Lateral resolution tells you that things at the same depth are side by side.

AXIAL VS. LATERAL RESOLUTION
Axial Transducer
Lateral Transducer
Beam width at a given depth is the most important determinant of lateral

resolution. If the beam is smeared out all over the place, you can’t tell
one thing from the other, but if the beam is narrow, you will be able to tell
things apart.
Also important in lateral resolution is the focus of the beam. A beam of

ultrasound has a near field, then the beam diverges and you have a far
field. The focus is best where these two fields meet. Your best lateral res-
olution is right there, at the focus.

BEAM FOCAL ZONE
See best here

Focal
zone
Transducer
Near field
Far field
ARRAYS
To get the vast amount of information necessary for a “movie of the

heart,” you could have one “supertransducer” sweeping back and forth.
That doesn’t fly, though; instead, modern TEE relies on a bunch of trans-
ducers spread out and all looking in the same direction. Some kick-ass
mathematics and computer stuff straighten all those signals out.

ARRAY OF TRANSDUCERS
Beam
The most likely transducer you will use is the phased array. So if some
know-it-all asks you what kind of transducer you have in your hand, say
“a phased array”.
The way it works is in the diagram above. Basically, crystals that are lined
up fire in sequence. Where the individual waves meet (summation front)
is a point, and this forms a single line or sector. Put a whole bunch of
sectors together and you have the pie-shaped image we are so familiar
with.
The biggest complication is the hardest to quantify—distraction. I kid

thee not, people will glue their eyes to that echo screen and ignore a
blood pressure of 60 or a heart rate of 140, they get so mesmerized by
the image. Especially when first learning, make sure someone is “guard-
ing the fort” while you tiptoe through the ultrasound airwaves.
Mechanical damage to teeth or upper airway and (most dreaded of all)

esophageal rupture are also complications. Patients may also complain
of difficulty swallowing post TEE insertion.
INSTRUMENTATION
A quarter-million-dollar rolling TV?
More knobs than Miami Beach has sand granules?
That’s MY summary of TEE instrumentation, but the test may go into

more detail than that. The scope itself is a modified gastroscope with the
precious transducer at the end. Ancient probes, unearthed in Pompeii,
had only one plane or two planes, but all the modern ones have the
omniplane capability.
14 Board Stiff TEE
The ultrasound TV and its associated rat’s nest of knobs, video connec-
tions, and computer connections is called a platform. You cannot get
Walking Dead on the TV, no matter how much you roll around the track
ball, so satisfy yourself with ultrasound images.
The test may zoink you on how the knobs work. The next time you do an
echo, make a point of wiggling every damn knob every which way and
seeing what happens on the screen. On the test, they may, for example,
pull the knobs to very high gain at a certain depth on the Depth Gain
Compensation knobs and give you a streak of snow halfway down the
picture and ask you, “What just changed?”.
Here’s a rundown on the knobs, taken from the (cutely named) “Knobology”
Lecture at the TEE conference. (This stuff is dry as toast and easily goes
into the Insta-Forget sulcus of your brain, so do what I said before: play
with the knobs on your machine and know what each one does.)
Depth
Usually the depth is 12 cm, but you can adjust this. For example, if you
want to look real closely at the aortic valve (pretty close to the trans-
ducer), go to more shallow depth. If the patient has an enormous heart,
you may need to go to a deeper depth, otherwise you might not be able
to see all the heart.
Frequency
Higher frequency = better resolution but less depth

Lower frequency = less resolution but better depth
This came up a million times during the TEE meeting and (I’ll bet my bot-
tom dollar) will appear somewhere on the test.
Gain
Increases the strength of the signal you already received.

Too much gain = snow and clutter
Too little gain = too dark

Depth Gain Compensation
Controls gain at various depths in the field. This is the line of knobs like
you used to have a line of knobs on your stereo equipment.
A Million More
There are dozens of other knobs. Work them all, so when they ask you
something about some knob you at least have a clue. The most practical
ones to know are the ones mentioned above, Depth, Frequency, Gain,
and Depth gain compensation.
DISPLAYS
(I’ll be honest, I’m not quite sure what they’re driving at here, but this is
my guess.)
The image we get is displayed upside-down relative to the patient.

That is, the image as we see it, with the pointy part of the pie slice
at the top of the image, shows the patient as if we were looking at a
prone patient from the top of the bed. The tip is the left atrium. The
left side of the screen is the patient’s right side, and the right side of
the screen is the patient’s left side. If the omniplane angle goes 180
degrees around, then the right/left situation is reversed. The patient’s
right side is the screen’s right side, and the patient’s left side is the
screen’s left side.
Think of a patient lying prone

That’s how you’ll “see” the heart
When the omniplane is at 90 degrees, then the patient’s inferior aspect is

on the left and the anterior aspect is on the right of the screen.
B-MODE, M-MODE, AND TWO-

DIMENSIONAL ECHOCARDIOGRAPHY
B-mode
The “B” stands for “brightness.” This would just show different brightness
at various interfaces and isn’t of much use to us. It is an “ice-pick” view.
16 Board Stiff TEE
M-mode
If you roll a B-Mode out over time, then you can see the “ice-pick” view
of the heart go on over time. You could then, for example, see valve
movement over time. This is groovy, but we anesthesia types much pre-
fer the next mode so we can see stuff go on. Cardiologists understand
M-mode better than we do because they are smarter and tend to dress
better than anesthesiologists.
Two-dimensional
Here, an array of views gives us the familiar picture of the whole heart
moving in real time. This is the usual image you see:

IN THE MOOD FOR MODES
B-Mode M-Mode 2-D
I
love
TEE
Useless Only cardiologists

can understand. Aah
SIGNAL PROCESSING AND RELATED

FACTORS
Processing changes the appearance of the displayed image. You can, for
example, change the gain (too much = snow, too little = dark) to alter your
signal. Changing the gray scale or dynamic helps you adjust the image
to get sharper edges. No matter how you fiddle with the signal, it bears
repeating that “garbage in, garbage out”. For example, if you don’t empty
the patient’s stomach and a big hunk of pepperoni affixes itself to the front
of your probe, then no amount of signal processing will help you out.
QUESTIONS
1. Ultrasound output is suspended by pressing the freeze button. True or

false?
2. Lateral resolution is determined by:

A. Beam intensity
B. Power output
C. Sector angle
D. Beam width
E. The amount of resolution on the sides
3. The ultrasound probe you use every day is probably:

A. A linear array
B. A mechanical sector array
C. A phased array
D. A refurbished unit
E. A curvilinear array
4. The focal point of a transducer is:

A. About the zone of the specular reflectors
B. Between the near field and far field
C. On the edge of the focal zone
D. Focused on a point within the focal length
ANSWERS
1. True. When you press the freeze the machine stops sending signals.
This may help cool the probe if it is overheating.
2. D. Beam width is the major determiner of lateral resolution. Make your
whole scanning sector smaller for better resolution.
3. C. Phased array.
4. B. The focal point can be moved, but it is between the near field
and far field. It is in the focal zone, which begins right after the focal
length.
CHAPTER Equipment, Infection
4 Control, and Safety
Steven Ginsberg and Jonathan Kraidin
I am talking TEE, not TTE. It’s not ultrasound to find some flounder or
neck vein!
THE GOOD: SAFETY FIRST
Trust me its safe. It does freeze automatically nowadays (after about

5 minutes) to stop any heat emission. It’s not a cell phone. You shouldn’t
get cancer from regular TEE usage in the OR. There just isn’t that much
radiation going on here.
Latex: the skin of the probe should be latex free.
Set up an Echo Service
The Echo probes are expensive and fragile $$$$$
Before you make the investment or get new equipment (10–15 years)
make sure these are in place:
Who maintains the machine onsite?
Who brings it for cleaning?
What is the actual cleaning process?
Where do you keep the probes prior to insertion into the patient?
Where do you place the dirty probe?
Who fixes a problem with the machine?
Who regularly will reboot this electronic monster?
Where do you keep those bite blocks?
Where do you keep probe covers?
19
20 Board Stiff TEE
Move it from Place to Place
The clean probe should be left in a clean and labeled tube, or safely hung
from its bracket. It should not be bumped around.
Don’t drop this baby.
How about that nice case that came with it? Use it. Do not bend the
probe in half.
OOPs! I just put a clean probe in the “dirty” tube. Now that’s a problem!
You probably shouldn’t curl it into a nice ball prior to usage—you will
break a fine instrument.
THE UGLY (BAD WILL COME LATER):

CLEANING—YOU NEED A SYSTEM
What should we do with the probe to have it ready for the next case?
Have you considered cleaning it?
But there is lots of schmutz (not schmaltz) on this thing.
Wipe off any junk-food and organic material. Never use more that 70%
alcohol. Alcohol should not go onto the transducer; use it only on the
handle. Don’t saturate it; wipe it. Do not submerge the handle. Do not
submerge that electrical fancy do-hicky that gets plugged into the fancy
machine.
Place a plastic cover over the tip of the probe until it is in use.
Clean it with a soft cloth and remove the junk prior to a solution cleaning.
Then, consider soap and water with a soft cloth. Wipe it down. The
manufacturer has some directions, rules and recommended disinfectants
(neutral pH).
n Dry the thing
n Don’t store it around your neck
n Do not autoclave it
n Keep the tip straight when you store it
The Physical Probe: How’s it Look?
Eyeball the Probe

Watch for cracks, bulges, breaks. If you get a shock while holding the
TEE probe it is a problem. Get it out of the patient. Did the LIM alarm?
Watch out for the small cuts at the end of the tube.
I guess I should have used a bite block!

Chapter 4 Equipment, Infection Control, and Safety 21
It won’t Plug in?

Perhaps one of those expensive pins or connectors is dirty or bent. Is
it wet? Don’t even think of using a transducer from a different type of
machine or company.
Use the Probe

Be gentle and use a bite block. Oh, heavens, wear gloves! Don’t jam it in.
Don’t let it wrap around the ETT—this will lead to an untimely extubation
when you remove the probe at the end of the case.
Don’t figure that because your patient is paralyzed that you don’t have to
worry about those teeth scratching or cutting the probe. On the contrary,
when you take that baby out you will scratch it against those choppers,
so watch out. You use the bite block not so much because the anes-
thetized patient will bite the probe, but to protect the probe on removal.
It will run against those rabbit incisors and scratch! Your warranty won’t
work here.
Insert: How’s it Go?
Why can’t I place the probe?
I don’t know what I am doing
Patient has a trach
Patient has an esophageal diverticulum
Patient is biting the probe
Patient is bleeding from those varices and I can’t see a thing
Patient is not NPO and is puking on my fellow
Make sure that baby is “unlocked”—you want it to easily change direction

with the patient if needed.
Make sure the tip is in neutral position.
If the teeth aren’t loose then raise the lower jaw.
Watch out for the junior resident knocking those teeth out.
Maybe use a laryngoscope if you are having a tough time of it—it goes in
the hole on bottom.
Don’t force it. If you must have Echo then use a pedie probe!
When to consider NO: just had esophageal surgery, gastric bypass,

bleeding, it won’t go, radiation, radical neck.
Ergonomics
Don’t grip the transducer with excessive force. Try telling the surgeon
that you can’t do a TEE because his last case took so long that you
22 Board Stiff TEE
now have carpal tunnel! Don’t stand in one place while doing your echo.
Move around. Loosen up that back of yours and relax your shoulders.
This shouldn’t hurt.
THE BAD
What did I do to the poor patient?
Why did the patient croak?
Did I rupture a variceal with that locked probe?
Went through a tumor in the esophagus with the probe?
I perforated the esophagus—try to peg this one on the endoscopist?
I was too busy checking the Echo and did not notice the patient was
hypotensive or had a fatal arrhythmia—you pinched yourself and
woke up to treat in time.
n I broke his teeth
n Rarely vocal cord paralysis
n You bronched the patient—try the esophagus next time
n The patient desaturated because the TEE pushed the ETT in further
n Post-op complaints of dysphagia are possible
QUESTIONS (ECHO SAFETY)—TRUE/FALSE
1. Never place an Echo probe in the locked position?

2. After each use put the Echo probe in a tight circle so that its shape
retains memory for the next time?
3. Modern machines never have to be shut down?
4. The anesthesiologist should bring the probe, in cidex, to central
processing after each case?
5. Soaking the entire probe in cidex for 10–15 minutes is sufficient
maintenance?
6. It is possible that probe insertion can help to ensure a right main
stem intubation?
7. Post-op complaints of dysphagia will often go away on their own?
8. During long cases there is a concern for radiation exposure?
9. Direct laryngoscopy can help with a difficult probe insertion?
10. Small scratch marks may develop at the end of the probe when a
bite block is not routinely used?
Chapter 4 Equipment, Infection Control, and Safety 23
ANSWERS
1. T
2. F
3. F
4. F
5. F
6. T
7. T
8. F
9. T
10. T
CHAPTER Principles of Doppler
5 Ultrasound
Jonathan Kraidin, Steven Ginsberg, William Jian and
Kevin A. Jian
Doppler works with sound. Sound is a mechanical, longitudinal wave that

alternates between expanding and compressing the medium through
which it propagates. This is analogous to a wave moving through the
water. Normally, the ear perceives sounds up to 20 KHz. Higher frequen-
cies are referred to as ultrasound, and unless you are a dog or bat you are
not going to hear them. The rapid vibration of a piezoelectric crystal pro-
duces the ultrasound waves. The properties that describe the wave are1:
1. the period is the duration of each cycle
2. the frequency is the number of times the waves cycle per second
(this is the reciprocal of the period)
3. the wavelength is the distance between two wave crests of the
sinusoidal wave
4. the propagation speed, which is the speed the wave travels through
the medium as it compresses and expands
Doppler echocardiography allows the non-invasive assessment of blood
flow, velocity and direction.2 It is based on the principle that a moving
target will shift the reflected frequency higher or lower depending on
whether it is moving toward or away from the transmitter. Using this prin-
ciple, if one knows the frequency shift one can determine the velocity
and direction of the blood flow.
Waves of energy, such as light and sound, can be defined by the wave-
length and frequency. This gives us a third parameter, which is the propa-
gation speed through the medium.
The equation is

f*λ=c
in which f is the frequency, λ is the wavelength and c is the speed of

sound in tissue, which is 1540 m/sec.
When a pure frequency of sound hits a stationary object, the sound bounces
back at the same frequency. If the object is moving when the sound hits, the
returning wave will have a slightly different frequency. The difference in the
outgoing and incoming frequency is called the Doppler shift.
You can see the derivation of the Doppler Shift equation in the section,
Derivation of the Doppler Shift Equation. 25
26 Board Stiff TEE
THE DOPPLER SHIFT EQUATION
For a returning signal the equation is:

Fshift = f0 * Cos( θ ) * 2v/c
Let us break this equation down:
f0 is the original frequency of the ultrasound wave, v is the velocity of the

object hit by the wave, and c is the speed of the wave as it propagates
through the medium. Theta (θ) is the incident angle the beam makes with
the axis of flow.
This is not just theoretical physics. This stuff really happens. Recall
the sound of an approaching train. When the train is coming towards us, the
pitch is higher (v is positive); when the train is moving away from us the
pitch is lower (v is negative).
Let’s look at some real numbers:
c = 1540 m/sec
v (of blood) = 2 m/sec
f0 = 2 500 000 Hz (this is a typical frequency for the beam)
θ=0
Fshift = 2 500 000 * cos(0)*2*2/1540
Fshift = 6493 Hz
What can we do with this information? By knowing the Doppler shift, we

can use the equation in reverse and determine the velocity of the blood:

v = Fshift * c /[ 2 * f0* cos( θ )]
How is such a small change in the frequency measured? The truth is

that the frequency is not measured. The machine actually measures the
phase shift between the outgoing and incoming signal. The phase differ-
ence correlates with the Doppler shift as a first-order approximation.3
So, now that we have an understanding of the Doppler shift equation

and how the machine makes measurements, what can we do with this
information?
BASIC PRINCIPLE FOR TISSUE

RECONSTRUCTION USING ULTRASOUND
A sound wave is emitted from the transducer. When this wave encoun-
ters differences in density it gets reflected back. If you scream over the
ocean shore you don’t hear your voice reflected off of the air because
it has a constant density. If you scream across a canyon you hear an
Chapter 5 Principles of Doppler Ultrasound 27
echo because the sound encounters a change of density when it hits the
rocks, resulting in the sound getting reflected back. The amount of sound
that gets reflected not only depends on the change in density at the
interface, but on the orientation of the object. The orientation can scat-
ter the sound in different directions. Software analyzes the amplitude of
the sound at different times in order to reconstruct the tissue density at a
specific depth from the probe, giving an image.
B-MODE
This was originally called brightness mode. The brightness shown on the
display corresponds to the amplitude of the returning echo, and the loca-
tion is related to the position of the reflected tissue. Highly echogenic
objects reflect more of the signal back; this is represented by a brighter
point on the screen.
M-MODE
Once upon a time this stood for time-motion mode. It was shortened to
M-mode for motion mode. M-mode is multiple B-mode dots plotted on a
straight line. The amplitude of the signal is recorded at various times; each
time corresponds to a different distance from the probe. A vertical line is
constructed where the brightness of each pixel corresponds to the strength
of the echo at each point. The constructed line is moved leftwards and a
new scan line is created up to 1000 times/sec. Using this methodology,
time is represented on the x-axis and the distance of the tissue from the
probe is on the y-axis. This is useful for watching anatomical motion of the
myocardium and valves along a single line of sight. This is useful for timing
the movement of valve leaflets when assessing regurgitant blood flow.
TWO-DIMENSIONAL IMAGING
This is one line of B-mode swept through an arc. The result is a sector of
tissue called a frame. The frame image is rapidly refreshed between 30 to
60 times/sec allowing one to see motion of the tissue within the frame.
The frame rate, and thus the quality of the moving image, is affected by
sector width and depth.
The figure below sums this all up.

IN THE MOOD FOR MODES
B-Mode M-Mode 2-D
I
love
TEE
Useless Only cardiologists

can understand. Aah
28 Board Stiff TEE
COLOR DOPPLER
Remember the theory about Doppler shift? By sending a beam of sound

at moving blood cells one obtains blood velocities. The velocities are rep-
resented by colors. If the object is moving towards the probe the machine
tags it with a shade of red; if it is moving away it gets tagged with a shade
of blue (BART: blue away red towards). A jet of blood moving toward the
probe will appear as a red flame. The fastest part will be a bright red, which
will fade to a duller red as the velocity slows down. If the blood is swirling
(turbulent flow) the color will appear as a mosaic pattern because the veloc-
ity and direction are rapidly changing. The color will jump from red to blue,
and all the shades in between these two colors. The color representation of
the velocities is superimposed on a 2-D image of the underlying tissue.
Color Doppler allows one to get a rapid understanding of the blood flow
in a window of interest. One can determine that blood is moving in the
wrong direction, if the flow is laminar or turbulent, or if there is flow where
there should be none such as through a defect.
CONTINUOUS WAVE DOPPLER
Continuous wave (CW) Doppler allows one to measure fast blood veloci-
ties. CW Doppler is exactly as the name describes: a transducer continu-
ously transmits a beam of sound while a receiver continuously measures
the returning signal. As the transducer emits sound, the beam encoun-
ters moving blood cells at varying points. The returning sound contains
multiple shifted frequencies because it bounces off of blood cells at
different depths, moving at different velocities. CW Doppler is unable
to tell where these velocities are occurring; it can only report a range of
velocity values. These velocities are all mixed together in a velocity enve-
lope and occur along the line of sight of the probe.

How does this help if the machine is getting back a myriad of veloci-
ties? One uses CW when there is an interest in measuring fast veloci-
ties. True, all of the velocities are mixed together, but the operator only
cares about the fastest velocity. The peak of the envelope represents
the fastest velocity; everything inside the envelope represents all other
velocities, which one ignores. For example, if one is looking at a stenotic
aortic valve, the jet of blood traveling through the valve will give the fast-
est velocity. Even though the CW Doppler does not know where the
fastest velocity is coming from, the operator knows the fastest velocity
measured must be coming from the jet going through the stenotic valve.
PULSE WAVE DOPPLER
Sometimes one needs to know the velocity at a specific point. Pulsed

wave Doppler (PW), unlike CW, can give velocities within a specific vol-
ume of blood. PW Doppler sends out a pulse train (several pulses) of
sound at a fixed carrier frequency. The machine waits an appropriate
period of time for the pulse to travel a known distance and back before
looking at the shifted signal. By sampling the pulse at a fixed time inter-
val, and rejecting others, the operator can position a cursor at a specific
location and measure that velocity (see figure below). PW Doppler can
measure velocities close to 1.2 m/sec.

Look at it this way. You have three walls 1540, 3080, and 4620 meters
away. You ring a bell and the sound travels at 1540 m/sec. If you cover
your ears and listen only after 4 seconds you will hear the sound reflect-
ing back from the wall 3080 meters away; if you wait 6 seconds you will
hear sound bouncing back from the wall 6420 meters away. By waiting
just the right amount of time you can target from which wall you want to
hear the echo.
RANGE AMBIGUITY
Some of the sound will travel farther than the target and get reflected
back during a sampling interval. Also, some of the sound will get
reflected back sooner and get sampled with some of the pulses that
were sent out earlier. This will give some velocities at other ranges. When
velocity information is recorded at other locations and is mixed with the
sample, we call this range ambiguity (see figure below) because it is giv-
ing ambiguous information.

A 1 sec
1
770 m
B 1 1/2 sec
385 m 770 m
1
C 3/4 sec
2
385 m 770 m
D 1 1 sec
2
385 m 770 m
30 Board Stiff TEE
A: Sound sampled at 1 sec will obtain information about an object

770 m away.
B: If there is an object of interest 385 m away, information about the
object will be available 0.5 sec after it was sent out. Some of the
sound that had continued forward will hit an object at twice the
distance.
C: After the first pulse is received a second pulse is sent out. The new
pulse and traces of the first pulse reach the midway object at the
same time.
D: Both pulses arrive back at the receiver at the same time. Which
one has information about the midway object? This is range
ambiguity.
Other than the problem with range ambiguity, why is PW not used for
all Doppler measurements and just do away with CW? After all, it does
give information at a specific location. Sampling theory dictates that at
least two points are needed for each wave oscillation in order to recon-
struct the correct frequency. If the wall is 1540 meters away one needs
to wait 2 seconds before the Doppler-shifted sound comes back. This
corresponds to a frequency of ½ Hz. The sound will not travel any faster
than this. Two measurements take 4 seconds. This means that the shift
frequency can go no faster than ¼ Hz (frequency (Hz) = 1/time).
NYQUIST LIMIT AND ALIASING
If we do not take enough samples of the signal, the measured veloc-

ity direction will appear reversed, or aliased. The velocity waveform will
appear cut off at the top of the display and reappear at the bottom.

The figure is the strange-looking effect from not taking enough sam-
ples. Remember seeing a rotating wheel appear to spin backwards?
Remember the song: “the wheels on the bus go round and round…”.
Well, the bus wheels sometimes appear to spin in reverse. Let’s analyze
this by referring to the figure of a spinning wheel, where the top spoke is
marked (see figure below).

True Motion
Apparent Motion
Flash Flash Flash Flash
The wheel spins at 1 revolution per second clockwise in a dark room. If

we use a strobe light and send a flash once per second we will illuminate
the wheel when the top spoke is in the same position. By observing the
wheel in the same position each second we do not know if the wheel is
spinning once per second, twice per second or is even moving at all. If
we sample it every ¾ of a second we will first see the marked spoke ¾
of a revolution around. After the next strobe it will move another ¾ of a
revolution and we will see it half way around. The third strobe will occur
when the spoke is ¼ of the way around.
Even though the wheel is rotating clockwise it appears that the wheel is
moving counterclockwise. This is aliasing. In order to avoid this we need
to send out a strobe at least every ½ second, or twice the revolution fre-
quency. In this case, the Nyquist limit is ½ Hz, and if the wheel spins any
faster than 1 Hz it will appear to move backwards. Similarly, if the blood
velocity is fast enough to yield a shift frequency above the Nyquist limit,
the blood will appear to move in the opposite direction.
If you would like to see the derivation of the Nyquist limit please refer to
Derivation of the Nyquist Limit for PW Echo.
Just remember these points: Aliasing occurs when the sampling fre-
quency is below a calculated limit called the Nyquist limit. PW allows one
to measure the velocity of a volume of fluid at a specific depth from the
probe. Shifting the baseline or switching to CW Doppler enables one to
measure faster velocities, and work around the Nyquist limit. Sometimes
you can even use CW for fast velocities if the blood flow is isolated to a
small enough region.
HPRF (HIGH PULSE REPETITION

FREQUENCY) MODE3
Sometimes one wants to know a velocity at a specific location, but the

velocity is too high to get a true reading. What can one do? Many echo
machines have a HPRF mode that allows one to exceed the Nyquist
limit. It does not have a range as high as CW, but it is higher than plain
PW. How does it do it? Pulses are sent out before the time is reached
32 Board Stiff TEE
to send out the next allowed pulse. If the object is 770 meters away we
normally have to wait 1 second before sending another pulse so we are
sure it is an echo from that distance. If we send a pulse every ½ second
we can measure twice the shift frequency. The downside is that there is
some range-ambiguity: one will get a mixing of the velocity at two loca-
tions, shown by two cursor location markers.
BEAM ANGLE
The most accurate reading from the PW or CW interrogation is when the

beam is parallel to the flow. As the beam moves off of the axis of flow it
begins to underestimate the true value. The value is directly related to
the cosine of the angle between the beam and the blood flow. The effect
becomes significant when the angle is greater than 20 degrees, and this
corresponds to an underestimation error of about 6%. After 20 degrees,
the error gets significantly larger at a faster rate.

(WARNING: Math alert! Proceed with caution!)
Derivation of the Doppler Shift Equation
We are going to derive the shift equation in order to get a better under-
standing of it.
λ
3 2 1
C
C tnew
3 2 1
C
V tnew
λ
If the object is stationary, the wavelength seen by an observer positioned

on the object is unchanged. An observer on the object will encounter
each wave crest at the same time it is transmitted. If the object is moving
forward with a velocity v, the moving observer will encounter each wave
crest sooner. It will appear that the wavelength is decreased and the fre-
quency is increased.
t0 = λ/c is the time, t0, it takes for the next crest of our sound wave to hit
the stationary object.
tnew is the faster time that it takes for our object, moving at speed v, to hit
the next crest.
The object moves a distance v * tnew; the next wave crest moved a dis-
tance c * tnew. The sum of both distances, c * tnew + v * tnew, equals one
original wavelength, λ. The perceived wavelength is v * tnew.
Doing a little math we find:

c * tnew + v * tnew = c * t0

(c + v ) * f0 = c * fnew

f0 * (c + v ) / c = fnew
This means that the frequency has increased for our observer on the
moving object. But we are not interested in the shifted frequency seen
by an observer on the object; we are interested in the frequency that is
reflected back from this object.
We have already shown that the crest of the wave hits the moving object
in a shorter time, tnew, when the object is moving towards the source.
The listener on the object perceives a shorter wavelength. This is the
first Doppler shift. When a wave is reflected off of the object back to the
source, the distance between each wave crest is shortened once again,
giving a second Doppler shift. The wavelength is shortened a second
time because the object is following the reflected waves.
Here is another way to think of this: You are standing still and there is a
row of evenly spaced balls, traveling at the same speed, that are com-
ing towards you. The number of them that passes you each second is
the frequency. If you start to move towards the balls you will pass a new
ball faster than if you stood still. The frequency of passing a ball has
increased. This is the first Doppler shift, which is from the perspective of
the observer, and not the person sending out the balls.
Now imagine that you let the balls bounce off a board that you are
holding. If you are standing still the balls will travel away from you
at the same frequency as when they were coming towards you. The
34 Board Stiff TEE
spacing between each ball will also be the same. If you are walking
towards the incoming balls, and they bounce off a board you are hold-
ing, they will not move away from you as quickly as when you stood
still. This is because you are walking toward the ball as it recedes
from you. So not only has the distance between each oncoming ball
decreased because you are walking towards them (first Dopper shift),
but the distance decreases even further for the reflected balls because
you are walking toward the balls as they move away (second Doppler
shift). We can derive a mathematical relationship demonstrating
this fact.
λ
3 2 1
C
V
A
3 2 W1 1
C
B
C
W1 W2
λn V tnew
C tnew = λnew
Referring to the above figure, we see that, at time A, the first wave crest
hits the object, reflecting back wave W1. This wave moves towards
the left at a speed c. The original wave also moves towards the right at
speed c. The object moves towards the left at speed v and hits the next
wave crest at time tnew. We derived this value earlier. When the object
hits the next wave crest it reflects back wave W2.
Now, W1 moved a distance c * tnew during the time it took to hit the next
crest. The object moved a distance v * tnew. The difference, c * tnew –
v * tnew is the new wavelength, λn, of our reflected wave, and it moves at
the same speed, c. The frequency of the returning waves is

Fn = c / λn
Let’s bang out the derivation:

1. c * tnew – v * tnew = λn
2. c – v = λn * fnew
3. fnew = f0 * (c + v)/c (derived earlier)
4. c – v = λn * f0 * (c + v)/c (sub #3 into #2)
5. λn = c/Fn
6. (c – v)/(c + v) = f0/Fn (sub #5 into #4)
7. Fn = f0 * (c + v)/(c – v)
8. Fshift = Fn – f0
9. Fshift = [f0 * (c + v) – f0 * (c – v)]/(c – v)
10. Fshift = f0 * 2v/(c – v)
11. For c >> v → Fshift = f0 * 2v/c
And there it is. Bam!
Derivation of the Nyquist Limit for PW Echo
Carrier frequency = f, speed of sound = c, velocity measured = v
Time required for travel to and from a point at a fixed distance:

2*d= t*c

t = 2d / c → ftravel = c / 2d
Frequency of samples required is twice the shifted carrier frequency (also

called the pulse repetition frequency, PRF)

PRF = 2 * Fshift
We derived the Doppler shift equation earlier: Fshift = (2fv/c) * cos(θ). So,

PRF required = 2 * (2fv / c) * cos( θ ) → (4fv / c) * cos( θ )
One can not send out pulses faster than the time for the first pulse to
make a return trip. The PRF can not exceed Ftravel

Ftravel = c / 2d = 4fv cos( θ ) / c

v = c2 cos( θ ) / 8fd
What we see is that the maximum velocity we can determine decreases

as the measured point is further away from the transducer or the carrier
frequency increases. Now if you read all of this you deserve a candy bar
break. Go ahead, you earned it.
36 Board Stiff TEE
QUESTIONS (DOPPLER PHYSICS)
1. The speed of sound in body tissue is approximately:

A. 1.540 m/s
B. 15.40 m/s
C. 154.0 m/s
D. 1540 m/s
2. The equation that relates the speed of sound (c), frequency (f) and
wavelength (λ) is:
A. c = λ * f
B. λ = c * f
C. f = c * λ
D. f = 2 * c * λ
3. If the Doppler beam makes an angle of θ with the moving blood, the
measured velocity is less than the true velocity by what amount?
A. sin(θ)
B. tan(θ)
C. cos(θ)
D. sec(θ)
4. High Pulse Repetition Frequency is used when:

A. using PW Doppler and the blood flow is slow
B. using PW Doppler and the blood flow is fast
C. using CW Dopper and the blood flow is slow
D. using CW Doppler and the blood flow is fast
5. The beam angle becomes significant when it is over:

A. 1 degree
B. 5 degrees
C. 10 degrees
D. 20 degrees
TRUE OR FALSE
6. The Nyquist Limit increases as the scanning depth decreases

7. Pulse wave Doppler measures all velocities along a line of sight
8. Continuous wave Doppler is used to measure fast velocities
9. The Nyquist Limit is the highest frequency one can use to measure
the velocity
10. Color Doppler shows blood flow, represented by color,
superimposed on a 2D image
ANSWERS
1. D. The average speed of sound in tissue is 1540 m/sec

2. A. You can solve this by looking at the units: speed
(m/s) = wavelength (m) × frequency (1/sec)
3. C. The measured velocity will be less than the true velocity by cos(θ)
4. B. HPRF is used with PW Doppler and allows you to measure faster
blood velocities
5. D. The correction factor, cos(θ), becomes significant when the angle
is greater than 20 degrees
6. True. When the scanning depth decreases, it takes less time for the
sound to travel back
7. False. PW Doppler measures velocity within a specific volume
8. True. The measurement of fast velocities is the benefit of CW
Doppler
9. False. The Nyquist Limit is the fastest velocity one can measure, not
frequency
10. True. Color Doppler shows blood velocity, represented by colors, on
top of the 2-D image
References
[1] Barrick B, Podgoreanu M, Prokop E. Physics of ultrasound imaging. In: Mathew J, Swaminathan M,
Ayoub C, editors. Clinical manual and review of transesophageal echocardiography (2nd edn.).
New York: McGraw Hill; 2010. p. 1–8.
[2] Bulwer B, Shernan S, Thomas J. Physics of echocardiography. In: Savage R, Aronson S, Shernan S,
editors. Comprehensive textbook of perioperative transesophageal echocardiography (2nd edn.).
Philadelphia: Lippincott Williams & Wilkins; 2011. p. 26–30.
[3] Halberg LI, Thiele KE. Extraction of blood flow information using Doppler-shifted ultrasound.
Hewlett-Packard Journal 1986;34(12):35–40.
CHAPTER Quantitative M-mode
and Two-dimensional
6 Echocardiography
Varun Dixit, John C. Sciarra and Christopher J. Gallagher
M-mode provides a one-dimensional, “ice pick” view through the heart

and updates the B-mode images at a very high rate.1 Doppler record-
ings reflect blood velocity, whereas M-mode motion of cardiac structures
reflects volumetric blood flow. The two examinations are hemodynami-
cally complementary. In certain situations, M-mode recordings of the
valves and inter-ventricular septum can be particularly helpful.2 M-mode
is a superior method of examining the timing of the cardiac events espe-
cially when displayed with the electrocardiogram.
EDGE RECOGNITION
Seeing the edges is easiest when the signal hits the objects at
90 degrees. (Don’t get fooled here, Doppler does best at 0 degrees or
180 degrees, but the best 2-D images are picked up when the beam is
90 degrees to the object.) The clearest edges are right down the middle
of the image. Picking out edges along the side is trickier, less clear.
Knowing where the edge ends is important when you are looking at ven-
tricular function. Good function shows good wall thickening and good
chamber emptying. Without seeing the edges clearly, it’s hard to read
either wall thickening or chamber emptying.
M-mode gives you a good edge, but to make sense of those squiggles
I think you need the $250 Italian leather designer shoes and snappy silk
ties of the cardiologist.
EDGE COMPONENTS
When measuring “where is the real live edge” in the ventricle, the back of
the mid-papillary muscle view is the most appropriate. Then, the whole
deal centers on where does the blood stop and where does the ventri-
cle start. For this, you are best off using contrast, as noted above. Other
than that anemic explanation, I don’t know beans about how they’d ask
you a test question on “Edge Components”.
39
40 Board Stiff TEE
TEMPORAL RESOLUTION
Anything that takes more scan lines will slow down your temporal resolu-
tion. In other words, anything that makes the transducer process more
data will slow it down. That makes sense, if you think about it. Even your
PC at home, when processing a lot of stuff at once, slows down.
Deeper field?—That would take more information in, so temporal

resolution would be worse.
Shallower field?—That would take less information in, so temporal

resolution would be better.
Wider field?—More information coming in, therefore worse temporal

resolution.
Narrower field?—You’re getting it. Less info, therefore better temporal

resolution.
AORTIC VALVE IN M-MODE
The aortic valve can be evaluated in different views but one of the best
for M-mode is the mid-esophageal long-axis view. On the right-hand cor-
ner is the view through the ME AV LAX view and the cursor is through the
aortic valve. If you press the M-mode button on your ECHO machine,
you will get this image. Let’s try to make sense of this picture.
First you will see the chest wall. The next hypoechoic shadow is the
right ventricular outflow tract. The next ‘ice pick’ line you get is the
aortic anterior wall.
Chapter 6 Quantitative M-mode and Two-dimensional Echocardiography 41
The ‘box car’ represents the cusp separation of the aortic valve.
The second ice pick line is the posterior wall of the aorta. Behind the
posterior wall is the left atrium, depending your view.
The picture explains the same landmarks in greater details. Try to corre-
late the diagram shown below with the real life ECHO picture above.
The diagram shown on the left is of an aortic valve in case of aortic ste-
nosis. Try to appreciate the small cusp separation, and the thickened
cusps of the aortic valve (small box cars). Cusp separation below 8 mm
represents severe aortic stenosis. Always correlate the M-mode with the
EKG.
This diagram shows the aortic regurgitation in M-mode. Note continuous

flow during the two consecutive ‘box cars’ representing the leak in the
aortic valve.
MITRAL VALVE IN M-MODE
Again, the mitral valve can reviewed in various views, in fact it should be
evaluated in different views. One of the easiest is to get the mid-esophageal
four-chamber view and then get the curser through the mitral valve and hit
the M-mode button.
In the image shown above, the first hypoechoic image will be of the left
atrium. Then there will be the mitral valve leaflets.
Note, the two leaflets of the mitral valve move in M-shaped mirror image
pattern in diastole. At the onset of systole the two leaflets come together
and generate the first heart sound.
42 Board Stiff TEE
VENTRICULAR WALL ASSESSMENT WITH

M-MODE
If M-mode is performed in trans-gastric view, the left ventricular wall can

be evaluated during the systole and diastole. Try to get the inter-ventricu-
lar septum and the left ventricular wall. The first hypoechoic shadow is of
the right ventricle.
The next ‘ice picked’ line is the inter-ventricular septum (IVS). The IVS
will move inwards during the systole as the left ventricle contracts, and
at the same time the posterior wall of the left ventricle moves anteriorly
as it contracts. From this view the end-systolic and end-diastolic mea-
surments can be calculated. It is also possible to make measurements
of the left ventricular wall thickness. The left ventricular end-diastolic
dimension is measured at the onset of the QRS complex.
The end-systolic dimension is measured at the maximum movement of

the ventricular septum and postero basal left ventricular free wall. The
end-diastolic dimension is measured at the minimum movement of the
ventricular septum and wall.
In a normal heart the thickness of the inter-ventricular septum and the

posterior left ventricular wall is between 0.8 and 1 cm. Also note behind
the posterior wall pericardium and epicardium are closely placed.
In case of collection of pericardial effusion, the space between posterior

wall pericardium and the epicardium is increased and the collection of
fluid can be appreciated.
Note the paradoxical motion of the inter-ventricular septum (instead of

moving in, the septal wall is moving out). This wall motion abnormality
can be seen in post-cardiac surgery and right ventricular hypertrophy.
GLOBAL FUNCTION: MEASUREMENTS AND

CALCULATIONS
At last, something familiar!
Even someone with little echo experience can see pretty quickly that
the heart is functioning well but is empty (give volume!) or the heart is
functioning poorly (give inotrope, put in a balloon, do something!).

Without getting wild about specific measurements, the naked eye can
tell pretty well when the ventricle is pumping all its volume out and con-
tracting well, and when the ventricle is just sitting there, doing nothing.
Obviously, experience will improve your assessment over time but it’s
hard to miss the elephant in the room.
This is worth dwelling on for a moment, not so much for the test, but for real
life. Plus, you will hear this lesson over and over and over again in this book.
REAL LIFE NOTE You’re in the OR, or the unit, and a patient has unexplained
hypotension. Is it hypovolemic shock or cardiogenic shock? Or is this cardiac
tamponage? Or has the patient low SVR due to sepsis? Maybe you have a Swan,
but then the numbers might be ambiguous. Does a PA of 30/15 mean empty or full?
What were the baseline numbers? Is the Swan working OK? Maybe you don’t have a
Swan. Now, what do you delay while you try to get in a Swan? What if the Line Gods
are not with you and you have a hard time sticking the neck, or the subclavian, or the
femorals? Now what?
BINGO! Put in a TEE. Just like that you’ll SEE what’s going on and
won’t have to INFER anything! Tamponade? You’ll see it, you won’t
have to figure whether the numbers support it. LV failure? You’ll see
it. Empty (say your patient had an allergic reaction and the SVR is
zippo)? You’ll see it.
When you are in trouble, transesophageal echo may keep you from
crashing.
Now, on to more mundane stuff, the types of calculato-equationo-testo

stuff that might appear on the test.
With a true long-axis or short-axis view, you can get the fractional area of
the ventricle with the following equation:

(End diastolic) (End systolic)
Fractional area of contraction
End diastolic
You can trace an outline of the ventricle at diastole and systole and
run the numbers, but most often you just eyeball it and make your own
assessment. Errors in LVEF estimates can be diminished by increased
experience of the echocardiographer, the use of cine loop technology,
and frequent, continuous training for quality improvement.3
GEOMETRIC, SPECTRAL, AND OTHER

MEASUREMENTS
You can go a little more gaga on this measurement stuff. Measure, for
example, the area of the LVOT, measure a VTI there, then you’ll get the
following:

Stroke volume cross-sectional area ∞ velocity-time index
44 Board Stiff TEE
Once you have the stroke volume, multiply that by the heart rate and you
have the cardiac output. There you have it, a geometric way to calculate
the LV function.
Spectral? Things get a little hairier here. The fancy gadgets we have
nowadays can filter out the high-velocity, low-amplitude signals of blood
flow, and reveal the high-amplitude, low-velocity signals of cardiac tissue
itself. So instead of looking at how the heart moves the blood, you look
at how the heart itself moves.
Too cool.
From this examination of the heart tissue itself, you can judge strain (a
dimensionless quantity that shows the percentage change from a resting
state to one achieved following the application of a force [that force is
called stress]).
Strain rate measures the rate of deformation of a tissue segment and

is measured in s−1. Infarcted myocardial tissue does not demonstrate
shortening or lengthening activity and shows no or minimal systolic strain
rate or strain.4
The echocardiogram is that visual assessment of wall motion which relies

mainly on evaluation of inward motion of the myocardium (the transverse
component of the contraction). Strain measurement allows evaluation of
the longitudinal component as well, thus enabling identification of abnor-
malities that are not readily seen by the naked eye.5
QUESTIONS
1. Which is the best view to assess the left ventricular function:

A. Bicaval view
B. Deep trans-gastric view
C. TG mid short-axis view
D. ME long-axis view
2. The best angle to get a 2-D image is:

A. 60 degrees
B. 90 degrees
C. 120 degrees
D. 180 degrees
3. Which combination will give you best temporal resolution:

A. Deeper and wider field
B. Deeper and narrower field
C. Shallow and wider field
D. Shallow and narrower field
4. Calculate the fractional area of shortening with the following data

(without using a calculator or your 4-year-old): end-diastolic area
4.8 cm2, end-systolic area 3.6 cm2, right atrial diameter 3.4 cm, left

ventricular wall thickness 1.6 cm
A. 2/3
B. 1/3
C. 1/4
D. 1/2
5. A patient admitted for CABG has central crushing chest pain. You
place a TEE probe and, guess what, you got M-mode. What ECHO
findings will you see during systole?
A. Reduced wall motion
B. No systolic thickening
C. Normal ventricular thickness
D. All of the above
6. What do you see in this picture?

A. Aortic insufficiency
B. Aortic stenosis
C. Mitral stenosis
D. Aortic regurgitation
ANSWERS
1. C. The left ventricular function can be evaluated in number of views

but the trans-gastric short-axis view will give an impression of the
ventricular walls, which are supplied by all the three main coronary
arteries.
2. B. A quick revision: Doppler is best at 0 or 180 degrees, but 2-D echo
images are best viewed at 90 degrees.
3. D. Remember temporal resolution is like CA 1 resident, if you give him
too much information he will slow down. So tell him one thing a day
and give time to process. So a shallow and narrow field will give best
results.
46 Board Stiff TEE
4. C. Too bad!!! You already forgot the formula

FAC = EDA-ESA
i. EDA
5. D. All these are the findings of ischemia in ventricular walls. Note that
the ventricular wall should thicken during the systole; if there is normal
ventricular thickness it signifies ischemia. I even made a diagram for
you.
6. B. There is severe stenosis of the two cusps of the aortic valve, with
one cusp hardly moving at all.
References
[1] Perrino AC, Reeves ST. In: A practical approach to transesophageal echocardiography, 2nd ed.
Lippincott: Williams & Wilkins; 2003.
[2] Feigenbaum H. Role of M-mode technique in today’s echocardiography. J Am Soc Echocradiogr
2010;23(3):240–57.
[3] Mathew JP, Fontes ML, Garwood S, et al. Transesophageal echocardiography interpretation:
a comparative analysis between cardiac anesthesiologists and primary echocardiographers.
Anesth Analg 2002;94:302–9.
[4] Pellerin D, Sharma R, Elliott P, Veyrat C. Tissue Doppler, strain, and strain rate echocardiography
for the assessment of left and right systolic ventricular function. Heart 2003;89(Suppl. 3):iii9–iii17.
[5] Gila Perk Paul A, Tunick Itzhak Kronzon. Non-Doppler two-dimensional strain imaging by echo-
cardiography—from technical considerations to clinical applications. J Am Soc Echocardiogr
2007;20(3):234–43.
CHAPTER Quantitative Doppler
7 Christopher J. Gallagher, Christina Matadial
and Jadelis Giquel
TYPES OF VELOCITY MEASUREMENTS
Here I think they’re driving at pulsed-wave Doppler versus continuous-

wave Doppler. (It’s tough going through this and wondering “What are
they thinking?”) To review, then, pulsed-wave Doppler takes a specific
look at a specific velocity at a specific place. The pulse wave (PW) trans-
ducer is used as both a receiver and transmitter of ultrasound waves.
A complete cycle of transmission waiting and receiving is called the
pulse repetition frequency (PRF). The greater the depth of interrogation of
the pulsed ultrasound beam the longer the waiting period. Therefore, the
deeper the interrogation, the lower the PRF, and the lower the maximal
velocity that can be measured. Pulsed-wave ultrasound is used to pro-
vide data for Doppler sonograms and color flow images.
Continuous-wave Doppler, in contrast, takes velocity measurements along

the entire length of the beam, allowing you to measure high velocities, but
not allowing you to know exactly where that measurement is made (also
known as “range ambiguity”). In this modality, ultrasound is continually
transmitted by one crystal and continually received by another.
HIGH-FRAME RATE-DOPPLER
Another thing they might be driving at here is PISA, the proximal iso-
velocity surface area.

THE LEANING SEMICIRCLE OF PISA
Gradually
narrowing
flow
(broad river)
Flow here PISA

all at
aliasing Stenosed valve
velocity so (narrow gorge)
color changes
This, too, is gone over ad nauseum in Chapter 3, but here goes. As blood
flow converges toward a tight spot (Analogy? Think of a broad river com-
ing to a narrow gorge), the flow will speed up. At a certain concentric 47
48 Board Stiff TEE
area, the flow should all be at the same speed as the “chaos” of a broad
river becomes the “organized tightness” of a narrow channel. This area
will, when measured by color flow Doppler, hit the Nyquist limit and will
start aliasing. Red flow will become blue, for example, in a semicircle.
You can measure the area of this by the equation

Area = 2 × pi × radius squared × angle / 180
This will come in handy as you do volume measurements and try to

assess valve areas. At the risk of sounding like a broken record, go to the
hemodynamic section to see these ideas put into action. (And into the
kind of thing that would appear on an exam.)
VOLUMETRIC MEASUREMENTS AND

CALCULATIONS
This gets into the realm of the material in Chapter 3, the volume equa-
tions you use to measure valve areas, cardiac outputs, stroke volumes,
and the like. The sample problems in that chapter illustrate better than
this explanation, but here goes.
The main volume you will lug around through the heart is best thought of
as a cylinder of blood. You will make various area measurements (area is
0.785 × diameter squared) and “length” measurements (the TVI, or time-
velocity integral, which you get by outlining the flow through an area,
and then the echo machine computer spits out a TVI, the integrated area
under the flow curve).

MEASURING A BLOOD “CYLINDER”
Area 0.785 × Diameter2
Length Measure the TVI
A million times, you will make these measurements and apply them to
get valve areas. Yeah, verily, I say unto you, do all the problems in the
hemodynamics section and you will see what all of this means.

GETTING DIAMETER AND TVI
Diameter TVI
Put calipers
Measure flow
there
Outline flow—get TVI

Chapter 7 Quantitative Doppler 49
VALVE GRADIENTS, AREAS, AND OTHER

MEASUREMENTS
The gradient, or change in pressure, across a valve is measured by the

Bernoulli equation:

Delta pressure = 4 × velocity squared
The real Bernoulli equation is understood only by “brilliant French physi-

cists at the turn of the 18th century”. You know, when all this stuff was
figured out. Here are a few examples of Bernoulli’s equation in action:
Example 1: The velocity across a stenotic mitral valve is 4 meters/sec-

ond. What is the gradient?

Delta pressure = 4 × (4 meters / second) squared = 64 mmHg
Note that the velocity has to be in meters/second to get a pressure in

mmHg. Ask Bernoulli if you want to know why.
Example 2: The velocity going back across a regurgitant valve is

2 meters/second. What is the gradient?

Delta pressure = 4 × (2 meters / second) squared = 16 mmHg
So how does all this cool stuff translate into valve areas? Look no fur-
ther than the continuity equation (which was mentioned at least 4 million
times during the meeting). The continuity equation says this:
A quantity of blood passing here will pass there.
No more, no less. A cylinder of blood that you calculate passing through

one valve will (if no VSD or ASD or regurgitant flow “diverts” it) pass
through another valve. In equation-ese:

Area × length ( through one valve) = area × length ( through another valve)
Characteristically, you will have the area at one place and a velocity
(which you can then outline, get a TVI, and thus have a “length”) at the
same place. Then you get a velocity (which you again outline and thus
get a “length” by the same TVI gig) at an unknown valve, and solve for
that valve area by cross multiplying and dividing.
A typical example involves the LVOT (where you can figure the area and
get a TVI) and the aorta (where you can get a TVI but don’t know the
area):

Area LVOT × TVI LVOT × TVI aortic valve × area aortic valve

50 Board Stiff TEE
ESSENCE OF CONTINUITY
will equal
The cylinder the cylinder
of blood of blood
out the through the
aortic valve mitral valve
(Area × TVI) (Area × TVI)
The unknown in this equation is the area of the aortic valve.
You can flip it, turn it, bake it, braise it, blacken it, serve it with tartar
sauce or salsa—the continuity equation is always a variant of this theme.
Even in the “spooky” realm of PISA, you are still just doing the same
thing, using the continuity equation:

Area PISA × velocity PISA = velocity other valve × area other valve
The unknown is the area of the other valve. You cross multiply and divide
and there you have it. Note that in PISAville, you don’t use the TVI; rather,
you use a velocity. All is well, though, because you use a velocity on the
other side of the equation, too, so the units cancel out. But you’re still
working the continuity idea.
CARDIAC CHAMBER AND GREAT VESSEL

PRESSURES
Figuring this stuff (again, see examples in Chapter 3) requires the

Bernoulli equation and one commonsense principle. In the problem you’ll
wrestle with, you’ll be given a valve with a velocity across the valve. Use
the Bernoulli equation to figure what the pressure gradient is across that
valve. So far so good.
Now, use your common sense and figure this out: Where is the high-
pressure end of this gradient, and where is the low-pressure end? Recall
that this will be specific to the cardiac cycle. So, for example, if you have
mitral regurgitation, then during systole, you will have high pressure in
the left ventricle, a gradient across the mitral valve as the blood flows
backward into the atrium, and a low “leftover” pressure in the left atrium:

Ventricular systolic pressure − pressure lost across regurgitant valve
= left atrial pressure
If you have, say, mitral stenosis, then during diastole, the high-pressure
area will be the left atrium, the pressure gradient will be “pressure lost”
crossing the mitral valve as blood struggles to get into the left ventricle,
and the “leftover” pressure will be the left ventricular pressure. (Assuming
no aortic regurgitation muddies the waters.)
Left atrial pressure – pressure lost across stenotic valve

= left ventricular pressure
As long as you think of:

n Where is the high pressure?
n Where is the pressure lost crossing a valve?
n Where is the low pressure?
then you can figure any of these “what’s the pressure in chamber or ves-
sel X?” questions.

ESSENCE OF GRADIENT
High Pressure
Pressure lost at Through a

“choke point” = 4V2 “choke point”
Low Pressure
(Whatever pressure is “left over”)
TISSUE DOPPLER
Tissue Doppler looks at movement of the cardiac walls themselves,

rather than the blood racing around in the chambers. Tissue moves
about 10% as fast as blood, but our magical machines can tease out tis-
sue movement from blood movement. What will they think of next?
In systole, as seen on tissue Doppler, the heart tissue moves away from
the transducer. The first movement, S1, is isovolumic contraction. The
second movement, S2, is systolic shortening velocity.
In diastole, there are also two velocities. Both are toward the transducer.
The first diastolic movement, E velocity, corresponds to the rapid filling
of the ventricle in early diastole. The second diastolic velocity, A velocity,
corresponds to the atrial contraction.

TISSUE DOPPLER
Systole (away from transducer) Diastole (toward)
S1–Isovolumic contraction E–Early diastole

S2–Systolic shortening A–Atrial contraction
Myocardial velocity is not the be-all, end-all of cardiac imaging, because

it can get goofed up by “tethering” and translational movement.
During the meeting they showed some tissue Doppler, but not too much.
Just know that it exists and know what S1, S2, E velocity, and A velocity are.
52 Board Stiff TEE
QUESTIONS
1. What is the major advantage of pulse wave Doppler?

A. Range ambiguity
B. Range resolution
C. Acoustic impedance
D. Temporal resolution
2. Pulse wave Doppler is best to determine which of the following:

A. RVSP
B. Peak mitral regurgitation velocity
C. Severity of the dynamic outflow obstruction
D. Peak pulmonary vein systolic forward flow
3. CWD is best to determine which of the following:

A. Mitral annular velocity
B. Velocity though a small restrictive VSD
C. Left ventricular systolic volume
D. Diastolic flow reversal in the descending aorta
4. In calculating cardiac output using Doppler method, the LVOT

area × LVOT flow velocity equals:
A. Cardian output
B. Stroke volume
C. Time velocity integral (Stroke distance)
D. Flow rate
5. Which of the parameters (measured incorrectly) will most likely affect

calculation of the cardiac output:
A. LVOT TVI
B. AV TVI
C. MV deceleration time
D. LVOT peak velocity
ANSWERS
1. B. The major advantage of pulse wave Doppler is the ability to

determine the Doppler shift at a precise location. This ability is called
range resolution or range discrimination.
2. D.
3. B. The major advantage of continuous wave Doppler is the ability
to accurately measure high velocities of blood flow. The major
disadvantage is range ambiguity.
4. B. SV (cm3) = CSA (cm2) × VTI (cm)
5. A. See 4.
Bibliography
Gorcsan III J, Diana P, Ball BS, et al. Intraoperative determination of cardiac output by tranesopha-
geal continous wave Doppler. Am Heart J 1992;123:171–6.
Haltle L, Angelsen B. In: Doppler ultrasound in cardiology: physical principles and clinical applica-
tion. Philadelphia: Lea & Febiger; 1982.
Heimdal Andreas. Doppler based ultrasound imaging methods for noninvasive assessment of tissue
viability. NTNU 1999.
Muhiuden IA, Kuecherer HF, Lee E, et al. Intraoperative stimation of cardiac output by tranesopha-
geal pulsed Doppler echocardiography. Anesthesiology 1991;74:9–14.
Powis RL, Schwartz RD. In: Practical Doppler ultrasound for the clinician. Baltimore: Williams &
Wilkins; 1991:171–172.
CHAPTER Doppler Profiles and
8 Assessment of Diastolic
Function
TEST NOTE Anyone who ever took the test will attest to one thing:
DIASTOLIC DYSFUNCTION IS A BIG PART OF THE TEST. Repeat, DIASTOLIC
DYSFUNCTION IS A BIG PART OF THE TEST.
TRICUSPID VALVE AND RIGHT VENTRICULAR

INFLOW
The big Mammas of the valve world are the mitral and aortic, with whole
lectures dedicated to each one individually. The tricuspid and pulmonic
valves usually get lumped together, like third-class steerage passengers
on the Titanic. It’s a safe bet that you should put your efforts into the
mitral and aortic valves. But, let’s soldier on through the tricuspid valve.
The tricuspid valve has (duh) three cusps. Set in a (normally) low-
pressure system, the tricuspid doesn’t “have to” function perfectly. You
will normally see some regurg here. Think about it; sometimes the tricus-
pid valve is removed and not even replaced, and the heart continues to
function. Try that with the aortic valve!
You get a dandy view of the tricuspid in the “easiest” view to get, the ME
four-chamber. The ME RV inflow–outflow view also gives you a shot at
the tricuspid.
Focusing your Doppler on the tricuspid valve will tell you just how severe
the tricuspid regurg is. The regurg is severe if:
n The jet area is greater than 10 cm squared
n The jet area-to-right atrial area is greater than 67%
n The vena contracta width (narrowest width of the regurgitant jet) is
>6.5 cm squared
n The tricuspid jet intensity is >65% of antegrade flow
n The tricuspid annular dimension is >34 mm at end systole
Also, if the hepatic vein flow profile shows systolic flow reversal, that also
indicates severe tricuspid regurgitation. If you think about it, that makes
sense. When the heart contracts, if the tricuspid valve doesn’t work, the
blood flows back into the right atrium and just keeps on flowing backward,
55
56 Board Stiff TEE
backward, backward, all the way back into the inferior vena cava and back
further into the hepatic vein (which feeds into the inferior vena cava).

LOOKING AT THE TRICUSPID
ME 4 Chamber ME RV Inflow Outflow
Tricuspid emphasized Tricuspid emphasized
PULMONARY VALVE AND RIGHT

VENTRICULAR OUTFLOW
Look at your model of the heart again. The pulmonary valve is the far-
thest away valve in the heart. No surprise, then, that you sometimes have
a hard time getting a good look at it. And getting a good Doppler study
through it can be a real pain.
Fortunately, a kind Providence has given us a few good views of the pul-
monic valve. The ME RV inflow–outflow view works. If you get that aortic
valve in a good en face view (the Mercedes Benz sign), then you will get
a 90-degree view of the pulmonic valve.
Another view (not quite as easy to get) is the UE aortic arch SAX view.
This view gives you a better chance at getting a Doppler shot down the
pipe of the pulmonic valve.
PULMONIC VALVE
ME RV Inflow Outflow UE Aortic Arch SAX
PV PV
When you Doppler-ifize the pulmonic valve, you will see some regurg,
especially if there is a PA catheter straddling the valve. As with other
valves, you can get an impression of the degree of regurg by looking at
the size and depth of the regurgitant jet. A big jet means a lot of regurg,
a little jet means a little regurg. (Aren’t you glad you went to school for
years and years to be able to figure out such complex stuff?)
Since the pulmonic valve lies far afield from the echo probe, getting more
quantitative than that just ain’t in the works.
Chapter 8 Doppler Profiles and Assessment of Diastolic Function 57
When you see PR, it’s worth thinking about what might be causing it. As with
other valves, a poorly functioning valve (endocarditis, carcinoid syndrome,
congenital defect) may account for the blood flowing backward. Also, high-
pressure “downstream” of the valve (pulmonary hypertension, pulmonary
embolus) may “overwhelm” a normal valve and cause regurgitation.
MITRAL VALVE AND LEFT VENTRICULAR

INFLOW
TEST NOTE THIS IS THE BIGGIE. THE DOPPLER PATTERNS OF INFLOW

FROM THE MITRAL VALVE INTO THE LEFT VENTRICLE ARE EXTREMELY
TESTABLE. THESE PATTERNS REVEAL ALL-IMPORTANT DIASTOLIC
DYSFUNCTION. ENTIRE LECTURES IN THE REVIEW COURSE ARE DEDICATED
TO DIASTOLIC DYSFUNCTION. IF TIME IS SHORT, FOCUS ON THIS
MATERIAL AS YOU WILL SEE IT IN SPADES ON THE TEST.
How the blood flows into the ventricle tells a lot about the ventricle’s
function during diastole. If the heart is healthy, springy, and not stiff, then
the blood will flow in easily. If the heart is sick, stiff, and nonresilient, then
the blood will have to “work hard” to fill the ventricle.
THE KARMA OF DIASTOLIC DYSFUNCTION
Groovy Ventricle Bad Ventricle
LA LA Tough
Easy to
flow get
LV LV blood
in there
Judging by the puzzled looks in the diastolic dysfunction lectures, it was

evident to me that this whole idea is a little hard to absorb. For some rea-
son, the idea of systolic dysfunction is easy to grasp:
The pump doesn’t work, but the concept of diastolic dysfunction is tough.
The loading of the pump doesn’t work.
The world would be a nice place if the mitral inflow patterns were a
simple
Diastolic function OK—one pattern
Diastolic function no good—another pattern
But noooooooooooooooooooooooooooooooooooooooooooo! Life is not

so. Understanding these confusing patterns is the whole crux of under-
standing diastolic dysfunction.
First, I’ll blast through the patterns, then I’ll go back and try to drag you
through the reasoning. PLOW THROUGH THIS STUFF SLOWLY, AND
58 Board Stiff TEE
LOOK FOR THE EXPLANATION IN A FEW DIFFERENT BOOKS, FOR

DIASTOLIC DYSFUNCTION IS A TOUGHIE.
Now, the reasoning behind the patterns. (The first part is easy—the
second is a bit sticky.)
Side note: to acquire the E/A ratio, place the pulse wave circle thing at
the tip of the mitral leaflets. For the pulomonary flow go way to the top of
the left atrium and put the PW there. You may have to ask a professional
for help with this.

MV TO LV FLOW
E A E A E A E A
Normal Impaired Pseudo- Restrictive

relaxation normal or
really
bad!
THE GROOVY HEART
When you do a Doppler interrogation of the inflow into a nice compliant

ventricle that has no stiffness, no diastolic dysfunction, no nothing.
The E wave shows the rapid inflow of blood into the ventricle when the
mitral valve opens. This E wave then peters out, there is a time of diasta-
sis (no pressure difference, hence no flow), then the atrium contracts and
there is a second inflow of blood called the A wave.
THE HEART WITH IMPAIRED FILLING
In your mind’s eye, make the heart a little stiffer, a little less compliant.
When the mitral valve opens now, the blood has a harder time rushing
into the left ventricle (like trying to blow air into a stiffer balloon; it’s just
harder to do, so less goes in). The E wave, then, is blunted. Now the
atrium, which didn’t empty too well, is still sort of full, so when the atrium
contracts, the A wave will be a little bigger.
The E-to-A ratio has reversed, as seen in the second pattern in the figure
at the top of this page.
It would be great if things just stopped right here, because up until now,
it’s quite easy to follow.
Compliant heart, this pattern.
Noncompliant heart, that pattern.
Boom. Done.
Alas, from here on out, it gets a little tougher. This is where it pays to look
at a bunch of different books (Otto; the TEE review course syllabus) and
see how this is explained.
THE YET-MORE-NONCOMPLIANT HEART
Now, let time pass and the heart gets yet more noncompliant and yet
stiffer. Now, the atrium really fills up a lot, from a long-standing battle to
push blood into the ventricle. When the mitral valve opens, blood now
rushes in, not due to a compliant ventricle accepting the blood easily,
but from an overfilled atrium ramming the blood down the ventricle’s
throat. Then, when the atrium contracts, some more blood is added to
the ventricle.
Net result? The third pattern in the figure at the top of page 58, pseudo-
normalization of the E-to-A ratio.
But wait, that E-to-A ratio looks just like the first pattern, that of the
groovy heart with good compliance! It looks normal, but how can that be,
because we know it’s abnormal!
Right you are! That pattern is called a “pseudonormalization of the

E-to-A ratio.”
Every test-taker in the galaxy just asked himself or herself the same
question:
“On the test, and for that matter in real life, how do I know the difference between
a normal and a pseudonormal pattern?”
There are a few ways.
History and Physical
If you do a history and physical (gasp!), a normal pattern is seen most

often in a normal person. A pseudonormal pattern is seen in a sick per-
son. How’s that for a whap of common sense upside the head?
Size of the Left Atrium
Most people with diastolic dysfunction have an enlarged left atrium. No

surprise. You have, in effect, “mitral stenosis” not at the level of the valve,
but at the level of the entire left ventricle.
Valsalva Maneuver
If you perform a Valsalva maneuver and cut off venous return to the
heart, a pseudonormal pattern will go “back one step” to a noncompli-
ant pattern (the easy-to-understand blunted E wave). Why? By cutting
60 Board Stiff TEE
off venous return with your Valsalva maneuver, you don’t let the atrium
“supercharge” with volume and “overwhelm” the noncompliant ventricle.
Sit and think about that for just a minute. If you can really satisfy your-
self that that works, you go a long way toward really understanding this
whole diastolic dysfunction mess.
No, really, take a minute to suck that up.
Inflow Pattern of Pulmonary Veins
Another way to tell is to look at the inflow pattern of the pulmonary veins.
Normally, the pulmonary veins have the pattern shown in the figure below:

PULMONARY VEIN FLOW TO THE RESCUE!
E A
Normal or Pseudonormal?
Look at PV flow
S D A Blunt S S D A
Big D
Big A
But when the heart is noncompliant, then the pulmonary veins can’t rush
blood forward so well during systole, so the S wave is blunted and the D
wave is heightened. (You can think of this “blunted” pulmonary venous
pattern as similar to the blunted E wave and heightened A wave of the
“first stage of diastolic dysfunction” that you see in a mitral flow pattern.)
To recap:
Normal E-to-A ratio and normal pulmonary venous flow = normal
Normal E-to-A ratio and “blunted” pulmonary venous flow

= pseudonormal
Another aspect of the pulmonary venous inflow is this: the small amount
of flow reversal in the normal heart (causing a small A wave) becomes a
big amount of flow reversal in the stiff heart (causing a large A wave).
Others
There are a bunch more indicators that you can use to know the differ-
ence between normal and pseudonormal, but they’re a killer to memo-
rize (your humble author having tried and failed to do just that). If you
go over the reasons given above and really understand what’s going on,
then you’ll “get” diastolic dysfunction.
THE STIFF-AS-HELL HEART: NO KIDDING

END-STAGE DIASTOLIC WIPEOUT
Let more time pass and make that heart just as stiff as stiff can be. Now
the pattern gets distinct enough to differentiate from the normal pattern,
as shown in the fourth pattern in the figure at the top of page 58: restric-
tive or really bad.
What you are seeing is a thin spike of high pressure as a totally over-
amped atrium fires into a rock of ventricle. Pressure rises high and fast
and falls off fast. Note how thin the E wave is. Then the A wave is just
a tiny little thing, because the atrium is so stretched out that it doesn’t
have much “oomph” of its own left over.
For completeness’ sake, study the Doppler patterns of the other valves,
but FOCUS ON THESE MITRAL PATTERNS. THEY ARE THE KEY TO
DIASTOLIC DYSFUNCTION AND WILL APPEAR ON THE TEST.
Now we have spoken of the EA ratio, and the SD (systole, diastole) of

the pulmonary vein flow. It is time to put it all together. Here is the dia-
gram you must memorize. And when we say memorize, that means you
should be able to draw this in all its detail from memory. If you can, that
means you understand the relations of blood flowing into the LV and how
it relates to blood flowing into the left atrium. Now don’t rush thru this.
Each little detail is important.
DT
E A
inflow
Mitral
IVRT
IVRT
Bigger! Like a
S2 Down! dagger!
S1
Tissue Pulmonary
Doppler vein flow
S D
Bigger!
Ar
E A (Diastolic (Pseudo- (Restrictive)

(Normal) dysfunction normal)
or
relaxation
abnormality)
Notice how the IVRT (isovolumic relaxation time) changes. See how
the D wave in the pulmonary vein flow dips in diastolic dysfunction,
then goes up in pseudo-normalization. Pay attention to the PV-Ar (the
atrial reversal part of pulmonary vein flow). Look at how the DT (decel-
eration time) changes during the E phase of the mitral inflow. Try to
imagine these flows happening in the heart and memorize these subtle
differences.
This table is graphic and quite precise, but each drawing has a number
associated with it. On a test, you may see the image on a screen, or you
may just be given the numbers. So here is a table of the numbers. Note,
these are not iron clad. Textbooks argue over absolutes, so you may see
different numbers in different texts.
62 Board Stiff TEE
The diastolic dysfunction table of numbers

NORMAL DIASTOLIC PSEUDONORMAL RESTRICTIVE
DYSFUNCTION
MITRAL INFLOW
E/A 1 to 2 <1 1 to 2 greater than
or equal to 2
DT (ms) 150–220 >220 150–220 <100
IVRT (ms) 60–100 >100 >100 <60
PVF
S/D >1 greater than or <1 <1
equal to 1
Ar (cm/sec) <35 less than or greater >35 >35
than 35
TISSUE DOPPLER
E’ (ms) >8 less than or greater <8 <8
than 8
AORTIC VALVE AND LEFT VENTRICULAR

OUTFLOW
You don’t really interrogate the LVOT to determine diastolic dysfunction,

so this part of the outline is a bit of a “misnomer.” But you do need to
look with the Doppler at the aortic valve. The trouble is, to get a good
“up the pipe” view of the aortic valve, you need to align the aortic valve
in the deep transgastric long-axis view.
AND GETTING THE DEEP TRANSGASTRIC LONG-AXIS VIEW IS HARD

AS HELL!
The first (and in my case, nearly every) time you try to get this view, you
will advance the probe deep, deep into the stomach, you will anteflex it,
pull back and…and…and you get a transgastric mid–short-axis view. The
bouncing donut view.
Damn.
You try again, you put that probe in so far you figure you’ll be seeing the
toenails soon, then you bend the probe back and you get…the stupid
transgastric view again!
Hell and damnation!
Try again. Here’s an example to help guide you. Say you’re in to 50 cm at
the teeth. Advance all the way to 60 cm, then anteflex all the way that the
handle can go and come back slowly, ever so slowly. You just might get
it. Keep in mind that, even in experienced hands, this deep transgastric
long-axis view is just not gettable in 30% of patients.
If you ever DO get the damned view, then you can lay your Doppler
right across the valve and get a reading. One problem? You would love
to get a specific flow at a specific point (which means you want pulsed
Doppler) but the flow through the aortic valve is very fast (pulsed Doppler
would alias) so you have to go with continuous wave when analyzing the
aortic valve. There is range ambiguity then, and if the flow is faster in
another spot (say the patient has subaortic stenosis), then you will get
the “fastest” signal from the subaortic spot rather than the valve itself.
TEST NOTE The pulsed wave versus the continuous wave comes up again and
again. Make sure each time you understand WHY you use WHICH ONE.
Absolutely cannot, cannot, get the deep transgastric long-axis view? You
can get a less-than-perfect but still usable view with the transgastric long
axis.
Note that the alignment isn’t as perfect as the true blue deep transgastric
long-axis view.
REAL WORLD NOTE Getting these views and reading a gradient across the
aortic valve is no ivory tower exercise. When surgeons do a myomectomy for IHSS
or place a new valve that “might be too small,” they really want to know those
gradients because it may determine the success or failure of the procedure. Make
sure you do a few gradients on routine cases before you “have to” after an aortic
valve or interventricular septum procedure.
NONVALVULAR FLOW PROFILES
This was already touched upon in the discussion of mitral valve inflow
and diastolic dysfunction, but it bears repeating.
An important nonvalvular flow pattern is pulmonary venous inflow. When

you have an ambiguous read on the mitral inflow (is that “normal” E-to-A
ratio actually normal, or is it pseudonormal?), then take a look at the
pulmonary veins. If they show a blunted S wave, an enlarged D wave,
and a large A wave, then that goes along with diastolic dysfunction. The
heart is stiff and the atrium is having a hard time pushing blood into the
noncompliant ventricle, so the normal inrush during systole is blunted
(blunted S wave), more blood rushes forward when the atrium finally
does empty (larger D wave), and more blood goes backward into the pul-
monary veins during atrial contraction (larger A wave).
Any other nonvalvular profiles that might come in handy?
Yes! Anytime you are wondering about a structure, you can always lay
a Doppler across it and see what gives. Especially when you wander up
into views of the aorta or other great vessels, you might see a circle or
tube and wonder, “Well, what the Sam Hill is that?” If a patient has dis-
torted anatomy (lymphomatous nodes squishing this and that), you can
get mixed up with “is that the aorta coming around, or an innominate
vein, or what?”. Doppler will at least tell you if you have an arterial or a
venous wave pattern.
64 Board Stiff TEE
Remember the tricuspid valve? When that has regurgitant flow (as
already mentioned above), then you can always interrogate the hepatic
vein. Reversal of flow in the hepatic vein is consistent with severe tricus-
pid regurgitation.
By that same logic, would it make sense to interrogate the pulmonary

veins to look for mitral regurgitation? Yes. Systolic flow reversal in the
pulmonary veins is diagnostic for 4-plus mitral regurgitation.
Whip that damned Doppler all over the place, it will tell you all kinds of
stuff.
QUESTIONS
1. The IVRT is:

A. Pronounced “eevert”, not “eye-vert”
B. The time of relaxation of the LV
C. The time between the closing click of the AV and the opening click
of the MV
D. The time just before the opening of the AV and the closing of
the MV
E. The time just after the IV is placed and before the RT hooks up the
ventilator
What best describes the following patients? Normal, impaired relation,

pseudo-normal, restrictive filling.
2. E/A = 1, PVF S/D = 1.1_______________________________
3. E/A = 1, PVF S/D = 0.9 _______________________________
4. E/A = 2.4, PVF S/D = 0.9_______________________________
5. E/A = 1, IVRT = 99 ms, _______________________________
6. E/A = 1.5, DT = 190 ms, IVRT = 110 ms_________________________
7. PVF S/D = 1.1, PV – Ar = 33 cm/s_______________________________
8. E/A = 2, PVF S/D = 0.9, PV – Ar = 36 cm/s_________________________
9. DT stands for:
A. Decompression time
B. Default time
C. Deceleration time
D. Down time
E. Adventure time
ANSWERS
1. C.
2. This guy is normal. Look at the diagram or the table. If you got this
one wrong, go back and draw the wave forms.
3. Here our E/A looks normal, but the PVF is abnormal, so it is pseudo-
normal relaxation.
4. The E/A ratio is huge so you hardly need any more information than
that—restrictive filling.
5. E/A is normal so this could be a normal patient or pseudonormal.

Check the IVRT and see it is in the normal range, so he is normal.
6. The E wave is in the normal range, but the DT and IVRT fall in the
pseudonormal range—so pseudonormal it is.
7. Normal.
8. Pseudonormal.
9. C. Deceleration time.
CHAPTER
9 Cardiac Anatomy
IMAGING PLANES
Time to go back to the model and the pie-shaped slice of imaging that
comes out of the echo probe.
And time to take another good look at a plastic model of a heart.
These imaging planes tie in with the BIG 20 views of the heart. These
are the 20 views detailed in THE ARTICLE by Shanewise et al on
echo.1 The 20 views are also detailed a million times over on differ-
ent internet sites. Google “University of Toronto: TEE” for a great tuto-
rial. This article and the 20 views detailed therein are the absolute crux
of the TEE experience. Photocopy those 20 views and tape them to
your TEE machine. Every time you examine a patient, try to get all the
20 views. Get in the habit of “examining everything every time”. If not,
you’ll just look at the “thing of interest” and you’ll miss something else.
Also, getting all 20 views will sharpen your TEE probe-wiggling skills.
Shanewise gives the lecture on the “standard exam”—meaning the 20
views—and he says he can do it in 7 minutes, before the patient is even
draped!
Shanewise has thrown down the gauntlet. Can you do it that fast?
Here is our version of the 20 views. Notice it is not labeled. That is your
job. As you read through this book label every structure on these 20
images. Yes, you can write on the book. You did buy your own, didn’t
you?
TEST NOTE EVERY LITTLE STRUCTURE, VALVE, FLAP, AND SPACE IN THESE
CARTOONS IS FAIR GAME ON THE TEST. SO DON’T SAY WE DIDN’T WARN
YOU.
67
68 Board Stiff TEE
0° 90° 120° 0°
RV S L I A
P AS
0° 60° 30°– 40°
120°–140° 90°–110° 0° 110°
60° 0°–10° 90°
0° 90° 0° 90°
TEST NOTE AND REAL LIFE NOTE Know these views cold. Know each structure
in each view. Imagine you are learning a new language that has a 20-letter
alphabet. These 20 views are the letters of that alphabet.
In each view, note the approximate omniplane angle!
The imaging planes for these views are divided into distinct “layers,”
though, in reality, you slide gradually from one view to another rather
than making jerky quantum leaps.
The planes are upper esophageal, midesophageal, transgastric, and

deep transgastric. Each plane takes in a few views, except for the pesky
deep transgastric, which takes in just one view.
Here’s your new alphabet:
A THE TEE “ALPHABET”
MV
TV
RA LA
Anterior
RV LV wall
Lateral
RV free
wall
wall
Interventricular Inferior
septum or ME 4 Chamber wall ME 2 Chamber
septal wall Best “initial” view Know those walls!
Important for coronary anatomy
Chapter 9 Cardiac Anatomy 69
B TEE ALPHABET
PM papillary
AV
AL papillary
Antero- RV
septal
wall
Posterior
wall LV
ME LAX TG Mid SAX
Anterior leaflet of MV— Great for LV function
Note how close to AV!
C TEE ALPHABET
Post. leaflet
MV
MV
LV Ant. leaflet
MV
Anterior
wall
TG 2 Chamber TG Basal SAX
This is just a TG mid SAX “Fish mouth” is MV.

rotated 90°. You’re are a little higher in LV.
TEE ALPHABET
D
P3
AV
A2
“Mercedes
P1 Benz”
Pulmonic
valve
RV LV
ME Mitral Commissural ME AV SAX
Good for identifying specific Note: En-face view of AV

parts of MV with “side” view of PV.
E TEE ALPHABET
MV AV
AV Doppler
“shot” for
AV gradient
ME AV LAX TG LAX
Easy view to get; If can’t get deep TG LAX,

Great for looking for regurgitation of AV. use this for Doppler of AV.
F TEE ALPHABET
Perfect Doppler IAS

shot up the LA
AV
IVC SVC
Aorta
RA
Deep TG LAX ME Bicaval
Tough to get this view! Renal tumors can creep up

that IVC.
A TEE ALPHABET
Aorta
just above AV
RA LA
RV
RV Tricuspid valve
RV
inflow outflow
RV RA
ME RV Inflow-Outflow TG RV Inflow
Just a little higher and The TG 2 chamber looks

back from the ME AV SAX at the left; this view the right.
B TEE ALPHABET
Right pulm.
artery PA
Aorta Main pulm. Aorta
artery
ME Asc. Aortic SAX ME Asc. Aortic LAX
Best PA view, might see PE here. Just turned ME AA SAX 90°.
C
TEE ALPHABET
Aorta Aortic
PA
arch
Aorta
PV
Desc. Aortic SAX Desc. Aortic LAX UE AA LAX UE AA SAX
Look for Here’s where you see Arch can be Can shoot Doppler
dissections. artifacts like double- hard to see due down pulmonic
barrelled aortas. to bronchi. valve here.
Go over these views in detail. Know how to express your findings as

related to the views, for example:
“In the bicaval view, I see an ASD.”
“In the 4-chamber view, I see a clot in the apex.”
“The ME 2-chamber view shows a new regional wall motion

abnormality; the inferior wall is not moving.”
That’s how you want to work with the “TEE Alphabet”.
CARDIAC CHAMBERS AND WALLS
The four-chamber view gives you your best “initial impression” and a
good look at most of the major stuff in the heart. It’s what you first see
when you’re just starting TEEology.
When you show this view, most medical people can immediately grasp
what’s going on because it looks like a drawing of the heart. If you
have a med student, ICU nurse, surgeon, or someone else looking on,
this view shows you all four chambers of the heart (hence the name),
the lateral and septal walls, and the mitral and tricuspid valves. What a
deal!
And, niftier still, if you just rotate the view 90 degrees, you get the two-
chamber view and see the inferior and anterior walls. Rotate 90 more
degrees, and you get the long-axis view, revealing the anteroseptal and
posterior walls. Voila! You’ve seen all the walls of the heart.
As time passes, you’ll get to know what each view can “do” for you.
Now go transgastric, and you see all this stuff in cross section.
This systematic look at the walls of the heart will help us later when we
study coronary anatomy. (Preview: By knowing which wall you’re look-
ing at and which coronary feeds it, you can tell which coronary vessel is
not working. Ischemia leads to wall motion abnormalities and bingo! You,
Sherlock Holmes, MD, will nail the diagnosis.)
Knowing which wall is which seems a little tough at first, but a little brutal
memorization early on will pay off handsomely later.
Need a little crutch? Try this. Draw a cross section first and get those
walls down. Then, draw lines connecting each to its opposite wall.
That will get you to link these walls in pairs and keep you from getting
mixed up.
72 Board Stiff TEE
“WALL PAIRS” IN CROSS SECTION
Inferior Anterior I Posterior Anteroseptal

Septal Lateral P
S
L
AS
A
Schematic of LV in Cross Section
We will break these walls down further into segments later on, in
(Segmental Left Ventricular Systolic Function) of this outline. But before
you can know the wall segments, you need to know the walls them-
selves, so work on just that for now.
CARDIAC VALVES
Back to Med School for a minute.
The mitral valve is between the left atrium and the left ventricle.
The aortic valve is between the left ventricle and the aorta.
The tricuspid valve is between the right atrium and the right ventricle.
The pulmonic valve is between the right ventricle and the pulmonary artery.
All valves have three leaflets except the mitral valve, which has two.
Too simple for you? Believe it or not, it’s worth reviewing because, in a
test or in a hairy case, you can and do get amped out and go, “Wait,
that’s the…uh…”.
It is comforting to know that there is nothing we are incapable of

forgetting.
CARDIAC CYCLE AND RELATION OF EVENTS

RELATIVE TO ECG
Again, this is Med School redux, but it’s worth rehashing to make sure
you have it all down ice cold.
Break it down into sections. Since it’s a “cycle”, you can start wherever
you want.
Let’s start at the P wave of the EKG.

Atrium contracts, blood flows through the mitral valve into the left
ventricle. And on the right side? Atrium contracts there, too, and
blood flows from the right atrium into the right ventricle. Is more going
on? Well, yes. There is some backward flow into the pulmonary veins
at the time of atrial contraction, too. And on the right side? Does it
make sense there might be a little backward flow there too? (There
are, after all, no valves to prevent it.) Yes, by golly, there is a little
backward flow there, too, into the two “feeders” of the right atrium,
the inferior and superior venae cavae. Should there be a little back-
ward flow down the coronary sinus? That, too, lacks any valves to
prevent backward flow. My guess (I never read this or heard it men-
tioned in any lecture) is yes.
God all fishhooks, Batman, all that going on just with the stupid P wave.
I thought this section would be simple!
On to the QRS complex.
First, recall how the electricity travels through the ventricle.
As the ventricle depolarizes, the ventricle contracts, slamming the mitral

and tricuspid valves shut, and opening the aortic and pulmonic valves.
Oh, that was easy, not nearly so complex as that damned P wave.
Now, the ST segment.
After the ventricles are done contracting, the aortic and pulmonic valves
close, and the ventricles continue to relax (isovolumic relaxation) until the
pressure falls so low that the mitral and pulmonic valves can open and
start filling the ventricles.
That’s what goes on with the heart itself. It’s worth taking a second look
at this stuff. This time we’ll look at the CVP and the SGC and review what
goes on and when.
All those descents and letters and stuff are a pain in the ass, no doubt.
(Sort of like the Kreb’s cycle; you memorize it a few times in school, then
promptly forget it after the test.) But, alas, the docs giving the TEE review
course went over these more than once, so it looks like you have to learn
it again.
A wave—pressure increases from atrial contraction
X descent—in systole, as the ventricle contracts, the atrium is sort of

“pulled down” and the pressure decreases
V ascent—venous blood flows into the atrium, increasing the pressure
Y descent—the tricuspid valve opens, pouring blood into the right

ventricle and decreasing the pressure in the right atrium
74 Board Stiff TEE
What makes this interesting, of course, is when things go wrong. Regurg,

stenosis, congenital malformations, all kinds of things can throw that
waveform off. But you have to know the normal wave to make sense of
the abnormal.
QUESTIONS
1. Regarding the sector to the right:

Structure A is: ______________
Structure B is: ______________
LA B
AML NCC
Ao
LVOT
RCC
LV
RVOT
2. In the figure titled “20 views” identify:

A:
B:
C:
D:
B D
A
C
3. In the figure titled “20 views”, the artery that supplies E is:
1. LAD
2. RCA
3. Circ
4. PDA
5. Palm treo PDA
4. In the figure titled “20 views”, the artery that supplies F is:
1. LAD
2. RCA
3. Circ
4. PDA
5. Femoral
B
A
F
C G
D
E H
ME mitral commissural ME AV SAX
5. In the figure to the right identify:

A:
B:
C:
D:
E:
F:
G:
H:
I:
ANSWERS
1. A: Way at the back is the oblique sinus.

B: In that space rarely seen is the transverse sinus.
2. A = P3
B = A1 or A2
C = P2
D = A2
3. The artery that supplies E is the circumflex.
4. The artery that supplies F is also the circumflex.
5. A = P3
B = A2
C = P1
D = Posterior wall
E = Ant-lateral wall
F = Non-coronary cusp of aortic valve
G = R or L pulmonary valve leaflet
H = Anterior pulmonary valve leaflet
I = Right coronary cusp of aortic valve
Reference
[1] Shanewise JS, Cheung AT, Aronson S, et al. ASE/SCA Guidelines for performing a comprehen-
sive intraoperative multiplane transesophageal echocardiography examination: recommenda-
tions of the American Society of Echocardiography Council for Intraoperative Echocardiography
and the Society of Cardiovascular Anesthesiologists Task Force for Certification in Perioperative
Transesophageal Echocardiography. Anesth Analg 1999;89:870–84.
CHAPTER Pericardium and Extra-
10 Cardiac Structures:
Anatomy and Pathology
Enrique Pantin and F. Luke Aldo
There are so many things surrounding the heart that no one pays atten-
tion to!
It is all about the heart though, so who cares about all that other stuff.
Right? Wrong!
Like a lot of things in life, we forget that it is not about the “prima donna”,
but about the team! After all, there is no “I” in team, but wait a second,
there is a “ME”. Alright, never mind, let’s move on!
THE PERICARDIUM
n Surrounds, protects, supports, limits chamber dilation, and

lubricates, allowing the free motion of the heart.
n Provides entry and exit passages to the heart.
n Is a medium-sized bag with lots of holes and tubes crossing it to
enter or exit the heart:
u superior vena cava (“A”)
u aortic root (“B”)
u main pulmonary artery (“C”)
u pulmonary veins (right “D” and left “E”)
u inferior vena cava (“F”)
B
C
D E
77
78 Board Stiff TEE
The aortic root (“B” in the image above) is one of the structures the peri-
cardium covers, so if the root decides to rupture, well that patient is so
out of luck… cold and dead! As in ruptured aortic root dissection with
exsanguination into the pericardial sac→pericardial tamponade→that
light at the end of the tunnel…
There is a club composed by the “extra-cardiac structures team” whose

members can be seen by TEE most of the time but they are not too
happy with the lack of credit. Everybody talks about the heart, but what
about us?
n Ascending aorta.
n Aortic arch and its branches.
n Descending thoracic aorta.
n Upper abdominal aorta and its branches.
n Internal jugular veins.
n Innominate vein.
n Azygos vein.
n Trachea (yeah, we know you can’t see me but you know where I am
because I don’t let you see other guys!).
n Lungs, and pleural cavities.
n Thymus (in children).
n Spine, vertebral disks, and spinal cord (just bits of it can be seen).
n Stomach and its content or lack of it.
n Liver.
n Spleen.
n Kidneys.
n Other stuff like the tongue could be seen but it won’t be TEE but
oral ultrasound!
These are all members of the “extra-cardiac structures team”, they are
the majority, but this still sounds like a dictatorship by that narcissistic
heart!
As the TEE probe is advanced through the esophagus and into the stom-
ach we can image several structures besides the heart.
n Starting from the esophageal entrance we can see the main neck
vessels (the carotid arteries and internal jugular veins)
u can be used to guide central line placement, though I would NOT
recommend this in the awake patient!
n In the esophageal upper 1/3, we can see part or all of the arch
vessels
Chapter 10 Pericardium and Extra-Cardiac Structures: Anatomy and Pathology 79
u almost always the left subclavian, and sometimes the others

u distal aortic arch
u innominate vein
u left and right upper lung and pleural spaces
n In the mid 1/3 of the esophagus, the trachea creates a blind
spot, and we miss the distal ascending aorta, proximal arch, and
proximal to mid left pulmonary artery, but we can see:
u ascending aorta
u main pulmonary artery
u right pulmonary artery
u sometimes part of the left pulmonary artery
u proximal and mid thoracic aorta
u SVC
u right upper pulmonary vein

u transverse sinus
u left and right mid lung and pleural spaces
n In the lower 1/3 of the esophagus, we can see:
u pulmonary veins
u distal thoracic aorta
u IVC
u left and right lower lungs and pleural spaces

n From the transgastric window we can see:
u stomach and its contents
u liver
u upper abdominal aorta

u often the celiac trunk, SMA, spleen, and kidneys as well
Because the esophagus, our magic TEE window, is all the way in the
back of the chest, we decided to do a drawing from the esophageal
perspective. Then we took the back of our drawing away, including the
spine and rest of the bones, and applied some crude “X-ray” views to
see what lies in front of it. This is probably the only time the esophagus
finished first in a coronal view anatomical race. Congratulations Mr. “E”!
n trachea and lungs are gray
n stomach and esophagus are dotted gray/black
n rest of the structures are black
L = left and R = right; PA = pulmonary artery, P = pulmonary veins,

H = heart, L = liver, S = spleen, and K = kidney.
80 Board Stiff TEE
S
V
AA C
PA
B B
D P A PA
O
P A A R S RPA
V
P T C
L A P R
S A I L
O V
K C
K
n Did you understand the drawing?, I didn’t… If you didn’t, don’t

kill yourself over it, it is a pretty bad drawing. My partner did the
drawing, so call him and let him know you are happy he is a doctor
and not an artist!
n If you understood it, you are a genius!... then skip the following
sentence. If you did not understand it, then continue reading and
do as you are told. Go to your anatomy book and do a little review.
Now pretend you are the esophagus and try to imagine how all of
your neighbors look from where you are.
How can we see fluid on TEE?

n All potential spaces in the chest and abdomen (pericardial, pleural,
abdominal, sub-diaphragmatic, and hepato-renal) have the
potential for fluid accumulation.
n Depending on the location, amount, and speed of accumulation,
it can present as a clinically silent finding on TEE or it can cause
hemodynamic compromise.
n Fluid is usually seen as black on echo, but if the fluid has
solidified, as in the case of clotted blood, it can look just as the
liver or lung atelectasis does!
In a transgastric mid-short-axis view below, we can see lots of stuff

besides the heart!
n Gastric lining at the top, note the gastric rugae (those very tiny
indentations in the very top of the echo image).
n Left lobe of the liver (L).
n Pericardial reflection (that white line between “L” and the heart).
n Moderate-sized focal image “C”, suggestive of clotted blood:

u almost looks like liver does
u looks very similar to a layer of epicardial fat and can trick even
the experts!
u the history and additional findings will help define what the heck
this is.
n Right (R) and left (LV) ventricular cavities.
n Distal to the heart is more pericardium and lung.
There are very few important questions about the extra cardiac struc-
tures in the fast-paced world of anesthesiology and acute care. Usually
questions include:
n “Is there a pericardial effusion or not?” and if there is,
u “is it tamponade or not?”
n “Is there an aortic dissection?”
n “Is there a transection?”
n “Is there an aneurysm?”
n “Is there a clot in the pulmonary artery or other evidence of a
pulmonary embolism?”
n “Is there a pleural effusion?”
The rest is by far secondary, technicalities we really don’t care too much
about! After all, we are here to diagnose cardiac abnormalities and things
that can immediately affect cardiac function, not to determine if the
patient had filet mignon or penne a la vodka for dinner last night!
The Pericardium—we are back here again!

n Is 1–2 mm thick.
n Is difficult to see by echo unless there is fluid on both sides of it or
it is very thickened.
n Can elicit some extra brightness on echo like it has its own light.
n Has two layers (fibrous and serous).
82 Board Stiff TEE
n Serous layer has visceral and parietal aspects:

u serous parietal layer is tightly bound to the fibrous pericardium
that separates it from the rest of the chest structures
u serous visceral pericardium is attached to the epicardium.
n The layers extend a couple of centimeters, incorporating the aorta

and main pulmonary artery.
n Confines the total volume the heart can handle at one time creating
a closed volume relationship among all cardiac chambers.
n This limited volume relationship is the basis for the changes seen
during effusions and restrictive or constrictive pericarditis.
n There is normally a bit of pericardial fluid or “oil” (normally 5 to
10 ml and rarely up to 50 ml) that lubricates the heart so it can
dance without causing too much noise. Just like a car engine needs
motor oil, so does the engine of the human body. Luckily, we don’t
need oil changes every 3000 miles!
n When the oil is too thick because the sac gets inflamed
(pericarditis) or if the sac gets stiff, the pericardial layers rub as the
heart moves and make some weird noises.
n When the oil level is too high, we call this a pericardial effusion.
n Several types of “oil” can fill the pericardial space:
u serum, sero-sanguineous fluid, blood, pus, solid things like
metastatic tumors, fibrinous strands, etc.
n Excess “oil” can be due to:
u idiopathic causes, inflammation, infection, post heart attack,
systemic conditions, malignancy, post trauma, surgery, radiation,
congestive heart failure, etc.
n Pericardial effusion, like everything in medicine, we like to grade
it, but there are no prizes, and the higher the grade AND speed of
accumulation the worse!
u can be all around the heart (“E” in the image below) or just
localized in an area (focal accumulation or loculated)
u effusion can squeeze the whole heart or just a particular area
u pericardial fluid or “effusion” can be:
tiny (minimal)
small (<1 cm thick of fluid accumulation)
moderate (1–2 cm)
large (>2 cm).
u speed of fluid accumulation is a key factor to determine how
fast the symptoms appear. Acutely an accumulation thicker
than 1 cm could be considered significant, and usually causes
tamponade
u putting together the symptoms (hemodynamic compromise or
not) and the echo findings, a diagnosis of tamponade or not can
be made.
n Pericardial-cardiac filling pressures are intimately related to

breathing.
n Normally during SPONTANEOUS inspiration there is a drop in
intrathoracic and intrapericardial pressure. This facilitates right-
sided filling, right ventricle stroke volume and a drop in blood flow
out of the pulmonary veins, resulting in decreased left ventricular
stroke volume.
n Normally during SPONTANEOUS expiration, intrathoracic
and intrapericardial pressures increase causing a drop in right
ventricular filling and stroke volume. This provides more space to
the left ventricle and causes the squeezing of blood from the lungs
into the left ventricle, resulting in an increased left ventricular stroke
volume.
n This cyclic variation in stroke volume during SPONTANEOUS
breathing results in a less than 10 mmHg of inspiratory systolic
systemic pressure drop during normal conditions.
n If this systolic blood pressure variation exceeds 10 mmHg it is
called “pulsus paradoxus”. During conditions that increase
respiratory effort (COPD, acute asthma, etc.), hypovolemia, or
tamponade this pressure variation is greatly exaggerated.
n During MECHANICAL ventilation, the intrathoracic pump-
sucking effect created by the negative pressure during
SPONTANEOUS inspiration is lost and things get much worse for
the blood pressure if there is tamponade. During MECHANICAL
ventilation, the ventilation-pericardial pressure/cardiac filling
relationship is reversed and the inspiratory thoracic pump is
GONE! All this stuff is easily seen if the patient has an arterial
line (top tracing) and also if left ventricular filling patterns are
84 Board Stiff TEE
measured using PWD (middle tracing) through the mitral valve.

“I” = inspiration; “E” = expiration.

E I E I
n Normally the respiratory variation for tricuspid inflow velocity

(this is proportional to ventricular filling) is less than 25% and
for mitral less than 15%. This is all very scientific, but it is better
just to do simple math: symptoms + 2D echo finding = diagnosis.
n Cardiac chamber collapse during diastole is diagnostic of
tamponade. Usually tamponade is a clinical diagnosis with imaging
support, but sometimes chamber collapse can be seen before
symptoms are clearly seen. If a patient had a thick right ventricle,
collapse may be absent, despite having tamponade.
n If the pericardial sac gets stiff, due to inflammation, tissue
infiltration, or calcification, then it can affect the heart motion
and filling causing restrictive and/or constrictive pericarditis.
It is very hard to “see” pericardial sac thickening, stiffness, or
calcification by echo and most of the time we just see the effect of
the stiffness on the heart.
n CT and MRI are better diagnostic tools for pericardial layer imaging,
especially if there is no associated effusion.
THE AORTA
n Is the strongest tube we have, and one of the longest.

n Has six segments starting at the aortic valve annulus (annulus
located between “A” and “B” in the aortic figure), with a diameter of
about 3 cm, the sinus of Valsalva (at “B”), sinotubular junction (area
connecting segments “B” and “C”), ascending aorta (“B”+“C”, 5 cm
long), arch (segment “D”, from origin of innominate artery to end of
left subclavian artery), and descending aorta (segment “E”, starting
after left subclavian, and “K” ligamentum arteriosum and continuing
to the descending thoracic and abdominal aorta).
n The “aortic root” includes the aortic annulus up to the proximal
ascending aorta, and is included in the pericardial sac.
n The ascending is contained, with the pulmonary artery trunk, in the
pericardial sac and can be divided into the root with its sinus of
Valsalva, sinotubular junction, and ascending aorta.
n The aorta ends at the level of the 4th lumbar vertebra with about
1.75 cm in diameter as it bifurcates into the common iliac arteries.
n The coronary arteries are the only branches of the ascending
aorta.
n The arch gives origin to the innominate artery, left carotid and
left subclavian, although there are many anatomical variations that
these vessels can have.
n The descending aorta gives origin to intercostals and some
abdominal branches that often can be seen by TEE, like the celiac
trunk, superior mesenteric artery, and sometimes even the renal
arteries.
G H I
D
J
C K
E
F B
n The descending thoracic aorta in long-axis view looks like an evenly

sized black tube and it should have a smooth inner surface:
u the area at your left in the image below is distal and to your right
is proximal aorta
u distal in the screen we see again lung or just chest wall and ribs
depending on the esophageal to aorta alignment.
n CT and MRI provide excellent views of the aorta, its branches,

and of all extra cardiac structures, but they require IV contrast.
Additionally, the MRI/MRA requires lots of time. CT and MRI are
also both very “difficult” to do in the operating room!
86 Board Stiff TEE
n TEE can give a quick assessment of almost the entire aorta, from
origin to upper/mid abdomen. It is best to start your exam at the aortic
valve annulus and to try to follow the aorta all the way to the belly.
n It is best to examine the aorta in a short-axis view. This will prevent

you from missing something. Once an area of concern is identified
then a long-axis exam can add valuable information, such as length
of the pathology, which can help reconstruct a 3-D mental view of
the problem. We can actually do real-time 3-D views as well with
some machines.
n We are not going to give you the TEE multiplane angles
“recommended”. Instead you should try to:
u follow the aorta as you move from the aortic root to the
ascending
u once you lose the ascending aorta view, due to tracheal
interposition between the aorta and esophagus, turn the TEE
probe to the patient’s left (if you are standing at the head of the
bed) to find the proximal descending aorta
u once you find the descending aorta, by pulling/withdrawing the
TEE probe you reach the aortic arch
u after you have given a good look at the arch, try to find the arch
vessels, especially the left subclavian which is easily seen in
the distal arch. Make sure you do not pull the probe out of the
patient while looking at arch branches—we have done that!
u then, while reinserting the probe, try to follow the aorta down to
its most distal aspect in the abdomen
u sometimes the aorta can be tortuous and you must “follow” it by
turning the probe
u other times the aorta just disappears when you are following it
distally—it’s OK—these are just segments of the aorta that have
a poor echo window. In this situation, just prevent the probe from
turning left or right and continue to advance distally until the
aorta reappears
u NEVER advance the probe if you feel abnormal resistance.
Aortic aneurysm, dissection, and atheroma are the 3 big things. The
good thing is that we know what these things look like in the anatomic
specimen. With TEE it is only black-and-white images.
AORTIC ANEURYSM
n An aneurysm is a dilation greater than 1.5 times the normal size for
that structure.
n The ascending aorta is much larger than the aortic root and
sinotubular junction in the image below…what could this be? Yes,
you are correct an aneurysm it is!
n Sometimes we don’t know what the normal size is, but comparing
to other areas of the same structure usually gives us a hint that
things are bigger than they should be!
n Aneurysms can be isolated or associated with a cardiovascular
problem like HTN, aortic valve disease (AS/AI/bicuspid aortic valve),
Marfan’s, etc.
n Ascending aortic dilation can cause secondary aortic valve
insufficiency as well.
n Aneurysms greater than 5 cm or a rapidly growing (>5 mm/year) are
often used as indications for surgery. These are most commonly
CT- or MRA-based diagnosis.
n Patients with Marfan’s or other connective tissue disorders usually
have other cardiovascular anomalies. Thus a complete exam must
be done.
n Aneurysm of the sinus of Valsalva, like in any other portion of the
aorta, can also occur. Depending on which sinus is affected, it can
rupture into the right atrium (most commonly) or distort the annulus
and cause aortic valve insufficiency.
AORTIC PSEUDOANEURYSM
n Aortic pseudoaneurysm is a contained rupture of the aorta where

the aneurysm wall is made of non aortic tissues (surrounding
tissues).
n Usually has a narrow neck, like in the case of a ventricular
pseudoaneurysm.
n Can be spontaneous, secondary to an aneurysm, trauma, post
surgery, iatrogenic, or infection.
88 Board Stiff TEE
AORTIC DISSECTION
n Dissection occurs when a breach in the intima allows pressurized

blood to separate the intima from the medial layers. In the image
below note the double wall in the ascending aorta, typical of
dissection.
n Blood can propagate proximally, distally, or both between the

intima and medial layers.
n Can present as a clearly separated layer with a flow-like pattern,
often with several entry/exit points connecting the “true” and
“false” lumens (so called “fenestrations”).
n Sometimes it is difficult to find the “true” lumen, and color flow
Doppler can help in finding these fenestrations and define which
one is the perfusing lumen and which is not.
n The “true” lumen usually expands with systole and has a regular
shape (from circular to a flat tube).
n Dissections can also present as an intramural hematoma (5–10%)
and they must be differentiated from a smooth-layered atheroma.
Intimal layered calcifications (in the wall, below the plaque) and
close observation of the surface usually help distinguish the plaque
from intramural hematoma, where calcifications, if present, are in
the intimal layer of the hematoma.
n Dissection can be localized or diffuse, and occasionally it can
present as an intimal tear without dissection.
n Another way dissections can occur is of iatrogenic origin (cardiac
catheterization, post aortic cannulation, etc.), or when an ulcerated
atherosclerotic plaque suffers penetration into the intimal/medial layer.
n Dissections are classified as Stanford A or B (SA or SB) or DeBakey
I, II, or III (DB1, DB2, or DB3) types.
DB1 DB2 DB3

SA SA SB
u all dissections involving the ascending aorta or arch are

considered life-threatening emergencies and must be taken to
the operating room as soon as possible. These can rupture or
extend and cause tamponade, aortic insufficiency, myocardial or
cerebral ischemia or infarct, or exsanguination
u dissections occurring distal to the left subclavian artery
are managed medically unless there are signs of organ or limb
malperfusion. In this case, they can be managed by endovascular
techniques or operatively to restore compromised blood flow.
n Surgery of an aneurysm or a dissection:
u intends to prevent propagation of the dissection, its
complications, or rupture
u after repair of an ascending aortic aneurysm or dissection,
myocardial and aortic valve function must be assessed to make
sure coronary blood flow was not compromised and there is no
significant valve dysfunction
u if the dissection extended distally originally the distal false lumen
will persist after surgery, sometimes with flow in it. Chronic
thrombosis often occurs.
AORTIC PLAQUE
Aortic plaque or atherosclerosis is a common finding in our older or vas-

cular patients.
n Hypertension, diabetes, smoking, high cholesterol, and poor diet
(usually a Western diet; i.e. most of us!!!! I’ll take a Big Mac and
fries please. Oh and can you supersize that! STAT!) are all risk
factors.
n Plaque is often located in the arch and descending aorta, and is
less common in the ascending aorta.
n The most common site for plaque in the ascending is the right
sinotubular junction area and if calcified will give a nice black
shadow (see image below), as the ultrasound is pretty bad at
penetrating through calcium. As a result of the echo “shadow”,
we are not able to see beyond the calcification. If we want to see
what “lies beneath”, we will need to find this through alternative
imaging angles.
90 Board Stiff TEE
n Atheromas can take almost any shape and size, sometimes artistic,
mostly very scary! They can be flat, round, mountain looking,
pedunculated, mobile or not, as well as calcified or not.
n In this long-axis view of the descending thoracic aorta a large
atherosclerotic plaque can be seen, yes! that white blob attached to
the inner surface of the aorta.
n The bigger and more mobile they are, the higher risk for stroke and
embolic phenomena there is.
n We should define these plaques by their location, size (measure
from base to highest point), and if mobile or not.
n Aneurysm, dissection, and plaque can overlap in the same patient
making its management more complicated.
AORTIC TRAUMA
Aortic trauma is a distinct problem from dissection, but with the potential
of acute death as well—as opposed to chronic death? I tell you, my part-
ner was a bit sleepy when he wrote this stuff… .
n Most commonly occurs after blunt chest trauma, usually due to
high-speed impact.
n The aorta has several areas where it is relatively fixed (annulus to
heart, neck vessels, descending thoracic aorta fixed by intercostals)
to the chest and other areas where it is mobile (ascending and
arch).
n The aorta can rotate and twist at the aortic root, can bend at the
arch vessel area, and at the ligamentum arteriosum area.
n The aorta most commonly breaks at the root, arch vessel area, or at
its fixture at the ligamentum arteriosum area.
n If the transection is complete, kaput you are DEAD!
n Partial transections are what we see, and CT is the primary
diagnostic mode because it is part of the usual trauma workup.
n TEE can miss small tears in the arch and ligamentum area as they
are difficult to see with TEE due to tracheal interposition. Anyway
aortic shape disruption, adventitial hematoma, small evagination of
the wall, intraluminal hematoma, small flaps or tears can be seen.
n If you don’t see anything by TEE, but there is strong suspicion of a

transection, then a CTA or angiogram (much less used these days)
must be done.
n Aortic trauma can also be present with rupture of any other cardiac
structures: sinus of Valsalva into the right atrium, traumatic atrial-
septal defect, rupture of a papillary muscle (tricuspid or mitral),
aorto-caval fistula, etc.
AORTIC THROMBUS
n Aortic thrombi, are very rare, but we have seen them!

n They can form in the wall and look like a tumor.
n Usually discovered during workup for a source of emboli.
n They usually present as echo-dense, highly mobile structures.
AORTIC INFLAMMATION, COARCTATION,

AND INFECTION
Aortic inflammation, coarctation, and infection are such infrequent events

in the adult intraoperative echocardiography world that we will not com-
ment on them. Go read it elsewhere! But wait, sometimes you will see a
patient with Takayasu arteritis in the OR to be operated on for an aneu-
rysm. This inflammatory disease of the aorta occurs in young patients
and can involve the entire aorta.
PULMONARY ARTERY
Why do we care?
n It can tell us a bit about the chronic pulmonary vasculature
strain it suffers with chronic severe mitral regurgitation, pulmonary
hypertension (primary or secondary to asthma, COPD, etc.), acute
or chronic pulmonary embolism, etc. In all chronic cases it gets
BIG, and we don’t mean fat, but dilated like a nice round Italian
sausage.
n Did you know that a pulmonary embolism is one of the most
common causes of sudden unexpected intraoperative cardiac
arrest?!? But of course you knew! The other common causes
include acute myocardial ischemia, arrhythmias, tamponade, and
severe hypovolemia. ALL, but arrhythmias can have its diagnosis
“assisted” by TEE.
n As a rule made by us, the right (“R”) and left (“L”) pulmonary artery
should be 2/3 the diameter of the main pulmonary artery (“P”), and
the main PA and SVC (“S” = short-axis superior vena cava) should
be 2/3 of the ascending aorta (“A” = short-axis ascending aorta).
This “2/3” rule also applies to many other chambers and tubes in
the heart.
92 Board Stiff TEE
n In the image below, take note that the main PA has a similar
diameter to the ascending aorta, probably because there is some
chronic abnormality occurring with the PA.
n Sometimes we get lucky and can see an embolus occluding the

main or proximal PA branches, but most of the time we just see
signs of right ventricular strain. In cases of pulmonary embolism,
signs include PA dilation, RV dysfunction, RV dilation (“R”), tricuspid
insufficiency, dilated RA, bulging of the interatrial septum to the left,
and flattening of the interventricular septum (the so-called
“D”-shaped left ventricle (“L”) or a really squashed LV!).
Now what? We looked at the tubes going out of the heart. Now it’s time
for the incoming pipes.
SUPERIOR VENA CAVA, INFERIOR VENA

CAVA, AND THEIR COUSINS THE HEPATIC
VEINS
Once you get a nice 4-chamber view from the mid-esophageal window,
center the right atrium (“R”) in the middle of the screen and multiplane to
about 90 degrees. Most of the time you will get a nice bicaval view with
the SVC at the right of the screen and the IVC at the left of the screen. If
you multiplane a bit more, to around 120–140 degrees, you will see the
“modified bicaval view” like the beautiful one we got below.
In this modified bicaval view, we can see the left atrium (“L”), the inter-
atrial septum and its thinner/thinner area (the fossa ovalis), the right
atrium (“R”), the SVC (“S”), the IVC (“I”), the entrance of the coro-
nary sinus (“C”), and the right atrial appendage with its typical broad
base (“A”). The tricuspid valve (“T”) can also be partially seen, as well as
some of the right ventricle (“RV”).
If we advance the probe into the stomach following the IVC, we will see
the hepatic IVC (“I”) and the hepatic veins (“H”). Normally the IVC is less
than 2.5 cm in diameter. The hepatic veins can be used to assess the
inflow venous pattern as they lay parallel to the Doppler beam and thus
make it easier to evaluate with PWD or color flow Doppler.
The hepatic venous flow:

n Like the pulmonary venous flow, has 3 main waves, the “S”, “D”,
and “A” waves.
n Place the pulsed wave Doppler cursor, also called the “gate” or
“sampling volume”, 1 cm into the hepatic vein. Then we press the
PWD button and voila, a waveform for the hepatic venous flow is
displayed:
u “S” wave corresponds to ventricular systole. During this time,
the area of the heart with the closed tricuspid and mitral valves
(aka the base of the heart; I’d like to ask a few questions to the
person who named this!) is pulled down and a suction effect
facilitates forward flow to the atria
u Next the valves open and the “D” wave (diastolic) occurs as the
atrial blood volume emptying into the ventricles makes room for
more blood to move into the atria
u Finally, when atrial contraction occurs the “A” wave (atrial)
is generated because most of the blood is pumped into the
ventricles, but some is pumped retrograde into the hepatic or
pulmonary veins. This causes the “A” wave to inscribe below the
baseline. Yes, you figured it out! This is the so-called atrial flow
reversal and it is totally normal.
94 Board Stiff TEE
n In cases of severe tricuspid or mitral regurgitation, because the

valve is incompetent, blood flow is pumped into the atrium during
ventricular systole and from there into the hepatic or pulmonary
veins. The normal forward flow of the “S” wave is seen as totally
blunted or even reversed and inscribed below the baseline. This
tells us that blood is going into the hepatic or pulmonary vein in
ventricular systole instead of coming out of them and into the atria.
It’s pretty neat that we are able to follow blood flow in real time
without having to cut the heart open!
Well, well we are not done, but from here on it is much easier!
n The azygos vein, trachea, thymus (in children), and spine can be
seen, but add very little in acute care.
n For fun we can see the stomach and its contents thus having an
idea if there is some significant gastric content.
n From the gastric window, the liver and spleen are easily identified.
n Within the liver, the inferior vena cava has a normal diameter
change with respiration, suggestive of normal CVP.
u if there is a lack of IVC diameter change or the IVC is dilated this
is suggestive of elevated CVP. This is an easy way to have an
idea about what is going on with the right heart.
n The right kidney and the hepato-renal space (Morrison pouch),
as well as the subdiaphragmatic area, will show any fluid
accumulation in the right upper quadrant.
n We leave the lung and pleural space for last.
u TEE exam is never complete if we do not look at the left and
right pleural spaces
u lung can be seen with its typical aerated pattern
u if there is lung atelectasis or condensation it looks like liver.
Remember?
u pneumothorax is much more difficult to diagnose and we will
leave that for you to research!
u pleural effusions are easy to see, but we need to look for
them. The best view to start looking for pleural effusions is in
the descending aorta short-axis view. Anything we see in this
location, we will know belongs to the left chest, as seen in the
following image. This is a short-axis view of the descending
aorta with normal lung (“L”), atelectatic lung which looks very
similar to the liver in echo (“A”), pleural effusion (“E”), and the
chest wall with the ribs and all (“C”).
n After we are done with the left chest we have two options, you can
just rotate to the right at the level of the atria until you find a right
effusion or normal lung. You could also simply find the liver and pull
the probe straight back from there until you see the right lung. Be
careful not to pull out so much or the TEE probe will come out of
the patient’s mouth!
Now it is your turn to grab that TEE probe and start trying to find all the
cool stuff we talked about. Lots of extra-cardiac stuff and many things to
see, some more important than others, but all fun!
Bibliography
Armstrong WF, Ryan T. In: Feigenbaum’s echocardiography, 7th edn. Philadelphia: Lippincott
Williams & Wilkins; 2009.
Baumgartner H, Hung J, Bermejo J, et al. Echocardiographic assessment of valve stenosis: EAE/
ASE recommendations for clinical practice. J Am Soc Echocardiogr 2009;22:1–23.
Brown JM, O’Brien SM, WuChangfu et al. Isolated aortic valve replacement in North America com-
prising 108,687 patients in 10 years: changes in risks, valve types, and outcomes in the society
of thoracic surgeons national database. J Thorac Cardiovasc Surg 2009;137:82–90.
Isolated aortic valve replacement in North America comprising 108 687 patients in 10 years:
Changes in risks, valve types, and outcomes in the Society of Thoracic Surgeons National
Database.
Kisslo JA, Adams DB. Doppler Evaluation of Valvular Stenosis #3 <http://www.echoincontext.com/
doppler03.pdf>
Mathew J, Swaminathan M, Ayoub C. In: Clinical manual and review of transesophageal echocar-
diography, 2nd edn. New York: McGraw-Hill Professional; 2010.
Shanewise JS, Cheung AT, Aronson S, et al. ASE/SCA guidelines for performing a comprehensive
intraoperative multiplane transesophageal echocardiography examination: recommendations
of the American Society of Echocardiography Council for Intraoperative Echocardiography and
the Society of Cardiovascular Anesthesiologists Task Force for Certification in Perioperative
Transesophageal Echocardiography. J Am Soc Echocardiogr 1999;12:884–900.
Zoghbi WA, Enriquez-Sarano M, Foster E, et al. Recommendations for evaluation of the severity
of native valvular regurgitation with two-dimensional and Doppler echocardiography. A report
from the American Society of Echocardiography’s Nomenclature and Standards Committee and
the Task force on valvular regurgitation, developed in conjunction with the American College of
Cardiology, Echocardiography Committee, the Cardiac Imaging Committee Council on Clinical
Cardiology, the American Heart Association, and the European Society of Cardiology Working
Group on Echocardiography. J Am Soc Echocardiogr 2003;16:777–802.
CHAPTER Pathology of the Cardiac
11 Valves
F. Luke Aldo and Enrique Pantin
Cardiac valves… hopefully somewhere somebody talked about normal

valves…
Cardiac valves are like any other valve, they help direct flow in the
desired direction, and the cardiac ones have to do this about 3–3.5 billon
times without failing. I want the same warranty for my car!!! Simply, they
have to open completely and then close completely.
NORMAL VALVE AREA CM²

Aortic valve 3–4
Mitral valve 4–5
Pulmonic valve 3.5–4.5
Tricuspid valve 5–8
No matter which one we are talking about, the four cardiac valves all
have to do the same thing, open and close and nothing else… talk about
a boring job. The valves can only work if there is blood being pumped
through the heart, usually by the heart, but sometimes by a superhero
trying to save a life by pumping on the chest. There are only two main
problems with valves: insufficiency/leaky/open when it should be closed
and stenosis/narrowed/somewhat closed when it should be open. There
are however several reasons why they get messed up. Blood pumped
through relatively narrow holes (which the valves are) causes certain
blood velocity increases.
Normal systolic blood velocities through the valves are:
Aortic valve <1.4 m/s

Mitral valve <1.2 m/s
Pulmonic valve <1 m/s
Tricuspid valve <0.8 m/s
Valves and their supporting structures can sustain several types of dam-
age that can cause them to malfunction. For simplicity, valve dysfunction
has been categorized as stenosis or insufficiency. Before we continue
any further we must always make sure in cases of valvular stenosis that
the problem is at the valve level and not a sub- or supra-valvular ste-
nosis. It takes years to develop tight valves, and thus it takes a while to
cause problems. Leaky valves can occur over years, but also acutely. As 97
98 Board Stiff TEE
you can imagine, acute valve leakage is not well tolerated by the heart.
This often needs immediate medical intervention and usually surgical
repair as the heart has no time to compensate for the extra volume load.
Aortic valve stenosis due to senile calcific degeneration is the most com-
mon valve problem in the elderly (>65 years old). Is this really that old?!?
In the figure below we see a short-axis view of a normal aortic valve (A).
How nice and secure it looks closed, and when it opens a truck can drive
through its orifice! This figure is drawn anatomically correct, but as you
know when we do TEE, the top will be on the bottom, and the left will be
on the right. Unfortunately a lot of stuff in echo is not done anatomically
correct because some genius a long time ago decided to be fancy!
A B C D
Rheumatic heart disease (B) is the most common cause of mitral stenosis
in general, and is a common cause of aortic stenosis in less developed
countries. Rheumatic disease starts with commissural fusion at the leaf-
let coaptation points and works its way outward towards the perimeter of
the valve. This early commissural calcification often gives the so-called
“hockey stick” appearance. As we mentioned earlier, in developed coun-
tries nobody beats senile calcific aortic stenosis (C). Here calcification
starts at the perimeter of the valve and works its way in toward the leaf-
let edges, which is the exact opposite of rheumatic disease progression.
Congenitally defective aortic valves (bicuspid, unicuspid, etc.) can get tight
much sooner. A bicuspid aortic valve (D) is the most common cause of
aortic stenosis in patients less than 55 years old. Note the upper and larger
lower valve leaflets fused with a clearly seen raphe, and the smaller left
coronary cusp. The valve comes defective from the factory and you can't
return it. Where is the consumer protection! Nature is definitely smarter
than us because they have no lawyers involved in their business!
Too much, just see the table below for a list of causes of valvular prob-
lems, not necessarily in any particular order.
We are going to concentrate on the two valves that most commonly

develop problems, the aortic and the mitral. When assessing valves
we use 2-D imaging and Doppler-related measurements: continu-
ous wave Doppler (for faster velocities, usually greater than 2–2.5 m/s),
Chapter 11 Pathology of the Cardiac Valves 99
Table 1
STENOSIS INSUFFICIENCY
Aortic Calcific Calcific
Bicuspid Rheumatic
Rheumatic Myxomatous
Unicuspid Congenital
Infectious
Traumatic
Annular dilation
Dissection
Aneurysm
Mitral Rheumatic Annular dilatation
Degenerative calcification Leaflet perforation
Hyperparathyroidism Ruptured chord
LES Ruptured papillary muscle
Rheumatoid arthritis Rheumatic
Systemic carcinoid Dilated cardiomyopathy
Amyloid Prolapse
Post radiation Marfan
Traumatic
Tricuspid Rheumatic Annular dilation
Endomyocardial fibrosis Pulmonary hypertension
Carcinoid Right ventricular dilation
Rheumatic
Ebstein's anomaly
Carcinoid
Infectious
Marfan
Prolapse
Pulmonic Congenital Pulmonary hypertension
Rheumatic Annular dilation
Carcinoid Carcinoid
Sarcoma Marfan
Rheumatic
Infectious
Trauma
pulsed-wave Doppler (for slower velocities, anything less than 2–2.5 m/s),

and color flow Doppler (will give us an idea about what the blood flow
pattern is). We can also use 3-D, but this is a bit esoteric for us. We know
what the normal velocities through the valves are and that if the valve
gets narrower, in order to allow the passage of the same stroke volume
the blood velocity through the smaller orifice will increase proportionally.
This is valve stenosis in action. That is it, you’ve got it! End of chapter,
we can stop writing! You wish! Valvular regurgitation is diagnosed when
we see diastolic valvular flow in the opposite direction it should be going.
100 Board Stiff TEE
Now we are really done! Just kidding, we will explore stenosis and regur-
gitation a bit more.
You already have read that there are several formulas used to calculate
blood velocity using the Doppler effect. Well it is quite simple and we
really only need to memorize two Doppler-derived formulas:
Simplified Bernoulli equation

Pressure gradient through a narrow area 4 Doppler velocity 2

P = 4V 2
Continuity equation
In a tube with an area of focal stenosis:

Velocity1 Area1 BEFORE or AFTER the stenosis
Velocity 2 Area 2 AT the stenotic area
Integrating the area under the velocity curve obtained by Doppler we get
the Velocity Time Integral (using VTI gives us a more accurate result than
just the velocity).
This can also be written as:

Velocity Time Integral1 Area1 Velocity Time Integral2 Area 2

VTI1 A1 VTI2 A2
There are a bunch of images and numbers used to categorize the degree
of valvular dysfunction. You should always look at the supra-valvular, val-
vular, and infra-valvular areas. For the aortic valve the mid esophageal long
and short axis, and then the deep transgastric views are ideal. The first
two will provide a lot of anatomical data and the last one is the best for
Doppler measurements. In the ME AV LAX view (during systole and dias-
tole) the areas above, below, and at the level of the valve can be examined
in 2-D and then color flow Doppler. The first image below is named Mid
Esophageal Aortic Valve LAX (Long Axis) view and is usually obtained at a
multiplane angle of about 130 degrees. The image was taken in ventricular
diastole; note that the mitral valve is open, and the aortic valve is closed.
LA = left atrium; P = posterior mitral valve leaflet; A = anterior mitral valve
leaflet (the anterior mitral leaflet is always the closest to the aortic valve);
LV = left ventricle; AO = ascending aorta. The anterior mitral leaflet in this
image corresponds to a segment of the mitral leaflet called “A2”. “A2”
length measurement correlates very closely with the ideal mitral valve ring
size that needs to be used when a surgeon performs a mitral valve repair in
cases of mitral regurgitation. Hey, you can teach this to your surgeon! The
second image is in ventricular systole. Notice the closed mitral valve and
the amount of mitral leaflet coaptation (arrow), usually greater than 8 mm.
A measurement of the aortic valve annulus is taken during systole (white
line). This is the best view to measure the aortic annulus.

At the valvular region, the annulus and leaflets must be closely examined.
You also must take a look at the chamber above and below the valve to
see the effects of the valvular problem on these chambers. Finally, in cases
of mitral or tricuspid insufficiency you must see how the regurgitation
affects the pulmonary or hepatic venous flow into the left or right atrium.
If the venous flow is reversed into the pulmonary or hepatic veins during
systole, there is a high chance that the valvular insufficiency is pretty bad!
Because we know you have such an open mind, we are going to talk
about the two valve problems at once! Not really talk, but just put some
stuff into a table. What do you expect? Don't you know by now we want
to finish writing this stuff! Just take a look at the table below, and then
take a deeper look. Dissect it, enjoy it, and try to make sense of it! We
show you several ways, but not all the ways the valve pathology can
present. For example, there could be aortic insufficiency due to calcified
leaflets or annular dilation. We will not talk about cardiac symptoms or
speed of development of the valvular problem, otherwise we’ll be here
forever and most likely you will fall asleep!
Now that we have an idea of what to look for we will try to grade the
severity of the valvular problem. PLEASE always make sure to set your
CFD scale ≥50 cm/s to avoid over reading flow patterns and scaring the
s#@* out of your surgeon after a mitral valve repair! It might be humorous
to try on April Fools day, but I wouldn’t make a habit out of it unless you:
(a) enjoy watching your surgeon stomp his feet like a 2-year-old child
who can’t get their way
(b) like to see him launch a scalpel across the room like he’s playing a
competitive game of darts
(c) want to hear him curse like a truck driver
(d) want to make him realize he is not the omnipotent deity he thought
he once was
(e) all of the above.
Table 2
VALVE CHAMBER SYSTOLIC
PULMONARY
ANNULUS ANNULUS LEAFLET LEAFLET MOTION CFD BEFORE THE AFTER THE
VEIN FLOW
DILATION CALCIFICATION CALCIFICATION VALVE VALVE
AI NO NO YES Restricted Diastolic Dilated LV or Mostly normal Unchanged
normal LV
YES NO NO Normal but Tethered Diastolic Dilated LV or Mostly Dilated Unchanged
normal LV
AS NO YES or NO YES Restricted Systolic turbulent LVH Normal or
Dilated
AS + AI NO YES or NO YES Restricted Systolic turbulent LVH Normal or Unchanged
diastolic dilated
MR YES NO NO Normal Systolic to LA Dilated LA Mild dilated LV Unchanged
blunted or reversed
depending on
severity
NO NO NO Perforated Systolic to LA Dilated LA Mild dilated LV
NO NO NO Rupture chord or Systolic to LA Dilated LA Mild dilated LV
papillary
NO YES YES Restricted Systolic to LA Dilated LA Mild dilated LV
MS NO YES YES Restricted Flow convergence Dilated LA Normal size LV
to valve from LA
MS + MR NO YES YES Restricted Systolic to LA Dilated LA Normal or Similar to mitral
flow convergence dilated LV regurgitation
to valve from LA
AI = aortic insufficiency; AS = aortic stenosis; MR = mitral regurgitation; MS = mitral stenosis; LVH = left ventricular hypertrophy; CFD = color flow Doppler.
Ok, here we go!
We start by having practiced enough 2-D imaging to be able to obtain

the 20 standard ASE TEE views. If you can't, please STOP, and go back
until you can identify them and their components. Otherwise, you will say
our chapter stinks, when in fact it is you.
The following TEE web page is an AMAZING teaching tool, go there and
study it:
http://pie.med.utoronto.ca/tee/TEE_content/TEE_standardViews_intro.
html
Done? Can you obtain the 20 standard views? Can you do more?
Excellent, then let's move on! We will start at the Mid Esophageal Four-
Chamber (ME4C) view that is obtained at a multiplane angle of ZERO
degrees. In this view we can see the atria (size, smoke, clots, append-
age, and veins draining into them), mitral and tricuspid valves, and both
ventricles all in one shot. Are we efficient or what?!? Below is the ME4C
view in ventricular diastole: RA = right atrium; AS = tricuspid valve
(A = anterior leaflet; S = septal leaflet); RV = right ventricle; LA left
atrium; AP = mitral valve (A = anterior leaflet segment “A3”; P = posterior
leaflet segment “P1”); and LV = left ventricle.
From there we have to decide if we want to start with the mitral or tri-
cuspid valve. Whatever valve we decide to check first, we turn our TEE
probe to make sure we place it in the middle of the screen. Then we
take a look at all its components in 2-D first. You want to see if the valve
looks normal, if it opens and how much, if there is motion restriction, and
if things are hanging from it or ruptured. After the 2-D exam a CWD to
measure the maximum velocity across the valve should be done. This is
super important in stenosis. Let’s talk a bit more about mitral/tricuspid
stenosis. With the CWD information we can calculate the mean pres-
sure gradients across the valve, by tracing and integrating (with the TEE
machine software) the area under the curve for the mitral or tricuspid dia-
stolic pressure tracing.
Mitral inflow patterns obtained with CWD can be seen below. All tracings
shown below the baseline mean that flow is moving away from the trans-
ducer, and all shown above, duh, mean that flow is moving towards the
transducer! You feel pretty smart, don't you? We decided to place several
patients in one drawing. “A” and “B” demonstrate normal CWD tracings
104 Board Stiff TEE
through the mitral valve in diastole and systole. The Doppler cursor is
placed running through the middle of the mitral valve. Take a look at a nor-
mal valve tracing during ventricular diastole “A”. You did notice the two
peaks of the “A” tracing right? The early one called the “E wave” repre-
sents passive ventricular filling, and the late one, the “A wave”, represents
additional ventricular filling due to the atrial kick. Yes indeed, the “A wave”
is named after the atrial kick. When the mitral valve closes, during ven-
tricular systole, we see a normal mitral valve tracing “B” (no Doppler sig-
nal in diastole because the valve is 100% competent). The next patient is
Mr. C with a typical severe mitral stenosis tracing “C”. Note the increased
velocity, the little “E wave” deceleration slope, and the large area under the
curve for “C”. This is reflective of a high gradient across the mitral valve, all
indicative of significant mitral stenosis. Finally, in the case of mitral regurgi-
tation we see patient “D”.
6
A B C D
MITRAL STENOSIS GRADING BY DOPPLER MITRAL VALVE AREA

Mild <5 mmHg mean pressure gradient >1.5 cm²
Moderate 5–10 mmHg 1.5–1 cm²
Severe >10 mmHg <1 cm²
A mean pressure gradient >5 mmHg is suggestive of severe tricuspid

stenosis and an area of <1 cm².
Another calculation we can do with the aid of the TEE machine software
is the pressure half time. The deceleration slope of the mitral “E” wave
is traced from the mitral inflow envelope generated by CWD and the
machine calculates a pressure half time number. The longer, slower, and
less complete it takes the atria to empty, the flatter the slope will be and
thus the smaller the valve size. Mitral valve area = 220/mitral pressure
half time, and tricuspid valve area = 190/TV pressure half time.
Mitral and tricuspid regurgitation is much easier, especially to differenti-

ate between none or mild (we all can have a bit of leaking in these valves)
and severe leakage! The most helpful tool is the CFD. Remember to set
the color flow Doppler scale to ≥50 cm/s, otherwise we will be over read-
ing and calling things severe that are not. Starting from the ME4C view,
we look at the valve and multiplane to see all sides of the valve. In the
2-D image below, obtained in ventricular systole, it is pretty clear some-
one bit a piece off of the mitral valve leaflets and a gap can be seen. We
then turn on our secret weapon, CFD, and a large, gigantic, humongous
flare of color can be seen across the mitral valve. This is severe mitral
regurgitation. A wimpy barely visible flare across the tricuspid valve is
seen as well. This qualifies for trace tricuspid insufficiency. Please do not
panic, we all have a bit of tricuspid regurgitation and other flares as well.
Before you decide to make any "TEE diagnosis" make sure you interro-
gate the whole darn heart! Too often, we stand up with our heads held
high and announce to the world with a loud and proud voice that there is
no valvular problem or that the heart function is great! Then, a nanosec-
ond later we realize we missed the view that showed severe regurgitation
or that the patient had a humongous apical aneurysm and its effective
ejection fraction is only 5%!!!!!!!!!!!!!!
Before we go into fancy methods of valve assessment in the mid esopha-

geal 4-chamber view we need to center the mitral valve in the middle of
the screen and at zero degrees scan the entire valve. First, we slowly pull
out the TEE probe until the valve disappears and then advance it back in
until the valve disappears again. What we just did was scan the valve from
the most superior area of the valve, the so-called “Area 1”, then as we rein-
serted the probe we passed through "Area 2", and finally before we lost
the view of the valve we saw “Area 3”. The posterior mitral valve usually
has three clearly differentiated scallops, the most superior numbered “1”,
the middle, "2", and the most inferior, "3". The corresponding opposing
portions of the anterior leaflet are named the same way. This mitral valve
nomenclature allows for uniform communication among surgeons, cardiolo-
gists, and anesthesiologists. From the Transgastric Basal SAX (short-axis)
view of the LV, we can see these three mitral valve segments as well. This
view is obtained at ZERO degrees as well with the probe inside the stom-
ach and moderate degree of ante-flexion of the probe tip.
106 Board Stiff TEE
R = right ventricular outflow track; A = anterior leaflet of the mitral valve

with segments 1 (the most superior), 2, and 3 (the most inferior), and
P = posterior leaflet of the mitral valve. This view is great to localize
regurgitant jets, but not to grade them as the color Doppler is almost per-
pendicular to blood flow.
A few common ways to grade the severity of mitral and tricuspid regurgi-
tation are vena contracta measurements, regurgitant jet area, continuous
wave Doppler of the regurgitant jet, and pulmonary venous and hepatic
venous flows. If you want to get even sexier we can even obtain a PISA
(no, this has nothing to do with the Leaning Tower of Pisa…it stands for
proximal isovelocity surface area), which will be explained in another sec-
tion of this book, but if not then go read a more sophisticated echo book.
Vena contracta is simply a measurement of the narrowest portion of the
regurgitant jet, usually at the level of the leaflets. Obviously, the larger the
vena contracta the worse the regurgitation. The regurgitant jet area can be
obtained by simply tracing the jet with our magic trace button and track
ball on the TEE machine and the computer will spit out a number. It’s
that simple! CWD as we mentioned above will show different waveforms
depending upon the severity. A mild MR jet will have a soft density and will
be parabolic in shape, whereas a severe MR jet will be a very dense trian-
gular one. Lastly, we can explore flow reversal. If regurgitation is severe
enough it will affect even the veins draining into the cardiac chamber it is
leaking into. For example, normally during systole blood is flowing from
the pulmonary veins into the left atrium, but with severe MR, the regurgi-
tant jet is so powerful that it is actually reversing this flow and not allow-
ing the pulmonary veins to empty. Makes sense right? Of course it does!
The exact same thing applies to the hepatic venous flow when grading tri-
cuspid regurgitation. Now be careful, echocardiography is not about dis-
covering one finding in one specific view and slapping on a diagnosis. No!
Echocardiography is more like a murder mystery. You are Sherlock Holmes
and you are gathering as many clues as possible to solve the crime or in
this case make the diagnosis. The more clues you discover the more confi-
dent you can be in your diagnosis.
The pulmonic valve for TEE is like the red-headed step child that no one
likes. Why is this the case? The pulmonic valve is the furthest away from
our TEE probe and as a result, the hardest to image. In the case of pul-
monary regurgitation, there are no quantitative measurements to grade the
severity. We are left with making a qualitative assessment of the valve and
regurgitation. A thin jet with a narrow origin is likely mild and a large jet with
a wide origin is likely severe. Not very scientific we know. As for pulmonary
stenosis, a CWD can be shot down the valve to obtain a peak gradient.
Pulmonary stenosis can be graded depending on the PEAK pressure

gradient as:
Mild <36 mmHg
Moderate 36–64 mmHg
Severe >64 mmHg
The best view to shoot a CWD through the pulmonic valve is the upper
esophageal aortic arch short-axis view obtained at 90 degrees. One of
those 20 standard views that you are an expert at by now! This view is
nice because it allows for near parallel alignment of the CWD down the
pulmonic valve.
Wow, so many words! Finally we can discuss Mr. aortic valve. After get-
ting the valve in view we do the same stuff again. We evaluate the valve
with 2-D, look at the valve in a short and long axis, the annulus, and the
chamber before and after (LV and aorta). The Mid Esophageal Aortic
Valve SAX view of the aortic valve is obtained around 45 degrees of mul-
tiplane and allows for a pretty good view of the tricuspid and pulmonic
valves (“P”). Because the tricuspid is almost parallel to the Doppler cur-
sor, this view is commonly used to evaluate insufficiency or stenosis.
The aortic valve has 3 leaflets: a left coronary cusp (“L”), a right coronary
cusp (“R”), and a non-coronary cusp (“N”). Yes indeed, all are named
based upon the coronary arteries that originate from their location.
LA = left atrium; RA = right atrium; RV = right ventricle; and P = pul-
monic valve and main pulmonary artery.
Then again place the CFD over the valve. We will see systolic turbulent
flow after the valve in aortic stenosis, and diastolic blood flow across
the aortic valve if insufficient. In the picture below, we see the Mid
Esophageal Aortic Valve LAX view during ventricular systole. The two
following images are of the same patient, both in ventricular systole. On
your left, there is an aortic valve that does not visibly open, not even with
a microscope can we see an opening! We see that the mitral valve is
closed because… yes, you’re correct: the heart is in ventricular systole,
because the aortic valve does not open… not because it is lazy, but the
leaflets are stuck together… yes, correct again: this is how severe aor-
tic stenosis looks! The aortic valve leaflets are thickened and have areas
of calcification (top arrow) with posterior echo shadowing as the ultra-
sound has trouble seeing beyond the calcified area and thus the machine
just shows a black long triangular area after the severely calcified area
108 Board Stiff TEE
(bottom arrow). All of this is typical of senile calcific aortic stenosis. To

the right, color Doppler demonstrates a mosaic flow pattern after the
valve. This is typical of turbulent flow, and flow speed above the flow
scale limit aka the Nyquist limit.
In our next set of two images, aortic valve insufficiency is seen after plac-
ing the CFD interrogation box over the aortic valve. In the image on the left,
obtained during ventricular diastole, trace insufficiency is seen. The image
at the right demonstrates a large color pattern (we know there is no color
in this book, but imagine it!) starting immediately from the subvalvular area
and extending into the left ventricle occupying the entire CFD box. Look
closely and you will also notice that the anterior leaflet of the mitral valve
has been pushed into the semi-closed position by the regurgitant jet. We
can see this more so on the right image in severe cases of AI.
Wider and longer color usually correlates with a more severe problem. If
the ventricular function is poor, systolic flow will be decreased as well.
Now that we are done with 2-D and CFD, it’s time to do CWD across
the valve. The transgastric views are the best views to shoot a CWD
across the aortic valve, as they allow parallel alignment of the Doppler
beam with the valve. The Deep Transgastric LAX view, obtained at ZERO
degrees, is shown below with the Doppler cursor in ideal position across
the aortic valve; RV = right ventricle, LV = left ventricle, LA = left atrium,
and A = aorta.
CWD cursor is seen across the LV, aortic valve, and proximal ascending
aorta.
CWD systolic envelope with a peak velocity greater than 1.5 m/s is seen
in stenosis.
Aortic stenosis can be classified depending on the degree of peak veloc-

ity by CWD as:
Mild >1.5 m/s, but<3 m/s

Moderate 3–4 m/s
Severe >4 m/s
These velocities correlate with aortic valve areas of:
>1.5 cm² = Mild AS
1.5–1 cm² = Moderate AS
<1 cm² = Severe AS
These peak velocities are all nice, but if the ventricle is half dead (has
poor/crappy function) he is not able to generate large gradients even in
the presence of severe stenosis. One easy way to tell, besides looking
at the valve, is to measure the PWD at the LVOT and the CWD through
the valve. A ratio of LVOT velocity/aortic valve velocity close to 100%
is normal, >50% is indicative of mild stenosis; 50–25%, moderate, and
<25% is indicative of severe aortic stenosis. These Doppler measure-
ments along with a measurement of the LVOT cross sectional area (which
is easily obtained in the ME AV LAX view by measuring the diameter of
the LVOT and having the computer figure it out) can also be plugged into
the continuity equation, which we reviewed earlier, and an aortic valve
area can be calculated. Another quick and dirty measurement could be
made using planimetry in the ME AV SAX view. Planimetry is just a fancy
word used for tracing the aortic valve orifice and having the machine cal-
culate an area. It has tons of potential for error, especially in a stenotic
valve, and is no-where near as impressive as the all great and powerful
continuity equation!
110 Board Stiff TEE
Aortic insufficiency is best evaluated by looking at CFD in the ME AV

LAX and ME AV SAX views. It is considered mild aortic insufficiency if
the amount of color through the valve in relation to the LVOT is <25%;
mild/moderate if 25–45%; moderate/severe if 46–64%; and severe
if >65%. With the CWD the slope of the regurgitation waveform can
also be measured, usually using the deep transgastric window. The
insufficiency is considered severe if the slope is >3 m/s². A pressure
half-time of >500 ms = mild, 500–200 ms = moderate, and <200 ms =
severe aortic insufficiency. Again we can use vena contracta measure-
ments to grade the valvular insufficiency. A vena contracta <0.3 cm is
mild AI, 0.3–0.6 cm is moderate, and >0.6 cm is severe. In severe AI,
we will also see LV dilation from volume overload. Yet another diagnos-
tic clue for severe AI would be holodiastolic aortic flow reversal in the
descending aorta. This is simply done by obtaining a long-axis view of
the descending aorta and shooting a PWD down it, just as we looked
for reversal in the pulmonary veins for MR and the hepatic veins for TR.
Wow, this is all coming together and starting to make sense!
The following diagram contains CWD tracings through the aortic valve
from various patients, all bunched into one graph. Tracing “A” and “B”
correspond to one whole cardiac cycle in an aortic valve that is working
normally. We just like to make learning this stuff a bit more confusing for
you. Not really, we are just trying to save some space.
5
A B C D E
Tracings below the baseline represent systolic flow across the aortic
valve, and above, diastolic flow. Note also the “double envelope” in all
systolic flow patterns. The larger tracing of the “double envelope” repre-
sents flow across the aortic valve and the smaller one represents flow at
the LVOT. “A” and “B” = a normal systolic and diastolic (no flow across
the valve) flow pattern. “C” = severe aortic stenosis, with a peak velocity
of 6 meters/second, which is equivalent to a calculated peak pressure
gradient using the simplified Bernoulli equation of 144 mmHg! Yikes! The
double envelope relationship, LVOT/AV Doppler, is called the dimension-
less index as it is pretty independent of ejection fraction. Normally it
is >50%. An index <25% is considered criteria for severe aortic steno-
sis. “D” = mild aortic insufficiency. The deceleration slope is almost flat.
“E” = systolic flow across the aortic valve at 3 m/s, equivalent to a peak
gradient of 36 mmHg and moderate aortic stenosis. Finally “F” = severe

aortic insufficiency. Note the steep deceleration curve reaching the
baseline demonstrating rapid diastolic equilibration between the
ascending aorta and the left ventricle. This can only happen if there is a
BIG hole across the aortic valve in diastole, or just no aortic valve at all!
Well, well, well. If you are still awake and were able to get to this point
you will be happy to know we just decided to end it right here.
Final word: take it easy, learn what is normal very well, and then when
you see abnormal you will know something is cooking! Now we are done!
Out-freakin’-standing!!! You deserve a pat on the back!
QUESTIONS
1. What is the most common cause of aortic stenosis in patients <70

years old?
A. Unicuspid aortic valve
B. Bicuspid aortic valve
C. Rheumatic heart disease
D. Senile calcific degeneration
E. Endocarditis
2. What is the most common cause of mitral stenosis?
A. Hyperparathyroidism
B. Endocarditis
C. Senile calcific degerneration
D. Rheumatic heart disease
E. Radiation therapy
3. Which Doppler mode is used for velocities >2–2.5 m/s?
A. Pulsed-wave Doppler
B. Color-flow Doppler
C. Continuous-wave Doppler
D. 3-D Dopper
E. None of the above
4. Which of the following is NOT necessary to calculate the aortic valve
area using the continuity equation?
A. VTI of the LVOT by PWD
B. VTI of the MV by CWD
C. VTI of the AV by CWD
D. Cross sectional area of the LVOT
E. All of the above are necessary
5. Which view is best for doing a CWD measurement through the aortic
valve?
A. Deep TG view
B. TG LAX view
C. ME AV LAX
D. A and B
E. A and C
112 Board Stiff TEE
6. When evaluating mitral regurgitation and you see systolic flow

reversal in the pulmonary veins, how would you grade the MR?
A. Trace
B. Mild
C. Moderate
D. Severe
E. More information is needed
7. When evaluating valvular dysfunction with CFD, what should your
scale be set to in order to avoid overreading regurgitation or stenosis?
A. <20 cm/s
B. 20–30 cm/s
C. 30–40 cm/s
D. 40–50 cm/s
E. 50–60 cm/s
8. What is the best view to evaluate for subvalvular and supravalvular
causes of aortic stenosis?
A. ME AV LAX
B. ME4C
C. ME2C
D. ME AV SAX
E. TG SAX
9. When grading the severity of aortic stenosis using peak jet velocities
in a patient with an ejection fraction of 10%, how would you expect
your findings to compare to the true severity of the stenosis?
A. The severity of the aortic stenosis will be underestimated
B. The severity of the aortic stenosis will be overestimated
C. The severity of the aortic stenosis will be equal to the true severity
D. Peak jet velocities have no relation to the severity of aortic
stenosis
E. Planimetry is the only way to grade the severity of aortic stenosis
10. An IV drug abuser with endocarditis is most likely to have which
valve affected?
A. Tricuspid valve
B. Pulmonic valve
C. Mitral valve
D. Aortic valve
E. All valves can be equally affected
ANSWERS
1. B
2. D
3. C
4. B
5. D
6. D
7. E
8. A
9. A
10. A
Bibliography
Armstrong WF, Ryan T. In: Feigenbaum’s echocardiography, 7th edn. Lippincott: Williams & Wilkins;
2009.
Baumgartner H, Hung J, Bermejo J, et al. Echocardiographic assessment of valve stenosis: EAE/
ASE recommendations for clinical practice. J Am Soc Echocardiogr 2009;22:1–23.
Brown JM, O’Brien SM, Wu C, et al. Isolated aortic valve replacement in North America compris-
ing 108687 patients in 10 years: changes in risks, valve types, and outcomes in the Society of
Thoracic Surgeons national database. J Thorac Cardiovasc Surg 2009;137:82–90.
Kisslo J.A., Adams D.B. Doppler evaluation of valvular stenosis #3. <http://www.echoincontext.com/
doppler03.pdf>
Mathew J, Madhav Swaminathan M, Ayoub Chakib. In: Clinical manual and review of transesopha-
geal echocardiography, 2nd edn. McGraw-Hill Professional; 2010.
Shanewise JS, Cheung AT, Aronson S, et al. ASE/SCA Guidelines for performing a comprehensive
intraoperative multiplane transesophageal echocardiography examination: recommendations
of the American Society of Echocardiography Council for Intraoperative Echocardiography and
the Society of Cardiovascular Anesthesiologists Task Force for Certification in Perioperative
Transesophageal Echocardiography. J Am Soc Echocardiogr 1999;12:884–900.
Toronto TEE website: <http://pie.med.utoronto.ca/TEE/index.htm>
Zoghbi WA, Enriquez-Sarano M, Foster E, et al. Recommendations for evaluation of the severity of
native valvular regurgitation with two-dimensional and Doppler echocardiography. A report from
the American Society of Echocardiography’s Nomenclature and Standards Committee and The
Task Force on Valvular Regurgitation, developed in conjunction with the American College of
Cardiology Echocardiography Committee, The Cardiac Imaging Committee Council on Clinical
Cardiology, the American Heart Association, and the European Society of Cardiology Working
Group on Echocardiography. J Am Soc Echocardiogr 2003;16:777–802.
CHAPTER Intra-cardiac Masses
12 and Devices
Al Solina, F. Luke Aldo and Salvatore Zisa
Cardiac Masses: A mass by any other name, is still a mass. Or is it?
You may remember from high school physics that mass is simply a quan-
tity of matter. Under the right set of circumstances, it can even be con-
verted into a predictable amount of energy. But that’s not what we are
talking about here. Cardiac masses come in a variety of shapes, sizes,
locations, consistencies, and clinical significance. They can be charac-
terized primarily into real masses, and normal anatomical structures
that masquerade as masses. Real cardiac masses can be further char-
acterized as being benign or malignant, and as being primary or meta-
static. In order to differentiate between these possibilities it is important
to understand normal anatomy, the physics involved with imaging arti-
facts (see Chapter 5), and the characterization of real cardiac masses.
Echocardiography has been utilized to image cardiac masses since the
1950s, and can be used to characterize the anatomy and pathophysio-
logical consequences of the mass. Although a mass may be histologically
benign, it may muck up the normal function of the heart by interfering
with chamber filling or valve function, and therefore not be benign from a
physiological perspective.
MASSES THAT ARE NOT REALLY MASSES
Normal anatomic variants: these structures, although normal anatomic

features, may mimic cardiac masses.
Atrial Anatomic Variants
n Chiari network—having little to do with communications or

information technology, this network is a filamentous embryological
remnant located in the RA.
n Coumadin ridge—a finger-like projection of tissue in the LA, which
separates the left superior pulmonary vein from the left atrial
appendage. It is sometimes mistaken for a thrombus.
n Crista terminalis—not a train station in Rome, but rather a ridge
of tissue in the RA located at the junction of the SVC and the RA
appendage.
n Eustachian valve—an embryological remnant, located at the
junction between the IVC and the RA, and directed towards the
fossa ovalis of the interatrial septum. 115
116 Board Stiff TEE
n Foreign bodies—pacemaker and AICD leads, catheters, and

cannulae of all different flavors may parade around in the atria.
Additionally they may cause reverberations and side lobe artifacts
that further muddle things up.
n Lipomatous hypertrophy of the interatrial septum—this benign
variant is characterized by a sometimes dramatic thickening of
adipose tissue surrounding, but sparing the fossa ovalis of the
interatrial septum. It kind of looks like a dumbbell. Thick-thin-thick.
While not having any meaningful significance in terms of acute
pathophysiological consequence, it is easy to recognize and very
impressive to say.
n Pectinate muscles—line the RA in a perpendicular array.
Ventricular Anatomic Variants
n False chords—nothing false about them. They are real anatomic

structures. They are typically thin, well…chords running across
the LV, near the apex.
n Foreign bodies—as above.
n Papillary muscles—hard to confuse these for anything abnormal if
you know their standard anatomical location, and the fact that they
have the appearance of myocardium. These muscles are found
anterolaterally and posteromedially in the LV, and attach to the
mitral valve via the chordae tendinae.
n Trabeculations—muscular ridges, which can be quite prominent,
especially in the RV.
n Moderator band—this is not some politically correct hip-hop band,
it’s a muscular band of tissue that traverses the apical third of the RV.
It can be confused with a thrombus or tumor.
Valvular Anatomic Variants
n Nodules of Arantius—small nodules along the coaptation point of

the aortic valve.
n Lambl’s excrescences—filamentous structure on the systemic side
of the aortic valve, originating near the coaptation point.
Artifacts may appear for all the world to be true cardiac masses. It is
important to interrogate a suspected mass in different views to ascer-
tain its true anatomical nature. Artifacts tend to disappear with alternate
imaging planes. Be suspicious when you see a structure crossing normal
anatomic boundaries, this is another indication that you may be looking
at an artifact.
MASSES THAT REALLY ARE MASSES
“Benign” primary cardiac masses: these masses are “benign” in their tissue
characterization, but may misbehave and cause functional disturbances
attributable to their anatomical location!
Chapter 12 Intra-cardiac Masses and Devices 117
n Myxoma—most common primary tumor, seen most frequently

in the LA. Can be quite large and interfere with valvular function.
Have a non-homogeneous appearance. Female preponderance.
May commonly be seen attached to a stalk from the LA side of the
interatrial septum. May be associated with systemic embolization.
n Lipoma—second most common benign primary cardiac
mass. Usually found in the left ventricle and right atrium, are
homogeneous and hyperechoic in appearance. Not associated with
systemic embolization. Can be up to 15 cm in size.
n Fibroma—second most common benign cardiac tumor in children
(rhabdomyoma is first). Most frequently seen in the ventricle.
Although benign in tissue type, may be associated with impaired
ventricular filling and/or arrythmias.
n Vegetation—strange name really. Don’t think anyone really
considers these little nuggets to be edible. Bacteremic vegetations
are usually found in the left heart (except in the case of IV drug
abusers), and are usually located on the upstream side of the valve.
They can interfere with valve function and may be associated with
abcesses. Movement usually synchronized with valve motion as
they are attached to it.
n Papillary fibroelastoma—as the most common primary tumor
affecting valves, it resembles a small (<1 cm) vegetation, but is
usually seen on the downstream side of a valve. Found more
frequently in association with left heart valves in patients greater
than 50 years of age. Are sometimes associated with embolic
events.
n Rhabdomyoma—most common tumor in children, usually before
one year of age. May obstruct blood flow and can be associated
with arrhythmias and heart block. Frequently found in conjunction
with tuberous sclerosis.
n Thrombi—tend to occur in areas of slow blood flow such as the left
atrial appendage, LV apex, and ventricular aneurysms. One hint that
the blood is slow-moving is when you see slowly swirling streams
of blood movement, called “smoke”. Where there is smoke there
are thrombi! Thrombi are readily detected in the LA by TEE, but may
be more difficult to interrogate and define when they reside in the
ventricular apex.
Malignant Primary Cardiac Masses
n Angiosarcoma—is the most common primary malignancy of the

heart, and displays a fondness for the right atria of middle-aged
men. They may be either intracavitary or infiltrative. They are
associated with a grave prognosis.
n Rhabdomyosarcoma—male preponderance. Often multiple lesions,
involving any heart chamber. Most common cardiac malignancy in
children. May interfere with valve function.
n Mesothelioma—affecting men more often than women, is typically
seen between ages 30 and 50.
118 Board Stiff TEE
Schematic Representation of Common Cardiac

“Masses”
LA
Lipomatous
hypertrophy
Coronary sinus
Myxoma
Thebesian valve
Renal cell IVC SVC
carcinoma
RA
Eustachian valve
Crista
terminalis
Chiari network
Thrombus
Mural thrombus in
PA right atrial appendage
catheter
TV Pectinate muscles
Metastatic Cardiac Masses
n Lung cancer—most common source of metastatic cardiac tumors.

n Leukemia/lymphoma.
n Breast cancer.
n Malignant melanoma displays a particular penchant for spread to
the heart.
n Renal cell carcinoma—these puppies may actually grow in to the
right atrium, and require cardiopulmonary bypass and even deep
hypothermic circulatory arrest to resect. Makes for a complicated day!
n Carcinoid—more likely to have an effect on the right heart valves
that is mediated by substances secreted by primary carcinoid
tissue located in the liver. Direct metastatic spread is less likely.
Imaging Modalities Utilized to Characterize

Cardiac Masses
n 2-D—it is critically important to evaluate cardiac masses utilizing

a multitude of views in order to appreciate the true functional
anatomic features of the mass.
n 3-D—real time 3-D imaging has been demonstrated to better
elucidate the anatomical relationships of intracardiac masses, and
may alter surgery when utilized intraoperatively.
n Contrast echocardiography—contrast echocardiography may

be utilized to define the vascularity of a mass and enable
more precise categorization. For example, papillary-type atrial
mxyomas, which are friable and associated with neurological
events, demonstrate relative avascularity when compared to the
solid ovoid type.
QUESTIONS
1. Which is the most common primary malignant cardiac tumor in

children?
A. Angiosarcoma
B. Rhabdomyosarcoma
C. Rhabdomyoma
D. Mesothelioma
2. The most common primary tumor affecting valves is:
A. Papillary fibroelastoma
B. Nodules of Arantius
C. Lambl’s excresences
D. Fibroma
E. Lipoma
3. A filamentous embryological remnant located in the RA
A. Lambl’s excresences
B. Chiari network
C. False chords
D. Crista terminalis
E. Nodules of Arantius
4. Which of the following is/are true regarding angiosarcoma?
A. It is the most common primary malignancy of the heart
B. It displays a fondness for the right atria of middle-aged men
C. They may be either intracavitary or infiltrative
D. They are associated with a grave prognosis
E. All of the above
5. Which of the following statements is/are true?
A. Myxomas demonstrate relative avascularity
B. Carcinoid primarily affects the left side of the heart
C. Lung cancer is the most common type to metastasize to the heart
D. A and C
E. A, B, and C are correct
6. Which of the following is/are true?
A. The Eustachian valve is associated with the coronary sinus
B. Most vegetations occur on the right side of the heart
C. The Thebesian valve is associated with the junction between the
RA and IVC
D. A and B
120 Board Stiff TEE
7. Which is are true regarding papillary fibroelastoma?

A. The most common primary tumor affecting valves
B. It resembles a small (<1 cm) vegetation, but is usually seen on the
downstream side of a valve
C. Found more frequently in association with left heart valves in
patients greater than 50 years of age
D. Are sometimes associated with embolic events
E. All of the above
8. Which is/are true of fibromas?
A. Second most common benign cardiac tumor in children
(rhabdomyoma is first)
B. Most frequently seen in the ventricle
C. Although benign in tissue type, may be associated with impaired
ventricular filling and/or arrythmias
D. A and B only
E. A, B, and C
9. Which is/are true regarding lipomas?
A. Second most common benign primary cardiac mass, usually
found in the left ventricle and right atrium
B. Are homogeneous and hyperechoic in appearance
C. Not associated with systemic embolization. Can be up to 15 cm
in size
D. A and B only
E. A, B, and C
10. Which is/are true regarding thrombi?
A. They tend to occur in regions of relative stasis
B. They are usually right-sided
C. They are easier to interrogate and define in the LV apex than they
are in the LA
D. A and B only
E. A, B, and C
ANSWERS
1. B
2. A
3. B
4. E
5. D
6. E
7. E
8. E
9. E
10. A
Bibliography
Armstrong W, Ryan T. Masses, tumors, and source of embolus. In Feigenbaum’s
“Echocardiography”, 7th Edition, Chapter 23, Lippincott Williams and Wilkins, 2010.
Hari P, Mohamad T, Kondur A, et al. Incremental value of contrast echocardiography in the diagnosis
of atrial mxyoma. Echocardiography 2010;27(5):E46–9.
Kirkpatrick J, Wong T, Bednarz J, et al. Differential diagnosis of cardiac masses using contrast echo-
cardiographic perfusion imaging. J Am Coll Cardiol 2004;43(8):1412–19.
Muller S, Feuchtner G, Bonatti J, et al. Value of transesophageal 3D echocardiography as an adjunct
to conventional 2D imaging in preoperative evaluation of cardiac masses. Echocardiography 2008;
25(6):624–31.
Peters P, Reinhardt S. The echocardiographic evaluation of intracardiac masses; a review. J Am Soc
Echocardiography 2006;19(2):230–40.
Ragland M, Tahir T. The role of echocardiography in diagnosing space-occupying lesions of the
heart. Clinical Medicine and Research 2006;4(1):22–32.
CHAPTER Left Ventricular Systolic
13 Function
Eric W. Nelson
For some reason there is a lot of focus on the left ventricle and its evalu-
ation on TEE, both in the operating room and on the boards. This most
likely has to do with the fact that it’s pumping blood to the entire body,
thus keeping you alive. The easiest way to start your evaluation of the left
ventricle is to know what a normal left ventricle looks like.
The shape of the LV should look somewhat like a football. If you drop a
TEE probe in someone and the heart is closer to a basketball than a foot-
ball, something is wrong.
So, now you know how to eyeball the heart and tell grossly if it’s normal
or not, but what about an actual measurement? LV function is typically
measured numerically by the ejection fraction (EF). That is, how much
blood that goes into the LV goes out through the aorta?
Good Bad
EF can be calculated by measuring the fractional area of change (FAC)

of the left ventricle. A true long- or short-axis cross section is required
being careful not to foreshorten. Foreshortening is a term commonly
used by echocardiographers to describe the heart when it is compressed
because of the viewpoint taken. With modern TEE machines all you have
123
124 Board Stiff TEE
to do is outline the end-diastolic area and the end-systolic area and the
machine will crunch the numbers.
FAC = (end-diastolic area – end-systolic area)/end-diastolic area
You can also estimate EF via the eyeball method, which is what most
people do. On the test you should be able to look at an image and deter-
mine the difference between an EF of 25% and 55%. Which is pretty
easy!
One thing to keep in mind whether using the eyeball method or doing an
actual measurement is don’t jump to conclusions based on one view. A
single slice may look great, but remember it’s only part of the heart and
another part may not look so good. Also, if you are foreshortening or not
getting a “true” cut of the LV your read is going to be off. Make sure you
eyeball the LV with multiple omniplane angles and also in both the trans-
gastric and midesophageal views.
ABNORMAL LV SYSTOLIC FUNCTION
Naturally, the first thing that comes to mind is ischemia…if this wasn’t
your first thought you may want to retake your boards. There are also a
lot of other things that may cause abnormal LV function.
n Ischemia, just can’t say it enough.

n Ventricle—infiltrative diseases that cause restrictive physiology
such as amyloidosis cause global impairment.
n Pericardial space—tamponade either from an effusion or
blood. TEE is great at not only making this diagnosis, but also
locating where the effusion is around the heart and whether it is
loculated.
n Pleural space—tension pneumothorax causes decreased venous
return thus decreasing preload and ventricular function.
n Metabolic—hypoxemia, hypoglycemia, anemia, hyperkalemia, and
a vast array of other metabolic abnormalities.
CARDIOMYOPATHIES
Hypertrophic
There are four different types of hypertrophic cardiomyopathies, although

the most famous is septal hypertrophy leading to subaortic stenosis or
“hypertrophic obstructive cardiomyopathy”, which all the cool kids just
call HOCM (pronounced hokum).
HOCM is an inherited cardiomyopathy. It is autosomal dominant with

limited penetrance, unless of course you are the patient then it is a very
penetrating diagnosis!
Chapter 13 Left Ventricular Systolic Function 125
With hypertrophic cardiomyopathies systolic function typically is not the

problem, rather the heart has a hard time relaxing, like that one attending
we’ve all had with the vein in his forehead that seems to keep growing
and may pop at any minute!
An important point about HOCM is the picture you see on TEE. Some
people call this the “dagger sign”. When a continuous wave Doppler
is placed across the left ventricular outflow tract, or LVOT, and the AV
the outflow pattern will resemble a dagger rather than the nice rounded
appearance of someone without this problem. This is secondary to the
ventricle being so empty at the end of systole and the septum being so
huge an obstruction actually occurs.
AS HOCM
Keep in mind that patients with HOCM are also more prone to SAM
or systolic anterior motion of the mitral valve. Since the outflow tract
is already narrow, it’s easy for the anterior leaflet to get sucked in and
impede flow.
The definitive answer to relieving HOCM is surgical resection of the septum.

TEE plays an important role here in order to determine preop if the surgery
is necessary and postop if there was enough septum resected, not enough,
or too much. If not enough was taken the obstruction will remain, but if the
surgeon got a little greedy the patient may end up with a VSD. Also remem-
ber that there are conduction fibers running through the septum. It’s not
uncommon to have a heart block after this type of surgery.
Too Little Too Much Just Right

126 Board Stiff TEE
Medical management of HOCM involves keeping the heart full; remem-

ber that the obstruction occurs when the heart is empty; and also
decreasing contractility.
Restrictive
Sometimes the only way to tell the difference between a hypertrophic

and restrictive cardiomyopathy is by looking at the posterior basal wall
of the heart. This is best appreciated in the transgastric short-axis views.
Remember, in hypertrophic cardiomyopathies the posterior basal wall is
spared, but in restrictive cardiomyopathies it is not. Oh yeah, don’t forget
that a good history and physical can also help determine the type of car-
diomyopathy as well.
Restrictive Hypertrophic
Alright, we’ve determined that we have a restrictive cardiomyopathy,

but where’d it come from? Well, the list is long and distinguished. There
are a lot of things that can “sneak” into the myocardium and cause
restriction:
n amyloid
n sarcoid
n glycogen from patients with glycogen storage disease

n eosinophils from eosinophilic myocarditis (also known
as Loffler’s)
Like hypertrophic cardiomyopathies, restrictive cardiomyopathies
mainly present a problem in diastole that is the heart does not relax
well enough to accept blood. Remember to go over the various dia-
stolic E/A patterns and pulmonary venous flow because these do show
up on the test!
Patients with restrictive heart disease are also prone to thrombus forma-
tion even without a wall motion abnormality. Thrombi are typically found
in the apex. Remember, the apex of the heart is best visualized in the
mid-esophageal 2-chamber view and the mid-esophageal 4-chamber
view. Thrombi may also form under the posterior mitral valve leaflet,
which may lead to a bit of mitral regurgitation.
Dilated
Remember at the beginning of this chapter when I mentioned that the

heart shouldn’t look like a basketball? Well that’s exactly what this type
of heart looks like. It’s big, the walls are thin, and it really isn’t doing
much at all. Keep your eye out for thrombi, as there isn’t much going on
so clot formation is possible.
Clot
Like everything else there is a list of what causes dilated cardiomyopathy

n Ischemic
n Post viral
n Peripartum
n Alcohol
n Idiopathic (a doctor’s way of saying “I just don’t know”)

n And numerous others.
QUESTIONS
1. Which wall is spared in hypertrophic cardiomyopathy?

A. Inferiolateral
B. Posterior basal
C. Septal
D. Apical anterior
E. Anteroseptal
2. Which of the following may cause cardiomyopathy?
A. Pregnancy
B. Ischemia
C. Alcohol
D. Virus
E. All of the above
F. B and D
128 Board Stiff TEE
3. Where is the most likely place to find thrombus in the LV?

A. Apex
B. LVOT
C. Basal septal wall
D. Lateral wall
4. Treatment for HOCM includes all of the following except:
A. Surgical resection
B. Alcohol
C. Beta blockade
D. Inotropic agents
E. Increased preload
5. What causes hemodynamic compromise in patients with HOCM?
A. Anatomic outflow tract obstruction
B. Physiologic outflow tract obstruction
C. Decreased EF
D. Restrictive myocardium
6. Which of the following causes restrictive cardiomyopathy?
A. Concentric hypertrophy
B. Alcohol
C. Ischemia
D. Iron overload
E. Celiac disease
7. Which of the following patients are prone to LV thrombus formation:
A. Atrail fibrillation
B. Hypertrophic cardiomyopathy
C. Restrictive cardiomyopathy
D. Pericardial tamponade
E. Severe MR
8. A problem in which of the following spaces may affect LV systolic
function?
A. Pericardium
B. Pleura
C. Ventricle
D. Metabolism
E. A, B, and C
F. All of the above
9. True or false: It is possible to evaluate the ejection fraction of the
heart by one view on TEE
A. True
B. False
10. Which view is the best to evaluate HOCM
A. Mid-esophageal 4 chamber
B. Mid-esophageal 2 chamber
C. Deep transgastric
D. Transgastric short axis
E. A and C
ANSWERS
1. B
2. E
3. A
4. D
5. B
6. D
7. C
8. F
9. B
10. E
CHAPTER Segmental Left Ventricular
14 Systolic Function
John C. Sciarra and Christopher J. Gallagher
MYOCARDIAL SEGMENT IDENTIFICATION
Hear ye, hear ye. The Office of Homeland Security is not going to shoot
me for revealing any state secrets here. You will need to know these seg-
ments and you will need to know which coronaries feed which walls and
which segments.
I kid thee not.
I speak not with forked tongue.
This is a for sure on the test.
The first time you see it you’ll quasi freak, because it looks so complex,
but when you think of all the other stuff you memorized to get this far, it’s
not so bad. Plus there’s a logic to it, so don’t go off the deep end.
First, the whole thing, then we’ll back up and break it down.
A SEGMENTS—DON’T FREAK B DONUT AT EACH SLICE
Basal 6 I Not in
P apical
Mid 6
S L
Apical 4
Not in AS
apical A
C WHICH LEVEL IS DONUT? D WHICH WALL IS WHICH?
Basal? Septal
(see MV)
ME 4-Chamber
Lateral
Mid?
(see Paps) Inferior
ME 2-Chamber
Apical
(nothing) Anterior
ME LAX Posterior Anteroseptal
131
132 Board Stiff TEE
I found it easiest to start with the cross sections. That way you can at
least always know what’s “directly across” from you. Then you can take
the long views and start to put it together.
So, think of three of these lying on top of each other, starting at the top
of the ventricle, right next to the mitral valve. Three layers of six:
The basal 6 segments are next to the mitral valve.
The middle 6 segments are next down, at the level of the papillary
muscles.
The lower, or apical, 6 segments come next.
BUT WAIT!
Though it would make sense to do 6/6/6, the SCA (perhaps fretting

about the demonic number 666 from The Omen), only recognizes four
segments in the ever-narrowing apex.
Lose the posterior and the anteroseptal segments there. In the apical,
you just have inferior, anterior (across from each other, remember), and
septal and lateral (across from each other too).
Now, put it back together, piece by piece, until it makes sense. If you are
still confused, stay tuned for the 17 segment chapter.
CORONARY ARTERY DISTRIBUTION

AND FLOW
REAL WORLD NOTE Major, major importance that you know this. This ties in
with the extremely practical dilemma that you face on a daily basis: “Is the new
graft working?” If a wall fed by, say, the right coronary graft was working, and now
is not working, hey, look at the graft for kinks, disconnects, clots, dissections. It’s
a hell of a lot easier to recognize the problem and fix it now than to find out later
and lose a chunk of myocardium.
TEST NOTE Vintage testable material here, folks. A little brutal memorization
(come on, there are only three vessels, it’s not that bad) and you should nail these
questions.
Chapter 14 Segmental Left Ventricular Systolic Function 133
Pictures tell it all:

A CORONARY DISTRIBUTION
Right RV and Inferior Wall
Circumflex Posterior and Lateral
LAD Septal, AS, Anterior
B CORONARY DISTRIBUTION
LAD
Right
4-Chamber
Circumflex
Right
Know
2-Chamber these cold!
LAD
LAX
LAD
Circumflex
Let’s put it into words, just in case you’re less of a visual learner.
The right coronary feeds the inferior wall and right ventricle.
The left anterior descending feeds the anterior and septal walls. (No won-
der an LAD infarct is so problematic.)
The circumflex feeds the posterior and lateral wall.
Everyone studies the hell out of this issue, drawing the pictures over and
over again, flashcards, you name it. Get this stuff down but down.
Here is a little memory helper I made up, I call it the “coronary artery
memory helper”:
LM → LAD → Diags (the “D” in lad leads into the “D” in diagonals).
Circ → OMs (circumferential looks like the circumference of the “O” in

Obtuse Marginal).
RC → PDA (the right hand [RCA] writes on the palm pilot pda).
NORMAL AND ABNORMAL SEGMENTAL

DYSFUNCTION
Assessment and Methods
Keep your eyes open, that’s the method. The wall motion abnormali-
ties you see will not be subtle. Every test-taker since the dawn of time
emphasized that to me.
134 Board Stiff TEE
“You’ll see it moving, then BOOM, it ain’t moving.”
And in real life, that’s what you see too. As soon as a wall gets ischemic,
the motion disappears. Keep in mind, the normal movement of a wall is
thickening and an inward movement.
At the meeting, they get a little more scientific than this, saying “Normal
contractility results in 30% thickening of the wall, hypokinetic is 15%,
akinetic is, well, 0%, and dyskinetic means it bulges outward”.
Others gets a little more Gestalty:

n Normal is normal-looking.
n Hypokinetic is hypokinetic-looking.
n Akinetic is akinetic.
n Dyskinetic is dyskinetic-looking.
Golly.
All of this high-tech ranking is groovy, but you just have to look at a
bunch of echos and try to peg, “Which wall is not happening?”. This can
be harder than it seems, so be systematic about it. Look at one section
and (this according to the great Cahalan himself) say, “Systole, systole,
systole” and see if that particular section moves.
In the OR, I’ll put my finger in the center of the ventricle on the monitor
and see if different wall segments move in toward my finger.
One trick I stumbled upon is the value of fast forward. Tape a bit, then
rewind and look at the walls in fast motion. Believe it or not, when the
ventricle’s going super fast, the dyskinetic or akinetic wall stands out
better than at regular speed.
In your studying, look at either the tapes or the CDs. This is a total “mov-
ing picture experience”, for there is no other way than to drill these.
On the tapes from the 2002 meeting, they recorded the “Regional Wall
Motion Unknown” session. That is the best way I found to practice pick-
ing out the “mystery wall motion abnormality.” (Quit laughing as I men-
tion “tapes”, go online and look up a few examples of regional wall
motion abnormalities on the Internet.)
DIFFERENTIAL DIAGNOSIS
Well, gee whiz, what else could it be?
Wise counsel says, “Believe bad news and act accordingly”. Other than
a graft not working or a native vessel being occluded, there aren’t too
many other things it could be. The main aspect of the differential should
center on which catastrophe afflicted your graft:
n Air embolus (particularly after an open procedure).
n Spasm of the internal mammary (a surgeon at the meeting and in

the tapes points out that spasm of the internal mammary graft is an
oft-cited excuse. In reality, the graft was poorly placed, kinked, or
clotted off, and the all-encompassing excuse of “Oh, it must have
been spasm” is pulled out for public consumption.).
n Too long of a graft, leading to a kink.
n Too short of a graft, leading to a squinking shut of the graft as it’s
stretched flat as a pancake.
n Clot from, perhaps, hypotension and stasis (Eeek! That can be a
result of “Anesthetica Imperfecta”!).
n Dissection.
Whatever it may have been, when you see a new wall motion abnormality
that you thought you should have fixed, take a look-see.
CONFOUNDING FACTORS
Tethering can throw you off the hunt when examining regional wall
motion abnormalities.
TETHERING
Can’t move as well.
Infarcted./Dead and gone.
Can’t move as well.
A hypo-, dys-, or akinetic area can “hold back” a normal area. (You may
be able to run around pretty energetically, but if I jump on your shoulders
and say, “Yeehaa! Giddyap!”, your motion may slow down considerably.
You have been tethered by my bulk.)
The angle of your examination may throw you off too. If you get a really
foreshortened view of the ventricle, for example, you may not get a clean
look at one segment; rather, you’ll see a lot of segments at once and
won’t be able to make a clean diagnosis.
LEFT VENTRICULAR ANEURYSM
An aneurysm is a thinning of the entire wall of a structure. So, on echo,

a ventricular aneurysm is seen as a dyskinetic region (bulges outward in
systole) that has a diastolic contour abnormality (keeps bulging outward
even after systole is over). In other words, the damned thing is always
bulging out. Kind of the “love handles” of the heart.
Of specific diagnostic interest, an aneurysm has a smooth transition from

normal myocardium to thinned aneurysm. There is no sharp angle or neck
(as we’ll see with pseudoaneurysms or ventricular ruptures in just a minute).
136 Board Stiff TEE
The love handle analogy helps again. Love handles (however much they
may plague us, uh, more mature gentlemen) at least have an aestheti-
cally pleasing smoothness as they transition from the torso to the love
handle proper.
Aneurysms are most often found in the apex, though they can occur
elsewhere. And aneurysms, with their underlying stasis, can give rise to
thrombi.
LEFT VENTRICULAR RUPTURE
For a big-time ventricular rupture, skip the TEE. Grab a pathology text
and head for the refrigerated surgical suite in your hospital’s basement.
A survivable rupture through the myocardium but contained within a

“skin” of pericardium is called a “pseudoaneurysm”. On echo, you don’t
see the smooth transition of the true aneurysm; rather, you see a nar-
rowed neck at the site of the breakthrough.
PSEUDOANEURYSM
Ruptured
ventricle “held”
Narrow by pericardium
neck
Abrupt
If you want to get all quantitative and anal about it, the ratio of the neck to
the maximum diameter of the pseudoaneurysm should be less than 0.5.
But give me a break; if you know what happened, the difference between
an aneurysm and a pseudoaneurysm should jump out at you.
QUESTIONS
1. Regarding myocardial stunning:

A. Ischemia tends to produce more severe wall motion abnormalities
B. Stunned myocardium shows a gradual improvement and function
in the first minutes to hours following separation from bypass
C. Stunned myocardium may be recruited to contract with inotropic
stimulation
D. Inotropic stimulation may worsen function in an ischemic segment
E. All of the above
2. Concentric LV hypertophy is:
A. A really big heart
B. Commonly called “cow heart”
C. Wall thickness increased in proportion to the increase in
chamber size
D. Wall thickness increased out of proportion to chamber size
E. Wall thickness inversely porportional to chamber size
3. Eccentric LV hypertophy is:

A. A really big heart
B. Commonly called “cow heart”
C. Wall thickness increased in proportion to the increase in
chamber size
D. Wall thickness increased out of proportion to chamber size
E. Wall thickness inversely porportional to chamber size
ANSWERS
1. E.
2. D.
3. C.
CHAPTER
The 17 Segment Model
15 John C. Sciarra
(Update note: In the ancient history of the first edition, there were 16 seg-
ments. Apparently we have evolved a 17th segment!)
This chapter requires some artist skill. When I say some, I mean very lit-
tle. If you can draw a line and a circle you are, for the purposes of this
chapter, an artist.
The 17 segment model is the way we as doctors communicate which

sections of the heart we are talking about. It is also a great tool for
designing test questions. For example, the patient is a gunshot wound
victim, and he has a hole in segment 8. What coronary artery is spurting
blood? What leads on the ECG do you expect to see abnormalities? See
what I mean? Well, I am not going to tell you the answer; you just have to
read on—and draw. And draw you will. You will draw what I call:
“The 17 Segment Star”.
First off, draw a line. Just a straight line. As seen below this is a straight line.
A line
Wow, that was not so bad. Now comes the tricky part. You have to add
two more lines in a cross pattern as seen below. It kind of reminds me of
an asterisk, or star. That’s you–an echo star!
Grip your pencil tightly because I am going to ask you to do something

completely different. Draw a circle on top of your star. 139
140 Board Stiff TEE

Good job Picasso, you have drawn the basic foundation for the 17 seg-
ment model. Next we have to number the segments. Start in the lower
left, inside the circle, and do 1 thru 6, as seen below.
6 4
1 3
Always
start here 2
Now start again outside the circle at the same lower left and do 7
thru 12. It should look like this. If you are not drawing at this point and
just reading you are missing the point. Get out your pen and do it.
11
5
12 10
6 4
1 3
7 9
2
8
Chapter 15 The 17 Segment Model 141
13 thru 17 start close to your original starting point, which is the bot-
tom. Circle around and finish at the bottom with 17. 17 is the apex or
bottom of the heart, so that is where the number should be. It should
look like this:
15
11
5
12 10
6 4
16 14
1 3
7 9
2
13
17
That’s it. Now you have to practice this without looking. Go ahead. Find
a piece of paper and start with the line, and finish with 17. You should be
able to do this in 5 seconds. I am waiting…. Do it.
Now that you are an artist, you may feel like painting your living room.
Hold on, since we now need to go over how your master work relates
to the heart. Your 17 segment model is a segmental version of the cross
section of the heart as seen below, which you may recognize from other
sections in this book. Or a dozen other inferior books on TEE.

“WALL PAIRS” IN CROSS SECTION
Inferior Anterior I Posterior Anteroseptal

Septal Lateral P
S
L
AS
A
Schematic of LV in Cross Section

142 Board Stiff TEE
We start at the top of the heart and work our way to the bottom, number-
ing as we go. “Wait” you say. The number one is in the wrong place. This
is due to the fact that in TEE things are backwards from trans-thoracic
scanning. I just put these images here to show you how the numbers
relate to the levels: basal, mid, apical, and apex.
Apical Mid Basal
1
7
13 2 6
8 12
14 16
9 11
15 3 5
10
4
LAD RCA LCX
This is the image you might see in most cardiology textbooks—if you
ever dared to crack one open.

1
7
2 6
8 13 12
14 17 16
9 11
15
3 5
10
4
1. Basal anterior 7. Mid-anterior 13. Apical anterior

2. Basal anteroseptal 8. Mid-anteroseptal 14. Apical septal
3. Basal inferoseptal 9. Mid-inferoseptal 15. Apical inferior
4. Basal inferior 10. Mid-inferior 16. Lateral
5. Basal inferolateral 11. Mid-inferolateral 17. Apex
6. Basal anterolateral 12. Mid-anterolateral
Alright, let’s get back to the world of anesthesia. This next image is the
one that has the positional planes lined up as the heart sits in the chest
and as the probe is at the back of the heart. Our orientation is the top
of the page is the back of the heart—the inferior portion—and the front
of the heart is at the bottom of the page or TEE image—anterior. This
should all be crystal clear in the cool exploded 3-D image I made below,
which I drew from an actual exploded heart.
Inferior
SEGMENTS
Septal Posterior
1–6
Anterior Lateral
septal
7–12
RV
13–16
17
Anterior
To review the coronary anatomy. Which really shouldn’t be neces-

sary—but what the heck:
LM → LAD → Diags (the “D” in LAD leads into the “D” in diagonals).
Circ → OMs (circumferential looks like the circumference of the “O” in

Obtuse Marginal).
RC → PDA (the right hand writes on the palm pilot pda).
(I hope those little memory hints help.)
This appears in another portion of the book. Learning thru repetition is

a time-honored teaching tool they say. And they say it over and over for
some reason.

A CORONARY DISTRIBUTION
Right RV and Inferior Wall
Circumflex Posterior and Lateral
LAD Septal, AS, Anterior
B CORONARY DISTRIBUTION
LAD
Right
4-Chamber
Circumflex
Right
Know
2-Chamber these cold!
LAD
LAX
LAD
Circumflex
144 Board Stiff TEE
So let’s answer our question from the beginning. Remember gunshot to

segment 8? Look at your drawing. Segment 8 is right in the middle of the
anterior portion of the heart. Kind of a bulls-eye if you will. The anterior
wall is the distribution of the LAD. See how easy that was. So he as a
hole in his LAD! Quick, get a doctor!
At this point I should be able to shout out a segment, and you shout out
a coronary artery—and vice versa. If not, go back to the beginning and
start reading again. And this time draw it out. Lastly, I want to explain
how some of the TEE planes relate to my 17 segment star. If you draw
some dashed lines in between the lines of the star, these represent the
planes of the TEE probe in certain views. The four-chamber view slices
thru segments 3 and 6, for example. Next is the two-chamber view with
the plane going anterior to inferior. Last is the ME long-axis cutting seg-
ments 7 and 4 among others.
I
S P
AS L
A
al
Inferior
Posterior
ept
rior
tal
t. s
l
era
Sep
Ante
An
Lat
LAD LCX RCA
So there you have it. The star makes it all come together. I recommend
trying to draw the 17 segment star in a few days to see if you remem-
bered it. Then in the future, during say, some exam, you see a question
involving the coronary arteries, wall segments, or ECG changes, just
draw the star and figure it out. Nothing will stop your star power!
QUESTIONS
1. Ischemia in the RCA would give wall motion abnormalities in

segment 2 or 5?
2. Segment 14 is hyperkinetic. You tell the surgeon which graft is
down?
3. The patient from the beginning of the chapter gets better, gets a
gun and goes all gangster on his shooter for revenge. He aims for
the LAD. Does he hit segment 2 or 12?
ANSWERS
1. Quick draw your 17 segment model, and look at the back wall.
Hmmm… must be 5.
2. Quick draw your 17 segment model... and it looks like 14 is lateral,
so it must be the circumflex.
3. Quick draw your 17 segment model, and guess he is accurate and
hits 2 which is anterior.
CHAPTER Assessment of Perioperative
16 Events and Problems
Ricardo Martinez-Ruiz and Christopher J. Gallagher
HYPOTENSION AND CAUSES OF

CARDIOVASCULAR INSTABILITY
REAL WORLD NOTE Let’s face it, cowboys and cowgirls, this is the real crux of
the whole deal with echo. All the cool physics and gradients and Doppler stuff are
necessary for the test. And if you’re going to do cardiac echo, you need to know all
the neato-frito valve details. But as TEE gets more and more common, the day will
come when every single anesthesiologist or ICUologist will need to know at least
the basics of TEE to figure out what’s going on when a patient gets unstable.
The TEE is the anticrash weapon of choice.
When badness happens (and we’ve all seen it happen), you might not
have a Swan or CVP. And even if you do, you’re still wrestling with num-
bers that tell you something, but not the whole picture. You are left with a
set of numbers from which you infer, or hope, you have the picture.
The TEE gives you the real picture, right now, no need for a leap of faith.
Cahalan points out in the tapes and at the meetings that, even with only a lit-
tle TEE experience, most people can diagnose the most common problems
in mere minutes. After all, when most patients go to caca, you want to know:
n Heart, full or empty?
n Ventricle, good or bad?
n Tamponade, yes or no?
For most problems, then, Cahalan gives us a nice, neat, easy-to-understand

and inherently obvious breakdown of the main causes of hypotension:
1. End-diastolic area decreased, ventricle contracting OK—You’re low
on volume. The heart is empty, so fill it.
2. End-diastolic area increased, ventricle contracting poorly—
You have a bad and already overfilled ventricle. Fix whatever’s
causing the global hypokinesis (Get a blood gas! Don’t forget the
basic stuff!), and once you’ve fixed what you can fix, it’s time for
inotropes or ventricular support of some kind.
3. End-diastolic volume normal or low, ventricle contracting well or
hyperdynamic—You have a problem with the volume not “going
where it’s supposed to go”. Either the volume is all going out into
a vastly dilated circulatory tree (anaphylaxis with low systemic 147
148 Board Stiff TEE
vascular resistance), or else some other channel is misrouting your

good cardiac output (severe mitral regurg or aortic regurg, or a
ventricular septal defect).

Full
Diastolic area >18 cm2
Empty
Diastolic area <10 cm2
Midpapillary views
The first two are easy to see with a glance at the TEE. The third is a little
trickier, but you can augment your TEE findings with other stuff. (Flushed
appearance and wheezing going along with anaphylaxis; murmurs or fur-
ther TEE views to find mitral regurg, aortic regurg, or a VSD.)
Then the final thing you want to know, “Tamponade, yes or no?”, is
figure-outable with your basic search for a pericardial effusion plus the
hemodynamics of tamponade.
Pericardial
effusion
Right cavities squeezed by effusion

Chapter 16 Assessment of Perioperative Events and Problems 149
If you take nothing else away from TEE (say you don’t want to bother
taking the TEE exam), if you at least know this, the differential for hypo-
tension, you will save somebody some day.
CARDIAC SURGERY: TECHNIQUES AND

PROBLEMS
Assessment of Bypass and Cardioplegia
How the hell do you use TEE to assess bypass and cardioplegia? Got
me. I have no clue what the Society of Cardiovascular Anesthesia folk
were thinking when they put this on their magical list.
Let’s stretch a little and try to figure this one out.

n Use your TEE to show that the heart is not beating at all—that
would mean the cardioplegia is working.
n Use your TEE to see that the heart is not blowing up like a
basketball—that would tell you that the cannulae are flowing in the
right direction and there is not some catastrophic flow reversal.
One thing is worth mentioning at this time. Disconnect your echo probe
while on bypass. That will allow the probe to cool down and prevent
esophageal burns. And remember that you do need to disconnect the
probe, not just put the image on FREEZE. Although the word FREEZE
implies a cool state of affairs, you have just frozen the image. You haven’t
actually frozen the probe and turned it into a big Fudgecicle.
Cannulas and Devices Commonly Used During

Cardiac Surgery
The main cannula you’ll be asked to visualize is the retrograde cannula

for cardioplegia. First, you need to know where the coronary sinus is (the
site of the retrograde cannula).
To see the coronary sinus on TEE, you need to get your ME 4-cham-
ber view and slowly advance the probe into the stomach and VOILA!!!
The coronary sinus shows up as a drak conduit that drains into the right
atrium (you can check with Doppler to see the coronary sinus blood
flow). Ocassionally you may have a valve (Thebesian valve) impeding
the easy positioning of the retrograde cannula, the cannula gets stuck
on it. It is pretty cool to tell your surgeon that the reason he is struggling
getting it in position is because of the valve.
150 Board Stiff TEE

RA Coronary sinus
Retrograde
cannula
Cannula to cross the threshold. Like all cannulas, the retrograde cannula
has a “double line” that tells you it’s a man-made thingamajig. And like all
cannulas, its 3-D reality will dive in and out of your 2-D picture, making
it sometimes a little tough to keep it entirely in view. In some occasions
you may see the stippled balloon at the end of the cannula: it looks like a
star cluster (yes…use your imagination!).
What else might Show up During Cardiac Surgery?
The aortic cannula is hard to see as it is often placed far into the ascend-
ing aorta, usually in the blind spot area.
But anytime an aortic cannula is in, a dissection (heaven forbid) could

occur, so you go ahead and examine the aorta and look for this dreaded
complication.
Look at the atrial cannula? Sure, why not? I suppose you could imagine
looking at the venae cavae, if the surgeons were having trouble cannulat-
ing, to see if there is a web or some bizarre thing holding them up.
The tip of your dual stage cannula should be just into the IVC.
Circulatory Assist Devices
It’s not a stretch to look for correct placement of an intra-aortic bal-

loon pump. You want to see the tip of the IABP at the takeoff to the
left subclavian artery. No higher (occlusion to the left arm) and no lower
(inadequate function of the balloon pump and potential occlusion of
renal arteries, oops). You should see the tip of the IABP, but no bal-
loon!, at the level of the takeoff of the Lt subclavian artery on the most
upper view of the descending thoracic aorta. As soon as you push the
probe deeper, the balloon should be visible with its characteristic up
and down, up and down… (you can also assess the quality of expan-
sion of the balloon).
Tip no balloon!
Further in ....
Balloon
It sc artery
and NO it
sc artery
Desc. aortic
SAX
Things can get more exotic, of course.
Left and right ventricular assist devices, and ECMO when things are
going really swell, all enter the cardiac realm in this Brave New World we
inhabit.
With an LVAD, you want to make sure the person doesn’t have a patent
foramen ovale or interatrial septal defect. You could, as the blood rushes
out of the left side into the assist device, “suck” blood from the right side
over to the left.
If this happens, then no blood goes out the right side, so no blood goes
to the lungs, so no oxygen enters the body. Unless your patient is a cya-
nobacterium, he or she will need oxygen.
So check for these PFO when you start an LVAD. You may also need to
make sure that there is no aortic regurgitation. If that happens blood will
“recirculate” in a circle of death >>>> from the LV >>> to LVAD >>>> to
aorta >>> back to LV.
Bad things!!
PFO/ASD
AI
VSD
LVAD
Once the LVAD is going, you can also use the TEE to confirm that the
aortic valve isn’t opening. At first that concept seems a little jarring.
152 Board Stiff TEE
“What, the aortic valve isn’t opening? But, golly Mr. Wizard, how can
the person live?”
Yes, usually that is the case, but remember, you’re not in Kansas any-
more, Dorothy. The LVAD is doing all the work now. You want all the
blood to leave the heart and go into the machine.
In testville, remember that the cannula that is draining blood out of the
body into the machine is the inflow cannula. (That is, inflow as far as the
machine is concerned. You could get faked out and think, well, relative to
the body, that is technically outflow, so… Don’t think that!)
There are two new gadgets for LV support that can be placed percutane-
ously >> the Tandem heart and the Impella. The Tandem inflow cannula
goes from the femoral vein into the IVC into the RA and then goes through
the interatrial septum into the LA! The LA blood is pulled into the centrifugal
pump located outside the body to be reinfused into the arterial system via
the femoral artery to provide systemic perfusion. You can check the place-
ment of the inflow cannula as it goes across the interatrial septum.

Tandem cannula
Inflow
LA
SVC
IVC
RA
The impella is different: it consists of a very small impeller-based pump

that its placed across the aortic valve (via the femoral artery most com-
monly) and sucks blood out of the LV and propels it back into the aorta.
This will provide for overall systemic perfusion needs and will also let the
LV decompress and recover. Neat stuff!!!

Aortic valve
Impella
LVAD
Outflow
Inflow
ECMO and RVADs? You can use TEE to check those cannulas too and
just make sure they seem to be in the right place.
Intracavitary Air
No biggie here. Air bubbles look like snowflakes swirling around in the
heart. You will want to look for these (the TEE is the most sensitive at
detecting air bubbles) after an open-chamber procedure to make sure
you de-aired the heart properly.
Air can hide out in the tangle of papillary muscles and chordae tendin-
eae. (When you think of a cardiac “chamber,” you think of this big, open
space, but it’s damned crowded in there.) Check along the septum and
down in the apex for “lurking air”.
Minimally Invasive Cardiopulmonary Bypass
(Perhaps more accurately called “Minimally done anymore cardiopulmo-

nary bypass”.)
As regular old off-pump CABGs work so well now, the days of MIDCABs
(such a puckish name) seem to be numbered. TEE was used to make
sure the fantastically complicated tangle of cannulas was all in place.
Thank God this ischemia-producing (in the anesthesiologist) procedure is

going the way of the 8-track cassette and the slide rule.
Off-pump Cardiac Surgery
Now this is more like it.
As a sign of the times, I looked back at the tapes for the 1999 TEE
course. People then were talking about doing off-pump cardiac sur-
gery in “select cases” and doing relatively small percentages of people
off pump. Well, of course, by now, everybody and their second cousin is
doing off-pump CABGs. McDonald’s will have a drive-thru window soon
where you can get off-pump CABG done.
One pain in the ass, actually THE pain in the ass, with off pumps is “the
hike”—when the surgeons lift the heart to get at those dim and distant
distals. Hemodynamically the patient’s blood pressure often takes a
hit with the hike, though the newer “holder thingies” and more surgeon
experience have made the whole process less devastating than in days
of yore. The hike also goofs up the echo, because now you may have air
between the heart and the probe.
No can do the transgastric view, no way.
Hike the heart, the view goes away.

154 Board Stiff TEE
The whole deal during off-pump surgery is, “Can we do this off pump?”
or “Are things getting SO BAD that we have to stop this charade, put in
cannulas, and do this on pump?”. Pertinent to us is the question, “Can
the TEE help me make that decision?”.
What tells you things are going to the dogs?

n Low blood pressure unresponsive to your usual blandishments.
n Ectopy so bad that you get ectopy.
n Ditto asystole.
n Rising CVP or PA pressures.
n Increasing mitral or tricuspid regurgitation.
n Regional wall motion abnormalities that persist and persist and
(when the hell are they going to finish the graft!?) finally make you
and everybody panic and say, “BASTA! The patient’s dying! Stop!”.
But during off-pump cases, you are actually looking at the wall right
there, with your own eyeballs. Even “hard to see” walls are hiked up for
you and the surgeon and everyone to see. You can, of course, confirm it
with the TEE, but your eyeballs do just as well in the OR.
TEE helps you to see the mitral and tricuspid regurg, of course. (Unless
you’re Superman, most of us can’t see inside the heart.)
So how much and how long of a wall motion abnormality is enough to

push you “onto the pump”?
Uh…
Jack Shanewise gives this talk at the TEE conference. (He’s a great
speaker, so don’t miss him. Remember, he spearheaded the big paper
that gave us the “big 20” views, so he knows from TEE.) He tells us he
usually sees signs of ischemia or wall motion abnormalities during these
off-pump cases, but that as long as things improve after the anastomosis
is complete, you’re usually (not always) OK.
Having heard the talk and done a bunch of off-pump cases, you’re still left
with a bit of a “by guess and by God” feeling about these off-pump cases:
1. They hike the heart.
2. They clamp the vessels to sew in the graft.
3. Things get bad, you limp along with volume, a little Neo maybe, you
hope things don’t get too bad.
4. TEE confirms that you are limping along, but you hope things get
better.
5. Things either get better or they don’t.
6. If they don’t, if the wall motion abnormality does NOT go away, then
you have to reexamine that graft and make sure it’s working OK.
(If you had an on-pump case and had a new regional wall motion
abnormality, you would reinvestigate your graft, wouldn’t you?)
How’s that for the state of the art?
I tell residents an off-pump case is like a labor epidural that’s just kind
of, sort of working. You pray and pray for the lady to deliver so that you’ll
just be done with it! Same with these cases: you pray and pray that they
get the grafts done so you’ll just be done with it!
CORONARY SURGERY: TECHNIQUES AND

ASSESSMENT
How will TEE help you in an on-pump CABG? (Since we talked about off-
pump just a second ago.)
Pretty much, the TEE will replace the Swan. (This debate will swirl around
for a long time, particularly the “What happens when the patient goes
to the ICU; do we put a probe in again each time we get in trouble? You
guys have it in the whole time in the OR, but we in the ICU don’t!”.)
With the TEE going in nearly all our patients (people at the meeting con-
firmed that, in a lot of places, heart surgery means a TEE, period), you
get most of your “Swan-like” information right there from the TEE. (We do
put introducers in everybody, so we can always put a Swan in later.)
n Heart empty or full? TEE tells us.
n Ventricle crummy, ventricle snappy? TEE tells us.
n Tamponade? TEE tells us.
In effect, this discussion is the exact same discussion as in Hypotension

and Causes of Cardiovascular Instability above. What, after all, are you
concerned about during a CABG? Hypotension and cardiovascular insta-
bility. So, boom, same exact analysis.
This helps you out at all points of the case. Hypotension and cardiovas-
cular instability can and do happen whenever they want to—at induction,
during the IMA dissection, coming off pump, whenever.
TEE also helps in regional wall motion abnormality analysis. This goes
right back to another previous discussion in Chapter 14 (see Coronary
Artery Distribution and Flow).
Examine the patient ahead of time, look for wall motion abnormalities.
See which grafts go in which distribution. If you see a new wall motion
abnormality, that is evidence a graft is not working.
This comes in especially handy once the chest is closed. The skin and
sternum are “in the way” and the TEE helps you see what your eyes no
longer can.
156 Board Stiff TEE
VALVE SURGERY: TECHNIQUES AND

ASSESSMENT
Valve Replacement: Mechanical, Bioprosthetic,

and Other
Not to sound like a broken record here, but TEE helps you during valve
surgery the same way it helps you during CABGs, that is, in the evalua-
tion of cardiac function and volumes, the management of hypotension
and cardiovascular instability.
TEE helps you keep the blood going round in circles in your patient, and
Oh be Joyful to that. How?
n Heart empty, heart full?
n Ventricle good, ventricle bad?
n Tamponade, yes or no?
Do we see a pattern here?
But in valve surgery, we go a little further than management of hypo-

tension and cardiovascular instability. We look at the valve itself, before
surgery, to confirm the diagnosis and assess severity, and after surgery,
to confirm good function of the valve and make sure there aren’t any
problems. And yes, once all is done, we go back like dutiful soldiers to
evaluating for hypotension and cardiovascular instability.
TEST NOTE You’ve got a little memorizing to do. You will need to know what
different valves look like on echo. Not the end of the world, but the hyphenated
double names of the artificial valves drove me cuckoo. Doesn’t any one person
ever design a valve?
Let’s plow through the various kinds of valves and how they look.
Different ones have different jets of regurg (you’ll need to know that too),
but one thing holds true for all valve replacements. You should not see a
PERI-valvular leak. You shouldn’t see leaking OUTSIDE the sewing ring.
That means bad news. All valves have some leaking INSIDE the sewing
ring, but not, repeat not, outside.
Another goody to know: prosthetic valves all need anticoagulation, tissue

valves don’t. Now, on to the specific valves.
NOTE get all the valve pics and make them smaller and put them together in
one pic.
Starr-Edwards
Ball-in-cage.
Oldest kind, can last a long time.
Kind of big and clunky, causes a lot of hemolysis.
Since flow goes around the sides, that’s where you’ll see a couple of jets
of regurg before the valve closes. (All valves have a little bit of regurg
before they close.)
Medtronic-Hall and Björk-Shiley
Tilting disc.
Complex flow pattern.
St. Jude and Carbomedics
(Always these double names! At least they settled on just one saint for
the St. Jude.)
Bi-leaflet, metallic >>> easy to see leaflet movement. These leaflets

can get stuck (by clot or tissue) and will produce severe MR.
Great durability, need anticoagulation.
They have signature regurgitant jet pattern to reduce clot formation.

LA
LV
Bileaflet mechanical prosthesis signature jets

158 Board Stiff TEE
Hancock and Carpentier-Edwards
(This really ticks me off, we already have a Starr-Edwards!)
Porcine bioprosthesis. They are getting better and better durability,

usually no need for long-term anticoagulation.
Has three metallic stents holding it in place, so you still see shadows.
They do have a built-in small central regurgitant jet.

LA
Small central jet
Ring
Struts
Leaflets
LV
Bioprosthesis signature jet
ROSS PROCEDURE
Take out the diseased aortic valve, take out the native pulmonic valve,
put the pulmonic valve in the aortic place, put a tissue graft in place of
the pulmonic valve.
TEST NOTE For me, the shadows from the tissue valve stents and the shadows
from the prosthetic valves can look pretty similar. Watch the video of this or study
the CD movies of these a lot because, on the test, you only have a minute or so to
look at these, and it can be pretty confusing. If there is one area where you can get
fooled, this is it.
There are stentless prosthetic valves. You won’t see the metal and their
reflections, but you may see a sewing ring. That is an extremely subtle
finding and easy to miss.
An issue with tissue valves is longevity. They tend to wear out faster.
You can measure gradients across these valves, but it can be challeng-
ing. You have to know where the tight spots are and you have to navi-
gate a straight shot through that spot. For example, for a Starr-Edwards,
you’ll have to slip your Doppler right through one of those regurgitant jets
around the sides of the ball.
A useful “Internal Medicine-y” thing to know about gradients: when you

are evaluating a valve and see a gradient you think is a little high, remem-
ber, all valves have some gradient. Try to find an old reading of the gradi-
ent before you ring the alarm bells. The thinking is the same as getting an
old ECG or CXR for comparison.
All valves are subject to embolism and endocarditis. So you’ll be look-

ing through some confusing reflections (try different angles to avoid the
metallic shadow) as you hunt for fistulas, abscesses, and clots.
VALVE REPAIR
Aortic Repair?
Doesn’t happen too often. A truly isolated injury to one cusp, maybe, but
surgeon enthusiasm for aortic valve repairs has faded a bit of late. More
often they replace the aortic valve.
Mitral Repair?
Now you’re talking. This is becoming to cardiac surgeons what appen-

dectomy is to the general surgeon.
First, you evaluate the mitral valve, looking to grade the severity. Four-
plus regurg pretty much mandates that “something be done,” often
a repair rather than a replacement. How do you know it’s 4+? Look for
systolic flow reversal in the pulmonic vein; that is diagnostic/pathogno-
monic/for sure for sure, good buddy, that the regurg is severe.

Pulmonary Vein Flow
le
e
to
ol
s
st
ia
Sy
D
l
sa
er
ev
lr
ria
At
Systolic reversal: grade IV MR
After the repair is done, you will look at the mitral valve again, making
sure, well, that the repair worked! Regurg gone (good), but not so gone
that you have moved all the way to mitral stenosis (not good).
160 Board Stiff TEE
Tricuspid Repair?
If the tricuspid valve has severe regurg, you will see reversal of flow in
the hepatic veins. (Similar to seeing systolic flow reversal in the pulmonic
vein with mitral regurg.) The surgeon may choose to repair it, though they
do this a lot less than mitral repairs.
After the repair is done, look for enough repair to stop the regurg (good),
but not so much that you have stenosis (not good). Sound familiar?
Pulmonic Repair?
Don’t see that much, though I suppose you could if you wanted to be
really cool.
With all these valves, what might you see that would make you NOT
want to do a repair?
Rheumatic, shortened, fused valves do not handle repairs well. Such a

valve needs replacement. You want to see a redundant valve, something
that gives you something to work with.
TRANSPLANTATION SURGERY
Heart
As far as TEE is concerned, there are only a few special things you’ll see
with a heart transplant. You’ll see extra-atrial tissue and see suture lines
that demarcate “the new from the old”.
From an anesthesia standpoint, one thing you will really be watching for
is signs of right heart failure—the big bugaboo of heart transplants. What
will you see, by way of review?
n RV enlargement
n Tricuspid regurg.
Of course you look for all the usual suspects—hypovolemia, global dys-
function, tamponade—as in every patient. Air, too, can bite you in the
butt, but it’s the right heart battling against “previously unseen” pulmo-
nary hypertension that will cause the most headaches.
Watch that RV!
Lung
Most lungs are, you sincerely hope, full of air, so it’s a toughie to exam-
ine them with TEE. Unless the lung is consolidated you might be able to
“see” the parenchyma > bad thing. Also with big pleural effusions you
can see the lung “floating” in the descending thoracic aortic views. You
can also see the presence of clot and fibrin in the fluid (pretty cool).
Aorta
Lung
Pleural effusion
So in those rare cases of lung transplants (not done too often or in too
many places), you’re left with doing the usual stuff—monitoring the heart
for signs of failure.
You will yawn when I say this, but you’ll be looking to monitor for hypo-
tension and cardiovascular instability; that is, you’ll watch for:
n Ventricle full or empty?
n Ventricle good or bad?
n Tamponade?
n Valves OK?
What more can I say—by now we keep coming back to the main things a
TEE does!
The TEE, your friend indeed in time of need.
Liver
If you put the TEE deep and turn it around, you can look at the liver,
though I don’t know of many observations you can make. (None were
mentioned at the meeting, or in the tapes or any books I read.)
I’ve been called into liver transplantation surgeries to put the TEE in and
look around. Of note, the varices that most of these patients have are
NOT a contraindication to placement of the probe.
You might want to take a look at the IVC as an index of fluid status and
Rt heart function>>IVC >2 cm in diameter suggests fluid overload (also
the lack of collapse with inspiration will confirm this).
162 Board Stiff TEE
QUESTIONS
1. When placing an LVAD you should look for, except:

A. Patent foramen ovalis
B. Mitral regurgitation
C. Atrial septal defect
D. Aortic regurgitation
2. The inflow cannula for the Tandem Heart is located in:
A. Right atrium
B. Femoral artery
C. Left atrium
D. Inferior vena cava
3. The mitral regurgitant jet of a bioprosthesis is, except:
A. Central
B. The severity is trace to mild
C. Is a washout jet to avoid clot formation
D. Comes from outside the ring
4. In the case of an anaphylactic shock the heart is/has:
A. Empty
B. Hyperdynamic
C. Low end systolic area in TG views
D. All of the above
5. In order to assess for contractility in an off pump CABG, you should,
except:
A. Wait for the surgeon to “drop” the heart
B. Look at the operative field to see how the heart is contracting
C. Use your filing pressures
D. The air behind the heart as it is elevated will interfere with the echo
image
ANSWERS
1. B
2. C
3. A
4. D
5. C
Bibliography
Perrino A, Reeves S. In: A practical approach to transesophageal echocardiography, 2nd edn.
Lippincott Williams & Wilkins; 2007.
Savage R, Aronson S, Shernan S. In: Comprehensive textbook of perioperative transesophageal
echocardiography, 2nd edn. Lippincott Williams & Wilkins; 2010.
Sidebotham D, Merry A, Legget M, Edwards M. In: Practical perioperative transesophageal echocar-
diography, 2nd edn. Elsevier Saunders; 2011.
CHAPTER
Congenital Heart Disease
17 Liliana Cohen and Daniel M. Shindler
“Oh, don’t ask why.”

—Jim Morrison–The Doors, Whiskey Song
TERMINOLOGY AND ASSOCIATIONS
Since cardiac embryology can be summed up as 9 months of looping

and unlooping, you can think of the congenitally malformed heart as hav-
ing taken the wrong turn at Albuquerque, and not just one time….
Where one congenital malformation can occur, others can occur.
So do a complete stepwise exam on everyone!!!
One congenital abnormality does not preclude another.
As a matter of fact, there are associations:
Atrial septal defect—pulmonic stenosis
Bicuspid aortic valve—coarctation of the aorta
Ebstein’s anomaly of the tricuspid valve—atrial septal defect.
You say pairs of associations are boring?
We say TETRAlogy:
1. Pulmonic stenosis—use transgastric and high esophageal views to
image the pulmonic valve, determine thickness and look for doming
(indicative of fused commissures).
2. Right ventricular outflow obstruction—mid esophagus 90 degree
views and transgastric views (when you get good).
3. Ventricular septal defect—120 degree mid esophagus, rotate your
wrist until you find it.
4. Overriding aorta—same 120 degree mid esophagus.
You should know the difference between overriding and straddling:
On the echo of tetralogy: the aorta “hovers over” the ventricular septum.
That is called overriding. 163
164 Board Stiff TEE
In atrio-ventricular canal defects an abnormal tricuspid valve “floats”

over the ventricular septum AND may have chordal attachments to
BOTH sides of the ventricular septum (like the legs of the rider on a
horse – it straddles the septum). The presence of straddling needs to
be sought during the TEE because it affects surgical repairability.
HISTORY
Before you start scanning, there is no shame in CHEATING. Talk to the

patient and get the history.
Was there a surgical repair?
Who did the operation (surgeon and institution)?
At what age?
For example, an operation done right after birth may be palliative and
just the first part of staged procedures. In patients born with hypoplastic
left hearts, a Blalock Taussig Shunt, may be followed by a Glenn Shunt,
followed by a Fontan. This is the Norwood heart. (Oh, don’t ask…).
Where is the scar—sternum or side of chest (ductus or coarctation repair)?
What year was the surgery?
There were no arterial switch operations for transposition until Jatene

and the Lecompte maneuver (aka zee French Connection) in 1975. The
surgeon maneuvers the pulmonary artery forward and then switches the
great vessels back where they belong.
But wait, there is more: the coronary arteries need to be moved back too.
If this is Greek to you, please know that before that time, transposition
of the great vessels was being repaired by the Mustard procedure (at the
Mayo Clinic—heh! heh!) using an intra-atrial baffle to redirect blood.
MUSTARD PROCEDURE
(Ake Senning did it first [without pants]—oh, don’t ask, just Google it.)
Think of the baffle as a pair of pants inside a single atrium—tailored by

a surgeon (possibly named Euripides Eumenides) to direct vena cava
blood into the “pant legs” of the baffle. The “waist band” of the baffle
directs the blood to the annulus of the venous atrio-ventricular valve.
By the way, anulus means “little anus” in Latin, maybe that is why we
prefer to spell it with two n’s.
PHYSICAL FINDINGS AND LABS
It’s gonna be bad if there is cyanosis, clubbing, or polycythemia!
Are the lungs clear or congested on that chest X-ray (that you never look at)?
Chapter 17 Congenital Heart Disease 165
MORE NAMES OF OPERATIONS
If you got a little befuddled by the name of an operation, here are more:
Glenn—cava to pulmonary artery shunt
Waterston—ascending aorta to pulmonary artery shunt
Potts—descending aorta to pulmonary artery shunt.
The original, modified, imitated, emulated, glorified, immortalized on film

(Alan Rickman and Mos Def), and still in use: Blalock-Taussig—subclavian
artery to pulmonary artery shunt.
Anything “Fontan” means only three heart chambers. There are no oper-
ations named Kermit (frog heart….three chambers…. Get it???).
Anything “Rastelli”—look for a conduit (or at least a patch).
You don’t need to know this.
Do not read it.
Damus Kaye Stansel (the WPW of heart operations—named after,

count them—three doctors).
Sometimes the name order is changed if Dr. Kaye’s or Dr. Stansel’s peo-
ple are operating.
It is an anastomosis of the distal part of the proximal pulmonary artery to

the side of the ascending aorta.
Blood flow to the pulmonary arteries is re-established by a graft from the

subclavian artery or from the thoracic aorta.
It is used to treat single ventricles with transposition of the great arteries

when there is obstruction of aortic flow due to subaortic stenosis.
We told you not to read this.
Identification and Sites of Venous and Systemic

Structures and Blood Flow
There is a “trick” to help you identify and follow the path of venous blood
through the congenitally malformed heart.
Inject some agitated saline into a vein. The saline contrast reflections show
the path of venous blood.
USING DESCRIPTIVE ECHOCARDIOGRAPHIC LINGO IN

TRANSPOSITION
Here are some suggestions for communicating with the grumpy person
holding the scalpel on the other side of the plastic curtain.
166 Board Stiff TEE
Transposition of the great vessels gets confusing real quick if you insist
on using certain terms.
Don’t say “right” ventricle—describe the ventricle instead.
The anatomic right ventricle may serve as the systemic ventricle but it
always has an infundibulum. This means that the atrio-ventricular valve is
separated from (not in fibrous continuity with) the semilunar valve.
Don’t say mitral valve—instead say: the atrio-ventricular valve that has
only two leaflets, that is shaped like the mitre of a bishop, and receives
blood from the (systemic or venous) atrium.
Don’t say pulmonary artery—say: the great vessel that bifurcates and has
no coronary ostia.
VENTRICULAR SEPTAL DEFECT
When it comes to ventricular septal defects your diagnostic mileage may

vary (making it appealing to test-writers and appalling to test-takers!).
The most common restrictive ventricular septal defect is the perimem-

branous defect.
So… always look for high-velocity systolic jets in the right ventricular
cavity.
The left-to-right shunt most frequently enters the right ventricle “peri-
where” the chordae of the septal tricuspid leaflets attach to the inter-
ventricular septum. The color flow jet is the Doppler equivalent of
the typical physical finding of a loud systolic murmur with a palpable
precordial thrill.
By the way, ventricular septal rupture is not congenital but it remains a

highly lethal complication of acute myocardial infarction with similar clini-
cal findings.
THE NATURAL HISTORY MAY FOOL YOU
Someone who had a loud systolic murmur during infancy (in the history
that you obtained, ha!), and now only has a soft diastolic decrescendo
murmur (on auscultation), may have closed a subaortic ventricular sep-
tal defect, but the aortic valve may not be adequately supported by the
healed septum. Say hello to my little friend: aortic insufficiency (caused
by a healed or healing ventricular septal defect).
But wait…there is more…
The lack of support in the area of the subaortic ventricular septal defect
may enlarge (or as President Bush would say: “aneurysmificate”) the
right sinus of valsalva.
Sinus of Valsalva aneurysms may rupture into the right ventricle.
This is where YOU come in:
Surgery to close a ruptured sinus of Valsalva aneurym may be

misguided by the echocardiographer who misses a persistent
ventricular septal defect that started the whole thing. The vsd signal
is masked by the rip-roaring systolic and diastolic Doppler signal
from the ruptured sinus of Valsalva aneurysm.
You tell the surgeon to close the ruptured sinus of Valsalva aneurysm,
but you find a persistent subaortic ventricular septal defect AFTER
they come off the pump and are ready to close the chest (rip-roaring
systolic and diastolic Doppler signal is not there to fool you anymore).
Still More VSD Pitfalls
Down syndrome is associated with partial, or complete, av canal defects.
As a result, the mitral valve may have a cleft—don’t forget to look for it.
It’s like a slice of pie was removed from the anterior mitral leaflet.
The tricuspid valve may send chordae (visible on TEE) to the crest of a
ventricular septal defect.
When it comes to chordal attachments to the interventricular septum, the

“septo-phobic” mitral says “no means no”; the “septo-phyllic” tricuspid
may straddle the septum on both sides making surgical repair a problem.
Patients with Eisenmenger’s may have no Doppler flow across a ven-

tricular septal defect; but there are clues… the pulmonary artery is way
bigger than the aorta, and there may be severe pulmonic insufficiency.
There is a rare ventricular septal defect known as a Gerbode defect, with

the shunt going from the left ventricle to the right atrium. The high-veloc-
ity systolic jet in the right atrium may be mistaken for tricuspid regurgita-
tion, and may be mistakenly used to diagnose non-existent pulmonary
hypertension (good thing you put the Swan in).
The mid-esophageal 75 to 90 degree TEE view can show three valves

simultaneously. A ventricular septal defect jet in this view can appear to
enter the right ventricle from the aortic valve. You are not going to fall for
that! If it originated in the aorta it would be a ruptured sinus of Valsalva,
and the color flow would be systolic AND diastolic.
The common perimembranous ventricular septal defect directs the

SYSTOLIC jet to the tricuspid valve. The less common subpulmonic ventric-
ular septal defect directs the jet (you guessed it) toward the pulmonic valve.
ATRIAL SEPTAL DEFECTS
Atrial septal defects may remain undiagnosed until adulthood. The mur-
mur is subtle and can be missed. Yes, yes, fixed splitting of the second
heart sound is a valuable clue.
168 Board Stiff TEE
You should know THREE different atrial septal defects.
The most common is the secundum defect. Surgeons love to fix these.
From the right atrium it looks like the circular center of a crater is miss-
ing. On TEE examination the thin membrane of the fossa ovalis is indeed
absent. To confirm the presence of a hole (as opposed to echo dropout),
use color flow Doppler and also look for a negative contrast effect when
you fill the right atrium with agitated saline. If it is not a hole but a flap,
then it is a patent foramen ovale. If the right atrium and right ventricle are
not dilated in an adult, it is not a hole. It’s a flap.
A defect of the “roof” of the right atrium, close to the sinus node, near
the entry of the superior vena cava into the right atrium is called a sinus
venosus atrial “septal” defect. It is associated with anomalous drainage
of a right pulmonary vein.
Lastly, primum atrial septal defect is due to failure of the atrial septum to
connect to the crux of the heart. This is part of the av canal defect and
is easily recognizable. However, you can easily miss an associated small
ventricular septal defect on a TEE.
Oh yes, we did say three, but… if you inject saline into a left arm vein
and the contrast shows up first in the LEFT atrium, you have got yourself
a persistent left superior vena cava with a fourth kind of “atrial septal”
defect—an unroofed coronary sinus.
PERSISTENT LEFT SUPERIOR VENA CAVA

(NO SHUNT)
Conversely, you can be born with a left superior vena cava that delivers
venous blood from the left side into the right atrium via an intact coronary
sinus. The coronary sinus gets dilated. Saline contrast that is injected
into a left arm vein will arrive in the coronary sinus and then in the right
atrium. There is no shunt, so there is no problem, right? An extra vein
never hurt anybody. Not so harmless if you use cardioplegia! W says:
“don’t cardioplegify a PLSVC”.
PULMONARY VALVE STENOSIS
Pulmonary valve stenosis may be isolated, or associated with other

lesions. It is part of the tetralogy of Fallot. It is also associated with atrial
septal defects. Tet + ASD = Pentalogy of Fallot (honest!). The normally
thin and notoriously difficult-to-image pulmonic valve may be thick (dys-
plastic) and it may dome—indicating fused commissures.
The physical exam of severe pulmonic stenosis includes a harsh, loud,

widely disseminated murmur. It sounds like you are clearing your throat.
Doppler examination parallel to the stenotic jet (harder to do than it
would seem from the high esophagus) gives the gradient. Look at the
pulmonic valve carefully before they start cutting the patient for a Ross
procedure. Right ventricular hypertrophy is also a clue to an abnormality
causing pressure overload.
BICUSPID AORTIC VALVE
This is the most common congenital heart defect in the adult. Caution!
Look at the aortic valve in systole. The diastolic appearance may be
deceptively similar to a normal trileaflet valve. In systole, both the thick
raphe and the fish-mouth orifice become easily recognizable.
Always look for associated coarctation. Aortic dissection should also be

kept in mind.
There is a rare abnormality called quadricuspid aortic valve. The four

cusps can make an “X” in diastole, and a square orifice in systole.
All stenotic valves with fused commissures exhibit a doming “hockey

stick” appearance.
LEFT VENTRICULAR OUTFLOW

ABNORMALITIES
We already looked at HOCM. Remember to pronounce it “Hokum”.

Cardiologists will all think you are hip. For the congenital stuff, think of
a washer under the aortic valve—a subaortic membrane. The old timer
stethoscope innuendo for subaortic stenosis on exam questions was
the conspicuous absence of an ejection click in a patient with “aortic”
stenosis.
In the age of echo, there is new stuff to confuse you with.
Who would think that a membrane UNDER the aortic valve would even-
tually cause aortic regurgitation? The turbulent systolic jet does just that!
The reason for operating to remove a subaortic membrane is to prevent
progressive destruction and consequent insufficiency of the aortic valve.
PATENT DUCTUS ARTERIOSUS
You know this one since cardiac embryology.
But how many have you diagnosed?
A small PDA may NOT be heard on auscultation. Observing diastolic flow

in the pulmonary artery may provide the initial clue to the diagnosis on
TEE. The flow originates at the pulmonary artery bifurcation, where it is
BOTH systolic and diastolic, and it is directed toward the pulmonic valve.
Pulses are prominent. Coarctation + downstream PDA + pulmonary
hypertension may reverse the shunt sending blue pulmonary artery blood
into the descending aorta. Physical finding: differential cyanosis (legs are
blue and right arm is pink).
Young hypertensives need TEE scrutiny of the aortic isthmus for

coarctation.
170 Board Stiff TEE
EBSTEIN’S ABNORMALITY OF THE

TRICUSPID VALVE
Mrs. Ebstein’s boy (the doctor) came up with this one—a while back in
the sixties (1866).
The normal tricuspid valve is more apically displaced than the mitral valve,
but the difference is normally much less than 10 mm. This becomes exag-
gerated in Ebstein’s with restricted motion of the septal tricuspid leaflet and
further (>10 mm) displacement of tricuspid coaptation into the right ventric-
ular cavity. It is associated with secundum atrial septal defect and can be
found with other complex congenital defects.
QUESTIONS
1. Which of these congenital abnormalities is most likely to result in a

dilated right ventricle?
A. Atrial septal defect
B. Pulmonic valve stenosis
C. Ventricular septal defect
D. Transposition of the great vessels (D-TGA)
E. Anatomically corrected transposition of the great vessels (L-TGA)
2. Which association is uncommon?
A. Pulmonic stenosis—atrial septal defect
B. Pulmonic stenosis—ventricular septal defect
C. Bicuspid aortic valve—coarctation of the aorta
D. Ebstein’s anomaly—atrial septal defect
E. AV canal—anomalous drainage of the left pulmonary vein
3. Sinus of Valsalva aneurysm ruptures into the:
A. Pericardium
B. Descending aorta
C. Right ventricle
D. Gerbode Windsock Thunderdome
E. Diverticulum of Kommerell
4. All the following require TEE evaluation of cardiac veins EXCEPT:
A. PLSVC
B. Scimitar syndrome
C. Sinus venosus ASD
D. “Snowman” chest X-ray
E. Aortopulmonary window
5. The following can be present AFTER “definitive” tetralogy repair
EXCEPT:
A. Pulmonic insufficiency
B. Dilated right ventricle
C. VSD
D. Lacerated coronary artery
E. Peripheral pulmonary artery stenosis
6. AV canal defects are associated with the following EXCEPT:
A. Down syndrome
B. Straddling tricuspid chordae
C. Overriding aorta
D. Mitral cleft
E. Goose neck
7. The following eponyms go with transposition EXCEPT:
A. Mustard
B. Senning
C. Jatene
D. Lecompte
E. Heinz
8. Least likely to permanently improve symptoms of hypertrophic
cardiomyopathy:
A. Alcohol
B. Myotomy
C. Myectomy
D. Beta blockers
E. Pacemakers
9. Atrio-ventricular discordance with ventriculo-arterial discordance
indicates:
A. Double outlet right ventricle
B. Tricuspid atresia
C. D—TGA
D. L—TGA
E. Truncus arteriosus
10. Single papillary muscle in the left ventricle is associated with:
A. Parachute mitral valve
B. Mitral valve prolapse
C. Cor triatriatum
D. Rheumatic mitral stenosis
E. Supramitral membrane
ANSWERS
1. Atrial septal defect results in dilatation of the right cardiac chambers

because of the right-side volume overload. Pulmonic valve stenosis
results in right ventricular hypertrophy because of the pressure
overload. Ventricular septal defect results in left ventricular
volume overload (oh, don’t ask why). Transposition of the great
vessels (D-TGA) needs to be repaired for survival, and will result
in dilatation of the systemic ventricle (anatomic right) with the now
abandoned Mustard repair. If D-TGA is repaired with the arterial
switch procedure, the right ventricle will be unaffected. Anatomically
corrected transposition of the great vessels (L-TGA) results in
dilatation of the systemic (anatomic right) ventricle.
How do you confuse an echocardiographer? Show him two shovels
and ask him to take his pick.
2. The longest one with the italics: E
3. Always pick C. You should Google E. D is like the Tooth Fairy, Santa,
and a cardiac surgeon with a sense of humor (non-existent).
172 Board Stiff TEE
4. E. Snowman cardiac shadow: the head of snowman is the superior

mediastinal shadow delineated by the SVC on the right, vertical vein
on left side and left brachicephalic vein superiorly. Body of snowman
is the heart. Snowstorm is brought to you courtesy of pulmonary
congestion.
Scimitar (shamelessly self-promoted): http://rwjms1.umdnj.edu/
shindler/scimitar.html
5. C. They usually do a good job closing the VSD. Thank God for small
favors.
6. C
7. E
8. E
9. D (fooled you)
10. A
AUTHOR’S NOTE: This may seem like “the ultimate bail”, but let me
emphasize—google any of these lesions/defects/operations and you will see
videos/power points/animations. If you want to learn this material, use this book
in conjunction with the wealth of material online.
CHAPTER
Artifacts and Pitfalls
18 Christopher J. Gallagher and Gian Paparcuri
When you are in the OR, you are forever asking yourself, “Is it real, or
is it Memorex?”. We get seduced by the great images, and you have
to shake yourself and say, “This is not a REAL LIVE picture, this is
an ULTRASOUND CREATION OF A PICTURE, and ultrasound can
fool you”.
Let’s grind through these monsters. Pay close, close, close attention to
the aortic dissection artifacts; that is what will scare the hell out of you in
the middle of the night.
Useful for any and all artifacts is the mantra, “Change the viewing
angle.”. That may allow you to see around a calcified or prosthetic valve.
Plus, if you see the same thing from a bunch of different angles, guess
what? It’s really there! (Maybe. We live in an uncertain world.)
Artifacts change their appearance and appear or disappear depending

on the view.
Real structures will remain constant and can be seen in multiple views.
n Error in imaging.
n Inconsistencies due to violations of the acoustic imaging
assumptions, equipment malfunction, ultrasound physics (physical
limitations of the modality), operator error (improper scanning
techniques), interpretation error.
n Interfere with image interpretation.
n Reflections not representing true anatomy.
n Part of an image will not represent the anatomic structure (reality)
accurately
u non-existing structures (not anatomically present) appear in an
image
u existing structures (anatomically present) missing from the image
u incorrect location, size, brightness of structures.
(See also CFD artifacts, pitfalls, and masses.)
173
174 Board Stiff TEE
Acoustic imaging assumptions (to assign the location and intensity of

received echoes):
n Reflections arise only from structures along the beam’s main axis.
Echoes detected originated from within the main ultrasound beam.
Problem: side lobes, grating lobes.
n Sound travels directly to a reflector and back (straight line).
Problem: refraction.
n Echo returns to transducer after a single reflection. Problem: mirror
images, reverberations.
n Sound (sound beam and its echo) travels in a straight line.
n Sound travels exactly at 1540 m/sec (constant, average
speed → time is distance). Problem: when the propagation speed
errors occurs, reflectors are placed in improper positions or at
incorrect depth (time is not equal to distance).
n The depth of an object is directly related to the amount of time for
an ultrasound pulse to return to the transducer as an echo (round
trip). The length of time for a single round trip of an echo is related
only to the distance traveled by the echo.
n Reflection’s intensity (strength) is related to tissue characteristics.
Problem: attenuation.
n Imaging plane is extremely thin. Problem: ultrasound beam has
some thickness in the perpendicular beam plane, reflections from
structures above or below a target reflector may be placed with the
target reflector on the display screen.
n Acoustic energy in an ultrasound field is uniformly attenuated.
ARTIFACTS
n Artifacts associated with US beam characteristics (beam width,

side lobe, grating lobe, edge shadow).
n Artifacts associated with multiple echoes (reverberations, comet tail
artifact, ring down artifacts, mirror image artifact).
n Artifacts associated with velocity errors (speed displacement
artifact, refraction, refraction artifact).
n Artifacts associated with attenuation errors (attenuation).
Artifacts Associated with US Beam Characteristics
US beam exits transducer as a complex 3-D bowtie shape (below

figure) with additional off-axis low-energy beams (side lobes and grat-
ing lobes). Strong reflector (highly reflective object) located outside
the main US beam (peripheral field) may generate detectable echoes
that will be displayed as having originated from within the main beam.
Misplaced echoes overlapping anechoic structure. Adjust focal zone to
the level of interest and place transducer at the center of the object of
interest.
Chapter 18 Artifacts and Pitfalls 175

Grating Side
lobe lobe
Focal zone Main

beam
Beam width: distal beam (widened beam) widens beyond the actual
transducer width (below figures).
Side lobe: multiple beams of low-amplitude ultrasound energy projecting

radially (off axis) from the main beam axis (from the edges of the trans-
ducer elements).
Multiple beams encountering same object duplicate the structure (false

targets), generating artifactual echoes of the true reflector, at its correct
depth but laterally from the true anatomy (the system assumes they origi-
nated from the main beam).
Weaker than the main beam, less acoustic energy, weaker returning echoes,
many are not actually seen (overshadowed by true echoes). Evident when
they do not conflict with real echoes or originate from strong reflectors.
If the beam is oscillating rapidly, the multiple artifactual echos produced

by the side lobes are displayed as a curved line at the same level as the
true object.
176 Board Stiff TEE
Options: reduce power (below figures).
Edge shadow: shadowing as a result of refraction at the edge of a cir-

cular structure (dropout phenomena). US beam intercepting tangentially
(poorly imaged around 10 and 2 o’clock).
Artifacts Associated with Multiple Echoes
In the presence of two parallel highly reflective surfaces, echoes may be

repeatedly reflected back and forth before returning to the transducer for
detection, displaying multiple echoes. The echo returning to the trans-
ducer after a single reflection will be properly displayed (proper loca-
tion). Sequential echoes will take longer to return and the processor will
erroneously place the delayed echoes at an increased distance from the
transducer (multiple equidistantly spaced linear reflections).
Reverberation artifact: echo signal returning to the transducer is reflected

back to the tissues by the surface of the transducer or a dense object
(two strong reflectors lying in the line, along the main axis of the ultra-
sound beam) creating multiple unreal superimposed images, equally
spaced, ladder-like appearance at ever increasing depth. Pulse bounces
back and forth between the two reflectors, sending multiple echoes back
to the transducer. The first two echoes arise from true anatomic struc-
tures in their correct position. Example: PAC, calcified aorta (strong
reflectors), makes sound wave ricochets (rebounding) back and forth
between transducer and structure. Readjust the angle; reducing gain or
the contrast might not eliminate ‘em.

178 Board Stiff TEE
Reverberation artefact
A A1
Linear reverberation: ascending aorta, mimics dissections.
Comet tail artifact (form of reverberation with a triangular, tapered shape):

reflective interfaces, sequential echoes and displayed images are so
closely spaced that individual signals are not perceived. The last echo
may have decreased amplitude secondary to attenuation (decreased dis-
played amplitude).
Ring down artifacts (supposed comet tail variant): main US beam

encountering a ring of bubbles with fluid trapped centrally. Resonant
vibrations from the pocket of fluid between air bubbles creates a con-
tinuous sound wave transmitted back to the transducer. Displayed as a
bright reflector with echogenic line (or series of parallel bands) extending
posteriorly (below figures).


Mirror image artifact (type of reverberation): duplicate of real structure.

Primary beam encounters a highly reflective interface (mirror-like spec-
ular reflector), the mirror redirects the ultrasound beam towards the
second reflector (the structure), the reflected echoes then encounter
the “back side” of the second reflector (the structure) and are reflected
back toward the reflective interface before being reflected back finally
to the transducer. The transducer “thinks” the sound is coming from the
original direction in which it was sent, but it takes longer to return, so
it “sees” the object farther, deeper. Duplicated echogenic lesion is mis-
placed distant—deeper—farther away and equidistant from the deeper
strongly reflective interface. Common at the level of the pericardium or
diaphragm, with the pleural–air interface acting as the strong reflector
(below figures). Options: change the angle (different orientation).

180 Board Stiff TEE

Artifacts Associated with Velocity Errors
The speed of sound within different materials (air 330, fat 1450, soft tis-
sue 1540, bone 4080 meters per second) depends on their density and
elastic properties. US image processing assumes a constant speed of
sound of 1540 m/sec. When sound travels through material with a veloc-
ity significantly slower than the assumed 1540 m/sec, the returning echo
will take longer to return to the transducer and will be displayed deeper
on the image.
Speed displacement artifact: the ultrasound system assumes a travel

velocity of 1540 m/s (since time is distance, if ultrasound beam travels
faster than assumed, faster speed equals earlier return, echoes will be
falsely displayed closer than they really are).
Refraction: change in direction (bending away from straight line path) of

sound wave traveling from one medium to another (≠propagation speed).
Occurs only when there is an oblique incidence—non-perpendicular
(Snells’s–Descartes’ law).
n Transmission angle/incident angle = propagation speed medium
2/medium 1 (when propagation speed in medium 2 is greater, the
transmission angle is greater than the incident angle).
Normal to surface
Incident ray Reflected ray
θ1 θ1
n1
n2
θ2
Refracted ray
θ1 (incidence angle) > θ2 (transmission angle) because n1 > n2
Incident Reflected
ray ray
θ1 θ1
V1
V2
θ2
Transmitted ray
θ1 (incidence angle) < θ2 (transmission angle) because V1 < V2

Angle of incidence
θ1
Surface Normal n1
n2
Angle of refraction θ2
sin θ1
RI =
sin θ2
182 Board Stiff TEE
Refraction artifact: based on the assumption that beam travels in a

straight line, returning echoes from refraction misplace their true location
(below figures).
C1
C2
Artifacts Associated with Attenuation Errors
Attenuation: absorption and scatter (greater distance traveled, more

attenuation). Compensation amplification (TGC) of echoes that take
longer to return to the transducer, that return later (>earlier returning
echoes) make image appear more uniform in he deep field.
Shadowing: when the US beam encounters a focal material that attenu-

ates the sound to a greater extent [or a lesser extent] than the surrounding
tissues (high acoustic impedance), the strength of the beam distal to this
structure will be weaker—shadowing—little US energy remains to image
deeper tissues [or stronger—increased through transmission].
Thus when US beam encounters a strongly attenuating or highly reflec-

tive structure (structure with high attenuation), the amplitude of the beam
distal to this structure is diminished (ultrasound beam is weakened), the
echo returning from structures beyond (deeper) the highly attenuating
structure will also be diminished, weakened (dark or hypoechoic band),

resulting in poor resolution within the shadow.
Calcified tissue and metallic valves eat up all the ultrasound waves (look-
ing white) and do not allow ultrasound to go further, throwing a distal
shadow.
Strong
attenuator
Loss of echoes (echo dropout) behind strong reflector.

184 Board Stiff TEE
Weak
attenuator
Color of the shadow can be black or white.

Near-field clutter: noise near transducer arising from high-amplitude

oscillations of piezoelectric elements. Problem: identify echogenic struc-
tures in the near field.
Electronic interface: linear “dot” artifact affecting the whole image

(electrocautery).
Incorrect gain: create and obscure information, reduces lateral resolution.

Erroneous appearance of spontaneous echo contrast (SEC), no “swirl-
ing” with grainy appearance.
Range ambiguity: At high pulse repetition frequency (don’t be afraid to go

back and look at the physics in Chapter 5 again), the ultrasound can get
fooled into thinking an object is in the wrong location. A second pulse is
sent out before the first one comes back, so the machine can’t tell where
the signal came from.
The end result of this chicanery? A Swan might appear in the left ven-
tricle (oops!), or an aortic valve might appear in the middle of a cham-
ber (how can the patient be so stable with his aortic valve sitting in the
middle of the left ventricle?). Change the depth of the image (that will
alter the pulse repetition frequency) and that should make the “mystery
object” disappear.
DOPPLER ARTIFACTS AND PITFALLS
The main Doppler headache, and a recurring point in the meeting and
tapes, is aliasing. You will hear a million times (and no doubt be asked)
to differentiate between continuous-wave Doppler (range ambiguity but
no problem with aliasing) and pulsed-wave Doppler (range certainty but
problems with aliasing).
As before, don’t be afraid to go through the physics in Chapter 5 again.

You finished physics a looooooooooooooooooooooooong time ago, and
this stuff can be a little tricky.
Aliasing: you can’t measure a maximum velocity.
Wrong angle: remember the cosine thing from long ago in a galaxy far,
far away? To get an accurate measure, you have to be looking “straight
up the pipe”.
If the angle is more than 20 degrees off kilter, your Doppler will be
inaccurate.
Beam width: this is the “Doppler equivalent” of the problem with side
lobes. You are trying to see, for example, the left ventricular inflow from
the left atrium, but your beam width is too wide and you also see an aor-
tic regurgitant jet at the same time, screwing up the signal.
186 Board Stiff TEE

DOPPLER BEAM WIDTH
Normal Aortic
mitral regurgitant
inflow flow
Can’t get
clean reading
Another problem with beam width is “the third dimension”. The beams
are not perfect 2-D structures. There is a thickness to them, so you may
get an abnormal signal from something “out of the plane” of the image,
but still “pick-upable” from the beam.
Mirror image artifact: A symmetric but weaker signal appears in the oppo-
site direction of what you measure.
When this happens, reduce the gain.
Ghosting: remember the old chestnut about seeing the “green flash” of
the sun just as it is setting? No doubt many a retina has gotten fried to a
crisp looking for that. Ghosting is sort of like that.
With color Doppler, if the patient has a strong reflector, like a metallic
valve, you can get a brief flash of blue or red that doesn’t correspond to
any flow pattern. It’s like, you know man, just like this big flash, so don’t
get all bent out of shape, man.
STRUCTURES MIMICKING PATHOLOGY
This is total Visual City, USA, and a lot of it you’ve heard of before.
All kinds of normal things and embryonic leftovers are floating around
the heart, gumming up the works and throwing you for a loop. The list is
quasi long, but each individual one just takes a little memory work and
pattern recognition.
Moderator band: A big muscle band in the apical third of the right ven-
tricle (never in the left). The moderator band has part of the conduction
system in it.
MODERATOR BAND
Thar
she
blows!
ME 4-Chamber
Pleural effusion: well, this isn’t exactly mimicking pathology, hell, it IS

pathology. But anyway, you see this lateral and posterior to the heart.
Since the heart is on the left side (usually), you usually only see left pleu-
ral effusions.
Nodulus arantii: kick ass name, huh?
NODULUS ARANTII
Cool, knobbly
dealies
ME AV SAX
Little knobby fibrous thingies at the center of the free edge of each cusp
of the aortic valve. Dig the Latin name.
Lambl’s excrescences: better name, even, than nodulus arantii. I hope I

never get excrescences anywhere.
Filamentous thingamabobs attached (usually) to the aortic side of the

aortic valve leaflets.
LAMBL'S EXCRESCENCES
Voila!
ME AV LAX
Coumadin ridge: atrial tissue dividing the atrial appendage from the left
upper pulmonary vein. Can look like a clot, but don’t fall for it.
I already drew this once, don’t get greedy.
Pectinate muscles: parallel ridges along endocardial surfaces of the left

and right atria, as well as both appendages.
188 Board Stiff TEE

PECTINATE MUSCLES
Great
pecs!
ME Bicaval
Crista terminalis: little valve-like thingie at the junction of the superior

vena cava and the right atrium (so you’ll see it to the right side of a bi-
caval view).
Eustachian valve: same kind of deal over on the other side, where the
inferior vena cava meets the right atrium.
Both of these were drawn a while ago. Re-read the book, if you missed it.
Thebesian valve: same kind of deal, but now at the entrance to the coro-
nary sinus. This can make it hard to place the retrograde cannula, since it
is, in effect, a valve.

THEBESIAN VALVE
Valve
“guarding”
coronary
sinus
ME 4-Chamber
(Insert)
Focus on IAS
Chiari network: kind of like a Lambl’s excrescence in the atrium.
Wall motion abnormality: this isn’t really an anatomic pitfall, but it’s worth
noting here, as Dr. Grichnik did in her lecture (and from which I hope she
doesn’t mind I stole everything!).
Epicardial pacing can make the septal wall appear hypokinetic or dys-
kinetic. The normal sequence of depolarization doesn’t occur, so you
could be fooled into thinking there was a coronary occlusion leading to
this regional wall motion abnormality.
QUESTIONS
1. If the artifact is in line with the axis of the transducer it is most likely:
A. A side lobe artifact
B. A mirror artifact
C. A displacement artifact
D. An acoustic impedance artifact
E. Best to ignore it
2. If the artifact is in line with the axis of the transducer it is least likely:
A. Reverberation artifact
B. Acoustic shadowing
C. Ring down artifact
D. Comet tail artifact
E. Range ambiguity
F. Mirror artifact
G. Most likely not a falsely real artifact
3. Ebstein’s anomaly is characterized by all of the following except:
A. Apical tricuspid valve
B. Atrialized right ventricle
C. Associated with Wolff-Parkinson-White syndrome
D. Right to left atrial shunts
E. All of the above
F. None of the above
G. Some of the above, but not quite all of the above
ANSWERS
1. B
2. E
3. E
CHAPTER Related Diagnostic
19 Modalities
Steven Gill, John C. Sciarra and Christopher J. Gallagher
STRESS ECHOCARDIOGRAPHY
Stress TEE is the same deal as a transthoracic stress echo. You get a
baseline reading, stress the heart with some dobutamine, kick up the
heart rate to marathon levels and do another exam. Besides seeing a
heart running like a race horse, you will also see the hyperdynamic heart
and any new wall motion abnormalities compared to the baseline rest-
ing heart. When you crank up the dobutamine, new wall motion abnor-
malities might pop-up revealing at risk myocardium, right? Well, not
always. Sometimes, low-dose dobutamine improves ventricular function,
but othertimes, you might see a biphasic response which is improving
response until reserve is exhausted. At which point you start to fall off
the old Starling curve and ventricular function declines to the point of
what we call scientifically—“Dead-as-a-doornail” myocardium. That is no
response to redbull levels of whipping the heart.
MYOCARDIAL PERFUSION SCANNING
Instead of looking for wall motion abnormalities, there are new dyes that
allow you to tag the blood and see the blood flowing to the myocardium
itself, thereby, healthy oxygen-demanding tissue shows up better then
ischemic tissue and at-risk myocardium can be identified.
EPICARDIAL SCANNING
You cannot do TEE on everybody because of things like esophageal

pathology or the 2% of people you can’t get a probe into. So you can
go with epicardial scanning. A probe is covered with a sterile sheath and
goop and passed onto the surgical field, placed on a sound conductive
spacer (remember: air does not transmit sound waves as efficiently as
goop), and is then placed directly on the patient’s chest. As mentioned
in another section, kiddie cardiac surgery often uses epicardial scanning.
You are not hindered by bronchi getting in the way, so you can get a look
all over the place.
The Gologorsky method of creating a spacer for epicardial scanning: just

fill the tip with gel and place in a sheath. Another common method is to
fill a sterile glove with gel or water and use that as a stand-off or spacer.
191
192 Board Stiff TEE
CONTRAST ECHO
Look at TEE images. There is a lot of dropoff and uncertainty around the
edges, especially off to the sides. With injectable contrast, the insides
light up! Making the endocardium definition much easier to identify. This
makes for easier measurements of cardiac output and wall motion calls.
UTILITY OF TEE RELATIVE TO

OTHER DIAGNOSTIC MODALITIES
You can look at this from a lot of different angles.
TEE VERSUS ECG
Regional wall motion abnormalities are the bomb when it comes to

detecting ischemia.
First perfusion is disturbed, then diastolic dysfunction occurs (hard to

pick up right away), then segmental wall motion abnormality occurs (TEE
to the rescue!), then later ECG changes occur, and then later than that,
chest pain occurs (unless, of course, the patient is denervated from dia-
betes or is post heart transplant).
So, to summarize, TEE is better than ECG to detect ischemia.
Of course, putting on an ECG ain’t no biggie and placing a TEE is.
TEE VERSUS TTE
Lot of pluses and minuses in this comparison.
TTE is easy to do in the awake patient and is comfortable. In the awake

patient, TEE requires topicalization, sedation, and all the spooky aspects
of a MAC anesthetic (oversedation, sympathetic stimulation—POP goes
the aneurysm!).
TTE provides a better look at the front of the heart, though the ribs and lungs
restrict your acoustic windows. The TEE provides a better look at the back
of the heart, though there are some limitations to the windows here too.
With just the right window, TTE can get a look at the aortic arch that the
TEE might miss. So in certain cases, TTE may be better at seeing a high
arch dissection.
TEE VERSUS CORONARY ANGIOGRAPHY
Angiography wins the “visualize the coronaries” contest all hollow.
Femoral artery sticks are invasive, and can lead to pseudoaneurysms,

retroperitoneal bleeds, and all kinda unholy terror. TEE obviates that,
though TEE has its own complications.
Chapter 19 Related Diagnostic Modalities 193
TEE VERSUS SWAN
TEE lets you see what’s wrong in a hurry. A Swan may be hard to get in a
hurry (CVP is low, can’t hit an IJ or a subclavian vein), and a Swan gives
you numbers requiring some leap of faith. But a Swan “stays in” and may
be useful for long-term ICU care. You can’t be popping an echo every
5 minutes, although there are some longer-term ICU-focused TEE probes
on the market.
What’s that up ahead, at the end of the yellow brick road? Is it the
Emerald City?
No.
It looks like there are a few questions.
QUESTIONS
1. You are performing epicardial scanning on a 2-month-old and cannot

obtain an image, reasons include:
A. The focus of the beam is too distal to the heart
B. You forgot a spacer to properly allow conduction of the beam
C. The patient’s heart is too small
D. The TEE machine is not plugged in
E. All of the above
2. Which modality allows for earliest detection of myocardial ischemia:
A. Swan ganz catheter
B. TEE
C. ECG
D. End tidal capnography
E. Blood LDL cholesterol level
3. Dobutamine can cause all the following except:
A. Increase in cardiac output
B. Decrease in blood pressure
C. Decrease in cardiac output
D. Myocardial ischemia
E. World peace
4. TTE may allow for better visualization of parts of the:
A. Heart apex
B. Aortic arch
C. Coronary sinus
D. Papillary muscle
E. Medulla oblongata
5. TEE usually can remain in the esophagus up to:
A. 1 hour
B. 6 hours
C. 72 hours
D. Until your shift ends
E. Indefinitely
194 Board Stiff TEE
ANSWERS
1. E
2. B
3. E
4. B
5. C
Bibliography
Bagur R, Rodes-Cabau J, Doyle D, et al. Usefulness of TEE as the primary imaging technique to
guide transcatheter transapical aortic valve implantation. J Am Coll Cardiol Img 2011;4:115–24.
Memtsoudis SG, Rosenberger P, Loffler M, et al. The usefulness of transesophageal echocar-
diography during intraoperative cardiac arrest in noncardiac surgery. Anesthesia Analgesia
2006;102:1653.
Öwall A, Ehrenberg J, Brodin L.-Å. Myocardial ischaemia as judged from transoesophageal echocar-
diography and ECG in the early phase after coronary artery bypass surgery. Acta Anaesthesiol
Scand 1993;37:92–6.
Shapiro SM, Young E, De Guzman S, et al. Transesophageal echocardiography in diagnosis of infec-
tive endocarditis. Chest 1994;105:377–82.
Youn H.-J., Foster E. Transesophageal echocardiography (TEE) in the evaluation of the coronary
arteries. Cardiology Clinics 2000;18:833–848.
CHAPTER Intraoperative 3-D
20 Echocardiography
Gian Paparcuri
Transesophageal echocardiography is probably the most frequently used

imaging technique in cardiac surgery. This powerful technology pro-
vides timely information, about cardiac structures (anatomy) and function
(hemodynamics) without disrupting the surgical workflow.
Developed decades ago, far from being a dead technology, echocar-

diography is a constantly evolving technique, requiring new skills and
expertise. Over the years echocardiography has evolved from 2-D into
3-D. Just like the movies. Some authors say that “3-D represents the
natural evolution of 2-D echocardiography”. But why do we need 3-D
echocardiography?
The answer is simple:
To provide more accurate information to the surgeon
To improve the communication with the surgeon.
3-D Echo:
n Enhances the illusion of depth perception.
n Offers a better appreciation of individual patient anatomy.
n Facilitates the understanding of complex cardiac pathology.
n Improves appreciation of the relationship between cardiac
structures by allowing visualization from different angles.
n Expedites the study of ventricular volumes by displaying
geometrically complicated chambers, such as the right ventricle.
n Eliminates the assumption of specific geometric shape of the
ventricles, when quantifying volume and ejection fraction. 3-D does
not assume the heart has a particular shape, because you see it as
it is (quantification is more accurate).
n Reduces measurement variability.
n Offers the potential to slice the dynamic cardiac structures in
infinite planes through the three dimensions.
With 3-D echocardiography, people who aren't echocardiographers can

appreciate valve anatomy and physiology in three dimensions. Surgeons
tend to very much appreciate 3-D images because the echo image looks
exactly like what they see when the heart is open. Finally, for those of
195
196 Board Stiff TEE
you taking the well-known echocardiography course in San Diego,

expect to see a lot of 3-D. It seems like the speakers are not allowed to
talk about echocardiography if they don’t complement their presentation
by adding some 3-D images.
Believe it or not, there are 3-D detractors out there. People are afraid of
change. But it is human to feel anxious when a new technology is trying
to be introduced. It is easier to welcome this new technology when limi-
tations of existing technology are appreciated.
n Mental reconstruction of a 3-D structure
n Assumptions
2-D echocardiography is the representation of a 3-D structure (the heart)

in 2 planes. The echocardiographer has to mentally visualize (cogni-
tive 3-D reconstruction) a complex 3-D structure based on a series
of 2-D views in order to obtain a 3-D object (the heart). Another limita-
tion is that 2-D echocardiography is based on a lot of assumptions. We
assume specific geometric shapes of cardiac structures for ejection frac-
tion quantification every day. Even worse, we assume the whole ven-
tricle behaves like the one displayed on the screen. Many times, these
assumptions fail because of the presence of RWMA.
To be honest, 3-D echocardiography is nothing new under the sun—it’s

been here for more than 15 years. But because of early limitations it was
not universally applied. In its beginnings 3-D echocardiography was a
tedious process: slow acquisition process, images acquired in 2-D had to
be reconstructed in 3-D using a program. It used to take a long time, sim-
ply because it was not really 3-D. Displaying 3-D images requires a huge
amount of data to process. More than 60 heart beats—images, acquired
over several hundred consecutive beats had to be gathered with the ECG
or respiratory rate for subsequent volume rendering and cropping. And after
this time-consuming process the computer was able to reconstruct (offline)
a 3-D image which very often was of poor quality with frequent artifacts. In
its early years 3-D echocardiography was very impractical in the operative
theater. New technology overcomes some of these limitations.
With real time 3-D gone is the need to sum information for 61 beats. What
is new about it these days is that instead of images that are acquired in 2-D
and then reconstructed into a 3-D image using software, the images can
be acquired in 3-D volumes and displayed in real time. The new technol-
ogy uses a special scanner (probe). The scanner used a unique matrix array
to scan a volume without physically moving the transducer. The transducer
gathers information from a single beat, resulting in a very low-latency display.
TEE PROBES
Non-3-D echocardiography probes use a limited number (64–128) of

piezoelectric elements (crystals) to scan tissue. Sequential (phased) acti-
vation of individual crystals generates an ultrasound beam that is steered
back and forth over a 90° angle to sweep a flat, “pie-shaped” scanning
plane or sector. 3-D echocardiographic probes have on their tips more
than 2500 active elements, incorporated onto the probe, conforming a
Chapter 20 Intraoperative 3-D Echocardiography 197
rectangular grid of 50 rows and 50 columns for a total of 2500 indepen-

dent piezoelectric crystals, generating a matrix array.
Individual piezoelectric crystals are activated and generate a US beam

that can be steered in the azimuthal (x-y) and the elevational plane (x-z)
over 90° to cover a pyramidal scanning volume.
How to create a 3-D display? How does it work? It’s a simple 4-step
process. 3-D echocardiography is based on volumetric techniques.
Ultrasonic data about a volume of tissue are obtained with the probe
scanner. This is the first step (data acquisition). The fancy scanner with
thousands of crystals (matrix array probe) is able to obtain all the infor-
mation required from the tissue in order to create this pyramid-shaped
volume. All in real time, in just one beat. Simpler and faster.
Step 2 involves temporary data storage within the computer random

access memory (RAM) of the US machine.
Step 3 is data processing, requiring the transformation of the scanned

raw data (volume of tissue) into a code (3-D dataset) necessary to gener-
ate 3-D objects on the display. This is actually 2 sequential, integrated
processes: conversion and interpolation.
n Conversion: raw data are placed into a Cartesian volume with each
point assigned x-y-z coordinates and an echo intensity value. The
product of this step is a group of points with distinctive echogenic
characteristics and a known position in space, called voxels or
volume of pixels, encrypting the physical characteristics and
location of the smallest cube in the dataset, similar to pixel size in
2-D image resolution. Large voxels are generated when raw data
are available for fewer points in the space and interpolation has to
fill wider gaps. Still not a clear 3-D image.
n Interpolation: filling the gaps or space between all the known points
in space with data points of similar characteristics. The result is a
smooth surface 3-D object.
Volume scanning generates a data stream using the computer RAM

and creates voxels while scanning, with near simultaneous conversion
and interpolation. The matrix array probe scans over the elevational axis
resulting in a pyramid-shaped volume with a curved base.
The surfaces and volumes are then rendered for display. Objects and
their relative positions in this 3-D space or coordinate system can be
quantified.
Finally, step 4 or 3-D image display: makes 3-D dataset visible.
3-D graphic reproduction is the product of a computer graphics render-

ing technique of the 3-D echo dataset (2 steps):
n 1st step is segmentation: separates the object to be rendered
from surrounding structures (differentiates between cardiac tissue,
blood, pericardial fluid, blood, air; given their diverse physical
properties and different ability to reflect US; this requires setting
198 Board Stiff TEE
a threshold of echo intensity). The program excludes from further

processing any point with echo intensity equal to or lower than
blood, and delineates the 3-D surfaces of cardiac tissue.
n 2nd step: The 3-D dataset undergoes 1 of 3 increasingly complex
rendering techniques to create a visible 3-D object: wireframe
rendering, surface rendering or volume rendering.
Wireframe rendering: The simplest technique. Defines and connects
equidistant points on the surface of a 3-D object with lines
(wires) to create a mesh of small polygonal tiles. Smoothing
algorithms refine the narrow angles making rudimental object
appear more real. This technique is used for relatively flat
surfaces such as the LV and the atrial cavities. It cannot display
objects/structures with complex shapes, such as valves (requires
greater anatomic detail for meaningful analysis). Processes
small amount of data (fast and efficiently performed on basic
computers).
Surface rendering: similar to wireframe but defines more points
on the surface of a 3-D object making the lines joining them
visible. Displays details of a 3-D surface and makes morphologic
assessment of the corresponding anatomic structure feasible.
Generates 3-D objects with rendered surfaces and a hollow core.
Volume rendering: displays 3-D objects with a rendered surface
and details of its inner structure. Enables the potential display of
every voxel of the 3-D object permitting a “virtual dissection”.
Although composed of voxels, 3-D objects are seen in the screen as pix-
els of a 2-D image. Perspective, light casting and depth color coding are
used to give a visual sense of depth and reality. Stereoscopic displays
and holograms may display a 3-D rendered object more realistically but
are currently used only for research purposes. Any volume-rendered 3-D
object can be freely rotated on the display screen to be viewed in any
orientation either as a static or a moving object.
3-D MODES
LIVE ZOOM FULL VOLUME

Acquired over a single Also live but magnified ECG gated over multiple
heart beat subsection of 3-D volume heart beats (4 to 7 beats)
Narrow angle (mid spatial Interrogates specific Loops of merged sub-
resolution) region, i.e. valve, inter-atrial volumes displayed “on
Good temporal resolution septum line” but not “live” (requires
(20–30 Hz) Provides high spatial time to stitch together each
resolution loop)
Lowest temporal resolution, Large 3-D volume created
lowest frame rate (<10 Hz) from sub-volumes stitched
but highest spatial together and synchronized
resolution to 1 cardiac cycle
Stitch artifact
Lowest spatial resolution
3-D images can be (post-processing) manipulated, rotated, cropped

(sliced along the 3 axes) at the will of the echocardiographer to analyze
anatomical details. The easily recognized AV is often used as reference
to orient the 3-D cardiac image in space.
Limitations: current technology does not allow even simple on-line mea-
surement of length and area within the 3-D image. A grid of dots (5 mm
apart) can be overlaid in real time (live or zoom) mode on any stored 3-D
image to estimate dimensions (see below).
MITRAL VALVE
3-D provides a “surgical view”—the same image that the surgeon will see
in the field. This is very important when repairs are being planned. It can
also accurately measure the size of the orifice. MV position within the
heart and its relationship to the esophagus allows perpendicular align-
ment of the TEE US scanning plane making the MV an easily imaged
structure!!! It is important for the ecocardiographer to provide the sur-
geon with detailed information of MV pathology, etiology, and a clear
understanding of individual patient (surgical planning).
The use of 3-DE has significantly contributed to a better understanding

of normal MV anatomy and the pathology of MV dysfunction:
n Spatial manipulation, assessment in anatomical and surgical
orientation for discussion with the surgeon.
n 3-D CFD for EROA.
The MV can be easily imaged using all the 3-D imaging modes
described:
n Live (from 2-D ME 4C) yields only a portion of the MV.
n Full volume.
n Zoom is the modality of choice to view detailed anatomy of the
entire MV with adequate temporal and spatial resolution. The zoom
acquisition starts with imaging the entire MV in 2-D, preferably
with the AV in view. The displayed pyramid-shaped 3-D image can
be manipulated on screen in real time to view the MV from any
perspective.
Stored MV 3-D images can be cropped on any plane to further delineate

leaflet morphology.
Typically, the MV 3-D image is presented “en face” in the surgeon’s

orientation as viewed from the LA with the AV at the top of the image
and the LAA to the left.
The role of 3-D transesophageal echocardiography is expanding to become

a powerful tool guiding surgical repair (treatment of choice for MR). In mitral
stenosis, 3-D echo can consistently identify MV commissural fusion and
200 Board Stiff TEE
predict the success of MV balloon valvuloplasty. Some authors have pro-

posed planimetry by real-time 3-D echocardiography as a “gold standard”
in the assessment of MS.
LV ASSESSMENT
n 2-D limitations: “eyeballing assessment”, time consuming,

geometrical assumptions, foreshortened views.
n 3-D benefits: largest cardiac structure (in normal hearts) and 3-D
(full volume) is the only imaging modality that can capture the
entire LV volume at sufficient frame rate (25 Hz) allowing dynamic
assessment.
LV VOLUME
n 3-D-guided biplanes: by simultaneously displaying 2 perpendicular

2-D planes (ME 4C and ME 2C combination minimizes LV
foreshortening) cutting the LV along its long axis at the true apex.
Allows calculation (by applying modified Simpson biplane methods
of disks to ES and ED frames) of LV volume, EF, mass. Limitations:
still relies on geometric assumptions.
n Direct volumetric analysis: rendering a cast of the LV cavity and
measure its volume throughout the cardiac cycle. Required
identification of 4 LV walls and apex derived from full-volume 3-D
dataset. Semiautomatic endocardial border detection creates
a dynamic cast of the LV endocardial cavity. EDV and ESV are
measured and SV and EF calculated. It is a more accurate method
for LV volume in patients with abnormal ventricular shape or
regional wall motion abnormalities due to a better alignment
through the cardiac apex—inclusion of more endocardial surface
during analysis and the lack of geometric shape assumptions (more
reliable especially for less experienced users).
LV volume 3-D quantification is more reproducible than 2-D, and cor-

relates well with MRI-obtained volumes. For regional LV function/wall
motion, the 3-D LV cast is automatically divided into 16 wedges plus an
apical cap and is based on a change in LV chamber volume over time.
High sensitivity and specificity. 17 segments! Where have we seen this
before? A full-volume 3-D dataset can be cut in multiple 2-D planes and
displayed simultaneously as a series of parallel SAX planes similar to a
MRI view.
RV ASSESSMENT
RV 2-D assessment is difficult because of its crescent shape and

complex geometry (a lot of assumptions). 3-D overcomes 2-D limita-
tions allowing full-volume 3-D dataset acquisition for RV size, volume
and function with good correlation with MRI and better reproducibility
than 2-D.
CONCLUSION
RT3-D is one of the most significant developments of the last decade

in cardiac US imaging. The challenges are that it requires new basic
skills to manipulate 3-D datasets and properly orient 3-D images.
Intraoperative real-time 3-D transesophageal echocardiography elevates
experience to a new fascinating and challenging dimension. Over time
there will be quicker acquisition of 3-D full-volume and 3-D color flow
Doppler. This combined with on-line automatic 3-D LV and RV recon-
struction will offer the most precise tool to assess and monitor LV and
RV volumes. The next generation of echocardiographers will, “grow up”
on 3-DE, and in the same way that 2-D echocardiographers today can't
imagine how people managed with M mode, the next generation is going
to say “how did we manage with 2-D?”.
CHAPTER The Structured TEE
21 Examination
(or guidelines for a comprehensive evaluation)
John C. Sciarra
When you do a TEE exam you gather information for yourself. So the
order in which it is done is your preference. But, if someone comes after
and wants to look at your exam, it can be difficult to sort out all the infor-
mation. That is why this chapter seeks to suggest a standard and logical
way to perform your exam. In addition, if you do it the same way each
time you will get more efficient. Plus the order suggested here just makes
sense. It is broken down into three sections. First is ventricular function,
second are the valves, and third are associated structures. This way you
can confidently blast through a comprehensive examination and be con-
fident you did not overlook a major item.
Preliminary checks:
n Confirm that there is no absolute contraindication for TEE insertion.
n Treat the probe gently (expensive), always use a bite block.
n ECG to be connected.
n Enter patient details—name, MRN, DOB in the machine using the
‘Patient I.D’ button.
VENTRICULAR FUNCTION
Left Ventricle
Studied in 4 views. In each view look for chamber size, wall thickness,
systolic, diastolic function, and wall motion abnormalities.
120° 0°
P AS
ME long axis TG mid short axis
The first view is the ME 4 chamber where both atria and ventricles are
seen with the two AV valves. The lateral and the septal walls of the left
ventricle and the free wall of the right ventricle are seen. The next view is
the transgastric short axis (TG SAX) obtained by advancing the probe
further down to enter the stomach and anteflex. Cross section of the LV/
203
RV (doughnut appearance) is seen at the level of the papillary muscles.
204 Board Stiff TEE
This is the most commonly used view to assess the systolic function
of the LV as it displays all the six regions corresponding to the distribu-
tion of the 3 coronary arteries. At this point record a loop of this view to
compare with the post-operative study. The TG 2 chamber is seen by
increasing the angle to 90 degrees.

90°
I A
ME 2 chamber
The next view is the ME 2 chamber where the left atrium, the anterior
and inferior walls of the left ventricle are seen. This is also a good view
with which to see the left atrial appendage and the left pulmonary veins
to the left of the screen and, finally, the long axis of the left ventricle is
seen in the ME LAX where the posterior and the anteroseptal walls are
seen along with the LV outflow tract. Both the mitral and aortic valves
are seen. Examine with color flow to see any valve lesions and also any
obstructive pathology at the outflow tract.
TEE ALPHABET
Aorta just
above AV
LA
RA
RV RV
inflow outflow
RV
ME RV Inflow-Outflow
Just a little higher and

back from the ME AV SAX
Right Ventricle
One of the most common views is the ME 4 chamber where the free wall
of the right ventricle is visualized. Look for chamber size, dilatation, and
contractility in relation to the left ventricle. Another common view is the
ME RV inflow/outflow with both the tricuspid and pulmonary valve
seen. Note the RV size and contraction. Color flow to be used across
both the valves to look for any stenosis/regurgitation; the long axis of the
right ventricle is also studied in the TG RV inflow view.
Chapter 21 The Structured TEE Examination 205

90°
I A
ME 2 chamber
VALVES
Mitral Valve

0°
S
RV L
ME 4 chamber
This is the most complex of all valves. A detailed examination in different

views is essential to define the mitral valve pathology. The following three
views are essential. In the ME 4 Chamber the anterior A1 A2 ( medial)
and posterior P1 P2 (lateral) leaflet is seen.

60°
ME mitral commissural
Note the leaflet morphology, motion, and coaptation. Examine with

color flow. In the ME 2 Chamber view the anterior leaflet (lateral) is
seen with all three scallops A1, A2, A3, and P3 seen medially. In the ME
Commissural view, all 3 scallops of the posterior leaflet are seen, with
P2/A2 in the center and P1, P2 on either side with their chordal attach-
ments. The coaptation of both leaflets can be studied in detail in the TG
basal SAX view, called the “fish mouth”.
206 Board Stiff TEE

30°–40°
ME aortic valve short axis
Aortic Valve
The aortic valve is examined in the ME and transgastric views.

120°–140°
ME aortic valve long axis
In the ME SAX view the 3 cusps are seen (the Mercedes Benz sign) the
non-coronary near the interatrial septum, the left cusp on the left, and
the right cusp anteriorly. Look at the number of cusps (tri/bi/uni-cuspid),
morphology, coaptation. Examine with color flow.

0°
Deep TG long axis
In the ME LAX, the long axis of the aorta is seen with the LV outflow and
the mitral valve. Note the leaflet morphology, coaptation, and dimensions
of the annulus, sinus, sino-tubular junction and ascending aorta. Examine
with color flow. Look for any pathology in the outflow tract. This view is
also used to study the A2, P2 of the mitral valve which are commonly
associated with prolapse. Advance the probe further into the stomach,
ante flex and go beyond the short axis of LV to visualize the Deep TG
view of the aortic valve which is seen at the bottom of the sector. This
view is used to measure the pressure gradient across the valve as the
Doppler is in line with the blood flow. If getting this view is difficult, the
Chapter 21 The Structured TEE Examination 207
gradient can also be measured in the TG LAX obtained by rotating the

angle to 90 degrees from the TG mid papillary view.

0°
S
RV L
ME 4 chamber
Tricuspid/Pulmonary Valve
The right-sided valves are seen in the ME 4 chamber view; note the mor-
phology, coaptation. Use color flow to quantify the regurgitation/stenosis.
The other view is the RV inflow/outflow. This view is used for both the
tricuspid and the pulmonary valve, and also for Doppler study across the
valve to grade the regurgitation and to indirectly measure the PA pres-
sure from the peak pressure of the regurgitant flow.
TEE ALPHABET
Aorta just
above AV
LA
RA
RV RV
inflow outflow
RV
ME RV Inflow-Outflow
Just a little higher and

back from the ME AV SAX
OTHER STRUCTURES
Atrium
Look for the size, appendages, and presence of masses (thrombus/tumor).

90°
UE aortic arch short axis

208 Board Stiff TEE
The following views are obtained to study the left atrium ME 4CH, 2 CH,
RV inflow/outflow, Bicaval.

110°
ME bicaval view
In the ME Bicaval view the SVC is seen on the right and the IVC on the
left; both atria and the atrial septum are well visualized. A good view to
identify atrial septal defect and patent foramen ovale.
Aortic Arch

0°
Decending aortic short axis
With the probe in the upper esophagus, and rotated to the left, the short
axis of the aortic arch is seen with the origin of the subclavian artery to
the left. Look for dilatation, dissection flap/atheroma. This view is used
to check the position of the intra-aortic balloon. Decreasing the angle
to 0 degrees gives the UE LAX view of the ascending aorta.
Descending aorta is scanned by advancing the probe further down to

follow the aorta. Note the lumen diameter, presence of any dissection
flap/atheroma/intra-aortic balloon. Increasing the angle to 90 degrees
gives the UE LAX view of the descending aorta.
The ascending aorta, which is difficult to visualize due to the proximity of

the large airways, can be seen in the UE SAX and LAX.
In other structures, you can add any odd pathology you may know
about—such as VSD, or persistent left superior vena cava. There you
have it—1, 2, 3, your basic exam is done. With practice this should take
you no more than a few minutes.
Now that you have covered the basics, you can go back and study the
diastolic dysfunction or tissue strain rates, etcetera, etcetera….
CHAPTER
Sonographic Formulas
22 John C. Sciarra
Ok, there is really no other way to put it. Memorize these!!!!!!!!!!!!!!!!!!!

Some you probably already know, others are Greek. So just write them
out over and over until you have them memorized.
CO = SV × HR
CI = CO/BSA
Gradient = 4 × Velocity squared
Volume = Area × TVI
Flow = area × velocity
Area of a cylinder thing = 0.785 × D squared
Area of a triangle = 0.433 × Side squared
MV area = 220/P 1/2t
Deceleration time mv area = 759/DT (ms)
Pisa area = 2 pi R squared × alpha angle/180

(angle stuff is one if no angle)
Pisa flow = 2 pi R squared × Aliasing Velocity
Pisa MV area = 2 pi R squared × alpha/180

× Aliasing Velocity/Peak Velocity
Continuity equation: what goes in comes out. (Note: you can sub peak
vel for TVI.)
c = f × λ c = 1540 m/s
Z = p × c
Here I will go over some that are not quite obvious. The hemodynamic
section will explain most of these again.
209
210 Board Stiff TEE
Volume = area × TVI…This formula describes a tube. The volume is the

space inside the tube. The area is the end of the tube. The TVI (or time
velocity integral) is the length of the tube. So, for example, what is the
stroke volume? Just measure the diameter of the LVOT, and calculate
the area of that circle. That is Area. Use Doppler to get a TVI through
the LVOT, and that is in cm. Thus the area of the circle times the TVI
gives you a tube of blood passing out the LVOT at one beat—the stroke
volume.
Area of a triangle = 0.433 × side squared…use this if you need to cal-

culate the area of the aortic valve, given one side.
MV area = 220/P 1/2t…This is the quick and easy way to get a mitral
valve area. 220 divided by the pressure half-time. If you want to know
how to get the pressure half-time—ask your attending or tech.
Pisa area, Pisa flow…These are just parts of the big Pisa MV area
equation. Understanding them as separate components is helpful.
CHAPTER
Hemo-dynamo Doc
23 Christopher J. Gallagher
“Houston, we have a problem.”

—Famous misquote from the Apollo 13 Mission. Jim Lovett actually said
“Houston, we’ve had a problem”.
AUTHOR’S NOTE: This is the ONE place where “Go to the Internet” does not
solve the issue. You need pencil, paper, and a little concentrated thinking to get
this section. Old fashioned, but effective!
The crew of Apollo 13 solved their problems.
See if you can solve these.
The first time you see the quantitative problems of transesophageal echo-
cardiography, you will defecate a quart jar of tenpenny nails, not to be too
indelicate about it. But fear not, all is not lost. The math is no more com-
plex than algebra, and the same concepts come back over and over and
over again. The best way to show this is to plow through the problems
they showed at the 2003 hemodynamics workshop meeting. The first time
through (especially if you haven’t seen this stuff before), it will seem like
Greek. But by the end (once you see that the same equations reappear
like Jason in a Halloween sequel), you should get it.
Go through these problems, and you, too, can be a Hemodynamo-Doc.
Case 1
77-yo man having CABG surgery has an A-line, CVP, and (surprise) a TEE.
On echo, the AV appears sclerosed with restricted leaflet motion and trace
AR. His BSA is 2.0 m squared. The following measurements are made:
• Heart rate: 75 bpm
• Systemic BP: 105/65 mmHg
• CVP: 105/65 (Oops! The resident must have nailed big red! It’s really
10 mmHg.)
• Diameter LVOT: 2.2 cm
• TVI LVOT: 18 cm
• Peak velocity LVOT: 1.0 m/sec
• TVI AV: 62 cm
• Peak velocity AV: 3.4 m/sec
• Peak velocity TR: 2.8 m/sec
211
212 Board Stiff TEE
Your job, should you decide to accept it, is to calculate:

• Stroke volume
• Cardiac output
• Cardiac index
• Peak right ventricular systolic pressure
• Peak aortic valve area
• Peak aortic valve gradient
• Peak left ventricular pressure
If you saw this problem ice cold, and thought the TEE exam was just a mat-
ter of looking at some videos and saying, “Yeah, there’s a dissection”, or
“There’s mitral regurg”, then you would no doubt die right here and now.
Fortunately, forewarned is forearmed; you KNOW this stuff will be on the
test, so let’s grind through it.
N.B. There will be a LOT OF REPETITION here as we go through these
problems. That is a good thing for it should POUND THIS STUFF
THROUGH YOUR THICK SKULLS. At the echo course in San Diego, they
emphasize that the course repeats and reinforces the main ideas.
Redundancy is a good thing.
And you can say that again.
Calculation of Stroke Volume:

Volume of a cylinder area of the cylinder length of a cylin
nder
The stroke volume going through the heart is thought of as a “cylinder of

blood,” so you look for a place that has both an area that you can measure
(lo and behold, the LVOT fits the bill) and a length that you can measure
(the LVOT TVI, which is a “length”). TVI stands for time-velocity integral,
and is measured by putting the pulsed-wave Doppler (the one that mea-
sures velocity at a specific place) right in the LVOT. Then you trace the out-
side of the velocity curve. The computer in the TEE machine will give you a
time-velocity integral, which is the length that the blood moved.
There is a little leap of faith here, with only engineers and pencil-necked
geeks understanding exactly the nature of “integration” turning a velocity
in cm/sec into a length of cm. Suffice it to say, TVI gives you the length
that the cylinder of blood moved.
Volume of a cylinder of blood moving through the heart (which is the
stroke volume) = area at a specific place (here, the LVOT) × length at a
specific place (here, the TVI of the LVOT).
Cleaning up a little:

Stroke volume area LVOT TVI LVOT
Area of a circle, you recall from 8th grade or so, is pi × radius squared.
Since pi is 3.14 and since radius = diameter divided by 2, then the area
Chapter 23 Hemo-dynamo Doc 213
equation can be simplified to area = 3.14 × diameter squared/2 squared,

or 3.14 × diameter squared/4. Crank out a little division and you come up
with:

Area 0.785 diameter squared
For some reason, in the TEE review course, they always go with
area = 0.785 × diameter squared, they never go with pi × radius squared.
Whatever, when in Rome, do as the Romans.
So let’s wander back to the stroke volume thing.

Stroke volume area LVOT TVI LVOT
0.785 (2.2 cm) squared 18 cm
3.8 cm squared 18 cm
68 cm cubed, or 68 mL
As you do these problems, pay attention to two things:

1. Units
2. Common sense
The units should come out properly, just like in chemistry or physics
class. We ended up with a stroke volume in units of cm cubed, or in other
words, mL. That makes sense. That is how you usually measure stroke vol-
ume. If, after your crafty machinations, you had come up with units of, say,
hectares per nanosecond per light-year, then you must ask yourself, “When
was the last time I measured a stroke volume in hectares per nanosecond
per light-year?”. The answer being, “Never”, you should go back and redo
the math.
Common sense should also play a part in your answer. This patient, ailing
though he was, had a stroke volume of 68 mL. That is not the greatest, but
is compatible with life in a human being. If, in blazing contrast, your calcu-
lated stroke volume came out to 3 mL, then you would have to ask yourself
“Just how long does your average human being live with a stroke volume
of 3 mL?”.
I wouldn’t sell such a person life insurance.
The flip side of the coin is, what if you calculate a stroke volume of
8900 mL? Either you are calculating the stroke volume of King Kong, or
you made a decimal point mistake in there somewhere.
Do your problem, then step back. Look at the units. Use common sense.
Calculation of Cardiac Output

Oh happiness, you don’t need any TEE chicanery to generate this number.
This is just plain old anesthesia knowledge stuff.
Cardiac output stroke volume heart rate

68 mL/heart beat 75 heart beats/min

5.1L/min
214 Board Stiff TEE
Does it pass the “units make sense” test? Yes. Does it pass the “common
sense” test? Yes. You’re in business.
Calculation of Cardiac Index

Would that it were all this easy! This goes back to Anesthesia 101.
Cardiac index cardiac output/surface area

5.1L/min divided by 2 m squared

2.5 L/min/m squared
Calculation of Peak Right Ventricular Systolic Pressure

Sorry, the free ride is over, you’ll have to put your thinking cap back on for
this one.
For this, you’ll need two things, one mathematical, and one
commonsensical/visual.
The Mathematical
The Bernoulli equation will appear a million times in any discussion of
TEE. The complicated form of this equation takes Sir Isaac Newton to deci-
pher, but the simplified version comes to us as the digestible.
Delta P (the change in pressure between two chambers in a flowing
system) = 4 × velocity squared (where the velocity is measured at a
“choke point” or narrowing between the two chambers)
So picture the place we’re interested in measuring, here the right ventricle.
Where is there a “choke point” or narrowing that leads into or out of the
right ventricle, we can measure a velocity. (Remember, the TEE can mea-
sure a velocity for you, but it cannot measure a pressure.)
Aha! The patient has tricuspid regurgitation, and there is a measurement
of the tricuspid regurg velocity that we can measure:

Peak velocity TR 2.8 m/sec
(Note well, the units for the Bernoulli equation work out as follows—use
the velocity in m/sec and your gradient will come out in mmHg.)
So let’s convert that TR velocity into a gradient:
Delta P (in mmHg) 4 velocity (in m/sec) squared

4 (2.8 m/sec) squared

31 mmHg
Now on to the second thing you need to solve this problem.
The Commonsensical/Visual
So we want to know the pressure in one place, we have a gradient, and we
have a pressure in a second place. Here’s where the common sense comes in.
There is a higher pressure place, the right ventricle (that’s what contracts,
after all). There is a lower pressure place, the atrium (the pressure in that
thin-walled chamber better be lower than the thicker walled ventricle).
Common sense tells you that you could set up an equation like this:
The higher pressure place the gradient you lose as you

go to
o the lower pressure place the pressure you
have left over in the lower pressure place
The right ventricle the gradient going back into the atrium
m
the pressure in the atrium
Unknown 31mmHg you lose going across the tricuspid valve

10
0 mmHg ( the CVP, or, the pressure in the right atrium)

Unknown 31mmHg 10 mmHg

Unknown 41 mmHg
In the TEE review course, they said:

Right ventricular systolic pressure CVP gradient
This may work for you, but I found it more useful to think through the
problem from the vantage of “here’s the high-pressure area, here’s the
low-pressure area, and here’s the loss of pressure between them”. That
way you’ll understand the way the pressure works, and you’ll be less likely
to, say, subtract the CVP from the gradient rather than add the CVP to
the gradient. Once you’re done, you can then draw your picture and see if
common sense holds up.
Calculation of Peak Aortic Valve Area

Here the continuity equation comes home to roost. At first baffling, the
continuity equation makes sense: it’s just a question of cross multiplying
and dividing, and shouldn’t make you lose much sleep.
Why bother? Why not just draw a line around the open aortic valve and let
the TEE machine do the area for you by planimetry?
Ah, grasshopper, things are not so simple as they seem.
Planimetry, as so many things in life, only works when you don’t need it!
(Kind of like the umbrella that never leaks unless it rains, or the life pre-
server that doesn’t let you drown unless you happen to fall into the
ocean.) When the aortic valve is crunchy and stenotic, planimetry (a two-
dimensional exercise), just cannot get a good handle on the exact orifice
area. You outline up here, but there is more stenosis below your outline, or
there is more stenosis above your planimetry, so the planimetry is just no
good.
Continuity Equation Idea: flow through one area of the heart equals flow
through another area of the heart.
216 Board Stiff TEE
Fluids are not compressible, so you can’t “squish” the blood. Also, blood
cannot just “disappear”, which brings up the BIG EXCEPTION to the conti-
nuity equation:
If a patient has noncontinuous flow (septal defect somewhere), then you
can’t use the continuity equation. To use continuity, have continuity!
So, if you can measure flow through one area, then that should equal flow
in another area.
Flow here = flow there. The essence of the continuity equation.
Recall from earlier that we “create” measurable flow by assuming a cylin-
drical amount of blood flow. (We did that in the original part of this prob-
lem, the stroke volume problem. Go back now and nail that down, because
that is the heart of the continuity equation.) We measure this cylindrical
flow by getting one area and multiplying it by the length (the time-velocity
integral), thus getting flow.

Area length area length
We know we want to know the aortic valve area, so where can we find
another place to measure stuff?
The left ventricular outflow tract, of course! (The LVOT is forever bailing
our mathematical asses out of trouble.)
So flow through the LVOT should equal flow through the aortic valve. So
plug in the respective three things that we DO have, and solve for the one
thing we don’t have:
Area of the LVOT blood flow “cylinder” length that the blood flow
“cylinder” goes area of the aortic valve “cylinder” length that
the aortic blood flow “cylinder” goes

Area LVOT TVI LVOT unknown aortic valve area TVI aortic vallve
You have the diameter of the LVOT, 2.2 cm, so use the area formula:
Area pi radius squared, or,

Area 0.785 diameter squared
0.785 (2.2 cm) squared

3.8 cm squared
So, plodding along,
3.8 cm squared (the area of the LVOT) 18 cm (TVI of the LVOT)

unknown (the area of the aortic valve) 62 cm (the TVI of the AV)
Cross multiply and divide, solving for the area of the aortic valve, and, voila!

Area of the aortic valve 1.1cm squared
Does this pass the units test? Yes. Aortic valve areas are measured in cm
squared.
Does this pass the common sense test? Yes, this fits the general size you
would expect of a stenotic aortic valve. You didn’t get an aortic valve area
the size of an electron, nor did you get an area the size of Comiskey Park.
Now hold on to your slide rulers and cyclotrons—there is, it turns out,
another way to get the aortic valve area.
Go back to the cylinder of blood idea (the gist of all these equations). If
you look just at the aortic valve, you could say:

Aortic valve area TVI aortic valve stroke volume through th he aortic valve
So, if you were of a mind to, you could calculate the aortic valve area that
way, could you not? (The first time you see this, you’ll go, “Huh? Aren’t
they cheating?”.) But it’s actually not cheating, because, in order to get the
stroke volume, you had to use the concept of the “cylinder of blood going
through the LVOT” (see above, where we calculated the very first part of
this problem, the stroke volume).
Take a second to digest this.
No, really, look back up there, don’t take this on faith.
Satisfied? Good.
So, here we go with the second way to calculate the area of the aortic valve.
Area of the aortic valve TVI of the aortic valve

stroke vollume Unknown (area of the aortic valve)
62 cm 68 cm cubed
Cross multiply and divide, and gee whiz golly, the aortic valve area is still
1.1 cm squared.
That shouldn’t surprise you, as this patient hasn’t aged much during this
problem.
What should surprise you is a second answer different from your first.
Since you were just grinding the same numbers through in different ways,
you should get a second answer the same as the first. If you don’t, go back
and rework it.
Calculation of Peak Aortic Valve Gradient

A little less Sturm und Drang here. Just use the Bernoulli equation:
Delta P ( the pressure gradient across a “choke point”

in a flowing system) 4 velocity in the “choke point” squared
Delta P 4 (3.4 m/sec ) squared
(Keep in mind, you need that velocity in m/sec to get a pressure in

mmHg!)

Delta P 46 mmHg
218 Board Stiff TEE

Units OK ? Check.

Common sense OK ? Check.
Calculation of Peak Left Ventricular Pressure

At the TEE course, they didn’t ask for this, but it’s worth doing just to get
that “high-pressure area, gradient loss, low-pressure area” idea down.
First, draw a picture of what you’re trying to find. (To repeat, getting the
concept down of where the high pressure should be, as well as where the
low pressure should be, is important. A good picture will make sure you
add where you should add and subtract where you should subtract.)
The high-pressure area should be the left ventricle in systole, because the
left ventricle has to overcome the “choke point” of the aortic valve, and still
have enough oomph left over to provide systolic pressure.
High pressure in the left ventricle (unknown) − pressure lost in the stenotic
aortic valve (the previously calculated gradient of 46 mmHg) = pressure left
over in the aorta (the systolic pressure of 105 mmHg)

Unknown 46 mmHg 105 mmHg

Unknown 151mmHg
Now, redraw the picture and see if it makes sense.
Case 2
48-yo man having CABG. Monitoring includes a finger on the pulse and an
anesthesiologist on the phone to Merrill-Lynch. OK, OK, sorry. Monitoring
includes an A-line, CVP, and TEE. LV appears dilated and hypocontractile.
There is a central jet of MR judged to be 2+ to 3+ in severity. The following
measurements are made:
• Diameter LVOT: 2.5 cm
• TVI LVOT: 13 cm
• Mitral annular diameter: 3.5 cm
• TVI mitral annular diameter: 11 cm
• PISA radius: 0.8 cm
• PISA alias velocity: 34 cm/sec
• Peak velocity MR: 574 cm/sec
• TVI MR: 172 cm
Calculate the following:
• LVOT stroke volume
• MV stroke volume
• MV regurgitant volume
• MV regurgitant fraction
• Regurgitant orifice area
• PISA calculations
• Regurgitant flow rate
• Regurgitant orifice area
• Regurgitant volume
• Regurgitant fraction
Before you regurgitate yourself at all this stuff, a few pointers.
On this, the math part of the test, they will just give you the various mea-
sures. They’ll lay LVOT diameter on a silver platter and hand it to you. In
other parts of the test, you will visually have to show exactly where you
would take this measurement yourself. And on the test the various places
are damned close to one another, so make sure you know where to take
these measurements.
Second, PISA makes the whole auditorium groan, it seems so esoteric at
first. But once you gird your loins and throw yourself into this stuff, you’ll
see that PISA is just the continuity equation in another form.

Flow through the PISA flow through another area
PISA’s area is a hemisphere, so that’s a little different.

PISA’s area is affected by its angle to the valve, so that’s a little different.
PISA implies you know what the hell aliasing is, so that’s a little different.
Alright, so PISA is a pain in the ass, what can I tell you? I didn’t make up
the exam!
Let’s take a little breather from the PISA monster, get as far along as we
can in the calculations, get a little confidence, then jump into the snake pit
of PISA-ness.
Calculation of LVOT Stroke Volume

Whew, this is review. If you got the karma of the first case, this should be
cake. I’ll go through it just as slowly, though, so we jam this stuff into your
sulci but good.
From the chaos and irregularity of a real-live stroke volume, we make up a
“pretend” stroke volume that magically looks like a perfect cylinder, with a
perfect area and length.
Next, we look at the LVOT, make our area calculation, then multiply it by
the length (the TVI):

Stroke volume LVOT area LVOT length LVOT

Stroke volume pi radius square TVI
220 Board Stiff TEE
Or, in TEE Course-speak:
Stroke volume 0.785 diameter squared TVI

0.785 (2.5 cm) squared 13 cm

Units make sense? Yes. Common sense rule checks out? Yes. (Make it a
habit to always do this two-part checkout.)
Calculation of MV Stroke Volume

Danger! Danger, Will Robinson! Remember, when you measure these, to
measure both the diameter and the TVI at the same place. In this problem,
be sure to measure both the diameter of the mitral valve and the TVI of
the mitral valve at the annulus. If you measure the diameter at the annulus
and the TVI at, say, the tips of the mitral valve, then you would get an inac-
curate result.
Stroke volume of mitral valve area of mitral valve

length of flow in mitral valve (the TVI)
So once again, we are invoking a “cylinder of blood flow”.

Though the mitral valve is more like an oval, for purposes of this problem,
we will consider it a circle:

Stroke volume pi radius squared TVI
Or, bowing to TEE convention:

0.785 (3.5 cm) squared 11cm

Units check? Yes. Common sense check? Wait a minute! Didn’t we just
calculate an LVOT stroke volume of 64 mL? Now where did this stroke vol-
ume of 106 mL come from? What about the Holiest of Holies, the continu-
ity equation?
Confused? Pause for a moment and think about what’s happening.
This patient has mitral regurgitation, so it makes sense that more should
go through the mitral valve than goes out the LVOT. Some of that mitral
volume is lost by going backward (as we’ll see below). Recall, too, that the
continuity equation doesn’t apply here, because the LVOT measurement
applies to blood flowing out to the aorta during systole. The blood flow
going forward through the mitral valve occurs during diastole.
Systole and diastole do not occur at the same time. They are
DIScontinuous so the continuity equation does not apply to them.
So, in review, the units check and the common sense also checks, once
you think about what is happening and when it is happening.
Calculation of MV Regurgitant Volume

Now it starts to come together.
Regurgitant volume through the mitral valve = total volume
that goes through the mitral valve – total volume that goes out through
the aortic valve
Another warning for Will Robinson.
This calculation only holds if there is no aortic regurgitation as well. The
extra flow that comes back during aortic regurgitation would mix in with
the blood regurgitating through the mitral valve, and all bets are off on vol-
ume calculations.
Adding aortic regurg to mitral regurg takes you from one equation–one
unknown to one equation–two unknowns, and that is a no-no.
Regurg volume 106 mL 64 mL

42 mL
Units check? Yes. Common sense check? Ye-e-e-es. (If you find yourself
hesitating, draw a picture to satisfy yourself that it does, indeed, make
sense.)
Calculation of MV Regurgitant Fraction

No rocket science here.
Regurgitant fraction of mitral valve
regurgitant volume MV/total volume through MV
42 mL/106 mL
0.4
or, in percentage terms, regurgitant percentage = 40%.

Units check? Yes, there are no units.
Common sense check? Yes, you can see a regurgitant valve tossing 40%
backward. That goes along with significant regurg.
You’ll note you didn’t come up with something impossible, like a regurgi-
tant percentage of 178% or a regurgitant percentage of −5%. Thank heaven
for small miracles.
Calculation of Regurgitant Orifice Area

This is a little hypothetical, as the regurgitant orifice area is not a fixed
thing that instantly appears, then instantly disappears. In reality, it’s more
like a door that is closed, opens at a certain speed, stays open for a length
of time, and then closes at a certain speed. This calculation looks at the
“door all the way open” and ignores the reality of the “opening period” and
the “closing period”.
But you’re not here to think. Just do the calculation and keep your trap
shut.
Go back to our cylinder of blood and start calculating.
222 Board Stiff TEE
Regurgitant orifice area length (the TVI of regurgitation)

stroke volume of regurgitation

Regurgitant orifice area 172 cm 42 cm cubed
Cross multiply and divide, you busy little hemodynamic beavers.

Regurgitant orifice area 0.24 cm squared
Units check? Yep. Common sense check? U-u-uh.

That makes sense. The mitral valve isn’t a complete waste case; it is regur-
gitant, but not wide, wide open, so it makes sense that a portion, not all,
of the valve effectively “stays open” during systole, allowing for the 40%
regurgitation.
PISA Calculations
Hunker down, cowboys and cowgirls, it’s not so bad as you think. Before
we go into the actual calculations in this case, let’s go over the main
aspects of PISAtology.
Look at the words that make up PISA, and draw pictures to illustrate the
point.
Proximal. That means the colorful and troublesome PISA radius will appear
on the upstream part of the “choke point”. So draw a few pictures. If the
patient has mitral regurg, and the flow is pouring from the high-pressure
left ventricle into the low-pressure left atrium, the PISA will appear where?
Proximal! That is, the PISA will appear in the left ventricle, the “near” side
of the “choke point”. The proximal area of the choke hold, not the far side.
That would be “distal isovelocity surface area”, and if you think of the cha-
otic flow on the far side of a “choke point”, that doesn’t make sense.
How about a case of mitral stenosis? Flow is trying to “squeeze” through a
tight mitral valve. Where would the PISA radius appear then?
Proximal! On the near side of the choke point, that is, in the left atrium.
Again, a radius on the far side of the choke point doesn’t make sense.
Isovelocity. All the flow at that area is the same. Recall that flow Doppler is
a pulsed-wave, not a continuous-wave, phenomenon. At a certain velocity,
the color of the wave will change. Conveniently for us, the aliasing velocity
(the velocity where color change occurs) is listed on the machine.
Well, why should the isovelocity thing line up so perfectly for us. Why isn’t
the isovelocity thing scattered all over the map?
Think of water going toward a narrow sluice gate. The velocities are all over
the map, until you get real close; then the pressure bearing down on the
water is all the same. The velocities “organize” as the water gets closer
to the sluice gate, and you get a hemisphere of water all going the same
speed toward that narrow opening. That is why you get a hemisphere of
“isovelocity-ness” that appears on the TEE screen.
Surface Area. Unlike earlier equations, which used the area of a circle
(pi × radius squared), this area is that of a hemisphere (2 × pi × radius
squared). Why? Look at the PISA thing. It is a hemisphere, not a circle.
So that’s where you get the 2 × pi × radius squared. In calculations done
at the conference, they give you the radius and you go with 6.28 (that is,
2 × 3.14) × radius squared.
So, once you believe in PISA, have the formula for area of a hemisphere
down, and recall the continuity equation, you are in business.
Calculation of Regurgitant Flow Rate by PISA

Just as in other valve calculations, invent the idea of a cylinder of blood
flowing along with a certain area and a certain length. This requires a little
mind bending, as you are used to looking at the area of a circle and multi-
plying it by the length. Here, with PISA calling the shots, you make an area
of a hemisphere and multiply it by the length.
Try not to think about it too much, you might pop an aneurysm. Just go
with the flow.

Regurgitant flow rate PISA area aliasing velocity
Wait, wait! Where did that aliasing velocity come from again?
That line, where the flow changes color, must all be going at the same
velocity—remember the water flowing towards the sluice gate? So read
the aliasing velocity right off your TEE screen (it’s listed right next to a
colored bar), measure the radius to that line change, and you know that
right there, the blood has to be going that fast, the aliasing velocity. And
you measured the radius right there, where the color change occurs, so
you are satisfying the demand that the area and the velocity be measured
at the same place. So,
Area (in one specific place) velocity (at that same specifiic place)
volume (at that specific place)

Regurgitant flow rate 2 pi (0.8 cm) squared 34 cm/sec
Wait, wait! In all the other stuff, we used TVI and got a length in cm. Now
we’ve got this aliasing velocity that has cm/second. Doesn’t that screw
everything up?
Don’t panic. Take a deep breath. The question asked for a regurgitant flow
rate (which implies a flow per unit time), so the aliasing velocity is-not-the-
same-as-TVI will not screw us up. But it’s good to see you fretting about
the units.
Regurgitant flow rate 6.28 (0.8 cm) squared 34 cm/sec

137 cm cubed/sec
Units OK? Check. (Again, you get Brownie points if you got nervous about
the aliasing velocity not being the same as the TVI.) Common sense? Yes.
224 Board Stiff TEE
Calculation of Regurgitant Orifice Area by PISA

Here we’ll keep an especially close eye on the units.
As before, area times velocity will equal flow. (Remember how we did the
same thing with other valves and other flows. It always goes back to the
same thing: area × velocity = flow. In earlier calculations, we didn’t have
the confounding variable of aliasing velocity, with its pesky cm/second.
Before, we always had a TVI with just cm. Watch closely.)
Effective regurgitant orifice area (of regurgitant mitral valve) × velocity
(through the mitral valve [recall, we can measure velocities directly, but not
pressures]) = flow (through mitral valve).
In shorter form,

ERO velocity MR peak flow (calculated by PISA)
Note, the velocity MR peak is in cm/second, and our flow by PISA is in cm

cubed/second, so that pesky second will cancel out:

ERO 574 cm/second 137 cm cubed/second
Cross multiply and divide and you get ERO = 0.24 cm squared.
Units OK? Yes. Common sense OK? Well now, I will be dipped in hot
fudge, stuck on a stick, and served up at the County Fair—the ERO turned
out to be the same thing! 0.24 cm squared. And this time we really did cal-
culate it a different way.
Who’d a thunk it.
Damnation.
Calculation of Regurgitant Volume by PISA

Area length, area length, area length.
Do you see a pattern here?
Regurgitant volume effective regurgitant area

TVI of the reegurgitant valve
0.24 cm squared (what we just calculated)
172 cm

41cm cubed
Units? Check. Common sense? Check. Recall, with the other way, we calcu-
lated a regurgitant volume of 42 mL. That is close enough for government
work.
Calculation of Regurgitant Fraction by PISA

Well, after jumping through all those other flaming hoops, this is nothin’
but nothin’.
Regurgitant fraction (PISA method) 41cm cubed/106 cm cubed

0.39
or, in percentage terms, 39%, which makes both units and common sense
sense. (Or, [sense] squared.)
Now that problem right there is a killer. If you can smack through that,
you can handle most anything in the hemodynamic front. Might be worth
going over this again a couple times, making sure you keep getting the
units all squared away, especially with PISA’s little twists and turns.
Case 3
60-yo obese female s/p cardiac arrest following total hip replacement.
Patient is brought to the operating room based upon a preliminary TEE
that suggests pulmonary embolus.
CONFERENCE NOTE: There was an entire lecture on TEE in the evalua-
tion of hypoxemia, and it focused on how TEEs help diagnose pulmonary
emboli. Though the embolus itself is rarely seen, the secondary signs—RV
dilatation, tricuspid regurg, all the signs of a right heart struggling to push
blood past an obstruction—are most helpful in making this slippery diag-
nosis of pulmonary embolus.
They did show one unbelievable clip of an enormous embolus that actu-
ally was in transit through the right heart. On screen, in real time, it came
unglued, shot up into the pulmonary artery, and the patient went on to die
soon after. Scary as hell. About as impressive a TEE as you’d ever care to
see. Or not see.
Vital Signs
• CVP: 16 mmHg
TEE Data
• Pulmonary artery diameter: 2.0 cm
• Pulmonary artery TVI: 10 cm
• Aortic valve TVI: 15 cm
• TR peak velocity: 4 m/sec
Calculate
• Stroke volume
• Cardiac output
• Aortic valve area
226 Board Stiff TEE
You’ve done two of these already, and you should have the equipment to
figure these out on your own, so give it a try before you read on. You will
note that the same stuff keeps coming up, the same ideas, the same equa-
tions. But it still doesn’t hurt to draw a picture or two to keep the big pic-
ture in mind.
This is a heart whose right side is “stopped up” with a plug in the outflow
from the right ventricle to the lungs. Status hemicardioconstipationatus
dextrus, if you prefer the Latin term. The tricuspid regurg shouldn’t sur-
prise you. As the right ventricle groans against a high pressure, some
blood will go backward through the tricuspid valves.
Calculation of Stroke Volume

Find an area, find a TVI, and create your cylinder of blood flow to give you
your volume. No problem, we’ve done it before.
OK, roll up the sleeves, find that LVOT diameter, find that LVOT TVI, and
plug them into the equation:

Flow area length
So,

flow 0.785 (diameter of LVOT) squared TVI of the LVOT
SCREEEEEEEEEEEEEEEEEEEEEEEEEEEEEEEECH!
What the hell? Where are my old favorites? How can this be? Has the
world turned upside down? It was so EASY to see it that way. You’re look-
ing right down the pipe of the left ventricular escape hatch. Out goes the
blood through the LVOT into the aorta and you’re there! What am I sup-
posed to do with the information I do have?
Here’s where you really need to understand the continuity equation. The
information you get is the pulmonary artery diameter and the pulmonary
artery TVI. If you really believe, I mean believe, brothers and sisters, in the
sanctity of the continuity equation, then you must convince yourself that
flow through the pulmonary artery will equal flow through the aorta.
That is, if the forward flow has no weird places the blood could disappear
to (ventricular septal defect, atrial septal defect, some weird AV malforma-
tion in the lung).
But! But! What about the tricuspid regurg? Doesn’t that “undo” the conti-
nuity equation?
No. The TVI you measure through the pulmonary artery is real-live, forward
flow. That flow has made it past the right ventricle. Whatever went backward
went backward, and we’ll measure that in our own sweet time. But the TVI
of the forward flow through the PA will rock right on straight through to the
lungs, the left atrium, and the left ventricle, and out into the body.
If no flow goes backward from the pulmonary artery on out (that is, the
pulmonary artery itself is not regurgitant), then the continuity equation
says, “the flow will flow”.
So, now that we’ve settled that, then we can calculate our stroke volume:
Stroke volume area of the PA TVI of the PA, or,

0.785 (2 cm) squared 10 cm

31 cm cubed, or 31mL
Units check? Yes. Common sense check? That forward flow seems pretty
small. In earlier patients we were getting stroke volumes of 68 mL and the
like. Only 31 mL? Pretty punky. But then, what does common sense tell
you? This patient has a big PE, a big blockage to flow out of her right ven-
tricle. It’s conceivable and understandable that a monster plug to the RV
could cut the “usual” stroke volume in half. So, yes, this passes the com-
mon sense test.
While you’re at it, turn the logic around. What if you calculate a stroke vol-
ume greater than normal, say, 90 mL? That wouldn’t jibe with the picture
of a pulmonary embolus and blocked forward flow.
Always check your numbers against common sense and what is really hap-
pening to the patient. You will be less likely to make a mistake. If you just
plug in numbers and hope against hope that you’re right, you’ll stumble.

Cardiac output is stroke volume × heart rate. Go back to your belief in the
continuity equation—the flow we measure going through the pulmonary
artery. IF FLOW CONTINUES STRAIGHT THROUGH WITHOUT MITRAL
REGURG, AORTIC REGURG, OR SOME SEPTAL DEFECT should be the
flow going through the aorta.
Cardiac output 31cm cubed/heart beat 100 heart beats/min

3.1L/min

Here again a picture will keep your signs straight. Whether on the right
side or the left side of the heart, think of what’s going on (here, systolic
flow from the right ventricle into the right atrium through the “choke
point” of the regurgitant tricuspid valve), think of where the highest pres-
sure should be (here, the right ventricle), the place where the gradient will
occur (the tricuspid valve), and the low-pressure place (the right atrium).
So, the equation will say:
Right ventricle (a high-pressure unknown) – gradient at the choke point
(the tricuspid valve) = pressure in the low-pressure place (the right atrium)
How to measure the “choke point”? We have a velocity (which TEE can
measure). Plug in Bernoulli:

Delta P 4 velocity squared
Delta P 4 (4 m/sec) squared (Remember, velocity in m/sec

to get pressure in mmHg.)
228 Board Stiff TEE

Delta P 64 mmHg
Right ventricle peak pressure pressure gradient

low-pressurre atrium pressure

RV peak pressure 64 mmHg 16 mmHg

RV peak pressure 80 mmHg
Units check? Yes. Common sense? Yes.

Now, apply your common sense to the clinical scene. Here’s a patient with
a PE big enough to give her cardiac arrest. She has little forward flow (bad
stroke volume, bad cardiac output). Her right ventricle, which in a normal
patient generates peak pressures of, say 25 or 30 mmHg, is now generating
a whopping 80 mmHg. And with that high a right ventricular pressure, is
it any wonder that the tricuspid valve (with a whiff of regurg in the best of
times) is pouring blood backward?
It all fits. The numbers match the clinical reality. Isn’t science wonderful?
Calculation of Aortic Valve Area

Back to the continuity equation (didn’t I tell you you just keep doing the
same stuff over and over again?).
In days of yore, we did this with the LVOT, remember?

Area LVOT TVI LVOT area AV (the unknown) TVI AV
Then you just cross multiply and divide. Well, as noted above, we ain’t got
no LVOT. We got the PA. There is tricuspid regurg, but that doesn’t con-
cern us now. We’re past that level of the regurg, and if, from the PA for-
ward, there is no stop to forward, continuous flow, we should be able to
use the continuity equation.
Plug in:
Area PA × TVI PA = area AV (the unknown) × TVI AV

0.785 (2.0 cm) squared 10 cm area AV 15 cm
Cross multiply and divide, you get AV area = 2 cm squared.

Units check? Yes. Areas are in cm squared. Common sense check? Yes,
2 cm squared puts this woman’s aortic valve area in the normal range. And
nowhere was there mention of aortic stenosis. She’s got enough trouble
already, what with a PE and cardiac arrest. Let’s not give her more worries.
Go back to Case 1. Remember how we worked out the AV area another
way?

Aortic valve area TVI AV stroke volume
We can do that here, also:
Aortic valve area 15 cm 31cm cubed

2 cm squared
As before, this shouldn’t come across as some miracle, as you are just
regrinding the numbers in a different path to get to the same result. Of
course, if you regrind and come out with a different number, perhaps you
need to look things over and mend the error of your ways.
Case 4
60-yo male with acute aortic dissection and aortic insufficiency.
Vital Signs
TEE Data
• LVOT diameter: 2.0 cm
• LVOT TVI: 30 cm
• MV diameter: 3 cm
• MV TVI: 10 cm
• AI TVI: 160 cm
• AI end-diastolic velocity: 3 m/sec
Calculate
• Mitral valve stroke volume
• Aortic regurgitant volume
• Aortic regurgitant fraction
• Aortic regurgitant orifice area
• Cardiac output
• Left ventricular end-diastolic pressure

Some things never change, ain’t it grand.
Make your cylinder of blood flow. Get the area of the LVOT − pi × radius
squared, or, 0.785 × diameter squared. Then get your length of your cylin-
der of blood, the TVI −30 cm.
LVOT stroke volume 0.785 (2.0 cm) squared 30 cm

94 cm cubed
It’s worth reminding yourself where you get all these numbers from. You
measure the LVOT about 5 to 10 mm proximal to the annulus of the aortic
valve. You measure the LVOT velocity (around which you draw your cursor
to get the TVI) at the EXACT SAME PLACE, using… well, you tell me. Do
you use continuous-wave Doppler or pulsed-wave Doppler?
230 Board Stiff TEE
(Play the theme from Jeopardy here.)

Right, pulsed-wave Doppler. Pulsed wave gives you a specific velocity at
a specific place, unlike continuous wave, which gives you ALL velocities
along a line. (If this is still a mystery to you, review the difference between
continuous wave and pulsed wave in Chapter 2; you need to know this ice
cold.)
Calculation of Mitral Valve Stroke Volume

Same deal here. Create your cylinder of blood, get an area, get a length,
and you’re in business. Again, we’ll “round out” the “what is really oval”
mitral valve.
Mitral valve stroke volume 0.785 (3.0 cm) squared 10 cm

71cm cubed
Let’s step outside the numbers again to make sure we got the numbers
from the right place.
You measured the mitral valve, where, the annulus or the tips of the
leaflets?
The annulus.
Where do you measure the velocity?
Same place. Get the stuff at the same place, not different places!
Which kind of Doppler did you use?
Pulsed wave, because we wanted a specific velocity at a specific place.
Calculation of Aortic Regurgitant Volume

Note well, young budding TEE’ogists. To calculate the aortic regurgitant
volume, you must assume there is no mitral regurgitation going on either.
Again, you need one equation, one unknown. Put in one equation and two
unknowns, it won’t work.
So, to the numbers:

Regurgitant volume aortic valve mitral valve stroke volume LVOT SV
The ventricle is “loaded” with two volumes during regurgitation, the blood
pouring backward from the incompetent aortic valve, and the blood flow-
ing forward through the mitral valve. Then WHOOSH, both these volumes
go blasting out the aortic valve.

Regurgitant volume aortic valve 71mL 94 mL
Regurgitant volume AV 94 mL 71mL

23 mL
Still not convinced the mitral valve has to be competent? Let’s load up the
ventricle then WHOOSH it out both valves.
Regurgitant volume AV MV stroke volume LVOT SV

MV regurgitaant volume
Unknown regurgitant volume 71mL 23 mL

unknown MV regurgitantt volume
No way, Jose. Too many unknowns.

Think about what’s really happening in these problems. On the exam, they
are sure to throw some kind of curve at you, so if you understand the phys-
ical reality of what’s flowing where, you should handle it. If you think you
can just “plug and forget”, you’ll get tripped up.
Calculation of Aortic Regurgitant Fraction

What amount of the total ejected blood ends up going backward?

Blood going backward/blood going forward regurgitant fraction
Regurgitant volume aortic insufficiency/forward volume through LVOT =

regurgitant fraction

23 mL/94 mL 0.24 (or, by percentage, 24%)
Units check? (Do it every time) Yes. Common sense check? Yes.
Calculation of Aortic Regurgitant Orifice Area

Back to the cylinder of blood moving around. Get an area, multiply it by a
length, and that gives you the volume of your cylinder of blood. Make sure
the area and the velocity (recall that the velocity, when outlined, yields your
TVI, or, length), are measured at the same place.

Aortic regurgitant orifice area TVI aortic regurg regurgitaant volume AI
Think it through: you have an area (of regurg), a length (of regurg), and a
volume (of regurg). It all makes sense, so now grind the numbers:
Aortic regurgitant orifice area 160 cm 23 cm cubed

23 cm cubed/160 cm

0.14 cm squared
Units? Good. Common sense? Um. That’s pretty tiny for an aortic valve,
but wait, this is the area where regurgitation is occurring, not the entire
valve area. You can picture that this patient has an aortic dissection, so
the aortic root is stretched, making the aortic valves not able to completely
reach each other, and leaving a small area “uncovered” in the middle.
Through that, 23 mL of blood per beat flows back into the heart. Then, yes,
the aortic regurgitant orifice area of 0.14 cm squared makes sense.
232 Board Stiff TEE
Say you had come up with an aortic regurgitation orifice area of 1.2 cm
squared. That would leave a gigantic gap. Blood would go like a house afire
into the ventricle, giving an enormous regurgitant volume and, in all likeli-
hood, a moribund patient.

You are interested in what goes forward here. Regurgitant flow is not really
output, it’s “backward-put”. So to calculate cardiac output, you need a real,
live stroke volume that actually gets “out there,” and as well you need a
heart rate.
Cardiac output 71mL (the SV of the MV) 80 bpm

5.6 L/min
Whoa! You say, wait just a darn tootin’ minute here, partner, who said any-
thing about the mitral valve? I thought, well, I thought we wanted cardiac
output, like as in from the left ventricle out to the body. Who gives a damn
about the “cardiac output” from the left atrium to the left ventricle?
Back to the continuity equation. We are talking about uninterrupted for-
ward flow. The amount of blood that leaves the left atrium and doesn’t
come back (recall the mitral valve is OK), must be the amount that leaves
the ventricle. As long as the forward flow is not diverted in its forward
movement.
Look at flow in a different way to convince yourself that the continuity
equation holds.
Pretend 71 mL of blood enters the left ventricle from the left atrium; then
71 mL do NOT go forward and out of the heart. Say only 50 mL goes out of
the heart with each beat, and then 71 mL keeps entering the left ventricle
through the mitral valve.
With each beat of the heart, the left ventricle gets 21 mL bigger. At the
end of a minute, the heart will have 1600 mL of blood just hanging
around, looking for a good time. At the end of the hour, your heart will
be 96,000 mL bigger, or 96 L big. Echo findings in such a case would be
remarkable, to say the least. Even the most vigorous patient might find
handling such a volume load to be beyond his or her capacity.
Let’s say you were given this problem and I said the patient had a VSD.
Could the continuity equation come to the rescue? No. Do a sample prob-
lem to satisfy yourself of this.
Pretend that you magically know that 71 mL of blood enters through the
mitral valve and 23 mL enters through regurgitation. That is, 71 mL of blood
enters the left ventricle from the mitral valve, and 23 mL enters the left ven-
tricle from regurgitant flow, so now the total ventricular volume of 94 mL
goes WHOOSH! But how much goes out the aortic valve, and how much
goes out the VSD? No way of knowing.
Calculation of Left Ventricular End-Diastolic Pressure

You’ll have a high-pressure chamber, a choke point where a certain amount
of pressure is lost, and a low-pressure area with the “leftover” pressure.
We’re in diastole, so the ventricle is relaxing; that’s the low-pressure

area. The aorta just got a blast of blood, so there’s high pressure there.
The choke point is the regurgitant valve. We can get the pressure from the
measured velocity (using our old buddy, Bernoulli).
Aortic pressure in diastole (the high-pressure area) − the pressure lost in
the choke point (the velocity of aortic regurg, which we’ll use to get a pres-
sure gradient by delta P = 4 × [velocity] squared; remember, velocity in
m/sec to get pressure in mmHg) = left ventricular end-diastolic pressure
(the low-pressure area, and our unknown).
Now, to make it more mathematical and less wordy:

Systemic diastolic pressure gradient across aortic valve LV
V EDP

60 mmHg 4 (3 m/sec ) squared LV EDP

60 mmHg 36 mmHg LV EDP

LV EDP 24 mmHg
Units check? Check. Common sense check? Yes. Blood flowing into the
left ventricle through regurgitation should create some pressure there.
Nothing ridiculous. (Say you came up with an LV EDP of 130 mmHg; that’s
higher than systolic pressure, and during diastole? No way.) So, this value
satisfies the common sense test.
Case 5
70-yo male with worsening dyspnea on exertion.
Vital Signs
• CVP: 12 mmHg
TEE Data
• LVOT TVI: 20 cm
• MV TVI: 90 cm
• MV pressure half-time (PHT): 300 ms
• Peak trans-mitral end-diastolic velocity (EDV): 2.0 m/sec
• Pulmonary insufficiency EDV: 2.5 m/sec
234 Board Stiff TEE
Calculate
• Mitral valve area by pressure half-time
• Mitral valve area by continuity equation
• Pulmonary artery diastolic pressure
Calculation of Mitral Valve Area by Pressure Half-time

Area 220/PHT
Where the hell did pressure half-time come from?

The rate of pressure (not velocity, but pressure) decline across the stenotic
mitral valve orifice is determined by the cross-sectional area of the orifice.
A tiny pinhole of a mitral valve would take a long time to empty. A totally
normal, enormous mitral valve would allow the blood to fall through in no
time flat. The picture tells the quantitative story.
The quantitative equation has been empirically worked out:

Area 220/PHT
How? Doppler half-times were compared to cath lab studies, and this
magic number appeared.
Draw a line down the E wave of mitral flow; make that line go right to 0.
Ignore the A wave. Find the halfway point down the slope that corresponds
to the pressure (recall, delta pressure = 4 × [velocity] squared); that is
the halfway point. Do not go to the halfway point as far as velocity is con-
cerned. As luck is with us, the computer on the TEE can do this.
So, back to the problem, what is the mitral valve area by PHT?
Area 220/300 millisec

0.7 cm squared
Units check? Yes. If you use this equation, and use milliseconds, you get
cm squared. Common sense? Yep. That’s a tight mitral valve, and that
goes along with the clinical picture of worsening dyspnea on exertion.
Calculation of Mitral Valve Area by Continuity Equation

So, we have a cylinder of blood in which we can measure the flow through
our old friend, the LVOT:

Flow through LVOT area of blood cylinder length of blood cyylinder
That, by continuity, must equal the flow through the mitral valve, so let’s
create that cylinder of blood:
Flow through mitral valve area of mitral valve (our unknown

n)
length of that cylinder

Flow through mitral valve area MV TVI MV
If we believe in continuity, and, amen, amen, by now you must believe, then
set the flow through the mitral valve equal to the flow through the LVOT:

Area MV TVI MV area LVOT TVI LVOT

Area MV 90 cm 0.785 (2.0 cm) squared 20 cm
Cross multiply and divide and you get:

Area MV 0.7 cm squared
Hot damn! Just like the pressure half-time way! Well bend me over an
Adirondack chair and spank me with a two-by-four ‘til I say “Mama!”.
Calculation of Pulmonary Artery Diastolic Pressure

Remember, we’re in diastole. Know where the high-pressure area, the
choke point (where we’ll get a gradient), and the low-pressure area with its
“leftover” pressure are.
In diastole, the high pressure is in the pulmonary artery. It just received a
blast of blood from the right ventricle. The right ventricle, in contrast, is
relaxing after a hard day at the systole office. The choke point is the pulmo-
nary artery, where blood is pouring back into the right ventricle.
• High-pressure area: pulmonary artery
• Choke point: pulmonic valve
• Low-pressure area: right ventricle

PA diastolic pressure choke point in pulmonic valve RV EDP

Unknown 4 (2.5 m/sec) squared RV EDP
Uh, er…Where is the RV EDP? Have we got one equation, two unknowns?
I cry foul!
Hold on, professor. Let’s find a good approximation of the RV EDP. How
about the CVP? Well, think about it.
If there is no big pressure gradient between the right atrium and the right
ventricle (there is no mention made of tricuspid stenosis), then, yes, in
diastole, with the tricuspid valve open, the prevailing pressure in the right
atrium should reflect the pressure in the right ventricle. So put 12 mmHg
into the right ventricle:

PA end-diastolic pressure 4 (2.5 m/sec) squared 12 mmHg
PA EDP 25 mmHg 12 mmHg

37 mmHg
Satisfy yourself that the units and the common sense hold true.
236 Board Stiff TEE
Case 6
54-yo man is having MV surgery. A-line, Swan, TEE. TEE shows thickened
MV leaflets with diastolic doming and restricted opening. There is 2+ MR
and no AI. You get the following:
Vital Signs
• Thermodilution cardiac output: 3.8 L/min
TEE Data
• MV pressure half-time: 215 millisec
• Peak trans-mitral E velocity: 240 cm/sec
• Mean trans-mitral velocity: 194 cm/sec
• TVI mitral inflow: 55 cm
• TVI MR: 85 cm
• MS PISA radius: 1.4 cm
• PISA alias velocity: 30 cm/sec
• MV alpha angle: 120 degrees
Calculate
• Peak trans-mitral pressure gradient
• Mitral valve area by pressure half-time
• Area of PISA
• Mitral valve area using PISA
• Mitral valve stroke volume
• Mitral valve regurgitant volume
• Mitral valve regurgitant fraction
• Effective MV regurgitant orifice area
Yipes. Killer.
Just start pounding, it’ll unfold.
Calculation of Peak Trans-Mitral Pressure Gradient

OK, this is not the end of the world. We’ve used velocities to give us gradi-
ents before. The trusty old warhorse of Bernoulli comes trotting out.
Delta P 4 velocity squared

4 (2.4 m/sec) squared

23 mmHg
Note that they tried to fake you out by giving you the trans-mitral E velocity
in cm/second. You need, in the Bernoulli equation, to have velocity in m/
second to get the answer in mmHg. If you had said

Delta P 4 (240 ) squared
you would have ended up with a gradient of 57600 mmHg. If you see such
a patient, DUCK, for his atrium is about to blow that wing of the hospital
to smithereens.
Calculation of Mitral Valve Area by Pressure Half-time

Our new friend, area = 220/PHT, comes in here.
Area 220/215 millisec

1.0 cm squared
Units OK? Yes. Common sense OK? Yes, this is a small mitral valve,
which goes along with the TEE findings of diastolic doming and restricted
opening. Just as an exercise, pretend he had a good mitral valve, one that
opened right up and emptied real fast. What would you see?
A faster pressure half-time, say, 110 milliseconds to empty half way. And
that means what? An area of 220/110, or 2 cm squared. A bigger valve.
Faster emptying. Makes sense.
Calculation of Area of PISA

PISA area = 2 × pi × radius squared when the PISA hemisphere is flush
and flat against the mitral valve. But when the PISA is at an angle to the
mitral valve annulus plane, then the PISA area is less. The area of the PISA
is then
PISA area 2 pi radius squared alpha angle/180

2 pi (1.4 cm) squared 120/180

8.2 cm squared
If that angle is giving you trouble, consider two extreme examples to sat-
isfy yourself that the angle does, indeed, decrease the area of the PISA
hemisphere.
Consider 180 degrees; in other words, there is no angle. Then the “angle
part” of the equation is 180/180 or 1. And the area is just that of a hemi-
sphere, 2 × pi × radius squared.
Consider 90 degrees. That looks like, and does, cut the area off by half.
Area 2 pi radius squared 90/180

2 pi radius squared 0.5
Now consider a ridiculous angle, 0 degrees. That means there IS no PISA

radius at all, and the area should be 0.
Area 2 pi radius squared 0/180

0
238 Board Stiff TEE
Calculation of Mitral Valve Area Using PISA

Um. Wait a minute here. Time and again, we’ve used the cylinder idea. You
have an area; multiply it by a length (the TVI), and you get your stroke vol-
ume. The units work out right, common sense usually prevails, Ford’s in
his flivver, and all’s right with the world.
But, er, we don’t have a length measured in handy units of cm. Now we
have an aliasing velocity in cm/second and a velocity of the mitral valve
flow in cm/second. Well, wait, that will work out.
Area PISA × velocity (aliasing) will give us the volume/second going
through the mitral valve. Well and good.
Area MV × velocity (MV peak) will give us the volume/second going
through the mitral valve. By the grace of continuity, these amounts have to
be the same. So we can set them equal to each other.
In earlier problems, we had set two cylinders of blood equal to each other
(LVOT area × LVOT length = mitral valve area × mitral valve length). Now we
have just taken it a step further by setting two cylinders/second equal to each
other (PISA area × PISA velocity = mitral valve area × mitral valve velocity).
To review, then, this problem yields:
Area PISA velocity PISA area MV (the unknown)

velocity MV 8.2 cm squared 30 cm/sec
area MV (the unknown) 240 cm/sec
Cross multiply and divide and you get:

Area MV 1.0 cm squared
Holy consistency, Batman, the area turns out the same, even after all that
work!
Calculation of Mitral Valve Stroke Volume

Things look a little more familiar here. Back to our “cylinder” of blood. No
bothersome extra “/seconds” to worry about.

Area mitral valve length mitral valve stroke volume mitral valve

Area MV TVI MV SV MV

1.0 cm squared 55 cm SV MV

SV MV 55 mL
Units OK? Yes. Common sense OK? Yes: 55 mL is a decent stroke volume.
Not super, but not ridiculously low or high.
Calculation of Mitral Valve Regurgitant Volume

Hubbada bubbada, what do we need to get this one? This does not jump
off the page and drip obviousness.
OK, think about what’s going on. Way back a hundred years ago you read
that the patient has mitral regurg but no aortic insufficiency. So we load
the left ventricle; where does the blood go?
There are only two “doors” into the left ventricle, the mitral valve pouring
blood in during diastole, and, what else, how else could blood get in there?
Blood could roll back into the left ventricle through the aortic valve. But no,
look:
“There is 2+ MR but no AI.”
“…no AI.”
So, forget that. The only blood going into the left ventricle is the stroke
volume passing the mitral valve, that is, the SV MV. That amount is 55 mL.
Now, what paths do we have OUT of the ventricle?
We still have the same two doors, the aortic and the mitral. Unlike during
diastole, though, this time BOTH of the doors are open. The aortic valve
functions its normal way, and pumps out a certain stroke volume, and the
mitral valve is incompetent, so blood flows out that way too.
A ventricle filled with 55 mL divides its two exit pathways into two:

55 mL volume out the aorta volume out the mitral valve
But how much goes out the aorta? Where is our “usual” LVOT diameter
and LVOT TVI? The bastards, they’ve left us high and dry.
Hold back your despair. It’s time to go back, long ago, to a galaxy far,
far away, where you used to figure stuff out without a TEE. Call this
retro-cardio-technology.
You have a cardiac output, right, remember, from that Swan thing that
they must have ordered from the Smithsonian? And you have a heart beat.
(God, they probably actually felt a PULSE! How’s that for a blast from
the past? Why don’t we all put on polyester leisure suits and head out to
Studio 54?)

Cardiac output out the aorta heart rate stroke volume out the aorta

3.8 L/min 100 beats/min stroke volume out the aorta

Stroke volume out the aorta 38 mL
So now we go back to what we were looking for:
55 mL (the amount loaded into the left ventricle) 38 mL out the aorta
X mL out the incompetent mitral valve

55 mL 38 mL regurgitant volume

55 mL 38 mL regurgitant volume

Regurgitant volume 17 mL
240 Board Stiff TEE
So, figuring this problem out was like the things every bride should wear,
“Something old, something new, something borrowed, something blue,
and a penny in her shoe”.
Only without the blue and penny stuff.
Calculation of Mitral Valve Regurgitant Fraction

Nothing earth-shattering here:

Regurgitant fraction regurgitant volume/total volume sent through MV

Regurgitant fraction 17 mL/55 mL

Regurgitant fraction 0.31, or, as a percentage, 31%
Units, common sense? Yeah, yeah, yeah. When will this chapter ever end?
Calculation of Effective MV Regurgitant Orifice Area

Cylinderville:

Area of regurgitation through the MV length of regurg volum
me of regurg

MV regurgitant area (the unknown) TVI MV regurg regurgitantt volume MV

MV regurgitant area 85 cm 17 mL
MV regurgitant area 17 mL/85 cm

0.2 cm squared
Makes sense, right units, so rock on. If this is starting to get repetitive, that
is fine and dandy, sugar candy. These should be so drilled into you that
you should be able to do these problems standing on your head. There are
only a few ideas (move a cylinder of blood; know which way the blood is
flowing; continuity; Bernoulli; area × length = volume; high-pressure area
loses pressure in a gradient, which goes to the low-pressure area). And, no
matter how the question is phrased, you get back to the same principles.
If you go through the nine problems from their workshop, and understand
how you got everything, you should ace this part of the test.
And if not, well hell, there’s always next year.
Case 7
56-yo man presents for AV surgery.
Vital Signs
• CVP: 14 mmHg
• BSA: 1.98 m squared
TEE Data
• LVOT TVI
• LVOT diameter
• Aortic valve mean gradient
• Aortic valve TVI
• TR peak velocity
Calculate
• Cardiac output and index
• Pulmonary artery systolic pressure
No kidding, by now you should be able to nail this stuff.

Move the cylinder, move the cylinder, move the cylinder of blood.

Stroke volume out the LVOT area of LVOT length(the TVI)
SV LVOT 0.785 (diameter LVOT) squared 23 cm

0.785 (2.2 cm) squared 23 cm

87 mL
which makes sense in terms of both units and normal physiology.
Calculation of Cardiac Output and Index

Puh-leeze! After jumping through the flaming hoops of PISA alpha angles,
this is downright pedestrian.

Cardiac output stroke volume TVI

Cardiac output 87 mL 23 cm

Cardiac output 1951cm to the 4th power
Units, um. Common sense, er… HEY, WAIT A MINUTE! Aha, so you see,
you can fall asleep at the wheel here and just grab any old number and
plug it in. Then, when your numbers and units come out phony baloney,
the klaxons should start clanging.

Cardiac output stroke volume heart rate
CO 87 mL/heartbeat 84 heartbeats/min

7.3 L/min
242 Board Stiff TEE
That’s more like it. That unit makes sense, and an output of 7.3 L/min
you’ve seen before in the OR.

Cardiac index CO/BSA
CI 7.3L/min/1.98 m squared

3.7 L/min/m squared

Continuity equation, here we come. The cylinder of blood going out the
LVOT = the cylinder of blood going out the aortic valve. We already have
the cylinder of LVOT blood.
LVOT SV (the cylinder of blood we calculated first) area off the aortic valve
(unbeknownst to us at present, but soon to yield to our astute powers
of calculation) length (TVVI of the aortic valve)

87 mL area of AV 122 cm
Cross multiply to get:
Area of AV 87 mL/122 cm

0.7 cm squared
Right units, right size for a fellow with aortic stenosis.
Calculation of Pulmonary Artery Systolic Pressure

Go with the concept of finding the high-pressure area, finding the choke
point where you lose pressure across a gradient, and the leftover low-pres-
sure area.
In systole, the right ventricle is the high-pressure area, and the right ven-
tricle is squeezing into the pulmonary artery. So, hmm, but they gave us
tricuspid valve regurg values and velocities.
Damn.
That’s, sort of, going the wrong way. Hmm. Think, think, think, like Winnie
the Pooh does.
We want to find the pulmonary artery pressure, darn the luck, but we seem
“at a remove” from what we want to find out. So we’ll have to approach
this from a more intellectual point of view.
The pulmonic valve, so we are given to understand, is OK, no stenosis
there. So, whatever pressure the right ventricle generates should go right
into the pulmonary artery. There is no “choke point” causing a gradient
loss.
That’s a start. The pulmonary artery systolic pressure will be the right ven-
tricular systolic pressure. Can we figure that out?
Yes! We are no longer “at a remove” from useful information. We have our
high-pressure area, our “choke point” where we lose pressure across a gra-
dient, and our low-pressure area.
RV pressure pressure lost across the tricuspid valve gradieent

low-pressure area in the right atrium (the CVP)

RV P 4 (3.6 m/sec) squared 14 mmHg

RV P 52 mmHg 14 mmHg

RV P 66 mmHg
Right units, makes sense that a right ventricle might have to generate a lot
of pressure in the face of a diseased heart. (He has a tight aortic valve plus
tricuspid regurg. Ay caramba! You think you’ve got problems.)
And, to answer the question, since the RV generates 66 mmHg, and the
pulmonic valve has no stenosis, then it makes sense that the pulmo-
nary artery “sees” all that pressure and thus the PA systolic pressure is
66 mmHg.
You CAN figure these things out, even when it’s not super obvious!
Case 8
78-yo man undergoing AAA surgery becomes hypoxic and hypotensive with
cross-clamping of the abdominal aorta. TEE reveals 1+ to 2+ MR, 1+ TR
without AS or AI.
Vital Signs
• CVP: 8 mmHg
TEE Data
• Aortic valve side: 2.3 cm
• Aortic valve TVI: 12 cm
• Peak velocity MR: 3.5 m/sec
• Peak velocity TR: 3.5 m/sec
Calculate
• Stroke volume
• Cardiac output
• Left atrial pressure
244 Board Stiff TEE

What’s with the side schtick? I got the cylinder thing down like nuthin’, and
now we got, what, Euclidean geometry, come on!
Chill. Like Avril Lavigne says in her song, “It’s all been done before”.
We have to turn ourselves in knots and avoid planimetry when the aortic
valve is diseased. Plain old (pardon the pun) planimetry can’t nail the aor-
tic valve area when the valve is all calcified, bumpy, irregular, and grotty
mundo. But hark, the case states the patient is “without AS or AI,” so it
turns out we can use planimetry.
Just when you had it all figured out, they throw in a normal one to screw
you up.
Call the aortic valve area an equilateral triangle, solve for the area of said
triangle, and you come up with:

Area 0.433 (side ) squared
Area of this aortic valve 0.433 (2.3 cm) squared

2.3 cm squared
Units make sense, and, wonder of wonders, the common sense works too,
because 2.3 cm squared is within the normal range. That jibes with “with-
out AS or AI”.
Calculation of Stroke Volume

Roll that cylinder, er, well, call it a kind of “triangular cylinder”? Either way,
the area of the blood × the length (TVI) of the blood will give us a volume,
however triangular we may envision it.

Area of AV TVI stroke volume

2.3 cm squared 12 cm SV

SV 28 mL
Units work out, and common sense, … whoa Nelly. Stroke volume of
28 mL. Not exactly irrational exuberance on the part of the heart is it? Does
that make clinical sense?
A 28-mL stroke volume is Bad News Bears Breaking Training. But look at
the overall picture — hypoxemic, hypotensive, old patient, just had the
aorta cross-clamped. Them’s a lot of reasons to be doing poorly. So, yes,
this result, though alarming, does satisfy the “common sense” criterion.

I won’t try to fake you out twice.

Stroke volume heart rate CO

29 mL 110 bpm 3.2 L/min
Bad, which goes along with the clinical picture.

Calculation of Left Atrial Pressure

Where is the high-pressure area? The left ventricle.
Where is the choke point? The mitral valve.
Where is the low-pressure area? The left atrium.
The left ventricle, with its systolic pressure, loses pressure (use Bernoulli)
across the mitral valve, which then lands in the left atrium.
LV systolic pressure − 4 × (3.5 m/sec) squared = left atrial pressure
85 mmHg (the systemic blood pressure, since the left ventricle creates the
pressure and goes out a nonstenotic aortic valve into the systemic circula-
tion) − 49 mmHg = left atrial pressure.

85 mmHg 49 mmHg left atrial pressure

Left atrial pressure 36 mmHg
Crikey (as the Croc Hunter says), this patient is overloaded and doing
badly. If things don’t get better soon, he may go Down Under.
Case 9
81-yo woman develops severe dyspnea and a harsh systolic murmur 8 days
after an acute MI. She gets intubated and rolls into an ICU near you. Stat
TEE shows a VSD with left-to-right shunting. Aortic and mitral valves are
normal.
Vital Signs
TEE Data
• LVOT TVI: 17 cm
• PA diameter: 2.4 cm
• PA TVI: 22 cm
• VSD peak velocity: 3.2 m/sec
Calculate
• Cardiac output
• Pulmonary artery stroke volume
• Pulmonary artery blood flow
• Shunt fraction (Qp/Qs)
246 Board Stiff TEE

Volume = area × distance (just in case you forgot, or in case you were
abducted by a UFO and had your brains sucked out).

Volume through LVOT area of LVOT length (TVI) of the LVOT
SV 0.785 diameter squared 17 cm

0.785 (1.8 cm) squared 17 cm

43 mL
Any hesitation on embracing this? Just the usual stuff, right? But what
about the VSD, does that gum things up? Remember, whatever may be
happening in the septum is below you. You measured the LVOT, which is
5 to 10 mm below the aortic valve. That area is real, and the TVI you mea-
sured with your precisely placed pulsed-wave Doppler is real. That LVOT
flow is the blood that has escaped whatever carnage is happening at
the ventricular septum. LVOT blood made good its escape from the left
ventricle.

Remember the anatomy; you can do the simple:

Cardiac output out the LVOT heart rate stroke volume of thee LVOT
Don’t sweat the VSD, you got past that, no worries, mate.

CO heart rate SV

CO 100 bpm 43 mL 4.3 L/min
Good units, good common sense.
Calculation of Pulmonary Artery Stroke Volume

Just sit back, relax, and let the cylinder of blood flow.

Area of PA (0.785 diameter squared) TVI PA (22 cm) PA SV

PA SV 99 mL
Right units. Now, that stroke volume looks a little larger than the stroke
volume we just calculated for the blood going out the LVOT into the sys-
temic circulation. Good Golly Miss Molly, has the inviolable truth of the
continuity equation been undone? Has the world gone mad?
The horror. The horror.
But wait, hope springs eternal. Remember, the continuity equation holds
ONLY IF the flow is uninterrupted. And we have an interruption here, a
VSD! We have another exit door out of the left ventricle.
Given that, then, this answer does make common sense.
Calculation of Pulmonary Artery Blood Flow

PA SV heart rate total flow through the PA

99 mL/heartbeat 100 bpm PA blood flow

PA blood flow 9.9 L/min
Units, good. Common sense? That’s a lot of blood zipping through the PA.
But then, if the right side is getting its “normal flow” (say 5 L/min or so),
plus a blast from the left side coming across the VSD (recall that the his-
tory mentions an MI with development of a VSD with left-to-right shunt-
ing), then 9.9 L/min does make common sense.
Calculation of Shunt Fraction (Qp/Qs)

Shunt fraction compares pulmonary flow to systemic flow.
Qp/Qs 9.9 L/min/4.3 L/min

2.3
No units, that works. More blood going through the pulmonary vascula-
ture than the systemic? Yes, that makes sense because the high-pressure
left side is squishing over to the low-pressure right side, “shorting” the
systemic blood flow and augmenting the pulmonary blood flow.

Where is the high-pressure chamber? The left ventricle. Since there is no
aortic stenosis, the systolic pressure in the left ventricle is all conveyed
to the aorta. So we can take the systemic pressure as our left ventricular
pressure.
Where is the choke point, across which the high-pressure area loses pres-
sure? The VSD. Bernoulli will tell us the pressure drop.
Where is the low-pressure point? The right ventricle. (Our unknown.)

LV systolic pressure 4 (3.2 m/second) squared RV systolic pressure

100 mmHg 41mmHg RV systolic pressure

RV systolic pressure 59 mmHg
And that, in so many words, is that. You are now a bona fide
Hemodynamo-Doc.
CHAPTER
Test Questions
24 William R. Grubb and Andrew T. Burr
QUESTIONS | Chapter 2: Principles of Ultrasound
2-1. Clinically useful ultrasound imaging waves are:

A. <20 kHz
B. Propagated in air
C. Between 1 and 10 MHz
D. Propagated faster in soft tissue than in bone
2-2. True concerning frequency of ultrasound signals include all but:
A. Higher frequencies provide better resolution
B. Higher frequencies are attenuated
C. Higher frequencies are used in the epicardial probes relative to
TEE probes
D. Frequency is directly related to wavelength
2-3. Wavelength is:
A. The time between cycles
B. Cycles over time
C. The distance between the onset of successive cycles (one cycle
compared to the next)
D. Speed (c) × frequency
2-4. Which is not a cause of attenuation?
A. Absorption
B. Reflection
C. Scatter
D. Refraction
2-5. Which is not true when describing the piezoelectric crystals?
A. Piezoelectric material creates an electrical change when
deformed
B. When changed by electrical current, a sound wave can be
produced
C. The piezoelectric crystal is the functional element of the
transducer
D. The lead zirconate titanate in an ultrasound transducer is stable 249
when autoclaved
250 Board Stiff TEE
ANSWERS | Chapter 2: Principles of Ultrasound
2-1. C
2-2. D
2-3. C
2-4. D
2-5. D
QUESTIONS | Chapter 3: Transducers and Instrumentation
3-1. The use of a damping material is applied to the transducer lens to

accomplish all the following except:
A. Shorten the length of an ultrasound pulse
B. Improve axial resolution for an imaging transducer
C. Results in a more homogeneous bandwidth
D. Results in a less homogeneous bandwidth for better image
acquisition
3-2. All true about axial resolution except:
A. SPL/2
B. Improved using a backing material
C. Improved with less bandwidth in a pulse
D. Improved with higher frequency transducer
3-3. True about spatial pulse length is:
A. Does not affect axial resolution
B. Determined by the number of cycles and the length of each
cycle
C. Effects beam width
D. Does not affect penetration of the beam
3-4. All true concerning the transition zone, except:
A. Occurs where the beam is narrow, at the end of the near zone
B. Is within the focal zone, where lateral resolution is best
C. Directly related to lens diameter squared and the frequency of
the transducer
D. Directly related to lens diameter squared and the wavelength of
the transducer
3-5. All true concerning phased array transducers, except:
A. Are used to create b mode images
B. Works by changing the frequency of the transducer
Chapter 24 Test Questions 251
C. Utilizes sequential firing of individual crystals in the transducer

D. Creates the pie-shaped image we see when the individual waves
in the sectors summate
ANSWERS | Chapter 3: Transducers and Instrumentation
3-1. C
3-2. C
3-3. C
3-4. B,D
3-5. B,C
QUESTIONS | Chapter 4: Equipment,

Infection Control, and Safety
4-1. Acceptable cleaning solutions for the active tip of TEE probe are
(multiple answers):
A. Soapy H2O
B. Glutaraldehyde
C. Hydrogen peroxide
D. Alcohol
E. Windex
4-2. If the insulation for TEE probe is broken, consequences can be:
A. Microelectrical shock
B. Faulty image
C. No image
D. Esophageal injury
4-3. The reason why a probe cannot be removed from a patient’s
esophagus:
A. Esophageal varicies
B. Probe locked in flexed position
C. Patient is not paralyzed
D. Not enough lubrication
4-4. It is possible to break TEE probe flexion lock by:
A. Pulling probe through bite block while in flexion
B. Excessive anterior flexion in stomach
C. Right main stem intubation
D. Retroflexed pharyngeal intubation
252 Board Stiff TEE
4-5. Which are contraindications for TEE? (multiple answers)

A. Recent esophageal surgery
B. History of gastric bypass surgery
C. History of radiation therapy to neck
D. History of radical neck dissection
ANSWERS | Chapter 4: Equipment,

Infection Control, and Safety
4-1. A,B,C
4-2. A
4-3. B
4-4. A
4-5. A,B,C,D
QUESTIONS | Chapter 5: Principles of

Doppler Ultrasound (True or False)
5-1. Focusing of the transducer beam is accomplished by the use of

lenses and electronic phasing
5-2. The intensity of the ultrasound beam decreases in tissue deeper
than the focal point of the system
5-3. The near zone length defines the furthest extent of the fresnel zone
5-4. Adding a damping material to a transducer will improve axial
resolution because the spatial pulse length decreases
5-5. The duty factor is the percentage of time the transducer is actively
putting signal into a tissue
5-6. The bandwidth of the transducer refers to the range of
frequencies over which the transducer can respond and is
determined by the difference between the highest and lowest
usable frequencies
5-7. A shorter pulse duration results in a broader bandwidth
5-8. Modalities that require good axial resolution, such as 2-D,
M-mode, and color Doppler, require fewer cycles in a pulse,
resulting in a short spatial pulse length
5-9. A 4 MHz transducer transmits a range of frequencies with an
average of 4 MHz
5-10. A single pulse from an ultrasound transducer contains a range of
frequencies
5-11. Increasing gain (transmit power) increases the voltage going
through the piezoelectric crystal producing a better signal to noise
ratio
ANSWERS | Chapter 5: Principles of Doppler

Ultrasound
5-1. T
5-2. T
5-3. T
5-4. T
5-5. T
5-6. T
5-7. T
5-8. T
5-9. T
5-10. T
5-11. T
QUESTIONS | Chapter 6: Quantitative M-Mode and

Two-Dimensional Echocardiography
6-1. True concerning M-mode:

A. Is not a form of B-mode echo
B. Best for examining the timing of cardiac events
C. Cannot work with color to determine velocities
D. Is old and useless technology
6-2. M-mode echo is useful to detect all the following except:
A. The function of the cusps of the mitral valve
B. The function of the cusps of the aortic valve
C. The thickening of the ventricle walls during systolic
D. Speed of passage of red blood cells through the aortic valve as
part of the continuity equation
6-3. Color M-mode technology is used to help assess diastolic function
in the following manner:
A. Measure tissue movement of the mitral annulus
B. Measure velocities of mitral inflow patterns
C. Create the estimation of velocity of propagation by measuring
the movement of a column of blood through the ventricle from
the mitral valve to the apex
D. Measure a deceleration time
254 Board Stiff TEE
6-4. M-mode assessment of the aortic valve in patients with aortic

insufficiency is notable in that:
A. Valve cusps seen in cross section do not approximate in diastoli
B. There is no appearance of the “boxcar”-like image
C. Valve cusps seen in cross section do not approximate in systoli
D. The anterior and posterior cusps do not approximate
6-5. Unique features concerning M-mode echo include all except:
A. It is a form of brightness mode in which amplitudes of returning
signals are displayed as degrees of brightness on a gray scale
B. It uses 1000–2000 scan lines per second to create high
sampling rates
C. High sampling rates lead to superior temporal resolution in
M-mode technology
D. It creates a 2-D image
ANSWERS | Chapter 6: Quantitative M-Mode and

Two-Dimensional Echocardiography
6-1. B
6-2. D
6-3. C
6-4. A
6-5. D
QUESTIONS | Chapter 7: Quantitative Doppler
7-1. Increasing the depth of data acquisition will:

A. Decrease the PRF
B. Change the frequency of the probe
C. Increase the PRF
D. Make the image clearer
7-2. True concerning PRF except:
A. It is the number of times the transducer is excited each second
B. It is the reciprocal of the PRP
C. It can be changed by the sonographer
D. It is inversely related to the duty factor
7-3. Range ambiguity is a feature of:
A. PW Doppler
B. Continuous wave Doppler
C. Color Doppler imaging

D. Tissue Doppler imaging
7-4. The velocity time integral is used in the continuity equation to
estimate:
A. Length that blood flowed over time in cm
B. Area of valves in cm squared
C. Volume of blood flow in cm cubed
D. Volume of blood over time
7-5. A cross sectional area multiplied by a VTI (estimated with a Doppler
determination of velocities over time) determines a:
A. Flow rate
B. Cardiac output
C. Stroke volume
D. Area of a valve
ANSWERS | Chapter 7: Quantitative Doppler
7-1. A
7-2. D
7-3. B
7-4. A
7-5. C
QUESTIONS | Chapter 8: Doppler Profiles and Assessment of

Diastolic Function
8-1. All are true about severe tricuspid regurgitation except:

A. Jet area greater than 10 cm squared
B. The vena contracta width is greater than 6.5 mm
C. There is systolic hepatic flow reversal
D. There is diastolic hepatic flow reversal
8-2. A basic concept of the study of diastolic ventricular function and
transmitral flow notes that:
A. Quicker rises in E-waves are associated with good diastolic
function
B. A stiff ventricle that does not relax results in changes in atrial
filling and the patterns of the pulmonary vein flows
C. Changes in the E-wave and A-wave peaks parallel each other
D. The area of the E-wave provides an assessment of diastolic
dysfunction
256 Board Stiff TEE
8-3. True concerning E/A ratios in diastolic dysfunction:

A. Differences in E/A ratios can distinguish normal from
pseudonormal function
B. A reduction in preload will help distinguish normal from
pseudonormal ventricles with similar E/A ratios
C. High E/A ratios are always good
D. A Valsalva maneuver will always change E/A ratio
8-4. A patient has an E/A ratio greater than 1, diastolic function can be
further distinguished by all the following except:
A. Calculating the VTI of the E-wave
B. Use of the Valsava maneuver
C. Noticing the speed of the atrial reversal blood flow Ar wave
D. Observing tissue Doppler velocities
8-5. In severe forms of ventricular diastolic dysfunction:
A. S:D ratios are <1, the A wave reversal speeds are greater than
35 cm/sec and the tissue Doppler E prime velocities are less than 8
B. S:D ratios are >1, the A wave reversal speeds are greater than
35 cm/sec and the tissue Doppler E-wave velocities are less
than 12
C. S:D ratios are <1, the A wave reversal speeds are greater than
35 cm/sec and the tissue Doppler E-wave velocities are less
than 12
D. S:D ratios are <1, the A wave reversal ratios are greater than 35
and the speeds of the diastolic relaxation are very fast
ANSWERS | Chapter 8: Doppler Profiles and Assessment of

Diastolic Function
8-1. D
8-2. B
8-3. B
8-4. A
8-5. A
QUESTIONS | Chapter 9: Cardiac Anatomy
9-1. The ME 4 chamber view of the perfusion to the ventricular

myocardium on the right side of the screen (the anterolateral wall) is:
A. RCA
B. Circumflex artery
C. LAD
9-2. In the ME 4 chamber view, the perfusion to the middle of the
ventricular display (the anteroseptal wall) is:
A. RCA
C. LAD
9-3. In the ME LAX135 degree view, the perfusion to the ventricular
wall on the right side immediately below the LVOT (the
anteroseptal wall) is:
A. LAD
C. RCA
9-4. In the ME 2 chamber view (90 degrees), the perfusion to the wall
on the left side of the display (the inferior wall) is:
A. RCA
B. LAD
C. Circumflex artery
9-5. In the ME TG SAX view, the perfusion to the myocardium at the
top of the screen (the inferior wall) is:
A. LAD
B. RCA
ANSWERS | Chapter 9: Cardiac Anatomy
9-1. B
9-2. C
9-3. A
9-4. A
9-5. B
QUESTIONS | Chapter 10: Pericardium and Extra-Cardiac

Structures: Anatomy and Pathology
10-1. The pulmonary veins are best imaged:

A. In the upper third of esophagus
B. In the deep transgastric window
C. In the mid esophageal transgastric view
D. In the lower one third of the esophagus
258 Board Stiff TEE
10-2. True concerning pericardial tamponade as seen with TEE:

A. Fluid appears echogenic and blood does not appear at all
B. Fluid appears echolucent (dark), but clotted blood appears like
tissue
C. Both unclotted and clotted blood are echogenic
D. Both unclotted and clotted blood are echo lucent
10-3. Normal pericardium is:
A. Greater than 5 mm thick on TEE
B. Echolucent (dark)
C. 1–2 mm thick on TEE
D. Never seen with TEE
10-4. True concerning normal pericardium includes all except:
A. Extends onto the aorta and main PA
B. Includes the transverse sinus
C. Can have a volume of 100 ml
D. Has a visceral layer attached to the epicardium
10-5. Pulsus paradoxus:
A. During spontaneous inspiration, a decrease in left-sided filling
resulting in a decrease in blood pressure
B. During spontaneous expiration, a decrease in blood pressure
C. During spontaneous inspiration, a decrease in left-sided filling
resulting in a decrease in blood pressure greater than 10 mmHg
D. During spontaneous expiration, a decrease in blood pressure
of greater than 10 mmHg
ANSWERS | Chapter 10: Pericardium and Extra-Cardiac

Structures: Anatomy and Pathology
10-1. D
10-2. B
10-3. C
10-4. C
10-5. C
QUESTIONS | Chapter 11: Pathology of the Cardiac Valves
11-1. True concerning normal aortic valve:

A. Peak velocity <1 m/sec and area 3–5 cm squared
B. Peak velocity <1.4 m/sec and area >5 cm squared
C. Peak velocity <1.4 m/sec and area 3–4 cm squared

D. Peak velocity <2 m/sec and area 3–5 cm squared
11-2. The most common cause of aortic stenosis in >55 yrs:
A. Rheumatic heart disease
B. Senile calcific degeneration
C. Bicuspid aortic valve
D. Marfan’s syndrome
11-3. All true about the continuity equation except:
A. At an instant in time, the VTI × area on each side of a stenotic
valve is equal
B. It is limited by estimation of the LVOT area
C. It is used to estimate aortic valve areas
D. Utilizes a pulse wave determination of velocity in the aorta and
a continuous wave velocity measurement in the LVOT
11-4. Mitral inflow patterns consist of:
A. Early A wave consistent with passive diastolic filling
B. Early E wave consistent with active diastolic filling
C. Early E wave consistent with passive diastolic filling
D. Early A wave consistent with active diastolic filling
11-5. All are true concerning the pressure half time determination of the
mitral valve except:
A. Uses the cwd determined deceleration slope of the E wave
B. Is normally less than 220 m/sec
C. Is normally less than 220 milliseconds
D. Is used to determine mitral stenosis
ANSWERS | Chapter 11: Pathology of the Cardiac Valves
11-1. C
11-2. B
11-3. D
11-4. C
11-5. B
QUESTIONS | Chapter 12: Intra-Cardiac Masses and Devices
12-1. All the following structures are seen in the right atrium except:
A. Chiari network
B. Coumadin ridge
C. Cristsa terminalis
D. Eustachian valve
260 Board Stiff TEE
12-2. All are true about myxomas, except:

A. Has a heterogeneous appearance as it often contains cysts
B. Most common pediatric intercardiac tumor
C. Often associated with the fossa ovalis portion of the interatrial
septum in the left atrium
D. Pedunculated but not fimbriate in appearance
12-3. All are true about intercardiac lipoma except:
A. Can be found in the left ventricle or the right atrium
B. Second most common benign primary cardiac mass
C. Usually sessile, homogeneous and hyperechoic
D. A small vegetation on the downstream side of a aortic valve
12-4. The most common intercardiac mass in the left ventricle is:
A. Renal cell carcinoma
B. Eustachian valve
C. Fibroma
D. Thrombus
12-5. All true concerning angiosarcoma except:
A. Most common malignant cardiac tumor
B. 80% seen in the right atrium
C. Extend into the pericardium and vena cava
D. Not associated with pericardial effusion
ANSWERS | Chapter 12: Intra-Cardiac Masses and Devices
12-1. B
12-2. B
12-3. D
12-4. D
12-5. D
QUESTIONS | Chapter 13: Left Ventricular Systolic Function
13-1. All true concerning HOCM, except:

A. Inherited autosomal dominant trait
B. Always includes SAM of the mitral valve
C. Diastolic function is impaired
D. Continuous wave Doppler ventricular contraction profiles are
characterized by late peaking “dagger-like” appearance
13-2. Treatments for HOCM include all the following except:

A. Surgical resection
B. Alcohol ablation of the septum
C. Beta blockade
D. Ionotropes
13-3. Causes of restrictive cardiomyopathy include all the following
except:
A. Sarcoidosis
B. Eosinophillic myocarditis
C. HTN
D. Viral etiology
13-4. Restrictive cardiomyopathy is associated with:
A. Systolic dysfunction only
B. Thickening of the posterior basal septal wall
C. Outflow tract obstruction of the LV
D. SAM
13-5. Thrombi are likely to be seen in these areas except:
A. At the LV apex
B. Under the posterior mitral valve leaflet
C. In the left atrial appendage
D. In the aortic sinus
ANSWERS | Chapter 13: Left Ventricular Systolic Function
13-1. B
13-2. D
13-3. C
13-4. B
13-5. D
QUESTIONS | Chapter 14: Segmental Left Ventricular

Systolic Function
14-1. LAD feeds what walls of the heart?

A. Posterior basal
B. Anterior and septal
C. Lateral
D. Inferior and basal
262 Board Stiff TEE
14-2. Normal movement of a LV segment during systole is:

A. Thickening and inward
B. Thickening and outward
C. Thinning and inward
D. Thinning and outward
14-3. Blood supply to the area highlighted in the figure below is:
A. LAD
B. RCA
D. PDA
14-4. Immediately post sternal closure the patient’s blood pressure
drops; arrhythmia ensues and TEE shows RWMA. The most
probable explanation is:
A. Air embolism
B. Coronary dissection
C. Kinked graft during closure
D. Dissection
ANSWERS | Chapter 14: Segmental Left Ventricular

Systolic Function
14-1. B
14-2. A
14-3. C
14-4. A,B,C,D
QUESTIONS | Chapter 15: The 17 Segment Model
15-1. In the 17 segment model, the anterior wall of the left ventricle
depicted in the figure below is composed of segments:
A. 2 basal, 4 middle, 6 apical

B. 2 basal, 8 middle, 13 or 14 apical and portions of 17
C. 2 basal, 7 middle, 12 apical
D. 2 basal, 8 middle, 12 apical and portions of 17
15-2. The segments (2 basal, 8 middle, 13 apical) in the above figure are
perfused by:
A. RCA
B. LAD
C. Circumflex
D. PDA
15-3. In the 17 segment model as depicted in the figure below the
inferior wall of the left ventricle is composed of segments:
A. 5 basal, 11 middle, 15 apical or portions of 16

B. 5 basal, 11 middle, 17 apical
C. 6 basal, 12 middle, 16 apical
D. 6 basal, 11 middle, 15 apical
264 Board Stiff TEE
15-4. The segments (5 basal, 11 middle) in the above figure (question

15-3) are perfused by:
A. RCA
B. LAD
D. PDA
15-5. The segments numbered 1,7 and seen in figure below in the 17
segment model, are perfused by:
A. RCA
B. LAD
D. PDA
ANSWERS | Chapter 15: The 17 Segment Model
15-1. B
15-2. B
15-3. A
15-4. A
15-5. B
QUESTIONS | Chapter 16: Assessment of Perioperative

Events and Problems
16-1. TEE assessment during CPB is performed to:

A. Visualize aortic cannulation site
B. Determine function of prosthetic valves
C. Assess venous cannulation sites
D. Determine that the left ventricle is not distending during
administration of cardioplegia into the aortic root
16-2. The coronary sinus:
A. Drains into the right atrium and is associated with the thesbian
valve
B. Derives from the aortic root

C. Carries arterial blood
D. Is never cannulated
16-3. The best method for determining dissection at the site of aortic
cannulation is
A. TEE
B. Epiaortic echo
C. Direct observation
D. Left arm blood pressure
16-4. The landmark arterial vessel for assessment of IABP
placement is
A. Innominate
B. Carotid
C. Left subclavian
D. Femoral
16-5. LVAD therapy will not work when
A. The patient has atrial fibrillation
B. The patient has interatrial septal defect
C. The patient has a foramen ovale
D. The patient has a prosthetic aortic valve
ANSWERS | Chapter 16: Assessment of Perioperative

Events and Problems
16-1. D
16-2. A
16-3. B
16-4. C
16-5. B
QUESTIONS | Chapter 17: Congenital Heart Disease
17-1. Tetrology of Fallot consists of the following features except:

A. VSD
B. Overriding aorta
C. Pulmonic valve stenosis and RVH
D. ASD
266 Board Stiff TEE
17-2. Persistent left superior vena cava includes all the following except:
A. Congenital anomaly with large coronary sinus
B. Venous injection of agitated saline appears first in the coronary
sinus and then in the right ventricle
C. Venous injection of agitated saline appears first in the left
atrium
D. Difficulty in establishing retrograde coronary cardioplegia flow
17-3. All true concerning coronary fistulas except:
A. Commonly involve the right coronary artery
B. Drain to the PA, coronary sinus, or superior vena cava
C. Commonly drain to the left heart
D. Are associated with a large or tortuous coronary artery
17-4. Most common congenital heart defect is:
A. PDA
B. Bicuspid aortic valve
C. ASD
D. VSD
17-5. Subaortic stenosis is associated with:
A. ASD
B. PDA
C. Bicuspid aortic valve
D. PLSVC
ANSWERS | Chapter 17: Congenital Heart Disease
17-1. D
17-2. C
17-3. C
17-4. B
17-5. C
QUESTIONS | Chapter 18: Artifacts and Pitfalls
18-1. Side lobes are created when ultrasound interacts with:

A. Objects deeper than the transition zone
B. Objects in the near zone
C. Objects outside the main ultrasound beam
D. Objects at the transition zone
18-2. Reflection occurs when:

A. The propagation speed of two mediums is the same
B. The incident angle is less than 90 degrees
C. The incident angle is 90 degrees
D. The incident angle is zero degrees
18-3. Reverberation artifact is caused when
A. The ultrasound interacts with a strong reflector or bounces
between the transducer surface and a structure
B. The gain is turned up
C. Ultrasound beam is absorbed by calcium in a structure
D. The probe orientation is changed through many different angles
18-4. The speed of sound is:
A. The same in all elements of the body
B. Faster in air than in bone
C. 1.54 m/sec in all tissues
D. Assigned a speed of 1540 m/sec in most soft tissues for ease
of calculating
18-5. When the ultrasound beam encounters the interface between two
mediums with different propagation speeds at an oblique angle:
A. Reflection occurs
B. Refraction occurs
C. Reflection, refraction, and absorption occur
D. Absorption occurs
ANSWERS | Chapter 18: Artifacts and Pitfalls
18-1. C
18-2. D
18-3. A
18-4. D
18-5. B
QUESTIONS | Chapter 19: Related Diagnostic Modalities
19-1. Advantages of epicardial echo include all the following except:

A. Ability to visualize the ascending aorta and pulmonic valve
B. Ability to detect plaque in the aorta
C. Can be used in patients with esophageal pathology when TEE
is contraindicated
D. Provides excellent imaging of the mitral valve
268 Board Stiff TEE
19-2. Best epicardial imaging of planar view of the aortic valve

A. Epicardial LAX
B. Epicardial 2 chamber
C. Epicardial LV SAX
D. Epicardial AV SAX
19-3. Best epicardial view for determination of velocity of flow with
Doppler
A. Epicardial LAX
D. Epicardial AV LAX
19-4. Best longitudinal epicardial view for determination of inferior wall
function:
A. Epicardial LAX
19-5. This epicardial transverse view shows the posterior papillary
muscle in the 9 o’clock position:
A. Epicardial LAX
ANSWERS | Chapter 19: Related Diagnostic Modalities
19-1. D
19-2. D
19-3. D
19-4. B
19-5. C
QUESTIONS | Chapter 20: Intraoperative 3-D

Echocardiography
20-1. Benefits of 3D TEE include all except:

A. Facilitates the assessment of complex cardiac pathology
B. Uses volumetric technique to display chambers such as the
right ventricle
C. Offers a better assessment of individual patient anatomy

D. Allows enhanced real-time velocity determinations
20-2. 3D TEE probes utilize:
A. 128 piezelectric crystals
B. 2500 active elements
C. A trapezoidal image
D. Movement of the transducer to create images
20-3. True concerning 3-D TEE
A. Dispersion is the technique when data are converted to
Cartesian coordinates
B. Extrapolation is the technique used to fill in data between the
coordinates
C. Data acquisition takes place, followed by RAM storage,
conversion, and interpolation
D. 2-D echoes are interpolated to form 3-D echoes
20-4. In 3-D imaging techniques, the poorest temporal resolution is
associated with:
A. Live
B. Live zoom
C. Full volume
20-5. True about 3-D imaging:
A. Volume techniques can be generated in one heartbeat
B. Current systems allow line measurements within a 3-D volume
C. A grid of dots can currently be overlaid on a 3-D image to
estimate length
ANSWERS | Chapter 20: Intraoperative 3-D

Echocardiography
20-1. D
20-2. B
20-3. C
20-4. B
20-5. C
QUESTIONS | Chapter 21: The Structured TEE Examination
21-1. In the ME 2 chamber view; the following walls of the left ventricle
are seen:
A. Anteroseptal and posterior
B. Anterior and inferior
270 Board Stiff TEE
C. Septal and basal

D. Posteroseptal and lateral
21-2. The ME commissural view of the mitral valve (60 degrees) is most
notable in that:
A. Only the a2 leaflet of the mitral valve is seen
B. P3 of the posterior, a2 of the anterior, and p1 of the posterior
are the most frequently seen cusps
C. Only the posterior leaflets are seen
D. The LV is seen in short axis
21-3. The view used to create the most parallel and precise continuous
wave assessment of velocity of blood flow in the ascending aorta is:
A. AV sax
B. Deep transgastric
C. AV lax
D. Epiaortic sax
21-4. The best view for simultaneous assessment of the tricuspid valve
and pulmonic valve is:
A. ME sax
B. ME lax
C. RV inflow outflow
D. TG short axis
21-5. The best view for identifying coronary sinus, IVC, SVC, and the
foramen ovale is:
A. 4-chamber 0 degrees
B. 2-chamber 60 degrees
C. ME lax 135 degrees
D. ME bicaval view
ANSWERS | Chapter 21: The Structured TEE Examination
21-1. B
21-2. B
21-3. B
21-4. C
21-5. D
QUESTIONS | Chapter 22: Sonographic Formulas
22-1. Stroke volume equals:

A. AVA × peak vel
B. AVA × TVIav
C. AVA × TVIlvot
D. CSAlvot × TVIav
22-2. All true about PHT except:
A. Rate of decline in pressure through a valve over time
B. Time for peak pressure in a system to decline to ½
C. Time of PHT = peak velocity/square root of 2
D. Equal to 0.29 × DT
22-3. MVA for stenotic valve:
A. 220/.29 × DT
B. 220 × PHT
C. PHT/220
D. 0.29 × DT
22-4. All true for PISA determination of MVA except:
A. Angle correction of alpha/180 is used because the mitral valve
is “tented” when closed and the isovelocity figure measured is
less than hemisphere in size
B. 2 pi r2 is the area of a hemisphere
C. ‘r’ is measured at the first isovelocity line
D. The determination is made during systolic
ANSWERS | Chapter 22: Sonographic Formulas
22-1. B
22-2. A
22-3. A
22-4. D
Epilogue: Smooth Sailing
“Nothing ever happens on my voyages.”

Edward Smith
Captain of the Titanic
There you have it. TEE in a nutshell.
Now, whether you decide to make TEE a part of your OR, ER, or ICU
practice, I wish you smooth sailing, just like Captain Smith had. (At least
for the first half of his trip.)
If you decide to take the PTEeXAM, best of luck.
I hope this simplified introduction helped to clarify a point or two about

the groovalacious world of transesophageal echocardiography.
See you under a bridge somewhere!
2013
273
Index
Note: Page numbers followed by “f ” and “t” refers to figures and tables respectively.
A ME AV LAX view 68f, 100–101, 101f,

107–108, 206–207, 206f
A (atrial) wave 73, 93
ME AV SAX view 68f, 107, 206, 206f
Abdominal aorta 84
insufficiency 78, 102t, 108, 110
Acoustic imaging, assumptions 174
leaflets 107–108
Air dilemma 5
left ventricle assist device (LVAD)
Air, intracavity 153
151–152
Aliasing 30–31, 30f, 31f
left ventricular outflow (LVOT) 62–63
‘Alphabet’, transesophageal
M-mode 40–41, 40f
echocardiography (TEE) 68f, 204f,
normal 110, 110f
207f
problems, causes 99t
Aneurysms
regurgitant fraction, calculation 231
aortic 87, 87f, 89
regurgitant orifice area, calculation
left ventricular 135–136
231–232
sinus of Valsalva 87, 167
regurgitant volume, calculation
ruptured 167
230–231
Angiosarcoma 117
repair 159
Anterior wall 68f, 71
stenosis 98, 102t, 107–108, 108f,
Anteroseptal wall 71
110–111, 110f
Aorta
classification 109
anatomy 84–86, 85f, 86f
senile calcific 98, 98f, 107–108, 108f
pericardial layers 82
stroke volume, calculation 244
see also Ascending aorta; Descending
systolic blood velocities 97
aorta
Arrays 12–13, 13f
Aortic annulus 100–101, 101f
Artifacts 173
calcification 102t
attenuation errors 182–185, 183f, 184f
dilation 102t
Doppler 185–186, 186f
Aortic arch (AA) 78–79, 85
mimics 116, 186–188, 186f, 187f, 188f
dissections 89
multiple echoes 176–180, 177f, 178f,
imaging 208, 208f
179f
descending short axis (SAX) view
types 174–185
208, 208f
US beam characteristics 174–176, 175f,
Aortic cannula 150
176f
Aortic conditions
velocity errors 180–182, 181f, 182f
aneurysm 87, 87f, 89
Ascending aorta 78–79, 84
inflammation/coarctation/infection 91
dissections 89
plaque 89–90
views, ME long axis (LAX)/short axis
pseudoaneurysm 87–88
(SAX) 68f
surgery 89
Atheromas 90
thrombus 91
Atherosclerosis 89–90
trauma 90–91
Atherosclerotic plaque 90
Aortic dissection 88–89
Atrial cannula 150
classification 88–89
Atrial reversal 61
Aortic root 77–78, 77f, 84
Atrial septal defects 163, 167–168
Aortic valve (AV) 72, 98–100, 107
primum 168
annulus 84
secundum 168
area, calculation 215–217, 228–229,
sinus venosus 168
242, 244
Atrio-ventricular valve 166
bicuspid 98, 98f, 169
Atrium
gradient, calculation 217–218
anatomic variants 115–116
imaging 100–101, 206–207, 206f
imaging 207–208, 207f
deep transgastric views 62, 68f,
ME bicaval view 208, 208f 275
108–109, 109f, 206–207, 206f
276 Index
Attenuation 6, 174, 182 malignant primary 117–118

errors, artifacts 182–185, 183f, 184f metastatic 118
Axial resolution 12, 12f mimics 115–116
Azygos vein 78, 94 valvular anatomic variants 116
ventricular anatomic variants 116
B Cardiac output, calculation 213–214, 227,
232, 241–242, 244, 246
BART (blue away red towards) acronym 28
Cardiac surgical techniques 149–155
Beam
bypass/cardioplegia assessment 149
angle 32–36, 32f
cannulas/devices 149–150, 150f
characteristics 174–176, 175f, 176f
circulatory assist 150–153, 151f, 152f
focal zone 12, 12f
cardiopulmonary bypass, minimally
formation 11
invasive 153
width 175, 175f, 185–186, 186f
intracavity air 153
Bernoulli equation 50, 214, 217, 236–237,
off-pump 153–155
245
Cardiac valves
modified 100, 110–111
anatomy 72
Bicuspid aortic valve 98, 98f, 163, 169
variants 116
Biplanes, 3-D guided 200
area 49–50, 97
Björk–Shiley valve 157
gradients 49–50
Blalock–Taussig operation 165
imaging 205–207
Blood flow reversal 106
normal values 98f
B-mode 15, 16f, 27, 27f
pathology 97, 99t, 102t
Bounce technology 4
surgery 156–158
Breast cancer 118
repair 159–160
Breathing, spontaneous 83
Bypass assessment 149, 153
valve types 156
see also Coronary artery bypass graft
see also specific valves
(CABG)
Cardiac walls, anatomy 68f, 71–72, 72f
Cardioplegia assessment 149
C Cardiopulmonary bypass, minimally
Calcifications 88 invasive 153
leaflet 102t Cardiovascular instability 156
senile aortic stenosis 98, 98f, 107–108, coronary artery bypass graft (CABG)
108f 155
senile degeneration 98 Carotid arteries 78
Calculations see Measurements left 85
Cancer Carpentier–Edwards valve 158, 158f
breast 118 Case studies 211
lung 118 Celiac trunk 79, 85
Carbomedics valve 157–158, 157f Central venous pressure (CVP) 73, 147
Carcinoid 118 Chiari network 115, 188
Carcinoma, renal cell 118 Chronic pulmonary vasculature strain 91
Cardiac anatomy 67 Cine loop technology 43
imaging planes 67–71, 68f Circulatory assist devices 150–153, 151f,
Cardiac arrest, unexpected intraoperative 152f
91 Clotted blood 80–81
Cardiac chambers CME Unlimited 1
anatomy 68f, 71–72, 72f Coarctation of aorta 163
collapse 84 Color flow Doppler (CFD) 28, 98–100,
pressures 50–51, 51f 102t, 186
Cardiac cycle 72–74 Comet tail artifact 178
Cardiac devices 149–150, 150f Comprehensive Review of Intraoperative
circulatory assist 150–153, 151f, 152f Echocardiography (echo meeting) 1
see also Cardiac masses Compression 3, 6f
Cardiac index, calculation 214, 241–242 Congenital heart disease 163
Cardiac masses 115 atrial septal defects 167–168
atrial anatomic variants 115–116 bicuspid aortic valve 169
benign primary 116–119 communication, intraoperative 165–166
common, schematic representation findings 149–150
118–119, 118f history 149–155
imaging modalities 118–119 left ventricular outflow abnormalities 169
Index 277
operation names 149–150 history 59

patent ductus arteriosus 169 left atrium, size 59
perimembranous 167 mitral valve (MV)/left ventricular inflow
persistent left superior vena cava 57–58, 57f
(PLSVC) 168 non-valvular flow 63–64
pulmonary valve stenosis 168 pulmonary valve/right ventricular
terminology 163–164 outflow 56–57, 56f
tricuspid valve, Ebstein’s abnormality pulmonary veins inflow 60, 60f, 63–64
170 tricuspid valve/right ventricular inflow
venous blood flow 165 55–56, 56f
see also Ventricular septal defect (VSD) Valsalva maneuver 59–60
Connective tissue disorders 87 see also Heart
Constrictive pericarditis 84 Diastolic pressure
Continuity left ventricular, calculation 232–233
equation 100, 215, 234–235 pulmonary artery 235
essence of 50f Dilated cardiomyopathy 127
Continuous wave (CW) Doppler 28, 28f, Dimensionless index 110–111
47, 98–100, 107 Displays 15, 15f
Contrast echocardiography 119, 192 Distraction 13
Conversion, raw data 197 Doppler Effect 100
Coronary angiography vs transesophageal Doppler shift equation 25–26
echocardiography (TEE) 192 derivation 32–35, 32f, 34f
Coronary arteries 85 Doppler ultrasound, principles 25
anatomy 143 artifacts/pitfalls 185–186, 186f
distribution 132–133, 133f, 143f B-mode 27, 27f
flow 132–133, 133f beam angle 32–36, 32f
memory helper 133 color flow Doppler 28, 98–100, 102t, 186
sinus, unroofed 168 continuous wave (CW) 28, 28f, 47,
surgical techniques 155 98–100, 107
Coronary artery bypass graft (CABG) 156 high pulse repetition frequency (HPRF)
off-pump 153 mode 31–32
on-pump 155 M-mode 27, 27f
Coumadin ridge 115, 187 Nyquist limit/aliasing 30–31, 30f, 31f, 35
Crista terminalis 115, 188 profiles 55
Crystal thickness 10 pulse wave (PW) 29, 29f, 35, 47, 98–100
quantitative 47
range ambiguity 29–30, 29f
D tissue reconstruction 26–27
D (diastolic) wave 61, 93 two dimensional (2-D) images 27, 27f
Dagger sign 124–125 Double envelope 110–111
Damping 11 Down’s syndrome 167
Damus Kaye Stansel operation 165 Dropout phenomena 176
Data processing 197
Data storage, temporary 197
Deceleration time (DT) 61 E
Deep transgastric (TG) plane 68 Ebstein’s anomaly of tricuspid valve 163,
long axis (LAX) view, aortic valve (AV) 170
62, 68f, 108–109, 109f, 206–207, Echo probes 19
206f cleaning 20–22
Depth 14 insertion 21
gain compensation 14 matrix array 197
Descending aorta 84–85 problems 20–21
long axis (LAX) view 68f three dimensional (3-D) 196–198
short axis (SAX) view 68f transportation 20
aortic arch (AA) 208, 208f use 21
thoracic 78, 84–85 Edge
Devices see Cardiac devices components, M-mode 39
Diagnostic modalities 191 recognition, M-mode 39
Diastole 51, 51f shadow 176, 176f
Diastolic function, assessment 55, 62t Eisenmenger syndrome 167
aortic valve (AV)/left ventricular outflow Ejection fraction (LVEF), left ventricular 43,
(LVOT) 62–63 123
278 Index
Electrocardiography (ECG) 72 see also Cardiac entries

vs transesophageal echocardiography cross section 141f
(TEE) 192 disease see Congenital heart
Electronic interface 185 disease
Embolism 159 images 142f, 143f
Endocarditis 159 impaired filling 58–59, 58f, 61f
Epicardial pacing 188 normal 58, 58f, 60, 61f
Epicardial scanning 191 pseudonormal 58f, 59–61, 61f
Equipment 19–20 restrictive flow 29f, 32–36, 61f
cleaning 20–22 transplantation 160
ergonomics 21–22 valves see Cardiac valves
see also Echo probes Hepatic veins 55–56, 64, 92–95
Esophagus 78–79, 80f flow 101
Eustachian valve 115, 188 Hepato-renal space 94
Examination, transesophageal High pulse repetition frequency (HPRF)
echocardiography (TEE) 203 mode 31–32
preliminary checks 203 High-frame rate-Doppler 47–48
structures 207–208 Holodiastolic aortic flow reversal 110
valves 205–207 Hologram displays 198
ventricular function 203–205 Hypertension 169
Expiration, spontaneous 83 Hypertrophic obstructive cardiomyopathy
(HOCM) 124–127, 125f, 126f
F Hypertrophy, lipomatous 116
False chords 116 Hypotension 147–149, 156
False lumens 88 causes 147–148, 148f
Fenestrations 88 coronary artery bypass graft (CABG)
Fibroelastoma, papillary 117 155
Fibroma 117
Fish mouth 68f, 169, 205–206 I
Fluid Image display
pericardial 81–82 3D 197
transesophageal echocardiography hologram 198
(TEE) 80, 81f stereoscopic 198
Focusing 11, 11f Impella 152, 152f
Fontan, defined 165 Incorrect gain 185
Foreign bodies Inferior vena cava (IVC) 77, 77f, 79, 92–95,
atrial 116 93f
ventricular 116 Inferior wall 68f, 71
Four-chamber view 71 Innominate artery 84–85
see also Midesophageal (ME) 4 Chamber Innominate vein 78–79
view Inspiration, spontaneous 83–84
Frequency 3, 4f, 14 Instrumentation 13–15
Insufficiency, valves 97–98
G aortic valve (AV) 78, 102t, 108, 110
Gain 14 causes 99t
Gastric lining 80 mitral valve (MV) 101
Gastric window 94 tricuspid valve 101
‘Gate’ 93–94 Interatrial septum, lipomatous hypertrophy
Gebode defect 167 116
Ghosting 186 Intercostals 85
Glenn operation 165 Internal jugular veins 78
Gologorsky method 191 Interpolation, raw data 197
Gradient Intra-aortic balloon pump 150–151,
essence 51f 151f
tissue valves 159 Intra-cardiac masses see Cardiac masses
Grating lobes 174 Intracavity air 153
Great vessel pressures 50–51, 51f Ischemia 124
Isovolumic relaxation time (IVRT) 61
H
Hancock valve 158, 158f J
Heart Jugular veins, internal 78
Index 279
K M
Kidney 78–79, 94 Malignant melanoma 118
Marfan’s disorder 87
L Matrix array 196–197
probe 197
Lambl’s excrescences 116, 187, 187f Measurements
Lanimetry 109 case studies 211
Lateral resolution 12, 12f M-mode 42–44
Latex 19 valve 49–50, 50f
Leaflet calcification 102t velocity 47
Leaflet motion 102t volumetric 48, 48f
Lecompte maneuver 164 Mechanical ventilation 83–84, 84f
Left atrium Medtronic–Hall valve 157
pressure, calculation 245 Melanoma, malignant 118
size 59 Memory wall motion abnormality 134
Left carotid artery 85 Mercedes Benz sign 56, 206
Left subclavian artery 85 Mesothelioma 117
dissections 89 Metabolic abnormalities 124
Left ventricle (LV) Metastatic cardiac masses 118
assessment 200 Midesophageal (ME) 2 Chamber view
assist device (LVAD) 151–152, 151f 68f
ejection fraction (LVEF) 43, 123 atrium 208
end-diastolic pressure, calculation left ventricle 204, 204f
232–233 mitral valve (MV) 205–206, 205f
hypertrophy (LVH) 102t Midesophageal (ME) 4 Chamber view 68f,
imaging 203–204, 203f, 204f 103, 103f
regional function/wall motion 200 atrium 208
shape left ventricle 203–204
dilated 123–124, 123f mitral valve (MV) 205, 205f
normal 123, 123f, 125 right ventricle 204–205
systolic pressure, peak 218 tricuspid/pulmonary valve 207,
volume 200 207f
Left ventricular inflow, mitral valve (MV) Midesophageal (ME) aortic valve (AV)
57–58, 57f, 61f long axis (LAX) view 68f, 100–101, 101f,
Left ventricular outflow tract (LVOT) 107–108, 206–207, 206f
49–50 short axis (SAX) view 68f, 107,
abnormalities 169 206, 206f
aortic valve (AV) 62–63 Midesophageal (ME) ascending aortic
stroke volume, calculation 219–220, view
229–230, 241, 246 long axis (LAX) 68f
Left ventricular systolic function 123 short axis (SAX) 68f
abnormal 124 Midesophageal (ME) bicaval view 68f
cardiomyopathies 124–127 atrium 208, 208f
segmental see Segmental left Midesophageal (ME) left ventricle long
ventricular systolic function axis (LAX) view 203f, 204
Leukemia 118 Midesophageal (ME) mitral commissural
Ligamentum arteriosum 84 view 68f, 205–206, 205f
Lipoma 117 Midesophageal (ME) plane 68
Lipomatous hypertrophy, interatrial long axis (LAX) view 68f
septum 116 Midesophageal (ME) RV inflow-outflow
Liver 78–79, 94 view 68f
left lobe 80 atrium 208
transplantation 161 right ventricle 204–205, 204f
Lumens tricuspid/pulmonary valve 207, 207f
false 88 Mimics
true 88 artifacts 186–188, 186f, 187f, 188f
Lung 78–79, 94–95 cardiac masses 115–116
atelectasis 94 Minimally invasive cardiopulmonary
cancer 118 bypass 153
right 95 Mirror images, artifacts 174, 179–180,
transplantation 160–161, 161f 179f, 186
Lymphoma 118
280 Index
Mitral valve (MV) 72, 98–100, 103, 166 P

area calculation
P wave 72
continuity equation 234–235
Papillary fibroelastoma 117
PISA (proximal isovelocity surface
Papillary muscles 116
area) 238
Patent ductus arteriosus 169
pressure half-time 104, 234, 237
Peak aortic valve (AV) area, calculation
gradient, calculation 236–237
215–217
imaging 205–206, 205f
Peak aortic valve (AV) gradient, calculation
ME 4C view 103, 105
217–218
ME AV LAX view 100–101
Peak left ventricular systolic pressure,
three dimensional (3-D) 199–200
calculation 218
inflow patterns 103–104
Peak right ventricular systolic pressure
insufficiency 101
214–215, 227–228, 247
leaflet 100–101, 101f
Peak trans-mitral pressure gradient,
left ventricular inflow 57–58, 57f, 61f
calculation 236–237
M-mode 41, 41f
Pectinate muscles 116, 187–188, 188f
problems, causes 99t
Pericardial space 124
regurgitation 64, 94, 102t, 103–106,
effusion 82–83, 83f, 148f
105f
fluid 81–82
regurgitant fraction, calculation 221,
reflection 80
240
sac thickening 84
regurgitant orifice area, calculation
Pericardial-cardiac filling pressures 83
221–222, 240
Pericarditis 82
regurgitant volume, calculation 221,
constrictive 84
238–240
restrictive 84
repair 159, 159f
Pericardium, anatomy/pathology 77–84,
stenosis 98, 102t, 103–104, 104t
77f, 80f, 81f, 82f, 83f, 84f
stroke volume, calculation 220, 230,
Perioperative events/problems 147
238
cardiovascular instability 147–149
coronary surgical techniques 155
M-mode 16, 16f, 27, 27f
transplantation 160–162
aortic valve (AV) 40–41, 40f
see also Cardiac surgical techniques
edge components 39
Persistent left superior vena cava (PLSVC)
edge recognition 39
168
measurements/calculations 42–44
Phased array 13
mitral valve (MV) 41, 41f
Piezoelectric crystals 196–197
quantitative 39
Piezoelectric effect 9–10, 9f, 10f
temporal resolution 40
PISA (proximal isovelocity surface area)
ventricular wall assessment 42, 42f
47, 47f, 50, 106
Moderator band 116, 186, 186f
PISA (proximal isovelocity surface area)
Morrison pouch 94
calculations 222–223
Multiple echoes, artifacts 176–180, 177f,
area 237–238
178f, 179f
mitral valve (MV) area 238
Mustard procedure 149, 164
regurgitant flow rate 223
Myocardial perfusion scanning 191
regurgitant fraction 224–225
Myocardial segment identification
regurgitant orifice area 224
131–132, 131f
regurgitant volume 224
Myocardial velocity 51
Planimetry 215
Myxoma 117
Pleural space 78–79, 94–95, 124
effusions 94–95, 160–161, 161f, 187
N Pneumothorax 94
Near field clutter 185 Posterior wall 71
Nodules of Arantius (nodulus arantii) 116, Potts operation 165
187, 187f A Practical Approach to Transesophageal
Nyquist limit 30–31, 30f, 31f, 107–108 Echocardiography (Perrino &
derivation 35 Reeves) 2
Pressure half-time calculation, mitral valve
(MV) area 234, 237
O Primum, atrial septal defect 168
Overriding Probes see Echo probes
aorta 163 Problems see Perioperative events/
defined 163–164 problems
Index 281
Pseudoaneurysm 87–88, 136, 136f mitral valve (MV) 221–222, 240

PTEeXAM 1, 11 PISA (proximal isovelocity surface area)
see also Examination, transesophageal calculations 224
echocardiography (TEE) Regurgitant volume, calculation
Pulmonary artery 79, 166 aortic valve (AV) 230–231
blood flow, calculation 247 mitral valve (MV) 221, 238–240
diastolic pressure, calculation 235 PISA (proximal isovelocity surface area)
main 77, 77f, 79 224
pathology 91–92 Regurgitation 98–100, 105
pericardial layers 82 blood flow 106
right 79 mitral valve (MV) 64, 94, 102t, 103–106,
shunt fraction, calculation 247 105f
stroke volume, calculation 246 pulmonary valve 106
systolic pressure, calculation 242–243 regurgitants 106, 106f
Pulmonary embolism 91 tricuspid valve 64, 94, 104–106, 105f
Pulmonary (pulmonic) valve 55, 56f, 72, 106 Renal arteries 85
continuous wave Doppler (CWD) 107 Renal cell carcinoma 118
imaging 207, 207f Rendering techniques 197–198
ME AV SAX view 107 Resonance 10
problems, causes 99t Restrictive cardiomyopathy 126, 126f
regurgitation 106 Restrictive pericarditis 84
repair 160 Retrograde cannula 149–150, 150f
right ventricular outflow 56–57, 56f Reverberation 174
stenosis 106–107, 163, 168 artifact 176–178, 178f
systolic blood velocities 97 linear 178, 178f
Pulmonary veins 77, 77f, 79 Rhabdomyoma 117
flow 61, 61f, 101 Rhabdomyosarcoma 117
inflow pattern 60, 60f, 63–64 Rheumatic heart disease 98, 98f
right upper 79 Right ventricle (RV) 166
systolic flow 102t assessment 200
Pulse repetition frequency (PRF) 47 imaging 204–205, 204f
Pulse wave (PW) Doppler 29, 29f, 35, 47, strain 92
98–100 systolic pressure, peak 214–215,
Pulsus paradoxus 83 227–228, 247
PV-Ar (atrial reversal part of pulmonary Right ventricular inflow, tricuspid valve
vein flow) 61 55–56, 56f
Right ventricular outflow
Q obstruction 163
pulmonary valve 56–57, 56f
QRS complex 73 Ring down artifacts 178–179, 178f, 179f
Ross procedure 158–159
R RT3D software 201
Range ambiguity 29–30, 29f, 47, 185
Rarefaction 3, 6f S
Rastelli, defined 165 S (ventricular systole) wave 93–94
Reeves, Scott T. 2 Safety 19–20
Reflection 5, 6f St Jude valve 157–158, 157f
Refraction 6, 6f, 174, 180–181 Sampling theory 29–30, 30f
artifact 182, 182f Sampling volume 93–94
Regional wall motion abnormality (RWMA) Savage, Robert 2
196 Scatter 6
Regional Wall Motion Unknown (tape) 134 Secundum, atrial septal defect 168
Regurgitant flow rate, PISA (proximal Segmental left ventricular systolic function
isovelocity surface area) calculation 131
223 aneurysm 135–136
Regurgitant fraction, calculation assessment, methods 133–134
aortic valve (AV) 231 confounding factors 135
mitral valve (MV) 221, 240 coronary artery distribution/flow
PISA (proximal isovelocity surface area) 132–133, 133f
224–225 differential diagnosis 134–135
Regurgitant orifice area, calculation rupture 136, 136f
aortic valve (AV) 231–232 segment identification 131–132, 131f
282 Index
Segmentation 197–198 vs transesophageal echocardiography

Senile calcific aortic stenosis 98, 98f, (TEE) 193
107–108, 108f Systole 51, 51f
Senile calcific degeneration 98 Systolic blood velocities 97
Septal hypertrophy 124 Systolic function see Left ventricular
17 segment model 139, 139f, 140f, 141f systolic function
transesophageal echocardiography Systolic pressure
(TEE) planes 144, 144f left ventricular 218
Shadowing 182 pulmonary artery 242–243
Shunt fraction, calculation 247 right ventricular, peak 214–215,
Side lobes 174–175, 176f 227–228, 247
Signal processing 16 Systolic pulmonary vein flow 102t
Sinotubular junction 84
right 89
Sinus of Valsalva 84 T
aneurysms 87, 167 Tamponade 84, 148
ruptured 167 Tandem heart 152, 152f
Sinus venosus, atrial septal defect 168 TEE: An Interactive Board Review (CD) 2
Snell–Descartes law 180–181 TEE ‘alphabet’ 68f, 204f, 207f
Society of Cardiovascular Anesthesiology TEE on CD: An Interactive Resource 2
1, 149 Temporal resolution, M-mode 40
Sonographic formulas 209 Tethering 135, 135f
Sound beam see Beam Textbook of Clinical Echocardiography
Speed displacement artifact 180 (Otto) 2
Spinal cord 78 Thebesian valve 188, 188f
Spine 78, 94 Thoracic aorta
Spleen 78–79, 94 distal 79
Spontaneous breathing 83 mid 79
expiration 83 proximal 79
inspiration 83–84 Three dimensional (3-D) images 195
ST segment 73 cardiac masses 118
Starr–Edwards valve 156–157, 159 functions 195
Stenosis, valves 97–98 left ventricle (LV)
aortic valve (AV) 98, 102t, 107–108, assessment 200
108f, 110–111, 110f volume 200
senile calcific 98, 98f, 107–108, 108f limitations 199
causes 99t mitral valve (MV) 199–200
mitral valve (MV) 98, 102t, 103–104, modes 198–199, 198t
104t probes 196–198
pulmonary valve 106–107, 163, 168 rendering technique 197–198
subaortic 169 right ventricle (RV), assessment 200
tricuspid valve 103 Thrombus 117
Stereoscopic display 198 formation 126, 127f
Stomach 78–79, 94 Thymus 78, 94
Straddling, defined 163–164 Time-velocity integral (TVI) 48–50, 48f
Stress echocardiography 191 Tissue
Stroke volume, calculation 212, 226–227 characterization 6–7
aortic valve (AV) 244 impedance 5
left ventricular outflow tract (LVOT) interactions 5–6
219–220, 229–230, 241, 246 propagation velocity 3
mitral valve (MV) 220, 230, 238 reconstruction 26–27
pulmonary artery 246 Tissue Doppler 51, 51f, 61f
Subaortic stenosis 169 Tongue 78
Subclavian artery, left 84–85, 89 Trabeculations 116
Subdiaphragmatic area 94 Trachea 78–79, 94
Superior mesenteric artery 85 Transducers 9
Superior mesenteric artery (SMA) 79 Transgastric (TG) 2 Chamber view 68f,
Superior vena cava (SVC) 77, 77f, 79, 203–204
92–95, 93f Transgastric (TG) basal short axis (SAX)
persistent left (PLSVC) 168 view 68f
Surface rendering 198 left ventricle (LV) 105
Swan–Ganz catheter (SGC) 43, 73, 147, mitral valve (MV) 205–206
155, 167, 185, 193 Transgastric (TG) long axis (LAX) view 68f
Index 283
Transgastric (TG) plane 68 long axis (LAX) view 68f, 208

view 71, 79 short axis (SAX) view 56, 56f, 68f, 208
Transgastric (TG) RV inflow view 68f, atrium 207f
204–205 Upper esophageal (UE) plane 68
Transgastric (TG) short axis (SAX) view Upper lung 79
203–204
mid 68f, 80–81, 203f V
Transplantation 160–162
V ascent 73
Transposition 164
Valsalva maneuver 59–60
Transthoracic echocardiography (TTE) vs
Valves see Cardiac valves
transesophageal echocardiography
Valvular regurgitation see Regurgitation
(TEE) 192
Vegetation, bacteremic 117
Transverse sinus 79
Velocity
Trauma, aortic 90–91
errors, artifacts 180–182, 181f, 182f
Tricuspid inflow velocity 84
measurement, types 47
Tricuspid valve 64, 72, 103
Vena cava see Inferior vena cava (IVC);
causes, problems 99t
Superior vena cava (SVC)
Ebstein’s anomaly 163, 170
Vena contracta 106, 110
imaging 207, 207f
Venous blood flow 165
ME AV SAX view 107
Ventilation, mechanical 83–84, 84f
ME4C view 103
Ventricle
insufficiency 101
anatomic variants 116
regurgitation 64, 94, 104–106, 105f
diseases 124
repair 160
see also Left ventricle (LV); Right
right ventricular inflow 55–56, 56f
ventricle (RV)
stenosis 103
Ventricular septal defect (VSD) 163, 166
natural history 166–167
True lumens 88
pitfalls 167
Two dimensional (2-D) images 16, 16f, 27,
Ventricular systole 93
27f, 39, 196
Ventricular wall assessment, M-mode 42,
cardiac masses 118
42f
Two-chamber view 71
Vertebral disks 78
see also Midesophageal (ME) 2 Chamber
Volume rendering 198
view
Volumetric analysis 200
data collection 197
U measurements/calculations 48, 48f
Ultrasound, principles 3
attenuation 6 W
compression/rarefaction 3
Wall motion abnormality 188
frequency/wavelength/tissue
Wall pairs, cross section 141f
propagation velocity 3
Waterston operation 165
reflection 5, 6f
Wavelength 3, 4f
refraction 6, 6f
Waves, ultrasound 5
scatter 6
Wireframe rendering 198
tissue
characterization 6–7
interactions 5–6 X
waves, properties 5 X descent 73
see also Beam; Doppler ultrasound,
principles Y
Upper abdominal aorta 78–79 Y descent 73
Upper esophageal (UE) aortic arch (AA)

@anesthesia Books 2013 Board Stiff

Uploaded by

Copyright:

Available Formats

@anesthesia Books 2013 Board Stiff

Uploaded by

Document Information

Original Title

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

@anesthesia Books 2013 Board Stiff

Uploaded by

Copyright:

Available Formats

What are the main topics covered in the book?

What are the main topics covered in the book?

What are some of the imaging modalities discussed in the book?

What are some of the imaging modalities discussed in the book?

https://t.

For additional online content visit

London, New York, Oxford, St Louis, Sydney, Toronto 2013

© 2013 Elsevier Inc. All rights reserved.

First edition 2004

No part of this publication may be reproduced or transmitted in any form or by any

ebook ISBN: 978-1-4557-3759-8

Printed in United States of America

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

Preface to the First Edition vii

CHAPTER 1 The Yellow Brick Road 1

CHAPTER 2 Principles of Ultrasound 3

CHAPTER 3 Transducers and Instrumentation 9

CHAPTER 4 Equipment, Infection Control, and Safety 19

CHAPTER 5 Principles of Doppler Ultrasound 25

CHAPTER 6 Quantitative M-mode and Two-dimensional

CHAPTER 7 Quantitative Doppler 47

CHAPTER 8 Doppler Profiles and Assessment of Diastolic Function 55

CHAPTER 9 Cardiac Anatomy 67

CHAPTER 10 Pericardium and Extra-Cardiac Structures: Anatomy and

CHAPTER 11 Pathology of the Cardiac Valves 97

CHAPTER 12 Intra-cardiac Masses and Devices 115

CHAPTER 13 Left Ventricular Systolic Function 123

CHAPTER 14 Segmental Left Ventricular Systolic Function 131

CHAPTER 15 The 17 Segment Model 139

CHAPTER 16 Assessment of Perioperative Events and Problems 147

CHAPTER 17 Congenital Heart Disease 163

CHAPTER 18 Artifacts and Pitfalls 173

CHAPTER 19 Related Diagnostic Modalities 191

CHAPTER 20 Intraoperative 3-D Echocardiography 195

CHAPTER 21 The Structured TEE Examination 203

Epilogue: Smooth Sailing 273

If you are doing cardiac anesthesia, cardiac surgery, or intensive care

You need to know TEE.

Board Stiff TEE is the perfect launch pad.

The book details

And final thanks to my daughter Rachel, who is a blast.

A long time ago in a galaxy far, far away…AND SO FORTH.

Daniel M. Shindler, MD FACC

The graying man pulled a Tony Roma’s pre-moistened towelette packet

“There,” he wiggled out of the box, “now I’m presentable.”

Both policeman and mailman said, “Uh-huh.”

Policeman and mailman both shook their heads, apparently unable to

The policeman and mailman looked at each other.

“Why yes,” the man said. “A book about transesophageal echo­cardio­-

“Oh, anyone who might want to save a patient in hemodynamic trouble:

n Intensivists of all flavors

“Thump! Thump!” “Thump! Thump!” Two more trucks passed overhead.

The man in scrubs went on, “Transesophageal echocardiography is

“And patients can crash anywhere!”

As if on cue, a driver on the bridge jammed on the brakes and a sicken-

But nothing happened. The policeman, mailman, and bescrubbed man

Above, a string of obscenities in Spanish crackled in the air, then an

“Follow the yellow brick road.”

(This chapter is included as a kind of time-capsule of how we thought

“Why yes,” the man said. “A book about transesophageal echocardio-

Think of a patient lying prone