A Practical Approach To Transesophageal Echocardiography 3rd Edition 2014 PDF

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A Practical Approach to
Transesophageal
Echocardiography
Third Edition

A Practical Approach to
Transesophageal
Echocardiography
Third Edition
Editors
Albert C. Perrino, Jr., MD
Professor, Anesthesiology
Yale University School of Medicine
Chief, Anesthesiology
VA Connecticut Healthcare System
New Haven, Connecticut
Scott T. Reeves, MD, MBA, FACC, FASE

John E. Mahaffey, MD, Endowed Professor and Chairman
Department of Anesthesiology and Perioperative Medicine
Medical University of South Carolina
Charleston, South Carolina

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Library of Congress Cataloging-in-Publication Data

A practical approach to transesophageal echocardiography / editors, Albert C. Perrino, Jr.,
Scott T. Reeves. – 3rd ed.
p. ; cm.
Includes bibliographical references and index.
ISBN 978-1-4511-7560-8 (alk. paper)
I. Perrino, Albert C. II. Reeves, Scott T.
[DNLM: 1. Echocardiography, Transesophageal–methods. 2. Heart Diseases–ultrasonography.
WG 141.5.E2]
616.1΄207543–dc23
2013016039
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❖
To Anita, Mary, Isabella, and Juliana for sustaining another of my
adventures and to Winston Churchill whose keen observation
also served as a source of support.
Writing is an adventure. To begin with, it is a toy and an amusement.
Then it becomes a mistress, then it becomes a master, then it becomes
a tyrant. The last phase is that just as you are about to be reconciled
to your servitude, you kill the monster and fling him
to the public. —Winston Churchill, ACP
❖
To My Savior, Jesus Christ, who gives me strength . . .
My wife, Cathy, who loves and puts up with me . . .
My children, Catherine, Carolyn, and Townsend, who give
me great joy . . .
My patients, who inspire me to do my best daily! — STR

Contributors
Heidi K. Atwell, DO Fabio Guarracino, MD
Assistant Professor Head
Cardiothoracic Anesthesiology Department of Anesthesia and Critical Care Medicine
Washington University School of Medicine in St. Louis University Hospital of Pisa
St. Louis, Missouri Pisa, Italy
Albert T. Cheung, MD Maurice Hogan, MB, BCh, MSc, MBA

Professor Department of Anesthesiology and Intensive
Department of Anesthesiology and Critical Care Care Medicine
Perelman School of Medicine Heart Center Leipzig
University of Pennsylvania University of Leipzig
Philadelphia, Pennsylvania Leipzig, Germany
Ira S. Cohen, MD Farid Jadbabaie, MD

Professor of Medicine, Director of Echocardiography Assistant Professor of Medicine (Cardiology)
Thomas Jefferson University School of Medicine Yale University School of Medicine
Philadelphia, Pennsylvania Director of echocardiography laboratory
VA Connecticut Healthcare System
Jörg Ender, MD West Haven, Connecticut
Director
Department of Anesthesiology and Intensive Care Colleen G. Koch, MD, MS, MBA
Medicine Professor of Anesthesiology
Heart Center Leipzig Cleveland Clinic Lerner College of Medicine of
University of Leipzig Case Western Reserve University
Leipzig, Germany Department of Cardiothoracic Anesthesia
Quality and Patient Safety Institute
Joachim M. Erb, MD, DEAA Cleveland Clinic
Senior Consultant Cleveland, Ohio
Department of Anesthesia and Intensive Care
Medicine A. Stephane Lambert, MD, MBA, FRCPC
University Hospital Basel Associate Professor, Department of Anesthesiology
Basel, Switzerland Division of Cardiac Anesthesiology and Critical Care
University of Ottawa Heart Institute
Alan C. Finley, MD Ottawa, Ontario, Canada
Assistant Professor
Department of Anesthesia and Perioperative Jonathan B. Mark, MD
Medicine Professor
Medical University of South Carolina Department of Anesthesiology
Charleston, South Carolina Duke University Medical Center
Chief, Anesthesiology Service
Susan Garwood, MBChB, FRCAInterim Veterans Affairs Medical Center
Division Head Durham, North Carolina
Division of Cardiothoracic Anesthesia
Department of Anesthesiology Andrew Maslow, MD
Yale University School of Medicine Director of Cardiac Anesthesia for Lifespan Hospitals
New Haven, Connecticut Associate Professor
Warren Alpert School of Medicine at Brown University
Donna L. Greenhalgh, MBChB, FRCA, FICM Providence, Rhode Island
Consultant Cardiothoracic Anaesthesia and Intensive
Care Medicine Joseph P. Miller, MD
Department of Anaesthetics Staff Anesthesiologist
University Hospital of South Manchester (Wythenshawe) Pacific Anesthesia, P.C.
Manchester, United Kingdom St. Joseph Medical Center
Tacoma, Washington
vi

Contributors vii
Wanda C. Miller-Hance, MD Manfred D. Seeberger, MD

Professor of Pediatrics and Anesthesiology Professor
Baylor College of Medicine Department of Anesthesia and Intensive Care
Associate Director of Pediatric Cardiovascular University Hospital Basel
Anesthesiology Basel, Switzerland
Director of Intraoperative Echocardiography
Texas Children’s Hospital Stanton K. Shernan, MD, FAHA, FASE
Houston, Texas Professor of Anesthesia
Director of Cardiac Anesthesia
Pablo Motta, MD Department of Anesthesiology, Perioperative, and
Assistant Professor of Pediatrics and Anesthesiology Pain Medicine
Baylor College of Medicine Brigham and Women’s Hospital
Staff Anesthesiologist Harvard Medical School
Texas Children’s Hospital Houston, Texas Boston, Massachusetts
Chirojit Mukherjee, MD Roman M. Sniecinski, MD, FASE

Senior Consultant and Fellowship Program Director Associate Professor of Anesthesiology
Department of Anesthesia and Intensive Medicine II Division of Cardiothoracic Anesthesia
Heart Center Leipzig Emory University School of Medicine
University of Leipzig Atlanta, Georgia
Leipzig, Germany
Scott C. Streckenbach, MD
Barbora Parizkova, MD Assistant Professor of Anesthesia and Director of
Consultant in Cardiothoracic Anaesthesia and Perioperative Transesophageal Echocardiography
Intensive Care Department of Anesthesiology and Critical Care
Papworth Hospital, NHS Foundation Trust Massachusetts General Hospital
Cambridge, United Kingdom Harvard Medical School
Boston, Massachusetts
Albert C. Perrino, Jr.
Professor, Anesthesiology Justiaan L.C. Swanevelder, MBChB, MMED(Anes),
Yale University School of Medicine FCA(SA), FRCA(Hon)
Chief, Anesthesiology Professor and Head of Department of Anaesthesia
VA Connecticut Healthcare System Groote Schuur Hospital
New Haven, Connecticut University of Cape Town
South Africa
Shahnaz Punjani, MD
Research Fellow Department of Cardiology Annette Vegas, MD, FRCPC, FASE
Yale University School of Medicine Director of Perioperative Echocardiography
New Haven, Connecticut Department of Anesthesiology
Toronto General Hospital
Scott T. Reeves, MD, MBA, FACC, FASE Toronto, Ontario
John E. Mahaffey, MD, Endowed Professor and Chairman Canada
Anesthesia and Perioperative Medicine
Medical University of South Carolina Michael H. Wall, MD, FCCM
Charleston, South Carolina Professor
Anesthesiology and Cardiothoracic Surgery
Rebecca A. Schroeder, MD Washington University School of Medicine in St. Louis
Associate Professor St. Louis, Missouri
Department of Anesthesiology
Duke University School of Medicine
Durham VAMC
Durham, North Carolina

Preface
T HE THIRD EDITION OF A Practical Approach to Transesophageal Echocardiography represents a remark-
able transformation for the highly regarded textbook. Most recognizable is that this edition has been exten-
sively reformatted and published as both an e-book and a portable manual. The e-book format takes full
advantage of the possibilities now available to clinicians with both tablet and personal computers. Readers
now experience full-motion video and extensive color artwork seamlessly embedded into each chapter. To
complete this transformation, the editors have recruited a new team of contributing authors who are inter-
nationally renowned and acknowledged for their independent contributions and teaching ability. These
authors were given the task of presenting a highly readable and clinically relevant survey of the current
practice of perioperative echocardiography. The editors are humbled by the “dream team” of talent drawn
to this project. Their enthusiasm, backed with the strong support of the publisher, has produced this book.
Three is a charm, and appropriately the third edition includes a feature chapter on three-dimensional
(3D) echocardiography. The uses of 3D techniques are embedded throughout the specific topic chapters,
particularly, its use during mitral valve surgery. A new chapter provides an up-to-date tutorial on the use
of echocardiography during mitral repair. In addition, the expanding use of echocardiography for percuta-
neous valve procedures has resulted in a dedicated chapter addressing this field. The evolving role of TEE
during coronary revascularization, including assessment of ventricular assist devices and TEE’s critical role
in clinical decision making, has resulted in a new chapter covering these topics.
The reader is guided through the physics, principles, and applications of two-dimensional (2D) imag-
ing and Doppler modalities for assessing ventricular performance and the clinical significance of valvular
disease. Updated practice guidelines by the American Society of Echocardiography (ASE), the Society of
Cardiovascular Anesthesiologists (SCA), and the European Association of Echocardiography for assess-
ment of valves and ventricles are discussed. Each chapter concludes with 20 self-assessment test questions
to further emphasize important teaching points.
Despite the notable comprehensive reference texts and case atlases available on this subject, this edi-
tion further establishes the reputation of A Practical Approach to Transesophageal Echocardiography as
the practicing clinician’s premiere resource to acquire the essential skills of TEE practice. The third edition
is not a mere refresh of its predecessor but a thoroughly updated manual supported by extensive original
color illustrations, figures, and full-motion echocardiographic images. The presentation, media, and con-
tent create a surprisingly portable text (both on tablet and as a printed handbook) that is conducive to rapid
appreciation of the critical elements in the use of TEE for a particular clinical challenge.
Certainly, the skills required to be an expert echocardiographer cannot be gained from textbooks alone.
In addition to clinical-based training, we recommend the excellent educational programs on intraopera-
tive TEE sponsored by the ASE, the SCA, the American Society of Anesthesiologists, and the European
Association of Cardiothoracic Anesthesiologists.
We hope this textbook will become a well-worn and valued asset to your echocardiography practice.
Albert C. Perrino, Jr., MD
Scott T. Reeves, MD, MBA, FACC, FASE
viii

Contents
SECTION I: ESSENTIALS OF 2D IMAGING
1. Principles and Technology of Two-dimensional Echocardiography .................................................................... 1
Andrew Maslow and Albert C. Perrino, Jr.
2. Two-dimensional Examination ....................................................................................................................................... 20
Joseph P. Miller
3. Left Ventricular Systolic Performance and Pathology ............................................................................................ 51
Shahnaz Punjani and Susan Garwood
4. Diagnosis of Myocardial Ischemia ................................................................................................................................. 82
Joachim M. Erb and Manfred D. Seeberger
SECTION II: ESSENTIALS OF DOPPLER ECHO

5. Doppler Technology and Technique........................................................................................................................... 102
6. Quantitative Doppler and Hemodynamics .............................................................................................................. 118
7. A Practical Approach to the Echocardiographic Evaluation of Ventricular Diastolic Function ............. 138
Stanton K. Shernan
SECTION III: VALVULAR DISEASE

8. Mitral Regurgitation ......................................................................................................................................................... 159
A. Stephane Lambert
9. Mitral Valve Stenosis ......................................................................................................................................................... 179
Colleen G. Koch
10. Mitral Valve Repair ............................................................................................................................................................. 194
Maurice Hogan and Jörg Ender
11. Aortic Regurgitation ......................................................................................................................................................... 224
Ira S. Cohen
12. Aortic Stenosis .................................................................................................................................................................... 240
Ira S. Cohen
13. Prosthetic Valves ................................................................................................................................................................ 258
Albert T. Cheung and Scott C. Streckenbach
14. Right Ventricle, Right Atrium, Tricuspid and Pulmonic Valves........................................................................... 286
Rebecca A. Schroeder, Barbora Parizkova, and Jonathan B. Mark
SECTION IV: CLINICAL CHALLENGES

15. Transesophageal Echocardiography for Coronary Revascularization ............................................................ 302
Donna L. Greenhalgh and Justiaan L.C. Swanevelder
16. Echocardiography for Percutaneous Aortic Valve and Mitral Clip Implantation ........................................ 327
Chirojit Mukherjee
17. Transesophageal Echocardiography of the Thoracic Aorta ............................................................................... 347
Roman M. Sniecinski
ix

x Contents
18. Critical Care Echocardiography .................................................................................................................................... 364

Heidi K. Atwell and Michael H. Wall
19. Transesophageal Echocardiography for Congenital Heart Disease in the Adult ....................................... 379
Pablo Motta and Wanda C. Miller-Hance
20. Cardiac Masses and Embolic Sources ......................................................................................................................... 424
Farid Jadbabaie
SECTION V: MAN AND MACHINE

21. 3D TEE Imaging .................................................................................................................................................................. 437
Annette Vegas
22. Common Artifacts and Pitfalls of Clinical Echocardiography ............................................................................ 456
Fabio Guarracino and Albert C. Perrino, Jr.
23. Techniques and Tricks for Optimizing Transesophageal Images...................................................................... 473
Alan C. Finley and Scott T. Reeves
APPENDICES
A. Transesophageal Echocardiographic Anatomy ...................................................................................................... 485
B. Cardiac Dimensions .......................................................................................................................................................... 488
C. Hemodynamic Calculations ........................................................................................................................................... 489
D. Valve Prostheses................................................................................................................................................................. 490
E. Classification of the Severity of Valvular Disease ................................................................................................... 497
F. Answers to End-of-Chapter Questions ...................................................................................................................... 501
Index ................................................................................................................................................................................................515

I ESSENTIALS OF 2D IMAGING
1 Principles and Technology of Two-dimensional

Echocardiography
TWO - DIMENSIONAL ECHOCARDIOGRAPHY GENERATES DYNAMIC IMAGES of the heart from reflec-
tions of transmitted ultrasound. The echocardiography system transmits a brief pulse of ultrasound that
propagates through and is subsequently reflected from the cardiac structures encountered. The sound
reflections travel back to the ultrasound transducer, which records the time delay for each returning reflec-
tion. Since the speed of sound in tissue is constant, the time delay allows for a precise calculation of the
location of the cardiac structures from which the echocardiography system can then create an image map
of the heart. Not surprisingly, successful cardiac imaging requires a firm understanding of the interactions
of sound and tissue. This chapter reviews the basic principles of ultrasound, its propagation through tis-
sues, and the technologies which create moving images of the heart.
PHYSICAL PROPERTIES OF SOUND WAVES
Vibrations
Sound is the vibration of a physical medium. In clinical echocardiography, a mechanical vibrator, known
as the transducer, is placed in contact with the esophagus (transesophageal echocardiography [TEE]),
skin (transthoracic echocardiography), or the heart (epicardial echocardiography) to create tissue vibra-
tions. The resulting tissue vibrations or sound waves consist of areas of compression (areas where mol-
ecules are tightly packed) and rarefaction (areas where molecules are dispersed) resembling a sine wave
(Fig. 1.1).
Amplitude
The amplitude of a sound wave represents its peak pressure and is appreciated as loudness. The level of
sound energy in an area of tissue is referred to as intensity. The intensity of the sound signal is proportional
to the square of the amplitude and is an important factor regarding the potential for tissue damage with
ultrasound. For example, lithotripsy uses high-intensity sound signals to fragment renal stones. In con-
trast, cardiac ultrasound uses low-intensity signals to image tissue, which produces only limited bioeffects.
Since levels of sound pressure vary over a large range, it is convenient to use the logarithmic decibel (dB)
scale:
Decibel (dB) = 10 log 10 I /I r = 10 log 10 A2/Ar2
= 20 log 10 A/Ar (1)
where A is the measured sound amplitude of interest and Ar is a standard reference sound level, I is the
intensity and Ir is a standard reference intensity.
More simply expressed, each doubling of the sound pressure equals a gain of 6 dB. The U.S. Food
and Drug Administration (FDA) limits the maximum intensity output of cardiac ultrasound systems
to be less than 720 W/cm2 due to concerns with possible tissue and neurologic damage from mechani-
cal injury (resulting from cavitation or microbubbles caused by rarefaction) and thermal effects. The 1

2 I. Essentials of 2D Imaging
Velocity
Amplitude
Wavelength (λ)
0.5 ms
FIGURE 1.1 Sound wave. Vibrations of the ultrasound transducer create cycles of compression and rarefaction in adja-
cent tissue. The ultrasound energy is characterized by its amplitude, wavelength, frequency, and propagation velocity. In
this example, four sound waves are shown in a period of 0.5 μs. The frequency can be calculated as 4 cycles divided by
0.5 μs and equals 8 MHz.
ALARA principle recommends that clinicians use exposure levels As Little As Reasonably Achievable
to protect patients.
Frequency and Wavelength

Sound waves are also characterized by their frequency ( f ), or pitch, expressed in cycles per second, or Hertz
(Hz), and by their wavelength (λ). These attributes have a significant impact on the depth of penetration of
a sound wave in tissue and the image resolution of the ultrasound system.
Propagation Velocity
The travel velocity or propagation velocity of sound (v) is determined solely by the medium through which it
passes. For example, the speed of sound in soft tissue is approximately 1,540 m/s. Velocity can be calculated
as the product of wavelength and frequency:
v =λ× f (2)
It becomes apparent that the wavelength and frequency are necessarily inversely related:
λ = v × 1/f (3)
λ = (1500 m/s)/ f (4)
Table 1.1 lists the corresponding sound wavelengths and frequencies commonly used in clinical ultraso-
nography.

1. Principles and Technology of Two-dimensional Echocardiography 3
TABLE 1.1 Corresponding Frequencies and Wavelengths in Soft Tissue
Frequency (MHz) Wavelength (mm)

1.25 1.20
2.5 0.60
5 0.30
7.5 0.20
10 0.15
WHAT IS SO SPECIAL ABOUT ULTRASOUND?

Several favorable physical properties of ultrasound explain its usefulness in clinical imaging. Ultrasound is
sound with frequencies greater than those of the audible range for humans (20,000 Hz). In clinical echocar-
diography, frequencies of 2 to 10 MHz are used. The high-frequency, short-wavelength ultrasound beam
can be more easily manipulated, focused, and directed to a specific target. Image resolution also increases
when higher-frequency sound waves are used (see later).
INTERACTIONS OF SOUND AND TISSUE

The propagation, or passage, of a sound wave through the body is markedly affected by its interactions
with the various tissues encountered. These interactions result in reflection, refraction, scattering, and
attenuation of the ultrasound signal. The exact manner in which sound is affected by the various tissues it
encounters determines the resulting appearance of the two-dimensional image (Fig. 1.2).
Attenuation
Refraction
Scatter
Reflection
FIGURE 1.2 Interactions of sound and tissue. Traveling through various tissues, sound energy is altered by four major
events. Specular reflection creates strong echoes directed back toward the transducer. Refraction bends the ultrasound
beam directing it in a new path. As the ultrasound beam travels deeper in tissue, attenuation occurs as the beam is dis-
persed and the sound energy is converted to heat. Scattering reflections from small objects such as red cells disperse the
sound energy in all directions.

TABLE 1.2 Acoustic Properties of Various Tissues
Acoustic Attenuation
Speed of sound impedance coefficient (cm-1 Half-power distance
Tissue/medium (m/s) (kg/m2 ¥ 106) at 1 MHz) (cm at 2.5 MHz)
Air 330 0.00004 — 0.08
Lung 600 0.26 — 0.05
Fat 1,460 1.35 0.04–0.09 —
Water 1,480 1.52 0.0003 380
Blood 1,560 1.62 0.02 15
Muscle 1,600 1.7 0.25–0.35 0.6–1
Bone 4,080 7.80 — 0.7–0.8
Reflection
Echocardiographic imaging depends on the transmission and subsequent reflection of ultrasound energy
back to the transducer. A sound wave propagates through uniform tissue until it reaches another tissue
type with different acoustic properties. At the tissue interface, the ultrasound energy undergoes a dra-
matic alteration, after which it can be reflected back toward the transducer or transmitted into the next
tissue, often in a direction that deviates from the original course. Precisely how the ultrasound beam will
be affected is predicted by factoring the acoustic properties of the tissues that create the interface and the
angle at which the ultrasound beam strikes this interface.
The Tissue Interface: Acoustic Impedance

An important acoustic property of a tissue is its capacity for transmitting sound, known as acoustic impedance
(Z). This property is largely related to the density (ρ) of the material and the speed which ultrasound travels (v):
Z = ρ× v (5)
As seen in Table 1.2, denser materials such as bones and fluids effectively transmit ultrasound, whereas
air and lung tissue have a low level of acoustic impedance and are poor transmitters of sound energy. This
property explains why an amplification system is required even for a small lecture hall, yet whales can hear
sound over great expanses of the ocean.
When sound reaches an interface of two tissues of similar acoustic impedance, the ultrasound beam
travels across the interface largely undisturbed. When the tissues differ in impedance, a percentage of the
ultrasound energy is reflected and the remainder is transmitted. The larger the absolute difference in the levels
of acoustic impedance across the interface, the greater the percentage of the ultrasound energy that is reflected.
Reflection can be calculated by using the reflection coefficient (R):
( Z2 − Z1 )2
Reflection coefficient = (6)
( Z1 − Z2 )2
The reflective properties of an interface are key factors in the imaged appearance of a structure. When
the absolute difference between the levels of acoustic impedance of the two interfacing media is large, as
when soft tissue interfaces with air or bone, more energy is reflected back to the transducer. These inter-
faces are represented by echo-dense or bright signals on the echogram. When the absolute difference is
small, as when soft tissue interfaces with soft tissue, the interface will not appear as bright and may even
be echolucent or dark.
Specular and Scattering Reflectors

The reflection of sound is also greatly affected by the size and surface of the tissue. Two types of reflection,
specular and scattered, are commonly encountered.

Specular reflection occurs when a sound wave encounters a large object with a smooth surface. Such surfaces
act like an acoustic mirror, generating strong reflections that travel away from the interface at an angle equal
and opposite to that at which the ultrasound beam traveled to the interface. Reflection is maximal when the
angle of incidence is 90 degrees—that is, the ultrasound beam and the object are perpendicular to each another.
With an angle of incidence other than 90 degrees, less energy is reflected back to the transducer. Because of the
important effect of strong specular reflection on image quality, echocardiographers adjust the position of the
TEE transducer so that the direction of its beam is perpendicular to the cardiac structure of interest.
Scattering reflection occurs when an ultrasound beam encounters small or irregularly shaped surfaces.
Such small objects, such as red blood cells, scatter ultrasound energy in all directions, so that far less energy
is reflected back to the transducer than in the case of a specular reflector. This type of reflection is the basis
of the Doppler analysis of red blood cell movement.
Both types of reflection contribute to the two-dimensional image. Although the strongest signals and best
images are obtained from interfaces that are perpendicular to the beam orientation, cardiac tissue is to a
large extent irregular and nonlinear in shape. Therefore, a significant component of the reflected energy
comes from scattering off the smaller irregular components of tissue. An example is imaging of the lateral
and septal walls of the left ventricle from esophageal windows. Although the ventricular walls are parallel
to the ultrasound beam, they can be imaged as a result of both specular reflection and scattering off the
irregular surfaces of the myocardium. However, the total amount of ultrasound returning to the transducer
is low, which accounts for the poor quality of images, which often include dark spots called echo dropout.
Adjusting the transducer angle or using a different echocardiographic window to orient the beam more
perpendicular to the structure of interest will often dramatically improve image quality.
Refraction
The portion of the ultrasound beam that is not reflected propagates through the interface, but its direction
is often altered or refracted. Refraction is most pronounced when the difference in sound velocities in the
two tissues is large and the angle of incidence is acute. When the angle of incidence is 90 degrees, or when
the difference in levels of acoustic impedance is minimal, refraction does not occur because the ultrasound
energy is either reflected or continues to travel in the same direction.
Refraction is an important factor in the formation of artifacts. Although the ultrasound beam may pro-
ceed in an altered direction, the transducer does not recognize this change.
Consequently, the refracted energy may interface with a cardiac structure outside the intended scanning
field. The reflected energy from this interface returns to the transducer, which then incorrectly displays the
structure alongside structures detected by the beam in its original course (Fig. 1.3). Altering the viewing
angle so that the ultrasound energy is perpendicular to the area of interest minimizes refraction and any
resultant artifact.
Attenuation
In addition to being reflected and refracted from tissue interfaces, the ultrasound signal is altered as it
travels through uniform tissue. Most notable is the steady loss (i.e., attenuation) in transmitted intensity
as a consequence of dispersion and absorption. The attenuation in ultrasound energy caused by dispersion
and absorption result in less energy returning to the transducer, and subsequently a weaker signal on the
display with a poor signal-to-noise ratio.
Dispersion occurs as the ultrasound beam diverges over a greater area in the far field. In addition, since
the cellular structure of tissue is irregular, scattering further disperses the ultrasound energy. The amount
of scattering varies greatly with tissue type.
Absorption occurs as frictional forces convert ultrasound energy into heat. Since friction is related to
the level of tissue movement, it is not surprising that the higher the frequency of the signal and the greater
the distance traveled, the greater the absorption (Fig. 1.4). The dependence of attenuation on frequency
and distance is reflected in the attenuation coefficient (dB/cm/MHz), which allows for a comparison of the
degree of attenuation between tissue types. The penetration of ultrasound can also be expressed by the
half-power distance specific for each tissue, which expresses the distance sound will travel until half of its
original energy is lost. The acoustic properties of various tissues are summarized in Table 1.2.

Ao
PA Catheter
A B
FIGURE 1.3 Refraction artifact. A: Refraction of a portion of the ultrasound beam in the near field (solid line) deflects
the beam laterally where it interacts with a strong reflector, a pulmonary artery (PA) catheter. B: The transducer is unable
to recognize that these scan lines have been refracted and incorrectly assumes that the returning reflections have origi-
nated from the original course of the beam. Echocardiography display illustrates the resulting artifact as the reflections
from the PA catheter are mistakenly positioned within the aorta (Ao).
As a result of these phenomena, the returning echoes from deeper structures are weakened. To decrease
the negative effects of attenuation during an examination, echocardiographers may choose to use a lower-
frequency signal (e.g., a 2.5-instead of a 7.5-MHz transducer frequency) and view the structure from a
window either closer to the structure of interest or that avoids a strong near field reflector (e.g., prosthetic
valve). In addition, the incoming signal can be enhanced by adjusting the gain controls to amplify the weak-
ened returning signals. These adjustments are discussed in greater detail in Chapter 21.
A B
FIGURE 1.4 Attenuation of ultrasound. The effects of transducer frequency and distance on signal strength are plotted in
decibels. A: The lower-frequency signals are less attenuated. B: The amplitude of a 1-MHz signal traveling through cardiac
tissue is plotted. Signals reaching the far field can be more than 60 dB less than those lying close to the transducer. These
effects warrant careful selection of the transducer frequency, imaging view, and gain settings to mitigate attenuation.

h
gt
len
lse
Pu
FIGURE 1.5 Transducer components: Creating a sound pulse. A brief transmission of alternating current from the elec-
tric connector causes charged particles within the matrix of the piezoelectric crystal to vibrate. The backing material helps
to dampen the crystal vibrations quickly, keeping the pulse length short; in this example, it is four wavelengths. An
acoustic lens aids in focusing the sound energy. The faceplate contains layers of material that match the acoustic imped-
ance of the esophagus, to avoid unwanted reflections and ensure excellent sound transmission. Epoxy filler secures the
working components to the probe.
TRANSDUCER DESIGN AND BEAM FORMATION
Transducer Components
The transducers used in echocardiography systems create a brief pulse of ultrasound that is transmitted
into the tissue (Fig. 1.5). To achieve this goal, most TEE transducer designs use the following components:
1. A ceramic piezoelectric crystal, which acts as an ultrasonic vibrator and receiver
2. Electrodes, which both conduct electric energy to stimulate the piezoelectric crystal and record the
voltage from returning echoes
3. Backing, which acts to dampen the vibrations of the crystal rapidly
4. Insulation, which prevents unwanted vibration of the transducer from standing waves or extraneous
incoming waves
5. A faceplate, which optimizes the acoustic contact between the piezoelectric crystal and the esophagus.
The faceplate may also include an acoustic lens to focus the beam
The following sections detail the inner workings of the modern ultrasound transducer and their effects
on the transmitted sound beam and the echocardiographic image.
Formation of Ultrasound Waves: The Piezoelectric Crystal

The heart of the transducer consists of a piezoelectric crystal, which contains polarized molecules trapped
within a matrix. The formation of the sound wave used in echocardiography is based on the principle
of piezoelectricity. When stimulated by alternating electric current, polarized particles within the crystal
matrix vibrate, generating ultrasound. Conversely, when an ultrasound wave strikes the crystal, the result-
ing vibrations of the polarized particles generate an alternating electric current. Therefore, a piezoelec-
tric crystal can function as both a transmitter and a receiver of ultrasound. This process is the hallmark

Reflected
signals
Transmitted
signal
A
FIGURE 1.6 Effect of pulse length on axial resolution. A: The transducer emits a long sound pulse. Since the length of
this pulse is greater than the length of the atrial septal defect (arrows), the reflections from the two tips of atrial septum
are smeared and the defect cannot be resolved. Consequently, the resulting two-dimensional echocardiographic display
(right) does not show the abnormality. B: The pulse length has been shortened and is now less than the length of the atrial
septal defect. The reflections from each interface are clearly identifiable, and the resulting display (right) shows the defect.
of piezoelectricity—that is, the transformation of electric energy into mechanical energy and the reverse
transformation of mechanical energy into electric energy.
For imaging purposes, the transducer emits a brief burst of ultrasound. Typically, two-dimensional
transducers emit a sound pulse of two to four wavelengths. As illustrated in Figure 1.6, the shorter the
length of the sound pulse, the better the axial resolution of the system. Therefore, the shorter the wave-
length, the shorter the resulting pulse length and the greater the axial resolution.
The Three-dimensional Ultrasound Beam

Near and Far Fields
The ultrasound transducer emits a three-dimensional ultrasound beam similar to the beam of a flashlight
Video 1.1 (Fig. 1.7, Video 1.1). The physical dimensions of this beam determine the following:
1. The specific area of the heart examined
2. The intensity distribution of ultrasound energy
3. The lateral (side-to-side) and elevational (top-to-bottom) resolution of the system

Far field
Near field
Far field
Focal zone
Elevational focus
Lateral focus
FIGURE 1.7 Three-dimensional beam. The ultrasound probe projects a three-dimensional beam. The dimensions of this
projection have important effects on imaging resolution and artifact. Typically, a narrow profile is preferred. A: Unfocused
beam. The beam is narrow in the near field and then diverges in the far field. B: Focused beam. Focusing has resulted in
a narrower beam in both the lateral and elevational planes, so that the imaging resolution of structures in the focal zone
is improved. Distal to the focal zone, the beam rapidly diverges, and the images of structures in this area will be of lower
quality. Video 1.1. Video 1.1
Narrower beams are preferred because they improve resolution, increase the intensity of returning
echoes, and reduce artifact. Most commonly, ultrasound beams have either a disk or rectangular shape and
comprise two main zones: The near field (Fresnel) and far field (Fraunhofer) zones. Beam manipulation and
image resolution are greatest within the near field. Also, ultrasound energy is more concentrated within
this zone, yielding stronger echoes and better imaging.
In the near field zone, the ultrasound beam is narrow. The length of the near field zone is proportional
to the diameter (D) of the transducer face and inversely proportional to the wavelength:
Ln = D2/4λ (7)
Distal to the near field zone, the ultrasound beam diverges, forming the far field zone. The angle of diver-
gence (θ) is inversely related to the diameter (D) of the transducer face:
sin θ = 1.22λ /D (8)
Accordingly, larger transducers with high-frequency (small λ) signals produce the most desirable beam
profile: A long, narrow near field and a less divergent far field.

Focusing
Focusing can further narrow the ultrasound beam. This is accomplished in three ways, as follows:
1. By creating a concave shape in the piezoelectric crystal
2. By gluing an acoustic lens to the front of the crystal
3. Electronically with the use of phased array transducers
The narrow beam at the focal zone enhances imaging at this location. However, the beam diverges
widely distal to the focal zone, reducing the intensity of the ultrasound energy and impairing imaging of
the far field.
Electronic Beam Focusing: The Phased Array

Modern echocardiography systems allow the echocardiographer to adjust the depth of the focal zone selec-
tively to optimize image quality. A single element transducer emits a wave front that diverges in a hemi-
spheric pattern. By aligning several crystals side by side in a linear array, the interaction of the individual
Video 1.1 sound waves emitted by each crystal creates a narrow, forwardly directed wave front (Fig. 1.8A, Video 1.1).
The beam’s shape can be focused further by electrically activating the crystals at the ends of the array before
those located at the center creating a concave wave front thereby focusing the beam at a selected distance
Video 1.1 from the transducer face (Fig. 1.8B, Video 1.1).
It is important to be cognizant of both the advantages and disadvantages of selecting the focus depth
of the beam. As discussed next, beam shape is of prime importance in determining the resolution of an
imaging system.
Resolution
Three parameters are evaluated when assessing the resolution of an ultrasound system: The resolution of
objects lying along the axis of the ultrasound beam (axial resolution), the resolution of objects lying hori-
zontal to the beam’s orientation (lateral resolution), and the resolution of objects lying vertical to the beam’s
orientation (elevational resolution).
Axial Resolution
Axial resolution is the ability of the ultrasound system to identify two separate objects that lie along the
path of the ultrasound beam axis. Axial resolution is determined by the bandwidth of the ultrasound pulse.
The bandwidth is the resonant frequencies that are emitted about the center frequency. High bandwidth
pulses are best for axial resolution as they are characterized by high-frequency signals of short duration. As
seen in Figure 1.6, short pulses of high-frequency ultrasound offer the greatest axial resolution. A general
rule is that the axial resolution of a system is approximately 1.5 times the wavelength of the system. There-
fore, for a 7.5-MHz transducer axial resolution is 0.3 mm. Improved axial resolution does not come without
a cost. The shorter the pulse, the lower its energy level, so that the penetration and returning echoes are
weaker. Similarly, high-frequency sound is quickly attenuated. Accordingly, the echocardiographer must
select these parameters based on the imaging needs.
Lateral (Azimuth) Resolution

Lateral resolution is the ability of the ultrasound system to distinguish between objects that are horizon-
tally aligned and perpendicular to the path of the ultrasound beam. Beam width is a primary determinant
of lateral resolution. Wide beams produce a “smeared” image of two such objects, whereas narrow beams
can identify each object individually. Signal frequency and transducer size impact lateral resolution, but for
typical cardiac ultrasound transducers the beam width is approximated as depth/50, yielding at 10 cm of
depth a beam width of approximately 2 mm.

7
+
6 +
5 +
Target
4 +
3 +
2 +
1 +
7 + Target
6 +
5 +
4 +
3 +
2 +
1
B
FIGURE 1.8 Phased array transducers. A: This illustration shows seven crystal elements in an array. The interactions of
the individual hemispheric wave fronts create a flat, profiled, forward-directed wave front. B: Phased array transducer.
Here, the crystals have been activated sequentially: Crystal 1 first, followed by crystal 2, and so on. This causes the beam
to be steered upward toward the target. Note that crystals 6 and 7 have been activated before crystal 5, creating a con-
cave wave front to focus the energy of the beam at the target. The ability to steer electronically and focus the beam is a
major advantage of the phased array system. Video 1.1. Video 1.1

Elevational Resolution
Elevational resolution is the ability of the ultrasound system to distinguish between objects that are vertically
aligned and perpendicular to the emitted ultrasound beam. Although two-dimensional images appear to
display a thin slice of cardiac anatomy, in actuality the information gathered from the entire thickness of the
beam is averaged and displayed. For this reason, the thinner the ultrasound beam, the better the elevational
resolution of the system (Fig. 1.7). Signal frequency and transducer size impact elevational resolution, but a
typical cardiac ultrasound transducer has a beam height approximated as depth/30. Accordingly, at 10 cm
depth the beam height is approximately 3.3 mm. Note that axial resolution offers fidelity of 50% greater than
that achieved in the lateral and elevational planes.
Optimizing Resolution
The interplay of the transducer size, signal frequency, and focal length and the distance of the structure of
interest determine beam width and height. The beam is narrowest in the near field or focal zone and diver-
gent in the far field. Resolution is therefore better in the near field and decreases in the far field. Factors that
lengthen the near field, such as a higher transducer frequency and a larger transducer radius, improve lat-
eral and elevational resolution. Focusing further decreases the width of the ultrasound beam and improves
lateral and elevational resolution at the focal point. However, focusing often increases beam divergence
distal to the focal zone, with an associated loss of lateral and elevational resolution. These factors explain
why it is preferable to position a transducer with a relatively high frequency (smaller wavelength) close to
the target of interest to optimize both lateral and elevational resolution. More precise measurements are
made along the axial plane due to the superior resolution in this orientation.
Extraneous Sound Beams

Side Lobes
Unfortunately, in addition to the powerful forwardly directed beam of sound energy produced by linear array
Video 1.1 transducers, additional beams of sound are emitted that travel off axis to the main beam (Fig. 1.9, Video 1.1).
These extraneous beams of sound, called side lobes, significantly affect imaging quality because the transducer
FIGURE 1.9 Ultrasound Beam Pattern: The spacial distribution of sound energy from a phased array transducer is char-
acterized by focal zone, near and far fields, as well as side lobes. A 6 crystal transducer is shown at the top of the image
(sharp peaks) and the emited waves interact causing constructive and destructive interference. The resulting pattern
includes the forwardly directed, high intensity main lobe with its focal zone showing both narrow dimensions and
peak intensity. Side lobes are also created and reflections from these off axis lobes reduce image quality and are a well-
described source of imaging artifact.

incorrectly processes their reflections as reflections of the main beam. Consequently, structures off axis to
the imaging plane appear incorrectly located on the two-dimensional image.
Grating Lobes
Grating lobes are side lobes generated with multielement array transducers. Each crystal of the linear array
can be considered a point source of sound emission. When these individual sound waves meet in phase and
off axis to the main beam (constructive interference), a grating lobe is created. The position of a grating lobe
is predictable as it is related to the spacing of the crystals and the wavelength of the signal.
Side Lobe Artifacts

Both side and grating lobes contain less energy than the main beam and usually do not significantly affect
the echocardiographic image. However, when these lobes of energy contact a highly reflective surface
(catheter, prosthesis, calcium), sufficient energy can be reflected back to the transducer to create an artifact.
The transducer believes these reflections have arisen from the main forwardly directed field and mistakenly
displays them together with those from the main beam. To reduce such artifacts, the echocardiographer
should minimize gain settings to decrease the likelihood of strong reflections from the weaker lobes. If they
persist, to differentiate an artifact from a real structure, the field should be imaged from another window.
An artifact is not likely to be reproduced in multiple planes.
SIGNAL RECEPTION AND PROCESSING

The conversion of reflected ultrasound signals into high-fidelity cardiac images is a complex process in
which returning ultrasound pulses are received, electronically processed, and displayed. Understanding
the basic principles of these steps is essential both to optimize image acquisition and avoid misdiagnosis
caused by artifacts.
Cycling of Transducer Transmit and Receive Modes

The ultrasound transducer acts first as a transmitter and then as a receiver of sound signals. An oscillator
signals the discharge of electric current to the piezoelectric crystal, thereby determining the rate of sound
pulse transmission. After emitting a short burst of ultrasound, the transducer switches to receive mode to
listen for the returning ultrasound reflections from the tissues.
Electrical Processing
Amplification: Gain Controls
The echoes that return to the transducer are converted from sound energy to a radiofrequency electric
signal by the piezoelectric crystal. A large portion of the sound energy is lost as the ultrasound wave travels,
and the electric signal must be amplified before it can be further processed. This amplification is controlled
by the system gain control. Furthermore, since signal attenuation is proportional to distance traveled, sig-
nals from distant structures can be 12 to 30 dB weaker than those from closer structures. Time gain com-
pensation allows the echocardiographer to selectively amplify signals from structures of varying distances
from the transducer. With this feature, signals from distant targets and weaker reflectors are boosted so
that their amplitudes more closely match those from nearby structures.
Compression and Display

The amplified and time gain-compensated electric signal must be processed before it can be displayed on a
monitor. The radiofrequency signal has a large dynamic range of more than 100 dB, far too large for moni-
tors to display. To reduce the dynamic range, two processes are commonly used. First, reject circuits filter
out low-amplitude signals, which typically represent background noise or speckle. The remainder of the
signal is then compressed, so that both low- and high-amplitude components can be displayed. Digital scan
conversion then converts the electric signal into a standard video format for display.

Distance
A B Time
mode mode
M-mode
FIGURE 1.10 Display formats. The ultrasound beam is directed through the aortic valve leaflets. Amplitude mode
(A-mode) display shows the resulting reflections as horizontal spikes. In the brightness mode (B-mode) display, the
spikes are replaced with pixels of varying brightness. Motion mode (M-mode) shows sequential B-mode frames to cap-
ture cardiac motion. The “boxcar” pattern depicts normal opening and closing of the aortic valve leaflets.
Preprocessing and Postprocessing

The digital scan converter requires the analog electric signal to be digitized so that it can be processed and
then converted to an analog video format. This process offers two important opportunities for the echocar-
diographer to control the display of the imaging data. By adjusting the preprocessing settings, which affect
the analog-to-digital conversion, and the postprocessing settings, which affect the conversion to analog video
format, the echocardiographer can modify the appearance of the displayed image. These adjustments can
be used, for example, to emphasize edge detection versus tissue texture or to improve the delineation of
weaker reflectors. Again, the choice of these settings is dictated by the examination and the personal prefer-
ences of the echocardiographer.
DISPLAY FORMATS
The Golden Rule: Time is Distance

Ultrasonic imaging is based on the amplitude and time delay of the reflected signals (Fig. 1.10). Since the
velocity in tissue is relatively constant, only the distance of the structure from the transducer alters the time
required for the ultrasound wave to travel to and from the reflected structure:
Distance = velocity × time (9)
As sound travels at a rate of 1,540 m/s through soft tissue, the round trip travel time for each centimeter
of separation between transducer and reflector is calculated as:
Travel time = 13 μ s/cm (10)
By timing the interval between transmission and return of the reflections, the echocardiography system
can precisely calculate the location of a structure.
Amplitude Mode
The original display format is amplitude mode (A-mode), in which the amplitudes of the returning signals
are represented as a series of horizontal spikes along the vertical axis of the display. The horizontal spikes
correspond to the distance of the reflecting tissue and the strength of the returning echoes.

FIGURE 1.11 Scan lines. Illustration of the arced sector from a phased array two-dimensional echocardiogram. Each
dotted line represents an individual B-mode (brightness mode) scan line. Any structure that interacts with a scan line will
create reflections (dark highlight); however, structures that lie between the scan lines are not interrogated, and the echo-
cardiography system averages the neighboring signals to fill in this defect. Accordingly, the closer the scan lines, the better
the image quality. With a phased array scan, the gap between scan lines increases with the distance from the transducer.
Brightness Mode
Current imaging is based on brightness mode (B-mode) technology. Instead of horizontal spikes, the ampli-
tudes of the returning echoes are represented as pixels of varying brightness along the vertical axis of the
display. The brightness correlates with the strength of the returning signal.
Motion Mode
Motion mode (M-mode) adds temporal information to B-mode by displaying a series of collected B-mode
images. M-mode echocardiography provides a one-dimensional, “ice pick” view through the heart and
updates the B-mode images at a very high rate, allowing dynamic real-time imaging. It is important to real-
ize that before it emits the next pulse of energy, the transducer element must first receive the reflected energy
of the previously emitted pulse. The frequency at which the B-mode images are updated is the frame rate
and is calculated as 1 s/round trip travel time. The frame rate with M-mode imaging is very high (>2,000
frames/s), affording a superior display of dynamic motion in comparison with other techniques. However,
M-mode imaging displays only axial motion and provides a limited view of cardiac anatomy. Because of
its superior dynamics and axial resolution, M-mode is the best mode for examining the timing of cardiac
events when displayed with the electrocardiogram.
Two-dimensional Echocardiography
Two-dimensional echocardiography is a modification of B-mode echocardiography and the mainstay of
the echocardiographic examination. Instead of repeatedly firing ultrasound pulses in a single direction, the
transducer in two-dimensional echocardiography sequentially directs the ultrasound pulses across a sec-
tor of the cardiac anatomy. In this way, two-dimensional imaging can display a tomographic section of the
cardiac anatomy, and unlike M-mode, it can show shape and lateral motion (Fig. 1.11).
TWODIMENSIONAL SCAN SYSTEMS

Both electronic and mechanical systems have been developed to sweep the beam across an area of inter-
est. Most commonly, the transducer consists of multiple crystals (or elements) aligned next to one another
in a linear array. The individual sound waves from each crystal combine to provide a unified wave front

that can be better focused and directed than that of a single crystal. Furthermore, with alterations in the
timing of the electric activation of each crystal in the array, hence the term phased array, the beam can
actually be steered without the transducer itself being moved. The advantages of an electronic system
over a mechanical one, including an absence of moving parts and easy manipulation (steering, focusing,
narrowing) of the ultrasound beam, have made it the dominant technology in echocardiography scanners.
The two commonly used electronic scanning systems in medical ultrasound are the linear scanners and
sector scanners.
Linear Scanners
The linear scanner uses a long transducer composed of several crystals. Groups of crystals are activated
sequentially from one end of the transducer to the other. The firing of each group of crystals images the
structures directly in front of them. With sequential firing of the groups of crystals, the anatomic features
under the entire transducer are imaged. However, the disadvantage of this approach is that the transducer
face must be large enough to cover a broad anatomic area effectively. The linear array is commonly used in
vascular and obstetric applications.
Sector Scanners
The phased array sector scanner is most commonly used in echocardiography. This is an electronic system that
by precisely timing the activation of the individual transducer elements is able to sweep the sound beam in
an arc across a predetermined field. With activation of the transducer elements in different sequences, the
ultrasound beam in the phased array system can be easily narrowed, steered, and focused (Fig. 1.8). The
ability to direct a series of beams electronically over an arced sector also makes it possible to use the smaller
transducer face required for TEE and transthoracic echocardiography.
CREATING THE TWODIMENSIONAL IMAGE
Imaging a Sector
To construct the two-dimensional image, the echocardiographic system records the B-mode data from the
first pulse, redirects the next beam, records the returning signals, and so on until the entire sector has been
scanned. Typically, the scanner images a sector of 30 to 90 degrees. The orientation of each B-mode line
(also called the scan line) is recorded so that the information can be displayed in the correct position on the
display screen. The two-dimensional scanner then repeats the entire process to update the image and cap-
ture motion. Each image created by a sector scan is a frame. Two-dimensional imaging typically requires
100 to 200 scan lines per frame, resulting in a frame rate of 30 to 60 frames/s. Since this rate is significantly
slower than that of M-mode echocardiography, two-dimensional imaging is not as precise for demonstrat-
ing dynamic motion or the timing of cardiac events.
Image Quality and Dynamic Motion

Two-dimensional imaging is characterized by several factors that are operator controlled and have impor-
tant (and often opposing) effects on image quality and dynamic motion. The proper settings vary depend-
ing on the particular examination at hand.
The pulse repetition frequency is the rate at which sound pulses are transmitted per second. The greater
the pulse repetition frequency, the greater the number of scan lines that are emitted in a given period of
time. The pulse repetition frequency is inversely related to the sector depth because a longer period of time
is required for the ultrasound to travel increased distances.
The frame rate is the frequency at which the sector is rescanned. Each frame consists of one or two scans
across the sector of interest. The information from two sweeps can be interlaced to improve image qual-
ity. A high frame rate improves the capture of movement. Typically, a frame rate greater than 30/s allows
the dynamic representation of some relatively fine movements (e.g., intermediate positions of the aortic
valve). The frame rate is critically dependent on the sector depth, which determines the time required for

each scan line to be received, and sector width, which increases the number of scan lines to be processed.
Consequently, increases in the sector size and depth come at the cost of a decreased frame rate.
The scan line density, calculated as the number of lines per degree of the sector, greatly affects the image
quality. Line densities should be maintained at 1.5 to 2.2 lines per degree. Doubling the scan lines essen-
tially doubles the lateral resolution. However, the cost is a decrease in the frame rate. The scan line density
is calculated by dividing the number of scan lines per sweep by the angle of the sector. The greater the
sector angle, the larger the area and the lower the line density. Since phased array transducers produce a
fan-shaped sector, scan line density and hence lateral resolution is greater, closer to the transducer, and
decreases in direct proportion to distance.
Image Quality Versus Dynamic Motion

It quickly becomes apparent that the echocardiographer must choose between the size of the imaging field
and the frame rate. If the frame rate is high (100 frames/s), the number of scan lines per frame is reduced,
resulting in a lower line density. Although the dynamics of the image may be excellent, the spatial image
quality is decreased. We caution against the practice of assessing several structures in a single large view
because it compromises both the dynamics and quality of the images. We recommend that the clinician
focus each part of the examination on a given structure of interest and select the imaging plane that best
delineates the structure in the near field. Motion can then be enhanced without costs in lateral resolu-
tion by decreasing the sector angle and depth. In situations in which the maximal frame rate is desired,
M-mode should be considered. This results in a very dynamic image with a high level of axial resolution.
For these reasons, M-mode echocardiography remains an important adjunct to both two-dimensional and
color Doppler echocardiography.
SUMMARY
Two-dimensional echocardiography is based on the interaction of ultrasound and the patient. Between the
generation of the ultrasound pulse and its subsequent reflection, reception, and display, a complex series of
events takes place. Echocardiographers who ignore the physical realities of the imaging process will suffer
two common causes of misdiagnosis: Inadequate imaging and artifacts. However, expert echocardiogra-
phers, by applying an understanding of the principles involved and selecting the most appropriate views
and machine settings, reliably optimize the imaging of a particular structure of interest. No patient or echo-
cardiographic system is ideal. Rather, echocardiographers must compromise between conflicting imaging
needs, such as between dynamic motion and the visual quality of an image, based on the primary diagnostic
goal. We expand on the important relationship between the echocardiographer and the echocardiography
machine in Chapter 23.
SUGGESTED READINGS
Geiser EA. Echocardiography: Physics and instrumentation. In: Marcus ML, Skorton DJ, Schelbert AR, et al., eds. Cardiac Imaging.
2nd ed. Philadelphia, PA: WB Saunders; 1991.
Weyman A, ed. Principles and Practice of Echocardiography. 2nd ed. Philadelphia, PA: Lea & Febiger; 1994:3–55.

QUESTIONS
1. Which of the following affects a sound c. They receive the reflected sound signals
wave’s propagation velocity? d. They are controlled by gain settings
a. Signal frequency
9. The length of the near field is:
b. Signal amplitude
a. Increased with large transducers and large
c. Tissue density
wavelength
d. Transducer size
b. Increased with large transducers and high
2. Sound waves propagate in all of the frequency
following except: c. Increased with small transducers and large
a. Vacuum wavelength
b. Blood d. Increased with small transducers and low
c. Bone frequency
d. St. Jude mitral valve
10. Typical cross-sectional beam dimensions
3. The speed of sound in soft tissue is at a distance of 10 cm from the transducer
approximately: equal:
a. 1,500 cm/s a. 1 mm2
b. 1,500 m/s b. 5 mm2
c. 1,500 km/h c. 15 mm2
d. 1,500 mph d. 50 mm2
4. High frequency sound waves are 11. Side lobe artifacts:
advantageous in cardiac imaging because a. Can be mitigated by increasing gain settings
they provide: b. Can be mitigated by increasing transducer
a. Better penetration through fatty tissue output
b. Better amplitude in the far field c. Do not occur in single crystal transducers
c. Smaller transducer face d. Are limited to the near field
d. Better focus
12. The transducer is most commonly operating
5. The signal amplitude is related to the: in transmit mode.
a. Square root of the intensity a. True
b. Intensity squared b. False
c. Intensity divided by sector width
13. Reject circuits are best employed to:
d. Intensity times sector width
a. Reduce white out
6. The sharply demarcated border between the b. Reduce background speckle
ascending aortic walls and aortic blood in c. Protect against electrical injury
the ME AV LAX view: d. Reduce side lobe artifacts
a. Results from specular reflections
14. Round trip travel time (time from emission
b. Results from scattering reflections
to return of reflected signals) in a TEE
c. Depends on the Nyquist limit
cardiac examination:
d. Is not affected by reflection coefficient
a. Varies significantly based on tissues encoun-
7. Factors in loss of ultrasound signal tered
amplitude include: b. Is impacted by sector width
a. Dispersion and reflection coefficient c. Equals 13 μs/cm
b. Absorption and sector width d. Is highest with high frequency signals
c. Frequency and pulse repetition frequency
15. The round trip travel time for a 10 MHz
d. Distance and gain settings
signal reflected from a target 20 cm from
8. Which of the following is false regarding the transducer is:
piezoelectric crystals? a. 3,080 μs
a. They transmit ultrasound b. 3,080 ms
b. They convert an AC electrical signal to c. 260 μs
ultrasound d. 2,600 ms

16. M-mode has higher temporal resolution 19. A freeze frame’s image quality is directly
than 2D ultrasound because: impacted by all of the following except:
a. M-mode employs higher frequency signals a. Pulse length
b. 2D employs sector display b. Scan line density
c. Effective depth of M-mode is one-half that c. Frame rate
of 2D d. Amplitude of returning signals
d. 2D employs B-mode
20. Dynamic motion appearance will be
17. Phased array: negatively impacted by:
a. Is a passing fad a. Increase in sector width
b. Is critical to M-mode display b. Decrease in signal frequency
c. Is an advancement over B-mode c. Decrease in depth setting
d. Features electronic control over the activa- d. Decrease in scan line density
tion of individual transducer elements
18. Frame rate is related to the pulse repetition
frequency.
a. True
b. False

2 Two-dimensional Examination
Joseph P. Miller
O VER THE LAST FEW YEARS there has been a great deal of emphasis on three-dimensional (3D) imaging
and new technology in general. Although it is easy to get caught up in the wave of excitement, not every OR
has a 3D machine and it will be a few years before this technology is ubiquitous and simple to use in all clini-
cal scenarios. Two-dimensional imaging remains the key clinical tool for intraoperative echocardiographic
imaging in the majority of clinical situations.
The purpose of this chapter is to demystify echocardiographic image orientation and provide a stepwise
approach to image acquisition. In the eyes of the novice, learning and applying transesophageal echocar-
diography (TEE) may seem like an insurmountable task. With the use of this stepwise approach, TEE will
quickly become an integral part of your practice and a valuable aid for intraoperative decision-making (1–6).
IMAGING PLANES AND ORIENTATION

Understanding the orientation of the imaging plane is crucial for both acquisition of the desired images
and correct interpretation of the displayed cardiac anatomy. Although TEE is limited to the confines of the
esophagus and stomach, the ability to alter the position and orientation of the ultrasound beam allows a
broad view of the cardiac anatomy.
PROBE INSERTION
The TEE probe is passed into the esophagus in the same manner in which an orogastric tube is placed.
The easiest way to insert the probe is to perform a jaw lift by grabbing the mandible with the left hand and
inserting the probe with the right. The probe is inserted with constant gentle pressure in addition to a slight
turning back and forth and from left to right to find the esophageal opening. If resistance is encountered,
the cause most often is excessive extension of the head and neck. Advancement of the probe is stopped
after the head of the probe has passed the larynx and cricopharyngeus muscle, where a distinct loss of
resistance is felt. The imaging head will lie in the upper esophagus.
PROBE MANIPULATION
The position and orientation of the TEE probe can be altered by several types of manipulation (Fig. 2.1,
Video 2.1 Video 2.1). By gripping the probe shaft near its entrance in the mouth, the probe can be advanced or with-
drawn. The degree of insertion can be easily determined by the depth markings imprinted on the shaft. For
cardiac imaging, the probe position ranges from the upper esophagus to the stomach. In the upper esopha-
gus, the structure closest to the TEE probe is one of the great vessels. In the midesophagus (ME), the struc-
ture closest to the TEE probe is the left atrium, and in the transgastric (TG) position, the structure closest
to the TEE probe is (most commonly) the left ventricle. Therefore, depending on the depth of insertion, the
structure at the apex of the imaging sector will be one of the great vessels, the left atrium, or the left ventricle.
The orientation of the ultrasound beam can be further adjusted by manually turning the probe shaft
to the left or right. The probe can be anteflexed or retroflexed by using the large knob on the probe han-
dle. The small knob on the probe handle will flex the probe leftward or rightward. These maneuvers allow
precise user control over the direction of the ultrasound beam to visualize the structure of interest.
20

2. Two-dimensional Examination 21
Turn to
the left
Turn to
the right
0 degree
Withdraw
180 degree
Rotate
Rotate
Advance forward
back
90 degree
Anterior Posterior Right Left
Anteflex Retroflex Flex to Flex to
FIGURE 2.1 Terminology used to describe manipulation of the probe and transducer during image acquisition. (From
Shanewise JS, Cheung AT, Aronson S, et al. ASE/SCA guidelines for performing a comprehensive intraoperative multiplane
transesophageal echocardiographic 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. Anesth Analg. 1999;89:870–884, with permission.)
MULTIPLANE IMAGING ANGLE

The first clinically useful TEE probes were capable of producing a single or monoplane cross section
of the heart. This imaging plane is generated perpendicular to the shaft of the probe and corresponds to
the typical transverse views obtained with transthoracic echocardiography. The biplane probes of the next
generation were able to produce two perpendicular views: The standard transverse cross sections and a
longitudinal cross section. Currently, most of the probes in use in adult TEE are multiplane probes. Through
an electronic switch on the probe handle, the operator selectively rotates the orientation of the imag-
ing plane from 0 degrees (transverse plane) to 180 degrees in 1-degree increments. This capability offers
many advantages with respect to image acquisition but can also generate tremendous confusion for novice
echocardiographers.
Experts rely on two key points to determine image orientation quickly. First, independent of the imag-
ing plane, the ultrasound beam always originates from the esophagus or stomach and projects perpendicu-
lar to the probe. Consequently, on the monitor the apex of the sector displays structures that are closest to
the TEE probe. As a general rule of thumb, structures seen near the apex of the image sector (i.e., closest
to the TEE probe) will be posterior structures, and those close to the arc of the sector (i.e., more distant
from the TEE probe) will be anterior structures.
Second, left and right orientation depends on the degree of rotation of the scan head. A simple way to
orient yourself is to place your right hand on your chest with your palm facing downward, your extended
thumb pointing leftward and anterior, and your fingers rightward and anterior. This is the orientation of

A B
FIGURE 2.2 A: Orientation of your hand, as described in text, for an imaging plane of 0 degrees. The red and green lines
correspond with the lines described in B. B: The top figure is a schematic representation of a transesophageal echocar-
diography (TEE) probe obtaining a midesophageal (ME) four-chamber view. The TEE probe lies in the esophagus poste-
rior to the left atrium. The imaging plane is projected like a wedge anteriorly through the heart. The image is created by
multiple scan lines traveling back and forth from the patient’s left (green edge of imaging sector) to the patient’s right
(red edge). The resulting image is displayed on the monitor with the green edge of the sector displayed on the right side
of the monitor and the red edge on the left. In the bottom image, the schematic is made transparent and the anatomy of
the heart is displayed in the orientation seen in an ME four-chamber view.
A B
FIGURE 2.3 A: Orientation of your hand, as described in text, for an imaging plane of 90 degrees. The red and green
lines correspond with the lines described in B. B: The top figure is a schematic representation of a transesophageal
echocardiography (TEE) probe obtaining a midesophageal (ME) two-chamber view. The probe is in the same position
as described in Figure 2.2. However, in this case the imaging sector is rotated so that the green sector edge has moved
clockwise and is now cephalad, and the red sector edge is now caudad. As previously described, the green edge is dis-
played on the right side of the monitor’s screen and the red edge on the left. In the bottom image, the schematic is made
transparent and the anatomy of the heart is displayed in the orientation seen in an ME two-chamber view.

LA
N L
RA R A
RV
B
A (0–45 degrees)
LA
RA
RV LV
C
B (0 degree)
LV
RV LV
RV Ao
C (0 degree) Transverse plane

C (120 degree) Longitudinal plane
FIGURE 2.4 Through simple manipulations, the transesophageal echocardiography (TEE) probe offers a multifaceted
picture of cardiac anatomy. Progressive advancement of the probe in the midesophagus provides a cross-sectional view
of the aortic valve (A) followed by a long-axis view of the cardiac chambers (B). Further advancement and anterior flexion
of the probe head (C) allow visualization of the left ventricle in the short axis. Rotation of the imaging plane expands
the imaging capacity of TEE. In this example, the left ventricle and its outflow tract are brought into view by rotating the
imaging plane to 120 degrees. LA, left atrium; RA, right atrium; Ν, nοncoronary cusp; L, left coronary cusp; R, right coro-
nary cusp; RV, right ventricle; LV, left ventricle; Ao, aorta.
the imaging scan at 0 degrees and the scan lines begin at your fingers sweeping right to left toward your
thumb. Consequently, your fingers point toward right heart structures that will be displayed on the left side
on the monitor as you look at the screen (Fig. 2.2). Note that this right-to-left display orientation is similar
to that of a chest x-ray.
Increases in the imaging plane angle proceed in a clockwise manner. For example, when the imaging
plane is rotated to 90 degrees, the imaging orientation is mirrored by rotating your hand clockwise 90
degrees (fingers pointing downward) (Fig. 2.3). Therefore, the scan now progresses from posterior to ante-
rior structures (longitudinal plane).
The combination of probe manipulation and imaging plane angle provides a powerful tool for cardiac
imaging (Fig. 2.4). For example, slight withdrawal of the probe and rotation of the imaging plane to 40
degrees provides a short-axis view of the aortic valve (Fig. 2.5). In contrast, advancement of the probe into
the stomach combined with anteroflexion with the imaging plane at 0 degrees provides a short-axis view
of the left ventricle (Fig. 2.6).
GOALS OF THE EXAMINATION

TEE examinations, whether comprehensive or abbreviated, should display all pertinent structures in the
heart. Each cardiac chamber and valve should be visualized in at least two orthogonal planes. All segments
of the myocardium should also be visualized. This approach helps ensure the diagnosis of any significant
abnormalities and minimizes the incorrect identification of artifacts.

FIGURE 2.5 The top figure is a schematic representation of a transesophageal echocardiography (TEE) probe obtain-
ing a midesophageal (ME) aortic valve short-axis view. The probe is in the esophagus but slightly above the position
in Figures 2.2 and 2.3. When the leaflets of the aortic valve are seen, the imaging plane is rotated from 0 degrees to
approximately 40 degrees when the aortic valve is seen in a true cross section. The image on the monitor is generated
from scan lines going back and forth from the green edge (right side of monitor) to the red edge (left side of monitor). In
the bottom image the schematic is made transparent and the anatomy of the heart is displayed in the orientation seen
in an ME aortic valve short-axis view.
Echocardiographers differ in their approach to a diagnostic TEE examination. Many prefer to start with
those views that examine known pathology. Others believe the examination should first systematically
examine for unknown pathology before the area of concern is evaluated. A common approach starts with
TG views of the left ventricle because of the frequent abnormalities detected with these views. Each of
these approaches has its advantages and disadvantages and there is no one correct way. However, the goal
of any approach must be a complete examination of all structures of the heart. A joint task force including
members of the American Society of Echocardiography and the Society of Cardiovascular Anesthesiologists
has published guidelines for performing a comprehensive intraoperative multiplane TEE examination (7).
However, additional views are often required to assess a particular abnormality and no consensus has been
reached regarding whether all 20 cross sections described in the guidelines should be acquired in every
surgical patient.
The examination described in this chapter is based on progressive esophageal advancement of the
probe to evaluate cardiac anatomy and function followed by progressive withdrawal for the evaluation
of the aorta. This approach minimizes manipulation of the TEE probe, thereby shortening the examina-
tion time. This author has not found the depth of probe insertion to be a reliable tool for identifying
intracardiac anatomy. The preferred approach is to report the location of cardiac anatomy/pathology
relative to known intracardiac structures and standard cross-sectional views. The progressive advance-
ment/removal of the probe provides a systematic anatomic orientation (avoiding disorientation as to
the displayed imaging plane) and allows for easy description of anatomy relative to other cardiac struc-
tures. Pathology in the aorta can be referred to the depth of probe insertion but this has more value in

FIGURE 2.6 The top figure is a schematic representation of a transesophageal echocardiography (TEE) probe obtaining
a transgastric (TG) midshort-axis view. The probe is advanced into the stomach and anteflexed until solid contact is made
with the gastric wall. The imaging plane is projected from the probe at 0 degrees. The image on the monitor is generated
from scan lines going back and forth from the green edge (right side of monitor) to the red edge (left side of monitor). In
the bottom image, the schematic is made transparent and the anatomy of the heart is displayed in the orientation seen
in a TG mid papillary short-axis view.
the long-term outpatient evaluation of lesions and, we believe, little value in the intraoperative exami-
nation.
The Comprehensive Examination

Midesophageal Ascending Aortic Short-axis View
From the initial position following passage into the esophagus, instead of advancing to the aortic valve,
the probe is only advanced slightly until the proximal aorta is seen. The probe angle is then rotated until
a true short axis is seen, usually between 0 and 45 degrees. The main pulmonary artery is seen bifurcat-
ing and the right pulmonary artery will lie posterior and perpendicular to the proximal aorta (Fig. 2.7,
Video 2.2). Video 2.2
This view is useful for identifying pulmonary artery catheter placement as well as for visualizing throm-
boembolism in the pulmonary artery.
Midesophageal Ascending Aortic Long-axis View

From the short-axis view, the probe angle is rotated to visualize the proximal aorta in the long axis. This
view may identify the proximal extent of a dissection, may allow for visualization of saphenous vein grafts
and can also be used to interrogate the proximal suture line of an ascending aortic tube graft (Fig. 2.8,
Video 2.2). Video 2.2

Superior vena cava Pulmonary

artery
Ascending aorta
FIGURE 2.7 Midesophageal ascending aortic short-axis view.
Midesophageal Aortic Valve Short-axis View

The probe is advanced until the leaflets of the aortic valve are seen. The imaging plane is then rotated to
approximately 45 degrees to obtain the ME aortic valve short-axis view. The size of the aortic valve in
comparison with the atrial chambers, in addition to the mobility of the aortic leaflets and any leaflet calci-
fication, are carefully noted.
The primary diagnostic goals of this view are to define the general morphology of the aortic valve (e.g.,
bicuspid vs. tricuspid) and to determine if aortic stenosis is present. The relative sizes of the aorta and
the atria should be noted. The intra-atrial septum can be observed for openings consistent with an atrial
septal defect or patent foramen ovale. In addition, look for continuous deviation of the septum away from
Video 2.3 an atrium with elevated pressures (Fig. 2.9, Video 2.3). If the probe is withdrawn slightly, with small left to
right turns, the origins of the left and right coronary arteries can be seen.
Midesophageal Right Ventricular Inflow–Outflow

After completion of the ME short-axis view of the aortic valve, the next three views are obtained at the level
of the aortic valve in the longitudinal plane. The first view is the ME right ventricular inflow–outflow view.
Start at the ME aortic valve short axis and, without moving the probe, change the rotation of the imaging

Right
pulmonary
artery
Ascending
aorta
FIGURE 2.8 Midesophageal ascending aortic long-axis view.
angle to approximately 60 to 90 degrees. The desired imaging plane will visualize the tricuspid valve, right
ventricular outflow tract, and proximal pulmonary artery. Note that the right atrium will be at the 10
o’clock position, the tricuspid valve at the 8 o’clock position, the right ventricular cavity at the 6 o’clock
position, and the pulmonary valve and pulmonary artery at the 4 o’clock position.
The primary diagnostic goals of this view are to gauge the right ventricular chamber and pulmo-
nary valve annulus size and to evaluate the pulmonic valve. This view is often superior to the ME four-
chamber view for Doppler interrogation of the tricuspid valve. In adults with prior congenital heart
surgery, evaluation of the right ventricular outflow tract and pulmonary valve may provide important
diagnostic information.
This view may be helpful in confirming the location of a pulmonary artery catheter if a diagnostic wave-
form is not identified. The echodense linear pulmonary artery catheter will be seen in the proximal pulmo-
nary artery if the catheter is in the correct location (Fig. 2.10, Video 2.4). Video 2.4
Midesophageal Aortic Valve Long-axis View

The ME aortic valve long-axis view is obtained by further rotating the imaging angle to approximately
110 to 130 degrees. A slight turn of the probe toward the patient’s right may be necessary to optimize this
image. The view is complete when the left ventricular outflow tract, aortic valve, and proximal ascending

Left atrium
Aortic valve
Right atrium
Right ventricle
FIGURE 2.9 Midesophageal aortic valve short-axis view.
aorta are displayed together. Additional structures to observe are the outflow tract itself, the sinus of Val-
salva, and the sinotubular junction.
The primary diagnostic goal of this view is to evaluate aortic valve function and annular and sinotubular
dimensions. The proximal ascending aorta should be inspected for calcification, enlargement, and protruding
atheroma. An important limitation of this view is that the aortic cannulation site in the distal ascending
aorta cannot be visualized. After completion of a two-dimensional examination, aortic valve function is
Video 2.5 evaluated further with color flow Doppler (Fig. 2.11, Video 2.5).
Midesophageal Bicaval View

The ME bicaval view is then obtained by turning the probe further to the patient’s right. This image is often
best with 5 to 15 degrees less rotation than in the ME aortic valve long-axis view. The key structures in this

−0
−5
−10
Left atrium
Aortic valve
Noncoronary
cusp
RVOT
Right
atrium
Tricuspid Pulmonary
valve valve
FIGURE 2.10 A: Midesophageal (ME) right ventricular inflow–outflow. B: Anatomic representation of the ME right ven-
tricular inflow–outflow view. The reader should compare this image to the adjacent echocardiographic image for a better
understanding of cardiac anatomy. (B from Patrick J. Lynch; illustrator; C. Carl Jaffe; MD; cardiologist, Yale University Center
for Advanced Instructional Media Medical Illustrations by Patrick Lynch, generated for multimedia teaching projects by
the Yale University School of Medicine, Center for Advanced Instructional Media, 1987–2000. Patrick J. Lynch, http://pat-
ricklynch.net Creative Commons Attribution 2.5 License 2006; no usage restrictions except please preserve our creative
credits: Patrick J. Lynch, medical illustrator; C. Carl Jaffe, MD, cardiologist. http://creativecommons.org/licenses/by/2.5/.)

Right
Left atrium
pulmonary
artery
Ascending aorta
Aortic valve
FIGURE 2.11 A: Midesophageal (ME) aortic valve long-axis view. B: Anatomic representation of the ME aortic valve
long-axis view. (B from Patrick J. Lynch; illustrator; C. Carl Jaffe; MD; cardiologist Yale University Center for Advanced
Instructional Media Medical Illustrations by Patrick Lynch, generated for multimedia teaching projects by the Yale
University School of Medicine, Center for Advanced Instructional Media, 1987–2000. Patrick J. Lynch, http://patricklynch.
net Creative Commons Attribution 2.5 License 2006; no usage restrictions except please preserve our creative credits:
Patrick J. Lynch, medical illustrator; C. Carl Jaffe, MD, cardiologist. http://creativecommons.org/licenses/by/2.5/.)
view are the left and the right atria, inferior and superior venae cavae, interatrial septum, and right atrial
appendage. Minor adjustment to probe depth and multiplane angle will often bring the tricuspid valve or
Video 2.6 coronary sinus into view (Fig. 2.12, Video 2.6).
The primary diagnostic goals of this view are to examine for atrial chamber enlargements and the pres-
ence of a patent foramen ovale or an atrial septal defect, and to detect intra-atrial air. If the integrity of the
intra-atrial septum is questioned, color flow Doppler or bubble contrast study should be performed.

Membrane of
fossa ovale
Left atrium
Interatrial
septum
Superior vena
Right atrium cava
FIGURE 2.12 A: Midesophageal bicaval view. B: Anatomic representation of the ME bicaval view. (B from Patrick J.
Lynch; illustrator; C. Carl Jaffe; MD; cardiologist Yale University Center for Advanced Instructional Media Medical
Illustrations by Patrick Lynch, generated for multimedia teaching projects by the Yale University School of Medicine,
Center for Advanced Instructional Media, 1987–2000. Patrick J. Lynch, http://patricklynch.net Creative Commons
Attribution 2.5 License 2006; no usage restrictions except please preserve our creative credits: Patrick J. Lynch, medical
illustrator; C. Carl Jaffe, MD, cardiologist. http://creativecommons.org/licenses/by/2.5/.)

Right atrium Left atrium
Left ventricle
Right ventricle
FIGURE 2.13 Midesophageal four-chamber view. LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.
This view may be helpful in the placement of pulmonary artery catheters in patients where entry into
the right ventricle is difficult. The pulmonary artery catheter is floated to 20 cm and the balloon inflated
and advanced. When the echodense-inflated balloon enters the proximal superior vena cava it will be seen
entering the right atrium. The catheter can be turned clockwise or counterclockwise to steer it toward
the tricuspid valve at approximately the 7 o’clock position in the atrium rather than the inferior vena cava
located at approximately the 9 o’clock position.
Midesophageal Four-chamber View

After completion of the ME bicaval view, the imaging angle is returned to 0 degrees and the TEE probe
is advanced to the mitral valve level. In the transverse plane, the ME four-chamber view is obtained (Fig.
Video 2.7 2.13, Video 2.7). This view allows visualization of all the chambers of the heart. The image rotation is
approximately 0 to 10 degrees with some retro flexion of the probe. Optimal position is achieved when

LA
AV
LVOT
LV
Left atrium
IS
Mitral valve
Aortic valve
Left ventricular
outflow tract
Left
ventricle
Right
Interventricular
ventricle
septum
FIGURE 2.14 Anatomic representation of a midesophageal five-chamber view with the corresponding echocardio-
graphic image. LA, left atrium; LV, left ventricle; AV, aortic valve; LVOT, left ventricular outflow tract; IS, interventricular
septum. (From Patrick J. Lynch; illustrator; C. Carl Jaffe; MD; cardiologist Yale University Center for Advanced Instructional
Media Medical Illustrations by Patrick Lynch, generated for multimedia teaching projects by the Yale University School
of Medicine, Center for Advanced Instructional Media, 1987–2000. Patrick J. Lynch, http://patricklynch.net Creative
Commons Attribution 2.5 License 2006; no usage restrictions except please preserve our creative credits: Patrick J. Lynch,
medical illustrator; C. Carl Jaffe, MD, cardiologist. http://creativecommons.org/licenses/by/2.5/.)
the tricuspid annulus is at its maximal diameter. The key structures to observe are the left atrium, left ven-
tricle, right atrium, right ventricle, the mitral and tricuspid valves, and the septal and lateral walls of the
myocardium. If a portion of the left ventricular outflow tract and aortic valve is displayed (the so-called
five-chamber view) (Fig. 2.14), retroflexion of the probe and slight advancement or rotation of the imaging
plane to 5 to 10 degrees should produce the ME four-chamber view. Remember that the aortic valve and
left ventricular outflow tract are anterior structures and these maneuvers will produce a true cross section
of the more posteriorly located ME four-chamber view.
The ME four-chamber view is one of the most diagnostically valuable views in TEE. The diagnostic goals
of this view include evaluation of chamber size and function, valvular function (both mitral and tricuspid),
and regional motion of the septal and lateral walls of the left ventricle. An additional important use of this
view is to look for intraventricular air following cardiopulmonary bypass. Air will appear as echodense
small bubbles at the junction of the septum and the apex of the left ventricle. After two-dimensional inter-
rogation of this view, color flow Doppler should be placed on the mitral and tricuspid valves to detect
valvular insufficiency and stenosis.
Midesophageal Mitral Commissural View

From the ME four-chamber view, the imaging array is rotated to approximately 60 degrees to display the
mitral valve in a characteristic (left to right) P3–A2–P1 appearance. In this view, both the posteromedial

Left atrium
Coronary sinus
Mitral valve
Left ventricle
FIGURE 2.15 Midesophageal mitral commissural view.
and anterolateral papillary muscles will be visible with chordae seen going to the anterior and posterior
leaflets. Small turns clockwise and counterclockwise as well as small amounts of ante- and retroflexion will
optimize the image and provide a broader perspective of the mitral valve anatomy.
Video 2.8 This view is especially helpful for localization of structural mitral valve pathology (Fig. 2.15, Video 2.8).
Midesophageal Two-chamber View

From the ME commissural view, rotate the imaging angle to approximately 60 to 90 degrees to obtain
the ME two-chamber view. This view is identified by the appearance of the left atrial appendage and the
absence of right-sided heart structures, and it allows visualization of the anterior and inferior walls of the
left ventricle. Occasionally, turning the probe shaft to the right will improve chamber alignment and this
is the best TEE view for visualization of the true left ventricular apex. The apex is less mechanically active
compared to the midcavity anterior and inferior segments which contract inward like the narrowing of a
V. If the apex rises with contraction, you are viewing a foreshortened left ventricle and not seeing the true

Left atrium
Left atrial
appendage
Mitral valve
Left ventricle
FIGURE 2.16 Midesophageal two-chamber view.
apex, and the probe position should be adjusted. Ventricular thrombus or hypokinesis at the apex is often
best appreciated in this view.
The primary goals of this view are to evaluate left ventricular function (especially the apex) and ante-
rior and inferior regional wall motion. It can also be used to look for thrombus of the left ventricular
apex and left atrial appendage. Another frequent use is to verify the correct position of a retrograde
cardioplegia catheter in the coronary sinus. The catheter will be seen as an echodense structure visible in
the coronary sinus located in the atrioventricular groove at approximately 9 o’clock in this cross section
(Fig. 2.16, Video 2.9). Video 2.9
Midesophageal Long-axis View

After evaluation of the ME two-chamber view, the probe is further rotated to approximately 120 degrees or
when the left ventricular outflow tract is seen. Small amounts of rotation and flexion will allow for maxi-
mizing the diameter of the outflow tract. This view often appears similar to the ME aortic valve long axis;
however, the ventricular inflow and outflow tracts are seen as well as a majority of the ventricular cavity.

Left atrium
Aortic valve
Mitral valve
Left ventricle
RVOT
FIGURE 2.17 Midesophageal long-axis view.
The mitral valve and the left ventricular outflow tract can be evaluated in this view. In addition, assess-
ment of regional wall motion and global function of the anteroseptal and inferolateral walls of the ventricle
Video 2.10 is possible in this view (Fig. 2.17, Video 2.10).
Transgastric Basal Short-axis View

From the ME long axis, the probe is rotated back to 0 degrees, advanced and anteflexed, and then with-
drawn to obtain the TG basal short-axis view of the left ventricle. This view is often difficult to obtain. If
the “fish mouth” view of the mitral valve is not obtained advancing to the TG mid papillary short axis, then
Video 2.11 withdrawing the anteflexed probe may allow visualization of the TG basal short axis (Fig. 2.18, Video 2.11).
Transgastric Midpapillary Short-axis View

The probe is then advanced, anteflexed, and withdrawn until contact is made with the wall of the stom-
ach and the TG midpapillary short-axis view is obtained. The key structures to visualize are the left

A3 P3
P2
A2
P1
A1 Mitral valve
FIGURE 2.18 Transgastric basal short-axis view.
ventricular walls and cavity in addition to the posteromedial and anterolateral papillary muscles. A true
short-axis cross section of the left ventricle is confirmed when the two papillary muscles are approxi-
mately of equal size. Fine-tuning this image may be challenging and is done in two phases. In the first
phase, the depth of the probe is altered, and in the second phase, the degree of flexion is adjusted. The
proper depth of the probe is obtained by focusing on the posteromedial papillary muscle, which is the
papillary muscle closest to the apex of the scan. If chordae tendineae are visible, the probe is too high
and should be advanced. If no papillary muscle is visible, most often the probe is too low and should be
withdrawn. Once the depth of the probe is appropriate, the flexion is adjusted to bring the anterolateral
papillary muscle to the correct position. If any of the anterolateral chordae tendineae is visible, the probe
is excessively anteflexed, and relaxation of the large wheel on the probe handle should bring the papillary
muscle to the correct position.
The primary diagnostic goals of this view are assessment of left ventricular systolic function, left
ventricular volume, and regional wall motion. Turning the probe rightward visualizes the right ventricle
(Fig. 2.19, Video 2.12). Video 2.12

Inferior wall, LV
Posterior
papillary
muscle
Lateral
wall, LV
Left Anterior
Right papillary
ventricle
ventricle muscle
Interventricular Anterior wall, LV

septum
FIGURE 2.19 A: Transgastric (TG) midpapillary short-axis view. B: Anatomic representation of a TG midshort-axis
view. (B from Patrick J. Lynch; illustrator; C. Carl Jaffe; MD; cardiologist Yale University Center for Advanced Instructional

Left atrium
Left ventricle
Mitral valve
Anterior wall of
left ventricle
FIGURE 2.20 Transgastric two-chamber view.
Transgastric Two-chamber View

After completion of the TG midshort-axis view, the imaging angle is rotated to approximately 90 degrees
and the TG two-chamber view is obtained; this provides a long-axis view of the left ventricle, with the apex
to the left of the display and the mitral valve to the right. The primary diagnostic goal of this view is analysis
of regional wall motion. This is the preferred view for evaluation of the support structures of the mitral
valve because they lie perpendicular to the ultrasound beam (Fig. 2.20, Video 2.13). Video 2.13
Transgastric Long-axis View

From the TG two-chamber view the probe is rotated to approximately 120 degrees. The left ventricu-
lar outflow tract and the aortic valve should come into view at the 4 o’clock position. This view is

Left ventricle Aortic valve
LVOT
RVOT Ascending
aorta
FIGURE 2.21 Transgastric long-axis view.
especially helpful in the spectral Doppler interrogation of the aortic valve and left ventricular outflow
Video 2.14 tract (Fig. 2.21, Video 2.14).
Transgastric Right Ventricular Inflow View

From the TG long axis, the probe is turned toward the patient’s right (clockwise) until the TG right ventricu-
lar inflow view is seen. This view is helpful in evaluating right ventricular wall thickening and tricuspid valve
pathology (Fig. 2.22). This is the one TG view where the left ventricle is not at the apex of the imaging sector.
Deep Transgastric Long-axis View

The probe is then rotated back to 0 degrees, advanced toward the left ventricular apex, then maximally
anteflexed and slightly withdrawn to obtain the deep gastric long-axis view. Leftward flexion of the probe is
often required. This view allows spectral Doppler interrogation of the outflow tract and aortic valves. Probe
Video 2.15 rotation may be necessary to optimize the Doppler interrogation angle (Fig. 2.23, Video 2.15).

Right
ventricle
Right atrium
Tricuspid valve
FIGURE 2.22 Transgastric right ventricular inflow view.
Aortic Examination
Descending Aorta Short-axis View
After completion of the evaluation of the ventricles, the probe is rotated to 0 degrees and the probe shaft
is turned to the patient’s left and slightly withdrawn until a transverse view of the descending aorta is
obtained (the descending aorta short-axis view). Key factors in imaging the aorta are its small size and its
proximity to the TEE probe head in the esophagus. Consequently, the following maneuvers are necessary
to optimize aortic imaging. First, the image depth is reduced to enlarge the displayed aortic image. Sec-
ond, the time gain compensation in the near field may have to be increased because it is often set at low
levels during the cardiac examination. Finally, the frequency of the transducer can be increased to enhance
resolution. In the author’s experience these changes in the settings have allowed the visualization of aortic
atheromas that were not evident before the adjustments were made. The aorta is then examined along its
course as the probe is slowly withdrawn. When the aorta begins to appear elongated, the probe has reached
the level of the aortic arch (Fig. 2.24, Video 2.16). Video 2.16

Left ventricle
LVOT
Aortic valve
Ascending aorta
FIGURE 2.23 Deep transgastric long-axis view.
Upper Esophageal Aortic Arch Long-axis View

At the level of the arch, the probe is turned rightward to visualize the distal ascending aorta and arch in
long axis. This view is often useful in evaluating the distal ascending aorta, especially for the presence of
Video 2.17 calcification and/or atheroma at the cannulation site (Fig. 2.25, Video 2.17).
Upper Esophageal Aortic Arch Short-axis View

The imaging angle is then turned to 90 degrees to obtain the upper esophageal aortic arch short-axis view.
Small left and right turns of the probe shaft will allow you to interrogate the arch for calcification, enlarge-
ment, and foreign bodies. You may see the origins of the great vessels at approximately 3 o’clock in the short
axis of the aortic arch. The innominate vein and the origin of the left subclavian artery are visualized in
this view. The pulmonary artery lies parallel to the imaging beam affording excellent Doppler interrogation
Video 2.18 (Fig. 2.26, Video 2.18).

Descending
aorta
Left lung
FIGURE 2.24 A: Descending aorta short-axis view. B: Anatomic representation of Descending aorta short-axis view.
(From Patrick J. Lynch; illustrator; C. Carl Jaffe; MD; cardiologist Yale University Center for Advanced Instructional

Aortic arch
FIGURE 2.25 Upper esophageal aortic arch long-axis view.
Descending Aorta Long-axis View

After completion of the aortic arch views, the probe is slowly advanced to obtain the longitudinal view of
the descending aorta (the descending aorta long-axis view). As the probe is advanced, small left and right
Video 2.16 turns of the probe permit better interrogation of the aortic walls (Fig. 2.27, Video 2.16).
AN ABBREVIATED EXAMINATION
The operating room is often a busy, hectic environment. Anesthesiologists are constantly multitasking
and often responsible for, not only the management of the anesthetic, but the simultaneous performance
and interpretation of the echocardiogram. A comprehensive examination may not be practical or indi-
cated in this environment especially during circumstances of hemodynamic instability. In such cases an

Aortic arch
Pulmonary artery
Innominate vein
Pulmonary
valve
FIGURE 2.26 Upper esophageal aortic arch short-axis view.
abbreviated or focused examination is more appropriate. An example sequence is found in Figure 2.28.
This examination can be completed in 3 to 5 minutes and focuses on pathologic conditions that require
immediate therapy. All chambers and valves (except pulmonic) are viewed in at least two planes. On the
basis of the findings, specific pathology can be further evaluated using additional two-dimensional and
Doppler techniques. In the intraoperative and critical care settings the abbreviated examination plays an
important role.
SUMMARY
Mastering the two-dimensional echocardiographic examination requires an understanding of the imaging
planes and practical experience. No two patients’ anatomy is identical and the images obtained in clini-
cal practice vary from the textbook examples. Some TEE views cannot be obtained in certain patients. A

Descending aorta
FIGURE 2.27 Descending aorta long-axis view.
common setback is disorientation with the displayed images. To recover your anatomic orientation, it is
often best to return the imaging plane to 0 degrees because many structures are more easily identified from
the transverse plane. Next, identify the structure at the apex of the scan. This structure will be one of the
great vessels (most often the aorta), the left atrium, or the left ventricle. Next, advance or withdraw the
probe until you can identify a major structure in the view (e.g., aortic valve). Finally, with the known struc-
tures in view, rotate the imaging plane. In this way, an unknown structure can be identified by its associa-
tion with the neighboring anatomy.
This chapter has described a stepwise approach to ensure an efficient yet systematic examination of the
pertinent anatomy. Whether performing an abbreviated or comprehensive examination a definable and
reproducible sequence should be followed. The habit of jumping around leads to the all too common error
of omitting views and missing clinically important and unrecognized abnormalities.

1. ME AV SAX 2. ME RV 3. ME RV Inflow-outflow
Inflow-outflow w/CFD of PV
~40 to 60 degrees ~60 to 80 degrees ~60 to 80 degrees
4. ME AV LAX 5. ME AV LAX w/ CFD of AV 6. ME Bicaval
~110 to 140 degrees ~110 to 140 degrees ~110degrees
7. ME 4C 8. ME 4C w/ CFD of MV 9. ME 4C w/ CFD of TV
~0 to 10 degrees ~0 to 10 degrees ~0 to 10 degrees
10. ME 2C 11. TG Mid SAX 12. TG 2C
~90 degrees ~0 degrees ~90 degrees
13. Desc aorta SAX 14. UE Aortic arch SAX 15. Desc aorta LAX
~0 degrees ~90 degrees ~90 degrees
FIGURE 2.28 The author’s recommended basic transesophageal echocardiography cardiac examination. ME, mid-
esophageal; AV, aortic valve; CFD, color flow Doppler; TV, tricuspid valve; RV, right ventricular; I-O, inflow–outflow; PV,
pulmonary valve; TG, transgastric; SAX, short-axis; LAX, long-axis; Desc, descending; 2C, two-chamber; 4C, four-chamber.
(Modified from Miller JP, Lambert AS, Shapiro WA, et al. The adequacy of basic intraoperative transesophageal echocar-
diography performed by experienced anesthesiologists. Anesth Analg. 2001;92:1103–1110, with permission.)

REFERENCES
1. Sheikh KH, De Bruijn NP, Rankin JS, et al. The utility of transesophageal echocardiography and Doppler color flow imaging in
patients undergoing cardiac valve surgery. J Am Coll Cardiol. 1990;15:363–372.
2. Sheikh KH, Bengtson JR, Rankin JS, et al. Intraoperative transesophageal Doppler color flow imaging used to guide patient
selection and operative treatment of ischemic mitral regurgitation. Circulation. 1991;84:594–604.
3. Stevenson JG. Adherence to physician training guidelines for pediatric transesophageal echocardiography affects the outcome
of patients undergoing repair of congenital cardiac defects. J Am Soc Echocardiogr. 1999;12:165–172.
4. Ungerleider RM, Kisslo JA, Greeley WJ, et al. Intraoperative echocardiography during congenital heart operations: Experience
from 1,000 cases. Ann Thorac Surg. 1995;60(6 suppl):S539–S542.
5. Savage RM, Lytle BW, Aronson S, et al. Intraoperative echocardiography is indicated in high-risk coronary artery bypass graft-
ing. Ann Thorac Surg. 1997;64:368–374.
6. American Society of Anesthesiologists. Practice guidelines for perioperative transesophageal echocardiography. A report by
the American Society of Anesthesiologists and the Society of Cardiovascular Anesthesiologists Task Force on Transesophageal
Echocardiography. Anesthesiology. 1996;84:986–1006.
7. 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
Perioperative Transesophageal Echocardiography. Anesth Analg. 1999;89:870–884.

QUESTIONS
1. Using the described standard 8. Which of the following views is not useful
nomenclature, which of the following for accessing pathology of the tricuspid
commands will move the center of the valve?
imaging sector toward the patient’s left? a. ME RV inflow–outflow
a. Anteflex–retroflex b. TG RV inflow
b. Forward rotation c. ME four-chamber
c. Turning d. ME two-chamber
d. Backward rotation
9. When standard orientation and terminology
2. If the imaging plane is set at 45 degrees, the is used, at 180 degrees, the image seen on
viewed cross section will run from: the right side of the display is:
a. Left shoulder to right hip a. On the patient’s left
b. Right shoulder to left hip b. On the patient’s right
c. Left side to right side c. Cephalad
d. Right side to left side d. Caudad
3. Which of the following structures cannot 10. Diagnostic uses of the TG basal short-axis
be seen at the apex of the imaging sector view include:
during a TEE examination? a. Assessment of mitral valve pathology
a. Aorta b. Assessment of papillary muscle function
b. Left atrium c. Assessment of apical LV regional wall motion
c. Left ventricle d. Assessment of mid LV regional wall motion
d. Right ventricle
11. When measuring thickness of the anterior
e. None of the above
wall of the left ventricle, which view will
4. Which view is necessary to identify the give you the best resolution?
specific cusp pathology of the aortic valve? a. TG Mid SAX
a. ME AV short axis b. ME four-chamber
b. ME AV long axis c. ME two-chamber
c. ME ascending aortic short axis d. TG RV inflow
d. ME ascending aortic long axis
12. Diagnostic uses of the UE aortic arch long
5. Measuring the AV annulus size is most axis include all of the following EXCEPT:
easily done in which imaging view? a. Evaluation for aortic atherosclerosis
a. ME AV short axis b. Evaluation for aortic dissection
b. ME AV long axis c. Inspection of aortic cannulation sight
c. ME ascending aortic short axis d. Evaluation of intra-aortic balloon pump
d. ME ascending aortic long axis placement
6. The tip of a correctly positioned intra-aortic 13. The origin of the pulmonary veins may be
balloon pump should be visible in which of seen in all of the views EXCEPT:
the following views? a. ME midshort axis
a. ME descending aortic long axis b. ME AV short axis
b. UE aortic arch short axis c. ME two-chamber
c. UE aortic arch long axis d. ME bicaval
d. UE ascending aorta short axis
14. The large and small knobs on the TEE probe
7. Which views are helpful in placing and/or control are:
determining the position of a pulmonary a. Anteflexion/retroflexion and left/right flex-
artery catheter? ion
a. ME bicaval b. Anteflexion/retroflexion and image rota-
b. ME RV inflow–outflow tion
c. ME ascending aortic short axis c. Left/right flexion and image rotation
d. ME ascending aortic long axis d. Image rotation and probe depth
e. All of the above

15. Which of the following views is useful for 18. Thrombus in the left atrial appendage is
placement of femoral cannula prior to the best seen in which view?
initiation of CPB? a. ME bicaval
a. ME bicaval b. ME two-chamber
b. ME four-chamber c. TG two-chamber
c. ME two-chamber d. ME four-chamber
d. TG midshort axis
19. Which of the following views are not useful
16. Which of the following views is useful for for spectral Doppler interrogation of the
the evaluation of pulmonary pathology in aortic valve?
an adult patient with a prior tetralogy of a. ME AV long axis
Fallot repair? b. TG long axis
a. ME RV inflow–outflow c. Deep TG long axis
b. UE aortic arch short axis
20. Left ventricular papillary muscles are
c. TG RV inflow
visible in each of the following views
d. a and b
EXCEPT:
17. Increasing the near-field time gain a. TG basal short axis
compensation may be necessary when b. TG midshort axis
evaluating all of the following EXCEPT: c. TG two-chamber
a. Aorta d. ME four-chamber
b. Left atrium
c. Left ventricle
d. Mitral valve

3 Left Ventricular Systolic Performance
and Pathology
Shahnaz Punjani and Susan Garwood
OF ALL THE INDICATIONS FOR echocardiography, the evaluation of left ventricular (LV) systolic func-
tion is perhaps the most common; in part because it is not only the best understood parameter of cardiac
function but also because it has consistently been shown to be a predictor of morbidity and mortality. Left
ventricular systolic performance is usually assessed in practically every echocardiogram, even if it is not
the primary focus of the examination. The American Society of Echocardiography (ASE) recommends
that every complete echocardiographic examination should include the evaluation of LV chamber size and
function and emphasizes the importance of these measurements for clinical decision making (1).
WHAT IS LEFT VENTRICULAR SYSTOLIC FUNCTION?

LV systolic function describes the contractility of the LV. Contractility of the myocardial fibers of the heart
is described by the Frank–Starling relationship whereby increases in preload (left ventricular end diastolic
pressure [LVEDP]) result in increased contractility. Therefore, contractility or systolic function is load
dependent and strictly speaking, should be assessed over a range of preload and afterload. This is not usu-
ally clinically feasible and true load-independent assessments of LV systolic function are difficult using
echocardiography. Consequently, the preload status at the time of the examination is frequently reported
along with the systolic function as the LV chamber dimension either as a diameter, area, or volume. LV
thickness or mass is also usually reported with systolic function and LV chamber size to complement the
overall estimate of LV systolic performance.
Quantitative Measures of Left Ventricular Systolic Performance

LV systolic performance may be assessed qualitatively or quantitatively with echocardiography. There are
a number of parameters which describe LV systolic function, the most commonly used being ejection
fraction. Ejection fraction is expressed mathematically as a fraction of a diastolic dimension minus the cor-
responding systolic dimension divided by the original diastolic dimension, where this dimension can be a
linear measurement, an area, or a volume. For example:
{(LVEDV – LVESV)/LVEDV} × 100%
where LVEDV is LV end diastolic volume and LVESV is LV end systolic volume. A normal ejection fraction
is equal to or greater than 55% for both men and women.
An echocardiographer may become quite efficient and accurate at visually estimating left ventricu-
lar ejection fraction (LVEF). However, accuracy and reproducibility are dependent upon the individual
interpreter’s skill and interobserver measurements may vary considerably. Consequently, calibrated mea-
surements are preferred, and the ASE recommends that even experienced echocardiographers regularly
cross-check qualitative evaluations against calibrated measurements (1).
Quantitative Evaluation of Left Ventricular Systolic Function—Linear Measurements

Linear measurements (whether made from motion mode [M-mode] or two-dimensional [2D] images) have
the lowest interobserver variability as compared to area or volume measurements, render quite accurate
estimates of systolic function in healthy subjects, but are probably the least representative of overall LV sys-
tolic function in cardiac diseases that produce regional abnormalities of the myocardium. Linear measure-
ments are preferably made from M-mode tracings, because the higher pulse rate compared to 2D provides
better temporal resolution. 51

Endocardial Fractional Shortening
Endocardial fractional shortening (%) = {(LVIDd − LVIDs)/LVIDd} × 100

Normal values: Men 25% to 43%, women 27% to 45% (1).
The measurements required for this quantitative estimate of systolic function are LV internal diameter
at end diastole (LVIDd, also called end diastolic diameter LVEDD) and LV internal diameter at end systole
(LVIDs, also called end systolic diameter LVESD). These are measured from endocardial border to endocar-
dial border (known as leading edge to leading edge) (2) from an M-mode tracing of a transgastric short-axis
(TG SAX) view taken just above the papillary muscles (Fig. 3.1).
Endocardial fractional
shortening
Distance 0.79 cm = LVIDs

Distance 2.50 cm = LVIDd
FIGURE 3.1 A: Transgastric mid short-axis view demonstrating M-mode measurements of ventricular cavity dimen-
sions in systole and diastole using the leading edge to leading edge technique. LVIDd, left ventricular internal diameter
at end diastole; LVIDs, left ventricular internal diameter at end systole; LV, left ventricular. B: Measurements made for the
calculation of endocardial fractional shortening may also be used to calculate end diastolic volume, end systolic volume,
and ejection fraction using the Cubed (Teichholz) formula.

3. Left Ventricular Systolic Performance and Pathology 53
Although fractional shortening gives a rapid and simple estimate of LV systolic function, it is not a
representative measurement in asymmetric ventricles such as those with regional wall abnormalities or
aneurysmal deformation (1).
Left Ventricular Wall Thickness

Normal values: Men 0.6 to 1 cm, women 0.6 to 0.9 cm (1).
Measurements of LV wall thickness are made using the TG mid-SAX view. Usually both septal wall
thickness at end diastole (SWTd) and posterior wall thickness at end diastole (PWTd) are reported.
Septal wall thickness is measured from the right septal surface to the left septal surface, whereas pos-
terior wall thickness is measured from epicardial surface to endocardial surface (being careful not to
include pericardial tissue), using leading edge methodology for M-mode (2) and trailing edge to leading
edge for 2D (1).
Relative Wall Thickness
Relative wall thickness (RWT) mm = (2 × PWTd)/LVIDd or (PWTd + SWTd)/LVIDd.

Normal values: Men 0.24 to 0.42 cm, women 0.22 to 0.42 cm (1).
Relative wall thickness (RWT) is often used in patients with LV hypertrophy. In transesophageal echo-
cardiography (TEE), the measurements are usually made in a TG SAX (just above the papillary muscles)
and may be calculated from either of the two formulae given earlier. RWT is expressed as a decimal and
used to describe LV hypertrophy and remodeling. An RWT equal to or greater than 0.42 denotes con-
centric hypertrophy (wall thickness is increased in the presence of a normal internal diameter) and an
RWT less than 0.42 denotes eccentric hypertrophy (dilated internal ventricular dimension). The distinction
between the two forms of hypertrophy is of prognostic interest, as concentric hypertrophy is associated
with a higher incidence of cardiovascular events than eccentric hypertrophy.
Quantitative Evaluation of Left Ventricular Systolic Function—Planimetric Measurements

Area measurements offer improvements in accuracy over linear dimensions, as more of the LV is repre-
sented in the measurement.
Fractional Area Change
Fractional area change (FAC) (%) = {(LVAd − LVAs)/LVAd} × 100

Normal values: Men 56% to 62%, women 59% to 65% (3).
The area of the LV cavity is measured at end systole (LVAs) and at end diastole (LVAd) and used to cal-
culate fractional area change (FAC). Most commonly these measurements are made from the TG mid-SAX
view of the LV, but when this view is suboptimal long-axis views can be substituted. The endocardium is
manually traced around the LV cavity ignoring the papillary muscles.
Alternatively, automated border detection obviates the need to manually trace cavity area and provides
real time, beat-to-beat measures of LVAd, LVAs, and FAC (Fig. 3.2). The acoustic properties of tissue and
blood are discriminated because they create significantly different backscatter and thereby signal strength,
allowing for automated detection of the endocardial border. A software package computes and displays the
area of the LV (blood pool) cavity, superimposes it upon a 2D display of the ventricle and calculates the FAC
on a beat-to-beat basis in the TG mid-SAX view. The echocardiographer adjusts the time-compensated
gain, lateral gain, and overall gain settings to ensure that the displayed automated border tracks the endo-
cardium throughout the cardiac cycle. For example, attenuation (or dropout) caused by the relative parallel
orientation of myocardial fibers in the septal and lateral walls to the ultrasound beam in the SAX view
decreases backscatter and therefore signal strength. Accordingly, adjustments to the lateral gain compen-
sation are used to enhance receiver gain in these areas and allow for better tracking of the borders by the
software.

FIGURE 3.2 Transgastric mid short-axis view demonstrating automated border detection measurement (red line) of
fractional area of change (lower panel ). AQ, acoustic quantification; EDA, end diastolic area; ESA, end systolic area; FAC,
fractional area of change.
Quantitative Evaluation of Left Ventricular Systolic Function—Left Ventricular Volumes

LV volumes measured at end systole and end diastole are used to calculate ejection fraction. However, LV
systolic volumes in and of themselves have prognostic value. Values greater than 70 mL are associated with
increased risk for morbidity and mortality.
Left Ventricular Volume, Volumetric Equations Using Linear Measurements
There are a number of formulae in use which derive a three-dimensional (3D) LV volume from linear mea-
surements. These are based on geometric models, which approximate the shape of a symmetric LV.
The Cubed formula (Teichholz method)
Cubed formula:
LV volume (mL) = (LVIDminor)3
This formula assumes that the LV is approximated by a prolate ellipse, which has an SAX (minor axis,
LVIDminor) equal to one-half of the long axis (or major axis, LVIDmajor) (Fig. 3.3). Measurement of the minor
axis can be performed in the midesophageal (ME) two- or four-chamber or the TG two-chamber view and
are taken at the mitral chordae level (1). Although the cube formula is the simplest formula, it compounds
measurement errors because of the cube function and overestimates the volume of dilated ventricles. This
occurs because the LV dilates primarily along the SAX, becoming more spherical in shape.
Volumetric Equations Using Planimetric Measurements

Again, these formulae are derived from geometric models which approximate a symmetrically shaped LV.
1. Single plane ellipsoid
Single plane ellipsoid method:
LV volume (mL) = 8 × (LVALAX)2/3πLVIDmajor
The LV volume is calculated assuming an ellipsoid shape. The long-axis diameter (LVIDmajor) and corre-
sponding LV cavity area (LVALAX) obtained from a single long-axis view (ME four- or two-chamber, or TG two-
chamber) are required for this formula (Fig. 3.4). The basal border of the LV cavity area is best delineated by
a straight line connecting the mitral valve (MV) insertions at the lateral and septal borders of the annulus (1).

FIGURE 3.3 Midesophageal four-chamber demonstrating left ventricle (LV) as a prolate ellipse, which has a short axis
(left ventricular internal diameter minor axis [LVIDminor]) equal to one-half of the long axis (or major axis LVIDmajor). The
minor axis is used for the cubed formula. LA, left atrium; RV, right ventricle; LVID, left ventricle internal diameter.
2. Biplane ellipsoid
Biplane ellipsoid method:
LV volume (mL) = (πLVIDmajor/6) × (4LVASAX/πLVIDminor) × (4LVALAX/πLVIDmajor)
This model incorporates the LV major axis diameter, LVIDmajor (acquired from an ME two- or four-
chamber view or TG two-chamber view, which are all long-axis views) and the LV cavity area from the same
image (LVALAX); plus the LV minor axis diameter (LVIDminor) acquired from the TG SAX of the LV view just
above the papillary muscles; plus the corresponding LV cavity area from the same image (LVASAX).
3. Hemisphere–cylinder or bullet formula
Hemisphere–cylinder (or bullet formula):
LV volume (mL) = 5/6 × LVASAX × LVIDmajor
FIGURE 3.4 Midesophageal two-chamber demonstrating the measurements required for single-plane ellipsoid for-
mula; a long-axis diameter (LVIDmajor) and the left ventricle (LV) area from the same long-axis view (LVALAX).·LA, left atrium;
RA, right atrium; RV, right ventricle.

Cylinder Hemisphere
(LV body) (LV apex)
1/2 LVID 1/2 LVID
LVASAX
FIGURE 3.5 Demonstrates how the geometry of a cylinder plus a hemisphere approximates the left ventricle (LV) as
a bullet. The length of the cylinder and the radius of the hemisphere are both equal to one-half of the left ventricular
internal diameter major axis (LVIDmajor). LVASAX, left ventricle area from the short-axis view.
This model approximates the LV to the shape of a bullet (Fig. 3.5). Volume is calculated from a long-
axis diameter (LVIDmajor) and the LV cavity area from the TG mid-SAX view (LVA SAX). This formula is also
known as the area length formula.
4. Method of disks (modified Simpson’s rule)
Modified Simpson’s rule:
LV volume (mL) = (π/4)∑(n=1−20)(LVIDnminor(ME 2 chamber) × LVIDnmnior(ME 4 chamber)) × LVIDmajor/20
In this method, the LV is described as a series of 20 disks from the base to the apex of the LV, like a stack
of coins of decreasing size. The views required for this calculation are ME four- (Fig. 3.6) and two-chamber
views. The computer software package calculates the volume of each disk as area × height and the volumes are
summated to give a total LV volume. Foreshortening of the LV will result in underestimation of volume (1).
Since biplane planimetry (area acquired using both the ME four- and two-chamber views) corrects
for shape distortion and minimizes mathematical assumptions, the method of disks is the recommended
technique for volumetric measurements of the LV, particularly in those patients with regional wall motion
abnormalities or an aneurysm (1). In cases where the endocardial border of the apex is not well seen, the
area length method becomes the method of choice (1). Since it assumes a bullet-shaped LV, the area length
method compensates for the inability to detect the apical endocardial borders.
Quantitative Evaluation of Left Ventricular Systolic Function—Left Ventricular Mass;

Linear Measurements
All LV mass calculations are based on the subtraction of the volume of the LV cavity from the vol-
ume encompassed by the LV epicardium. This leaves LV myocardial volume, which is then multiplied
FIGURE 3.6 Midesophageal (ME) four-chamber views demonstrating the left ventricle (LV) measurements required
for the method of disks (modified Simpson’s rule) to estimate LVEF. A: ME four-chamber view at end diastole; the endo-
cardium is manually traced and the software calculates the LVIDmajor and divides the LV cavity into 20 discs. B: ME four-
chamber view at end systole; the same measurements are made as in part A. These measurements are also required in
the ME two-chamber view. Note that there should be less than a 10% discrepancy between the long-axis measurement
of the ME four-chamber view in systole and the ME two-chamber view in systole (similarly in diastole). This ensures
against foreshortening in one of the views. LA, left atrium; RV, right ventricle; EDV, end diastolic volume; ESV, end systolic
volume; EF, ejection fraction. C: Three-dimensional echocardiography (3DE) may also be used for the calculation of left
ventricular volumes, mass, and ejection fraction. The two views required (midesophageal two-chamber and midesopha-
geal four-chamber) are generated simultaneously so that there will be no discrepancy between long-axis measurements.


TABLE 3.1 Normal Values for Echocardiographic Left Ventricular Systolic Parameters Published by the
American Society of Echocardiography (ASE)
Posterior wall thickness (mm) ɉ 6–10 Ɋ 6–9

Septal wall thickness (mm) ɉ 6–10 Ɋ 6–9
LV end systolic volume (mL) ɉ 22–58 Ɋ 19–49
LV end systolic volume/BSA (mL/m2) ɉ 12–30 Ɋ 12–30
LV mass (g) ɉ 88–244 Ɋ 67–162
LV, left ventricular; ɉ, men; Ɋ, women; BSA, body surface area.
Adapted from: Lang RM, Bierig M, Devereux RB, et al. Recommendations for chamber quantification: A report from the
American Society of Echocardiography’s Guidelines and Standards Committee and the Chamber Quantification Writing Group,
developed in conjunction with the European Association of Echocardiography, a branch of the European Society of Cardiology.
J Am Soc Echocardiogr. 2005;18(12):1440–1463.
by the density of myocardial tissue to calculate LV mass. The ASE recommends the following
formula:
LV mass (g) = 0.8[1.04{(LVIDmajor + PWT + SWT)3 − (LVIDmajor)3}] + 0.6 g
Increased LV mass is a stronger predictor than low ejection fraction (EF) for all-cause mortality and
cardiac event rates in both hypertensive and normotensive populations. Since LV mass increases as a func-
tion of body size (except those with morbid obesity), LV mass is preferably expressed as a function of body
surface area (BSA) (1). Normal values for LV mass are given as 67 to 162 g for women and 88 to 224 g for
men. Indexed to BSA this becomes 43 to 95 g/m2 for women and 49 to 115 g/m2 for men (1) (Table 3.1). LV
mass may be combined with RWT to categorize patients into various classes of hypertrophy (1) (see the
following section on “Left Ventricular Hypertrophy”).
Quantitative Evaluation of Left Ventricular Systolic Function—Left

Ventricular Mass, Planimetric Measurements
In the determination of LV mass using planimetric measurements, either the area length method or
the truncated ellipsoid method are recommended (1,4). Most current echocardiography machines
include the software to calculate LV mass by one or both of these two methods. The LV is acquired in
the TG mid-SAX view. An area tracing is made of the epicardial and endocardial borders. The difference
between the two areas is the area occupied by the myocardium. A major axis length is then acquired
from a long-axis view and the software calculates the mass of the LV according to the formulae used by
the vendor (1,4) (Fig. 3.7).
Quantitative Evaluation of Left Ventricular Systolic

Function—Rate of Ventricular Pressure Rise
The rate of rise in ventricular pressure (dP/dT) has been demonstrated to be well correlated with systolic
function. The greater the contractile force exerted, the greater the rise in ventricular pressure. Previously,
this could only be measured invasively with LV catheterization; however, continuous wave Doppler (CWD)
determination of the velocity of a mitral regurgitant (MR) jet allows calculation of instantaneous pressure
gradients between the left ventricle and the left atrium (LA). Left atrial pressure variations in early systole can
be considered to be negligible; therefore, the rising segment of the MR velocity curve during isovolumetric
contraction should essentially reflect LV pressure increase only. If the rate of rise in ventricular pressure is
reduced because of poor LV function, the rate of increase of the MR jet velocity will also be low.
To perform a dP/dT measurement (Fig. 3.8), the MR jet is interrogated with CWD. The cursor is
placed on the MR velocity profile at 1 m/s and then at 3 m/s and the time interval between the two points
is determined (5). Using the simplified Bernoulli equation, the pressure differential is [4(3)2] − [4(1)2] or
32 mm Hg. dP/dT is therefore 32 mm Hg divided by the time interval in seconds. Normal values exceed
1,000 mm Hg/s.

LVID major from

ME two- or four-chamber
TG mid-SAX
Area described Area described

by epicardium by endocardium
A
LVAd Endocardial 7.66 cm 2

LVAd Epicardial 27.40 cm 2
B LV mass 144 g
FIGURE 3.7 Left ventricular (LV) mass calculation. A: Diagram representing the views and measurements required for
planimetric LV mass calculation. B: The endocardium and epicardium are traced in the transgastric mid short-axis view
and the software calculates LV mass using left ventricular internal diameter major axis (LVIDmajor) (from a long-axis view as
in part A) and density of myocardial tissue. LVAd, area of left ventricular cavity measured at end systole.
Newer Echocardiographic Modalities for Assessing Left Ventricular Systolic Function

Three-dimensional Echocardiography
The advent of three-dimensional echocardiography (3DE) has revolutionized the acquisition and under-
standing of echocardiographic data. Currently there are two methods of acquiring 3DE images. One tech-
nique utilizes a set of 2D images which are then used to reconstruct the 3D image. This method requires
an “offline” reconstruction. Limitations of this form of 3DE include time for reconstruction and the need
for a regular cardiac rhythm during the acquisition period. The second technique employs a matrix array
transducer, which scans a pyramidal-shaped sector and displays the image in real time. Using this technol-
ogy, 3DE images of the LV can be acquired over one beat and displayed in real time (6).
The advantage of 3DE for measuring LV volumes and masses is that the LV can be acquired and dis-
played in its true shape avoiding the need for mathematical modeling. This means that regional function
can be included in the overall estimates, producing a more accurate measurement (Fig. 3.9, Video 3.1). Video 3.1
Furthermore, inaccuracies do not occur because of plane positioning errors and foreshortening. Three-
dimensional echocardiography is highly correlated with the gold standard of imaging (magnetic resonance
imaging [MRI]), producing a better agreement with lower inter- and intraobserver variations than 2DE in
normal subjects (7) and patients with regional wall motion abnormalities (8).

0
MR
1 m/s
2
3 m/s
m/s
4
Δ t (ms)
AO 100
LA + 36 mm Hg 80
60
mm Hg
LA + 4 mm Hg
40
A V 20
LA
LV X
Y 0
36 – 4 mm Hg
Δ p/Δ t =
B Δ t (ms)
FIGURE 3.8 A: Calculation of dP/dT. Place caliper on mitral regurgitant (MR) jet envelope at 1 m/s and again at 3 m/s to
measure the time for the instantaneous pressure gradient between the left ventricle (LV) and left atrium (LA) to rise from
4 mm Hg to 36 mm Hg. B: Upper panel—electrocardiography (ECG); middle panel—Doppler trace of MR jet (acquired
from transthoracic approach); lower panel—equivalent pressure recordings at catheterization. CWD, continuous wave
Doppler. (Part B from Pai RG, Bansal RC, Shah PM. Doppler-derived rate of left ventricular pressure rise. Its correlation with
the postoperative left ventricular function in mitral regurgitation. Circulation. 1990;82(2):514–520.)
Visual display of 3D systolic performance varies from vendor to vendor. The LV may be displayed as raw
images, a wire framework, or a reconstructed volumetric figure in which the walls of the LV can be visual-
Video 3.1 ized according to the American Heart Association (AHA)/ASE 17-segment model (Fig. 3.9, Video 3.1). The
contribution of each segment to volume and mass can be displayed as individual waveforms enabling an
assessment of global and regional performance from one image. Data can also be displayed as color-coded

FIGURE 3.9 A: Three-dimensional (3DE) echocardiography. Top panels: Midesophageal (ME) four- and two-chamber
views. Middle panels: Transgastric short-axis view and AHA/ASE 17-segment volumetric model. Bottom panel: Individual
segment contribution to overall left ventricular volume throughout the cardiac cycle. B: Mapping data from 3DE of left
ventricle with an anterior aneurysm. Upper panel: Timing of onset of contraction related to the mean value which is
depicted in green. Red denotes delayed contraction, blue denotes early contraction. Middle panel: Excursion of indi-
vidual segments toward the center of the left ventricle (LV). Blue denotes movement toward the center, black denotes
no movement (akinesia), and red denotes movement away from the center (dyskinesia). Color brightness denotes extent
of movement. Lower panel: Individual segment contribution to LV volume. See Figure 3.9(A) for color coding of the indi-
vidual segments. See also Video 3.1. Video 3.1

representations of regional LV segmental excursions superimposed on the standard “bull’s eye” display (Fig.
3.9B) assisting visualization of regional function.
Tissue Doppler Imaging

The high temporal resolution of Doppler imaging is specifically suited to the accurate measurement of veloc-
ities at precise locations in the heart. When Doppler is used in its original application to measure blood flow,
high-pass filters are employed to screen out the low velocities from the myocardium, valvular structures, and
vessel walls. In contrast, tissue Doppler imaging (TDI or tissue Doppler echocardiography, TDE) measures
the velocity of myocardial tissue using low-pass filters to screen out higher velocities generated by blood
flow. Unlike blood flow Doppler signals that are typified by high velocity and low amplitude, myocardial
motion is characterized by low velocity and high amplitude. Tissue motion creates Doppler shifts that are
approximately 40 dB higher than Doppler signals from blood flow and their velocities rarely exceed 20 cm/s.
To record low wall motion velocity, gain amplification is reduced and high-pass filters are bypassed.
During image acquisition, it is important to optimize temporal resolution by selecting as narrow
an image sector as possible, which increases frame rate (>150/s is recommended, Fig. 3.10). Equally
FIGURE 3.10 Tissue Doppler imaging (TDI). A: TDI of a midesophageal (ME) four-chamber view acquired as a full-sector
view; frame rate is 100 Hz. B: The same image is acquired but the sector is narrowed down to improve frame rates.
Note that frame rates have increased from 100 Hz to 223 Hz. LA, left atrium; RA, right atrium; MV, mitral valve; RV, right
ventricle; LV, left ventricle.

important is to select the appropriate velocity scale. These parameters should be optimized at the time of
imaging, as it is not possible to modify the frame rate and the velocity scale during postprocessing image
analysis.
In TDI, a small pulsed wave sampling volume measures the velocities of the myocardium as it moves
toward and away from the transducer. The sample volume is placed in the middle of a segment of the heart
and velocities within that area are measured. A velocity against time plot is displayed, using the convention
that tissue moving toward the transducer is positive. For example, during interrogation of the basal seg-
ment of the septum in the ME four-chamber view, as the heart contracts and thickens during systole the
atrioventricular ring moves toward the apex and thereby will move away from the transducer producing a
negative deflection.
Since this is a Doppler technique, TDI will underestimate the myocardial velocities if the angle of inter-
rogation is not parallel to motion (9). Although most ultrasound platforms allow for correction of the
Doppler equation for the angle of incidence, this is not recommended (7). Rather, it is recommended that
for an ME view, the wall to be interrogated is placed in the center of the imaging sector to better align the
angle of interrogation (Fig. 3.10).
Other errors encountered using TDI are caused by tethering as velocity imaging is confounded by
velocities from adjacent segments. For example, in an ME four-chamber view, an akinetic segment at the
basal part of the septum should by definition have a longitudinal systolic velocity of zero. However, if the
midventricular segment of the septal wall moves normally, the tethering effect will cause the akinetic basal
segment to move longitudinally.
In general, longitudinal measurements are made of the basal and midventricular segments, obtained
from the ME two- and four-chamber views. A gradient of systolic velocities exists from the base of the
heart to the apex. Peak systolic longitudinal velocities at the MV annulus (Sa) are greater compared to those
at the midventricular segments (Sm). Sm velocities are more representative of overall systolic function.
Annular velocities are difficult to acquire in patients with mitral annular calcification or with a prosthetic
valve or annuloplasty ring. Myocardial velocities are age and gender dependent (Table 3.2). From transtho-
racic studies, patients with normal global LV function have systolic velocities greater than 7.5 cm/s (10),
whereas velocities less than or equal to 5.5 cm/s indicate LV failure (11). Systolic velocities less than 3 cm/s
are associated with a significantly increased risk of cardiac death within 2 years (12). (Note that values are
positive because transthoracic measurements are acquired from the apex of the heart.)
The typical systolic TDI profile (Fig. 3.11) has two parts with a biphasic wave during isovolumic con-
traction (IVCa and IVCb) and a monophasic wave during systolic ejection. IVCa corresponds to the tim-
ing of the MV closure and represents early myocardial activation at the base of the heart, occurring 20 to
TABLE 3.2 Factors Affecting Tissue Doppler Imaging Velocity Measurements
Parameter Tissue Doppler velocities (cm/s)

Age differences in cardiac <65 years >65 years
Average Sa = 6.7 ± 1.8a Average Sa = 5.7 ± 1.7a
Gender differences in healthy Male Female
subjects with Sa lateral wall = 10.2 (9.6–11.0)b Sa lateral wall = 8.9 (8.4–9.5)b
mild hypertension
Point of interrogation i.e., Septum Lateral Posterior Anterior
longitudinal velocity Sa = 5.7 ± 1.6a Sa = 8.7 ± 2.4a Sa = 6.4 ± 1.1a Sa = 7.7 ± 2a
gradient (healthy subjects)
Sm = 4.3 ± 1.1a Sm = 7.9 ± 2.4a Sm = 5.4 ± 1.2a Sm = 6.3 ± 2.2a
Apex = 3.1 ± 1a Apex = 7.1 ± 2.4a Apex = 4.2 ± 1.4a Apex = 4.8 ± 2.5a
a
Mean ± standard deviation.
b
Mean (95% confidence intervals).
Sa, mitral annular systolic velocity; Sm, midventricular systolic velocity.
From: Bountioukos M, Schinkel AF, Bax JJ, et al. Pulsed-wave tissue Doppler quantification of systolic and diastolic function of
viable and nonviable myocardium in patients with ischemic cardiomyopathy. Am Heart J. 2004;148(6):1079–1084; Lim JG,
Shapiro EP, Vaidya D, et al. Sex differences in left ventricular function in older persons with mild hypertension. Am Heart J.
2005;150(5):934–940; Kowalski M, Kukulski T, Jamal F, et al. Can natural strain and strain rate quantify regional myocardial
deformation? A study in healthy subjects. Ultrasound Med Biol. 2001;27(8):1087–1097.

FIGURE 3.11 Typical left ventricle mitral annulus tissue Doppler imaging (TDI). LA, left atrium; RV, right ventricle; LV,
left ventricle; Ea, early diastolic peak tissue velocity; Aa, atrial contraction (late diastolic) tissue velocity; IVC, isovolu-
mic contraction; Sa, mitral annular systolic tissue velocity; IVCT, isovolumic contraction time; IVRT, isovolumic relaxation
time.
30 milliseconds earlier in the anteroseptal than the posterior free wall (13). The movement of the myo-
cardium at the annulus is inward and toward the apex. The second wave IVCb is in the opposite direction
caused by subsequent contraction of the apex making the base bulge up and outward just before ejection.
The monophasic systolic wave is directed inward and toward the apex and represents contraction of the
LV during ejection.
Color Tissue Doppler

In the same way that conventional Doppler can be color coded to provide a color map of blood flow pat-
terns, tissue Doppler can be color coded to display myocardial velocities, red depicting positive velocities
and blue for negative velocities. The display is of real-time 2D gray-scale images overlain by color-coded
myocardial velocities (Fig. 3.10).
Placing markers at various points along a ventricular wall produces a graphic representation of veloc-
ity against time called curved M-mode (Fig. 3.12). This form of color TDI combines spatial resolution with
high temporal resolution and can be displayed in real time. Color tissue Doppler measures mean velocities
and therefore has lower values for a given segment than tissue Doppler which measures peak instantaneous
velocities. The advantage of color tissue Doppler over tissue Doppler is the ability to utilize spatial infor-
mation and therefore assess regional and global LV function. The advantage of color tissue Doppler over
2D echocardiography is that the endocardial borders do not need to be clearly identified; dropout in walls
which lie parallel to the path of the ultrasound beam is no longer a limitation in assessing LV function.
Doppler Strain and Strain Rate

Doppler Strain (ε, change in length/original length or l/l0) and Doppler strain rate (SR) are an extrapolation
of TDI technology. Strain measures segmental myocardial deformation (or shape change) whereas SR mea-
sures the rate of this change. Strain is expressed as the percent change from the original dimension. Systolic
strain represents the magnitude of deformation between end diastole and end systole. SR measures the rate
of deformation of a tissue segment and is measured in s−1.
Deformation is the result of the complex interaction of intrinsic contractile force and extrinsic loading
conditions applied to a tissue with variable elastic properties. Changes in preload, afterload and myocardial
stiffness are important determinants of myocardial deformation. Therefore it follows that ε and SR are not
direct measures of contractility.
The use of ε and SR imaging overcomes some of the limitations inherent in using tissue Doppler veloc-
ity profiles because tissue Doppler myocardial velocities may be influenced by either global heart motion

FIGURE 3.12 Curved M-mode. Left lower panel: 2D midesophageal (ME) four-chamber showing placement of mark-
ers on lateral wall of left ventricle (LV). Left upper panel: tissue Doppler imaging ME four-chamber showing placement
of markers on lateral wall of LV. Right panel: Curved M-mode, displaying mean tissue velocities of the marked positions
(y-axis) against time (x-axis). MV, mitral valve; LA, left atrium; IVCT, Isovolumic contraction time; Sm, systolic tissue veloc-
ity; IVRT, isovolumic relaxation time; Em, early diastolic tissue velocity; Am, late diastolic tissue velocity. (From Maclaren
G, Kluger R, Prior D, et al. Tissue Doppler, strain, and strain rate echocardiography: Principles and potential perioperative
applications. J Cardiothorac Vasc Anesth. 2006;20(4):583–593.)
(translation and rotation) or by segmental motion induced by contraction of adjacent myocardial segments
(tethering).
By convention in strain imaging, an increase in myocardial length is denoted by a positive value, whereas
a decrease in myocardial length is denoted by a negative value. In the ME long-axis views, as the ventricle
contracts, the longitudinal length becomes smaller and ε and SR values will be negative. Conversely, during
diastole the ventricle elongates and ε and SR will have positive values. However, note that during systole
in a SAX view of the LV, the myocardium thickens, so that the measured myocardial length (thickness)
increases and ε and SR will have positive systolic values, with negative values during diastole as the myo-
cardium thins out (Table 3.3).
Modern echocardiographic machines color code Doppler strain such that positive strain is displayed as
blue and negative strain is encoded red (Fig. 3.13). Note that this is the opposite of TDI color coding. Akinetic
myocardial tissue does not change dimension (no strain) and is displayed in green. Since ε and SR are local-
ized measures of myocardial deformation and they do not suffer from the disadvantage of being influenced
by tethering as in TDI, ε and SR performs better at differentiating between infarcted and noninfarcted
myocardium. In a study of off-pump coronary revascularization, ischemia during transient occlusion of the
left anterior descending coronary artery was detected by a reduction in ε in the mid anterior wall segment
but not by TDI velocities or hemodynamic monitoring (14).
TABLE 3.3 Normal Strain and Strain Rate Patterns
Average value in normal

Wall subjects
Longitudinal strain (%) Lateral, posterior, anterior 18 ± 5
Septal 22 ± 5
Longitudinal strain rate (/s) Anterior, septal 1.5 ± 0.4
Lateral, posterior 1.2 ± 0.3
Adapted from: Kowalski M, Kukulski T, Jamal F, et al. Can natural strain and strain rate quantify regional myocardial deformation?
A study in healthy subjects. Ultrasound Med Biol. 2001;27(8):1087–1097.

FIGURE 3.13 Strain. Upper panel: midesophageal (ME) four-chamber color tissue Doppler imaging (TDI) with markers
placed on the septal wall. Middle panel: Color-coded strain imaging (deformation) of the left ventricle (LV) displayed for
each marker (y-axis) against time (x-axis); blue denotes positive strain (lengthening in diastole) and red denotes negative
strain (shortening in systole); green denotes zero strain (no change in length). Note that in the apical regions (# 3, # 4) the
myocardium contracts during diastole (postsystolic shortening). Lower panel: Individual strain values for each marker,
plus mean strain. LA, left atrium; PSS, postsystolic shortening.
Speckle Tracking Echocardiography (Tissue Tracking, 2D Strain, 2D-SRE)

A novel modality termed speckle tracking echocardiography (tissue tracking, 2D strain) utilizes routine gray-
scale 2D echocardiography images to calculate myocardial strain (15) (Fig. 3.14). Stable patterns of unique
acoustic markers (speckles or kernels) are identified in localized regions of the myocardium and tracked
LV SAX Y Representative speckle
Location: frame n + 1
dY
Location: frame n
dX X
Strain = Δ length/original length

+ ve
Percentage thickening
0%
− ve Percentage thinning
FIGURE 3.14 Tissue (speckle) tracking. Localized region of the myocardium is marked by box; speckles are identified
in frame (n) and tracked over time to frame (n + 1); velocity vector is calculated and used to derive strain. LV, left ven-
tricle; SAX, short axis. (From Suffoletto MS, Dohi K, Cannesson M, et al. Novel speckle-tracking radial strain from routine
black-and-white echocardiographic images to quantify dyssynchrony and predict response to cardiac resynchronization
therapy. Circulation. 2006;113(7):960–968.)

over time, measuring velocity and direction of movement. The image-processing software automatically
subdivides a user-defined region of interest into blocks of approximately 20 to 40 pixels containing these
stable patterns of speckles. Subsequent frames are then analyzed automatically by searching for the new
location of each of the speckles. The location shift of these acoustic markers from frame to frame (which
represents tissue movement) provides the spatial and temporal data which can be used to calculate LV
volume and ejection fraction. 2D-STE tracks endocardial border excursions better than AQ technology
and has significantly lower inter- and intraobserver variability than manually tracing 2D endocardial
borders (16). However, since speckle tracking is based on 2D imaging, accuracy will be affected by the
use of foreshorted longitudinal views. A further limitation of any 2D modality is the inability to track
motion in and out of the plane of imaging. Newly developed 3D real-time speckle tracking echocar-
diography (3D-STE) circumvents these limitations and has been shown to correlate well with LV areas,
volumes, and ejection fraction acquired by cardiac MRI which is considered the gold standard for these
measurements (17,18).
Spatial and temporal image processing of acoustic speckles in both 2D and 3D allows for the calcula-
tion of myocardial velocity, strain, and SR. Since speckle tracking does not rely on Doppler velocity mea-
surements, myocardial velocity, ε, and SR calculated from speckle tracking is independent of the angle of
interrogation. In comparison to Doppler ε and SR, which can only be measured in specific walls because of
this angle dependency, 2D- and 3D-STE ε and SR can be measured in any wall that can be visualized by 2D
or 3D echocardiography. Global longitudinal strain derived from speckle tracking is independent of both
geometric assumptions and endocardial border visualization (1).
Global longitudinal strain as measured by 2D and 3D-STE favorably compares with cardiac MRI-derived
LV volumes and systolic function and can reliably distinguish between normal and infarcted myocardium
(18,19). 2D and 3D-STE are also valuable in discriminating between normal and ischemic myocardium. A
2D-STE regional strain value of −4.5% discriminates between segments with viable myocardium and seg-
ments with transmural scar tissue on contrast-enhanced MRI (19). Regional longitudinal strain by 3D-STE
(but not by 2D-STE) differentiates nontransmural segments with <25% scar (18).
The ASE has issued a consensus statement on the methodology of and indications for TDI and speckle
tracking during transthoracic echocardiography (TTE) (20). A guide to image acquisition and analysis of
tissue Doppler and speckle tracking by TTE has also been published as open access (21).
Most of the work done on 2D and 3D-STE has been carried out in normal subjects and cardiology
patients using TTE. Some recent preliminary studies have evaluated the utility of TEE-acquired Doppler
or 2D-STE strain and SR for evaluating LV systolic function during cardiac surgery (14,22,23). Since it
is impractical to compare against cardiac MRI intraoperatively, TEE-acquired strain and SR have been
compared to TTE-acquired values with varying results (23,24).
Left Ventricular Synchrony

An important component of LV systolic function is synchronization of ventricular contraction. As LV
systolic function begins to fail, segments of the myocardium contract dyssynchronously, typically with
the posterior and lateral walls displaying delayed contraction. Dyssynchrony is caused by disease of the
conducting system itself (electrical dyssynchrony, classically left bundle branch block) or mechanical dys-
synchrony, caused by scarring from previous infarction which interrupts the electrical impulse within the
LV. The presence of LV dyssynchrony leads to inefficient LV contraction which shifts the blood volume
within the LV rather than contributing to effective ejection, resulting in a lower stroke volume. LV dys-
synchrony is recognized as an important predictor of poor outcome and patients with New York Heart
Association class III and IV heart failure have been shown to improve with cardiac resynchronization
therapy (CRT) (25).
To better identify patients with LV dyssynchrony and predict those who will respond favorably to CRT, a
number of echocardiographic approaches are in use. M-mode echocardiography has been used to measure
the mechanical delay between the septum and the posterior wall (septal to posterior wall motion delay)
where a delay of greater than 130 milliseconds between systolic motion of the septum and posterior wall
indicates severe LV dyssynchrony (Fig. 3.15).
TDI is the preferred screening tool for dyssynchrony and to stratify patients before CRT and during
follow-up. Using this method, a septal to lateral wall delay of greater than 65 milliseconds predicts

FIGURE 3.15 Left ventricular synchrony. Transthoracic M-mode of transgastric short-axis showing septal wall and pos-
terior wall. Identify maximal contraction of each wall and calculate time difference.
responders to CRT (25) (Fig. 3.16). However, as noted in the preceding text, segmental TDI velocities do
not indicate whether a segment is actively contracting or moving passively because of the tethering effect.
This may explain the fact that up to 20% of patients do not respond to CRT when screened in this man-
ner. This may be overcome by analyzing the velocity profile throughout the complete cardiac cycle during
a stress test where viable segments of myocardium will display an increase in systolic velocity whereas
infarcted and scarred areas will not. In addition, TDI can be used to detect postsystolic shortening which
represents myocardial contraction after closure of the aortic valve (AoV) during the isovolumic relaxation
time (IVRT) period. This form of dyssynchrony has deleterious effects on ventricular filling and subsequent
ejection (Fig. 3.13).
Three-dimensional echocardiography is particularly suited to studies of resynchronization (26). Since
the entire LV is acquired simultaneously, timing and excursion parameters of each of the 17 segments of the
LV enable temporal comparisons between segments. Objective measures of regional timing can be deter-
mined and used in planning therapy and measuring procedure effectiveness (Fig. 3.9B).
VENTRICULAR PATHOLOGY
Cardiomyopathies
Cardiomyopathy is a common diagnosis and encompasses a diverse range of cardiac disease states (Fig. 3.17).
A recent reclassification (27) divides cardiomyopathies into primary cardiomyopathies (disease confined to
the heart, which may be genetic, nongenetic, or acquired) and secondary cardiomyopathies (disease involves
the heart as part of a generalized process which also affects other organs).
Primary Genetic Cardiomyopathies

1. Hypertrophic cardiomyopathy (HCM). HCM forms a heterogeneous group of genetic cardiac diseases
characterized by a hypertrophied, nondilated LV which is not secondary to other disease processes such
as hypertension or aortic stenosis. Clinical diagnosis is made by the 2D echocardiography finding of LV
wall thickening with a small LV cavity in a patient without other causes for LV hypertrophy. Many HCM
patients have the propensity to develop dynamic obstruction of the left ventricular outflow tract (LVOT)
either under resting or provoked conditions. This LVOT obstruction is produced by systolic anterior
motion (SAM) of the MV in which the anterior mitral leaflet (AML) coapts with the bulging septum.
Several theories have been proposed to explain SAM, such as (i) the LVOT dynamic obstruction creates
a Venturi effect causing coaptation of the AML with the septum; or(ii) abnormally oriented papillary

Abnormal LV synchrony
Normal LV synchrony
FIGURE 3.16 Left ventricular synchrony. Left-hand side of upper and lower panels depicts a low left ventricular ejec-
tion fraction (dilated cardiomyopathy); markers are placed on the septal and lateral walls. Right-hand side of upper and
lower panels depicts individual strain waveforms for each marker. The upper panel shows a delay between septal and
lateral wall deformation (abnormal LV synchrony); this patient is therefore a candidate for cardiac resynchronization
therapy. RV, right ventricle; LV, left ventricle. (Mele D, Pasanisi G, Capasso F, et al. Left intraventricular myocardial deforma-
tion dyssynchrony identifies responders to cardiac resynchronization therapy in patients with heart failure. Eur Heart J.
2006;27(9):1070–1078.)
muscles secondary to LV remodeling; an abnormal AML which is elongated with an increased surface
area facilitating coaptation with the septum. Echocardiographic findings of SAM in HCM include AML
septal contact during systole, posterolaterally directed midsystolic MR associated with SAM which can
persist into diastole, a turbulent color flow Doppler pattern in the LVOT, a late systolic peaking velocity
profile on continuous wave interrogation of the LVOT, and systolic “notching” on the M-mode tracing
of AoV (premature closure of the AoV). Video 3.2a
HCM is caused by a number of mutations but is invariably expressed as an autosomal dominant Video 3.2b
inheritance. There are several phenotypic expressions that are recognized with the hypertrophy Video 3.2c
being concentric (Fig. 3.18, Video 3.2a–c), limited to the septum (Video 3.3) or to the apex of the LV Video 3.3

A B C
D E F
FIGURE 3.17 Cardiomyopathy variants. A: Normal. B: Septal hypertrophic cardiomyopathy (HCM). Note left ventricular
outflow obstruction (LVOT) causing increased LVOT gradient, systolic anterior motion of the mitral valve, and mitral
regurgitation. C: Concentric HCM. The posterobasal wall is frequently spared. D: Apical HCM. E: Dilated cardiomyopathy;
dilation may be confined to the left ventricle or biventricular with or without atrial involvement. F: Restrictive cardiomy-
opathy. Note thick ventricles with small intraventricular cavities and biatrial enlargement.
Video 3.4a (Video 3.4a,b). HCM limited to the septum, which may be either diffuse hypertrophy throughout the
Video 3.4b septum or only in the basal or mid wall regions, has also been known as asymmetric septal hypertrophy
(ASH) or idiopathic hypertrophic subaortic stenosis (IHSS). Asymmetry is expressed by a septal wall to
free wall (posterior wall) thickness ratio greater than 1.4. Although systolic function is usually preserved
in HCM until late in the disease, LV dyssynchrony is common in all forms.
FIGURE 3.18 Hypertrophic cardiomyopathy. Note hypertrophy of the right ventricle (RV) as well as the left ventricle
(LV). RA, right atrium; LA, left atrium. (Courtesy of Philips.)

FIGURE 3.19 Noncompaction of the left ventricle (LV) showing deep apical sinuses and enlarged trabeculae. RV, right
ventricle; RA, right atrium; LA, left atrium. (Murphy RT, Thaman R, Blanes JG, et al. Natural history and familial characteris-
tics of isolated left ventricular non-compaction. Eur Heart J. 2005;26(2):187–192.)
2. Noncompaction of the left ventricle (Fig. 3.19). Noncompaction of the LV is a congenital cardiomyopathy,
which involves predominantly the apex of the LV with deep sinusoids between enlarged trabeculae
caused by arrested embryogenesis of the LV. A cross section of the apex of the LV thereby resembles
the structure of a natural sponge. Noncompaction of the LV may be an isolated finding or may be
associated with other congenital heart anomalies such as complex cyanotic congenital heart disease.
Noncompaction of the LV results in systolic dysfunction and heart failure although arrhythmias and
sudden death are also frequent clinical presentations. Thrombi may form within the sinusoids and
being in continuity with the LV cavity may produce embolic events.
Primary Mixed (Genetic and Nongenetic) Cardiomyopathies

1. Dilated cardiomyopathy (DCM) (Fig. 3.20, Video 3.5a–c). DCM is a common cardiomyopathy with Video 3.5a
an estimated prevalence of 1:2,500; it is the third most common cause of heart failure and the most Video 3.5b
frequent reason for patients being listed for heart transplantation. It is characterized by LV enlargement Video 3.5c
and normal LV wall thickness despite the presence of increased cardiac mass. The LV becomes more
globular as dilation occurs preferentially along the SAX and the sphericity index (long axis/SAX) is
reduced from the normal (>1.5) and approaches 1. All measures of systolic function are abnormally low
and LV dyssynchrony is invariably present.
FIGURE 3.20 Dilated cardiomyopathy. ME, midesophageal; LA, left atrium; RV, right ventricle.

Frequent associated findings are mitral annular dilation, reduced excursion of the mitral leaflets
and abnormally oriented papillary muscles resulting in functional MR, a dilated right ventricle (RV),
biatrial enlargement, an apical thrombus, and diastolic dysfunction. DCM is associated with arrhyth-
mias, thromboembolic events, and increased cardiac-related death.
Approximately one-third of the patients with DCM are found to be familial, most frequently auto-
somal dominant. The DCM phenotype may also occur secondary to infectious agents (particularly
viruses), toxins (alcohol, chemotherapeutic agents, heavy metals), autoimmune diseases, collagen vas-
cular disorders, pheochromocytoma, neuromuscular, mitochondrial, metabolic, endocrine disorders,
and nutritional deficiencies.
2. Primary restrictive cardiomyopathy (RCM). Primary RCM is characterized by a normal or decreased
volume of both ventricles associated with biatrial enlargement, normal wall thickness and normal
valves, impaired (restrictive) diastology, and normal or near normal systolic function. Both familial and
sporadic forms have been described.
Acquired Primary Cardiomyopathies

1. Myocarditis. Myocarditis may be an acute or chronic inflammatory process caused by infective
agents, drugs, toxins, and a number of other less common agents. It typically results in DCM and
arrhythmias.
Video 3.6 2. Takotsubo (apical ballooning) cardiomyopathy (Video 3.6). Takotsubo cardiomyopathy (Fig. 3.21)
takes its name from the Japanese word for a traditional octopus trap, which resembles a vase with a
narrow neck and a ballooned outbase. This is a rapidly developing cardiomyopathy, typified by extensive
FIGURE 3.21 Takotsubo cardiomyopathy. LV, left ventricle; LA, left atrium.

myocardial stunning in the mid and apical segments of the LV. The apical half of the LV becomes akinetic
or dyskinetic ballooning out during systole mimicking extensive infarction, whereas the basal segments
are hypercontractile. It is apparently associated with extreme stress and high levels of circulating
sympathetic hormones and has a higher incidence in females than males. Treatment of the underlying
cause of stress and control of the sympathomimetic imbalance usually results in rapid and full recovery.
3. Peripartum cardiomyopathy. Peripartum cardiomyopathy is fortunately a rare cause of severe DCM
appearing at any time between the third trimester of pregnancy up to 5 months postpartum. Prognosis
is variable with approximately half the number of the women affected progressing onto persistent heart
failure whereas the remainder recover to normal function.
Secondary Cardiomyopathies
The list of causes of secondary cardiomyopathies is extensive and includes infiltrative diseases, storage
diseases, toxic exposure, inflammatory processes, genetic, and autoimmune diseases. Presentation may
be typified by signs and symptoms of either a hypertrophied or dilated left ventricle depending upon the
disease process.
Note that other myocardial pathologic processes and ventricular dysfunction such as that which occurs
with valvular heart disease, congenital heart disease, ischemic heart disease, and hypertension are not
included in this classification (15). Therefore the LV hypertrophy that occurs with hypertension is dis-
cussed in the subsequent text in the section on “Left Ventricular Hypertrophy.”
The Role of Echocardiography in Cardiomyopathies

Although echocardiographic findings in patients with symptomatic cardiomyopathy tend to be characteris-
tic of the specific phenotype, some of the more important roles for echocardiography in cardiomyopathies
are as follows:
1. Screening for cardiomyopathy in family members of affected subjects in cardiomyopathies of
genetic or familial origin. Most genetic cardiomyopathies do not display signs or symptoms until early
adulthood. Most of the traditional echocardiography parameters of systolic and diastolic function do
not distinguish between patients with cardiomyopathy and healthy controls until symptoms develop.
The more recent modalities of TDI, ε, and SR have proved useful in distinguishing between healthy
subjects, asymptomatic genetic carriers, and full-blown phenotypic expression in HCM (28).
2. Distinguishing between HCM and LV hypertrophy secondary to systemic hypertension or LV
hypertrophy in athletes. The distinction between these entities may be difficult on grounds of history
and examination. Again traditional echocardiographic markers are not able to distinguish readily
between HCM and athletes’ heart or HCM and LV hypertrophy secondary to systemic hypertension.
Newer echocardiographic modalities based on TDI may help differentiate between HCM and athletes’
heart (29).
3. Distinguishing between RCM and constrictive pericarditis (CP). The clinical distinction between
RCM (typified by amyloid infiltration of the heart) and CP is often very challenging because of the
similar clinical presentation and hemodynamic findings. Conventional M-mode and 2D images may
aid in the diagnosis by demonstrating a significantly thickened pericardium in CP or a pattern of
sparkling, granular LV in amyloid (RCM) (Fig. 3.22). Doppler blood flow patterns have proved helpful
in differentiating the two entities, and the respiratory variation in transvalvular velocity blood flow is
the most frequently used diagnostic parameter (Table 3.4). In CP, the total cardiac volume is defined
by the pericardium. During spontaneous inspiration, blood flows to the right atrium increasing right-
sided volumes, necessitating a reciprocal drop in left-sided volumes as the septum moves toward the
left ventricle (may be seen as septal flattening). These changes are reflected in the E wave (early diastolic
filling) across both the tricuspid valve (TV) and the MV. During inspiration, the tricuspid E wave
increases whereas the mitral E wave decreases. During expiration, tricuspid E wave decreases whereas
mitral E wave increases. These changes are most noticeable on the beat after the start of inspiration or
expiration. If the pulse wave Doppler (PWD) sweep speed is set to 150 mm/s, a characteristic undulating
increase and decrease of the height of the E wave can be seen to coincide with the respiratory pattern.

FIGURE 3.22 Amyloid restrictive cardiomyopathy. RV, right ventricle; LV, left ventricle; LA, left atrium.
TABLE 3.4 Two-dimensional and Doppler Characteristics of Constrictive Pericarditis and Restrictive Cardiomyopathy
Constrictive pericarditis Restrictive cardiomyopathya

■ Two-dimensional echocardiography or M-mode
Thickened pericardium +++ ±
Biatrial enlargement ± +++
LV chamber size ± Small
Wall thickness ± ↑↑
Myocardium Normal Sparkling, granular
Systolic function Intact Reduced
Septal movement Septal “bounce” = rapid anterior No ventricular interdependence
movement during early diastole;
clinically = pericardial knock.
Ventricular interdependence: Septum
moves toward LV during inspiration
IVC and hepatic veins Enlarged Enlarged
Mitral regurgitation ± Usually present
Tricuspid regurgitation ± Usually present
■ Doppler findings
E/A ratio May be normal or <1 >2.2
MV inflow deceleration time (ms) Low normal Shortened (<150)
Mitral E wave changes during >25% reduction in inspiration and Normal (−5%)
respiration increase in expirationb (reciprocal
changes seen in tricuspid E wave)
IVRT during inspiration ↑↑ No variation
Pulmonary vein flow (left-sided Inspiration S approximately = D, S < D, S/D ratio <0.5 deep and wide a
filling pattern) expiration produces ↑ D waves wave; no respiratory variation
Hepatic vein flow (right-sided W waveform (prominent a wave, Blunted systolic flow, deep atrial
filling pattern) prominently descent), with respiratory reversal, may be reversal during
variations (↑ diastolic flow during systole (2 degrees to significant TR).
expiration)
a
Findings in for example late cardiac amyloidosis.
b
In spontaneously breathing patient. Pattern would be reversed in positive pressure ventilation.
LV, left ventricle; IVC, inferior venacava; E, early diastolic filling; A, late diastolic filling; MV, mitral valve; IVRT, isovolumic relax-
ation time; TV, tricuspid valve; W waveform, reversal of flow in late systole and late diastole; TR, tricuspid regurgitation.

Note that in ventilated patients, the changes will be reciprocal because positive inspiratory pressure
reduces blood flow to the right side, thereby causing a decreased tricuspid E wave and an increased
mitral E wave. Respiratory variation also occurs in healthy subjects but the percentage difference in
mitral E waves between inspiration and expiration is usually less than 5%. A difference of greater than
25% in mitral E waves between inspiration and expiration is highly suggestive of CP. However, respiratory
variation is not invariably present in CP and also occurs in patients with chronic obstructive airway
disease, where the variation is somewhere in the range of 10% to 15% (30). TDI has proved useful in the
differential diagnosis of RCM and CP. An early diastolic mitral annular velocity (Ea) cutoff value greater
than 8 cm/s has a 95% sensitivity and 96% specificity for differentiating CP from RCM (31).
Left Ventricular Hypertrophy

LV hypertrophy is a compensatory adaptation of the ventricle to stress. Concentric hypertrophy is a thick-
ening of the ventricular wall as a consequence of parallel replication of sarcomeres without significant
chamber enlargement; it occurs secondary to chronic pressure overload of the ventricle, as in systemic
hypertension and aortic stenosis. The increased impedance to ejection causes marked rises in ventricu-
lar wall stress. Concentric hypertrophy is a compensatory response that reduces wall stress (the law of
Laplace) and enables the ventricle to develop the exaggerated intracavitary pressures necessary to con-
tract effectively against the increased afterload. Other physiologic alterations of the ventricle that occur
in concentric hypertrophy include a prolongation of isovolumetric relaxation, a reduction in compliance
that leads to diastolic dysfunction, and eventual worsening of cardiac function as compensatory limits are
reached. Echocardiographic analysis of concentric hypertrophy involves a determination of LV thickness
and LV mass which have both been described in the preceding text (Fig. 3.23).
Eccentric hypertrophy is an enlargement or dilation of the LV chamber as a consequence of serial repli-
cation of sarcomeres and occurs secondary to chronic volume overload of the ventricle; aortic regurgitation
is the classic example.
>0.42
Concentric Concentric
remodeling hypertrophy
Relative wall thickness
≤0.42
Normal Eccentric
geometry hypertrophy
≤95 ( ) >95 ( )
≤115 ( ) >115 ( )
Left ventricular mass index (g/m2)
FIGURE 3.23 Left ventricular mass may be combined with relative wall thickness to categorize patients into various
classes of left ventricle (LV) hypertrophy. (From Lang RM, Bierig M, Devereux RB, et al. Recommendations for chamber
quantification: A report from the American Society of Echocardiography’s Guidelines and Standards Committee and the
Chamber Quantification Writing Group, developed in conjunction with the European Association of Echocardiography, a
branch of the European Society of Cardiology. J Am Soc Echocardiogr. 2005;18(12):1440–1463).

Left Ventricular True Aneurysm

Most LV aneurysms are located at the apex and are predominantly a consequence of anterior myocar-
dial infarctions. Within 90 days of an anterior myocardial infarction, LV aneurysms develop in 22% of
patients (32). No new true aneurysms develop more than 3 months after myocardial infarction. Early
aneurysm formation, within the first 5 days of myocardial infarction, is associated with increased
mortality.
Two-dimensional Characteristics
A ventricular aneurysm is characterized as a dilated dyskinetic area with myocardial thinning. A narrow
band of myocardium lines a “true” aneurysm and distinguishes it from a pseudoaneurysm (discussed later).
Video 3.7a As demonstrated in Figure 3.24, Video 3.7a–c, a smooth, gradual transition is seen between the aneurysm
Video 3.7b and normal myocardium, with a gradual, obtuse tapering of the myocardium into a dilated, thinned area
Video 3.7c that has a wide neck or opening. The ratio of the size of the aneurysmal opening from the ventricle to the
maximal aneurysmal diameter ranges between 0.9 and 1 (33).
FIGURE 3.24 Left ventricular aneurysm. A: Transgastric mid short-axis view of inferior wall true aneurysm. Note wide
neck. B: TG long-axis view of posterobasal aneurysm. Note wide neck and gradual transition from normal myocardium to
the aneurysm. RV, right ventricle; LV, left ventricle; AoV, aortic valve; LA, left atrium.

Associated Findings
Intraoperative TEE is useful to detect thrombus formation within the aneurysm. Thrombus appears as an
area of increased echogenicity that can be clearly delineated from the endocardium and is a frequent find-
ing as a consequence of stasis of blood within the dilated aneurysm.
Left Ventricular Pseudoaneurysm

The ability to distinguish a true aneurysm from a pseudoaneurysm is critical because pseudoaneurysms
have a high incidence of spontaneous rupture and therefore require surgical correction (33). A pseudoan-
eurysm represents a chronic ventricular rupture contained by pericardium. Therefore, a pseudoaneurysm
is a saccular structure that communicates directly with the pericardial space.
Two-dimensional Characteristics
A pseudoaneurysm is characterized by a narrow orifice (neck) arising from the ventricular chamber; the
ratio of the size of the orifice to the maximal aneurysmal diameter is less than 0.5 (Fig. 3.25). The size of the
small neck rarely exceeds half the maximal parallel internal diameter of the aneurysmal sac (34). The LV
cavity size decreases in systole while the false aneurysm gradually expands.
Quantitative Doppler Characteristics

Doppler echocardiography has proved useful in diagnostically difficult cases and demonstrates bidirec-
tional flow of blood between the pseudoaneurysm and the LV. Color flow Doppler echocardiography
usually demonstrates mosaic jets exiting the LV in systole and entering the pseudoaneurysm cavity. In
diastole, this mosaic pattern occurs within the LV, confirming the turbulent ebb and flow of blood to
and from the pseudoaneurysm. One may also see a profound variation in maximal Doppler flow veloc-
ity throughout the respiratory cycle, with inspiration causing a significant increase in the maximal flow
velocity (34).
Associated Findings
Spontaneous echo contrast and thrombus within the pseudoaneurysm cavity are frequent findings.
FIGURE 3.25 Left ventricular pseudoaneurysm. Note narrow neck which is less than one-half of the parallel internal
diameter of the pseudoaneurysm. TG, transgastric; SAX, short axis; RV, right ventricle; LV, left ventricle.

CONCLUSION
LV systolic function is the most common assessment made during intraoperative echocardiography and a
number of parameters are available for measuring it. These vary in complexity from measurements made
on 2D gray-scale imaging through 3D representation and on to some of the newer modalities based on
TDI. Although subjective and qualitative assessment of LV systolic function have been shown to correlate
well with quantitative measurements and with clinical outcome, the ASE advises that even the most expe-
rienced clinician calibrates the findings against actual measurements on a regular basis.
Quantitative measurements of LV systolic function such as wall thickness and FAC can be easily
acquired by novice practitioners, producing meaningful data for use in daily practice. Current echocar-
diography software also assists in the rapid acquisition of some of the more complicated but more accu-
rate parameters such as LV mass and volume. Although the newer technologies based on TDI are rapidly
becoming the standard of care in echocardiography laboratories, their robustness has yet to be confirmed
in the operating room setting.
REFERENCES
1. Lang RM, Bierig M, Devereux RB, et al. Recommendations for chamber quantification: A report from the American Society
of Echocardiography’s Guidelines and Standards Committee and the Chamber Quantification Writing Group, developed in
conjunction with the European Association of Echocardiography, a branch of the European Society of Cardiology. J Am Soc
Echocardiogr. 2005;18(12):1440–1463.
2. Sahn DJ, DeMaria A, Kisslo J, et al. Recommendations regarding quantitation in M-mode echocardiography: Results of a
survey of echocardiographic measurements. Circulation. 1978;58(6):1072–1083.
3. Skarvan K, Lambert A, Filipovic M, et al. Reference values for left ventricular function in subjects under general anaesthesia
and controlled ventilation assessed by two-dimensional transoesophageal echocardiography. Eur J Anaesthesiol. 2001;18(11):
713–722.
4. Schiller NB, Shah PM, Crawford M, et al. Recommendations for quantitation of the left ventricle by two-dimensional echo-
cardiography. American Society of Echocardiography Committee on Standards, Subcommittee on Quantitation of Two-
Dimensional Echocardiograms. J Am Soc Echocardiogr. 1989;2(5):358–367.
5. Chung N, Nishimura RA, Holmes DR Jr, et al. Measurement of left ventricular dp/dt by simultaneous Doppler echocardiogra-
phy and cardiac catheterization. J Am Soc Echocardiogr. 1992;5(2):147–152.
6. Vegas A, Meineri M. Core review: Three-dimensional transesophageal echocardiography is a major advance for intraoperative
clinical management of patients undergoing cardiac surgery: A core review. Anesth Analg. 2010;110(6):1548–1573.
7. Gopal AS, Keller AM, Rigling R, et al. Left ventricular volume and endocardial surface area by three-dimensional echocar-
diography: Comparison with two-dimensional echocardiography and nuclear magnetic resonance imaging in normal subjects.
J Am Coll Cardiol. 1993;22(1):258–270.
8. Arai K, Hozumi T, Matsumura Y, et al. Accuracy of measurement of left ventricular volume and ejection fraction by new
real-time three-dimensional echocardiography in patients with wall motion abnormalities secondary to myocardial infarction.
Am J Cardiol. 2004;94(5):552–558.
9. Quinones MA, Otto CM, Stoddard M, et al. Recommendations for quantification of Doppler echocardiography: A report
from the Doppler Quantification Task Force of the Nomenclature and Standards Committee of the American Society of
Echocardiography. J Am Soc Echocardiogr. 2002;15(2):167–184.
10. Alam M, Wardell J, Andersson E, et al. Effects of first myocardial infarction on left ventricular systolic and diastolic function with
the use of mitral annular velocity determined by pulsed wave Doppler tissue imaging. J Am Soc Echocardiogr. 2000;13(5):343–
352.
11. Vinereanu D, Lim PO, Frenneaux MP, et al. Reduced myocardial velocities of left ventricular long-axis contraction identify
both systolic and diastolic heart failure-a comparison with brain natriuretic peptide. Eur J Heart Fail. 2005;7(4):512–519.
12. Wang M, Yip GW, Wang AY, et al. Peak early diastolic mitral annulus velocity by tissue Doppler imaging adds independent and
incremental prognostic value. J Am Coll Cardiol. 2003;41(5):820–826.
13. Garcia MJ, Rodriguez L, Ares M, et al. Myocardial wall velocity assessment by pulsed Doppler tissue imaging: Characteristic
findings in normal subjects. Am Heart J. 1996;132(3):648–656.
14. Skulstad H, Andersen K, Edvardsen T, et al. Detection of ischemia and new insight into left ventricular physiology by strain
Doppler and tissue velocity imaging: Assessment during coronary bypass operation of the beating heart. J Am Soc Echocardiogr.
2004;17(12):1225–1233.
15. Ingul CB, Torp H, Aase SA, et al. Automated analysis of strain rate and strain: Feasibility and clinical implications. J Am Soc
Echocardiogr. 2005;18(5):411–418.
16. Nishikage T, Nakai H, Mor-Avi V, et al. Quantitative assessment of left ventricular volume and ejection fraction using two-
dimensional speckle tracking echocardiography. Eur J Echocardiogr. 2009;10(1):82–88.
17. Nesser HJ, Mor-Avi V, Gorissen W, et al. Quantification of left ventricular volumes using three-dimensional echocardio-
graphic speckle tracking: Comparison with MRI. Eur Heart J. 2009;30(13):1565–1573.
18. Hayat D, Kloeckner M, Nahum J, et al. Comparison of real-time three-dimensional speckle tracking to magnetic resonance
imaging in patients with coronary heart disease. Am J Cardiol. 2012;109(2):180–186.

19. Roes SD, Mollema SA, Lamb HJ, et al. Validation of echocardiographic two-dimensional speckle tracking longitudinal strain
imaging for viability assessment in patients with chronic ischemic left ventricular dysfunction and comparison with contrast-
enhanced magnetic resonance imaging. Am J Cardiol. 2009;104(3):312–317.
20. Mor-Avi V, Lang RM, Badano LP, et al. Current and evolving echocardiographic techniques for the quantitative evaluation
of cardiac mechanics: ASE/EAE consensus statement on methodology and indications endorsed by the Japanese Society of
Echocardiography. J Am Soc Echocardiogr. 2011;24(3):277–313.
21. Teske AJ, De Boeck BW, Melman PG, et al. Echocardiographic quantification of myocardial function using tissue deformation
imaging, a guide to image acquisition and analysis using tissue Doppler and speckle tracking. Cardiovasc Ultrasound. 2007;5:27–
45.
22. Kukucka M, Nasseri B, Tscherkaschin A, et al. The feasibility of speckle tracking for intraoperative assessment of regional
myocardial function by transesophageal echocardiography. J Cardiothorac Vasc Anesth. 2009;23(4):462–467.
23. Marcucci CE, Samad Z, Rivera J, et al. A comparative evaluation of transesophageal and transthoracic echocardiography for
measurement of left ventricular systolic strain using speckle tracking. J Cardiothorac Vasc Anesth. 2012;26(1):17–25.
24. Kurt M, Tanboga IH, Isik T, et al. Comparison of transthoracic and transesophageal 2-dimensional speckle tracking echocar-
diography. J Cardiothorac Vasc Anesth. 2012;26(1):26–31.
25. Bax JJ, Bleeker GB, Marwick TH, et al. Left ventricular dyssynchrony predicts response and prognosis after cardiac resynchro-
nization therapy. J Am Coll Cardiol. 2004;44(9):1834–1840.
26. Lau C, Abdel-Qadir HM, Lashevsky I, et al. Utility of three-dimensional echocardiography in assessing and predicting response
to cardiac resynchronization therapy. Can J Cardiol. 2010;26(9):475–480.
27. Maron BJ, Towbin JA, Thiene G, et al. Contemporary definitions and classification of the cardiomyopathies: An American
Heart Association Scientific Statement from the Council on Clinical Cardiology, Heart Failure and Transplantation
Committee; Quality of Care and Outcomes Research and Functional Genomics and Translational Biology Interdisciplinary
Working Groups; and Council on Epidemiology and Prevention. Circulation. 2006;113(14):1807–1816.
28. De Backer J, Matthys D, Gillebert TC, et al. The use of tissue Doppler imaging for the assessment of changes in myocardial
structure and function in inherited cardiomyopathies. Eur J Echocardiogr. 2005;6(4):243–250.
29. Palka P, Lange A, Fleming AD, et al. Differences in myocardial velocity gradient measured throughout the cardiac cycle in
patients with hypertrophic cardiomyopathy, athletes and patients with left ventricular hypertrophy due to hypertension. J Am
Coll Cardiol. 1997;30(3):760–768.
30. Hatle LK, Appleton CP, Popp RL. Differentiation of constrictive pericarditis and restrictive cardiomyopathy by Doppler echo-
cardiography. Circulation. 1989;79(2):357–370.
31. Ha JW, Ommen SR, Tajik AJ, et al. Differentiation of constrictive pericarditis from restrictive cardiomyopathy using mitral
annular velocity by tissue Doppler echocardiography. Am J Cardiol. 2004;94(3):316–319.
32. Visser CA, Kan G, Meltzer RS, et al. Incidence, timing and prognostic value of left ventricular aneurysm formation after myo-
cardial infarction: A prospective, serial echocardiographic study of 158 patients. Am J Cardiol. 1986;57(10):729–732.
33. Brown SL, Gropler RJ, Harris KM. Distinguishing left ventricular aneurysm from pseudoaneurysm. A review of the literature.
Chest. 1997;111:1403–1409.
34. Roelandt JR, Sutherland GR, Yoshida K, et al. Improved diagnosis and characterization of left ventricular pseudoaneurysm by
Doppler color flow imaging. J Am Coll Cardiol. 1988;12:807–811.

QUESTIONS
1. Left ventricular ejection fraction can be c. Minor axis in the midesophageal four-
calculated from which of the following chamber view
parameters? d. Major axis in the transesophageal short-axis
a. Ventricular volumes view
b. Ventricular areas
8. Normal values for myocardial velocities
c. Ventricular diameters
measured in a healthy young adult male
d. All of the above
at the mitral annulus in the septal wall by
2. The area-length (“bullet”) formula for transesophageal echocardiography are
calculating LV volumes is most useful in approximately:
which of the following echocardiographic a. 3 cm/s
techniques? b. 5 cm/s
a. Transthoracic c. −3 cm/s
b. Epiaortic d. −5 cm/s
c. Transesophageal
9. Myocardial velocities as measured by tissue
d. Epicardial
Doppler imaging may be affected by:
3. The normal values for posterior wall a. Mitral annular calcification
thickness and septal wall thickness in a b. Tethering
healthy male subject are respectively: c. Angle of incidence
a. 7 to 12 mm and 7 to 12 mm d. All of the above
b. 7 to 12 mm and 6 to 10 mm
10. With respect to color coding and strain, an
c. 6 to 10 mm and 7 to 12 mm
akinetic segment is coded as:
d. 6 to 10 mm and 6 to 10 mm
a. Blue
4. Endocardial fractional shortening is b. Green
calculated from end systolic and end c. Yellow
diastolic measurements of: d. Red
a. Inferior wall
11. Using transesophageal echocardiography,
b. Anterior wall
the rate of left ventricular pressure rise
c. Minor internal diameter
(dP/dT) may be calculated from a:
d. Major internal diameter
a. Continuous wave Doppler profile of aortic
5. Endocardial fractional shortening is stenosis
measured from: b. Pulse wave Doppler profile of aortic insuf-
a. Endocardial border to endocardial border ficiency
b. Endocardial border to epicardial border c. Pulse wave Doppler profile of left ventricu-
c. Leading edge to trailing edge lar inflow
d. Trailing edge to trailing edge d. Continuous wave Doppler of mitral insuf-
ficiency
6. A calculated endocardial fractional
shortening of 48% in a healthy woman is: 12. To perform dP/dT, the time interval
a. Normal between which of the following velocities
b. Below normal is measured?
c. Above normal a. 0 and 4 cm/s
d. Very abnormal b. 1 and 3 m/s
c. 0 and 4 m/s
7. The diameter used for the cubed formula
d. 1 and 3 cm/s
can be the:
a. Minor axis in the midesophageal long-axis 13. Normal values of dP/dT are:
view a. <500 mm Hg/s
b. Major axis in the midesophageal two-chamber b. 500–1,000 mm Hg/s
view c. >1,000 mm Hg/s
d. >2,000 mm Hg/s

14. Match the following echocardiography 18. During the early stages of primary
modalities (a, b) to the correct method restrictive cardiomyopathy the ventricles
of measurement (i, ii). typically:
a. M-Mode a. Are dilated
b. B-Mode b. Have severely depressed systolic function
i. Leading edge to leading edge c. Have normal wall thickness
ii. Trailing edge to leading edge d. Have increased mass
15. With regard to systolic velocities measured 19. During end stage restrictive
by tissue Doppler imaging (TDI), which cardiomyopathy secondary to amyloid
of the following statements is correct there is typically:
in a healthy individual with normal a. Stage 1 diastolic dysfunction
systolic function and no regional wall b. Normal systolic function
abnormalities? c. Biatrial enlargement
a. Septal annular < lateral annular d. Significant variation of mitral E wave during
b. Septal annular < septal mid ventricular respiration
c. Septal annular > anterior annular
20. The most reliable echocardiographic
d. Septal annular (female) > septal annular (male)
modality for distinguishing primary
16. Myocardial velocities as measured by tissue hypertrophic cardiomyopathy from left
Doppler imaging (TDI) are: ventricular hypertrophy in an athlete is:
a. Gender independent a. Continuous wave Doppler of the left ven-
b. Inversely related to mortality tricular outflow tract
c. Age dependent b. Color flow Doppler of the mitral valve
d. Same value if measured by TEE or TTE c. Tissue Doppler imaging of the left ventricle
d. B-mode imaging of the left ventricle
17. For a given myocardial segment, color
tissue Doppler measures:
a. Peak instantaneous myocardial velocities
b. Mean myocardial velocities
c. Modal myocardial velocities
d. Absolute myocardial velocities

4 Diagnosis of Myocardial Ischemia
Joachim M. Erb and Manfred D. Seeberger
ANATOMY AND PATHOPHYSIOLOGY OF THE

MYOCARDIAL BLOOD SUPPLY
Coronary Anatomy
The myocardium has its own independent blood supply and drainage (Fig. 4.1). Two coronary arteries
originate from the aortic root: The left main coronary artery from above the left coronary cusp of the aortic
valve and the right coronary artery (RCA) from above the right coronary cusp of the aortic valve.
The left main coronary artery bifurcates at around 10 mm into the left anterior descending (LAD) and
the left circumflex (LCX) coronary arteries. The LAD runs along the anterior interventricular sulcus pass-
ing the ventricular apex to reach the posterior interventricular sulcus. On its way to the apex, it gives rise
to the diagonal branches and septal arteries. It thereby supplies the left ventricular (LV) anterior wall,
the apex, and the anterior part of the interventricular septum.
The LCX runs along the left atrioventricular sulcus and gives rise to a large marginal branch and the
posterolateral branches supplying the lateral wall. In patients with left dominant coronary distribution, the
distal LCX extends as a posterolateral branch to supply part of the inferior LV wall.
The RCA runs along the right atrioventricular sulcus, where its middle section gives off the right ven-
tricular (RV) acute marginal branches. These acute marginal branches supply the RV free wall and the
conduction system including the sinus and atrioventricular node. The RCA bifurcates into the posterior
descending artery and the right posterolateral branch. Their supply territory is the inferolateral RV wall, the
inferior part of the interventricular septum, and the inferior wall of the LV.
Ascending
aorta Left main coronary artery
Right Left
coronary anterior descending
artery
Left
circumflex artery
Branch to
SA node
Left cusp
Right cusp Left
Non-coronary
cusp marginal branch
Conus arteriosus
Left
Diagonal posterolateral
branch branch
Posterolateral
artery branch
Right marginal
branch
Posterior
descending
artery
FIGURE 4.1 Anatomy of the coronary arteries of the heart.

82

4. Diagnosis of Myocardial Ischemia 83
10˚
Basal
RCA Anterior
LAD 130˚ Anterolateral
LCX Anteroseptal
Apex
Mid
Inferior
Inferolateral
Inferoseptal
Lateral
Apical Septal
FIGURE 4.2 The 17-segment model of the left ventricle (inner ring) as demonstrated in the transgastric short axis
views. The outer ring shows the common (solid line) and variant (dash line) coronary artery distributions. RCA, right coro-
nary artery; LAD, left anterior descending artery; LCX, left circumflex artery.
Variations in Coronary Anatomy and Main Distribution Types

There are three major variations of coronary distribution. These distribution types affect the posterior
descending artery and posterolateral branch which supply the inferior septum and inferior wall of the LV
(Figs. 4.1–4.5). The right dominant coronary distribution type is the most common (80% to 85%), where
supply originates from the RCA. In left dominant systems supply is via the LCX artery. A balanced or co-
dominant type is present in about 5% of individuals, where the posterior descending artery and posterolat-
eral branch receive supply from both the RCA and from the LCX. Recent imaging studies, however, have
altered traditional concepts of coronary perfusion zones as well as reveal the significant individual variation
in coronary supply to the myocardial segments. For example, the apical segments are now understood in
the majority of cases to be supplied by the LAD with the LCX and RCA seen in a minority of individuals.
LCX
(or LAD)
RCA
(or LAD) L
Basal A
S T
E Mid
E
P R
RCA T Apical
A
A L
L
FIGURE 4.3 Segmental anatomy of the left ventricle in the midesophageal 4 chamber view and corresponding
coronary perfusion (common solid color, variant dashed color). LAD, left anterior descending; LCX, left circumflex; RCA,
right coronary arteries.

RCA
I A
N Basal N
F T
E Mid
E
R R
I Apical I
O LAD O
R R
FIGURE 4.4 Segmental anatomy of the left ventricle in the midesophageal 2 chamber view and corresponding coro-
nary perfusion. LAD, left anterior descending; RCA, right coronary arteries.
The greatest overlap in coronary artery distribution occurs in the inferolateral region corresponding either
to RCA or LCX territories, as well as the inferoseptal region that may be supplied by the LAD artery, RCA,
or even a left-dominant LCX artery. Figure 4.2 incorporates these recent findings and emphasizes the large
amount of myocardium supplied by the LAD artery and potential for substantial infarct size with LAD
occlusion (1). The coronary distribution can be defined by cardiac catheterization and this information is
valuable when communicating regional wall contraction abnormalities (RWCAs) to the surgeon.
Echocardiographic Assessment of Coronary Arteries

Two-dimensional Visualization of Coronary Artery Anatomy
Coronary ostia: From the midesophageal (ME) AV SAX view, the coronary ostia can be visualized by a
Video 4.1A small degree of anteflexion or withdrawal of the probe (Fig. 4.6, Video 4.1A+B) (2). The left coronary ostium
Video 4.1B and the full length of the left main coronary artery to its bifurcation into the LAD and LCX are visible in the
I
N LCX A
F RCA N
E (or RCA) T
R Basal E
O R
L O
A Mid S
T E
E Apical
P
R T
A A
L LAD L
FIGURE 4.5 Segmental anatomy of the left ventricle in the midesophageal long axis view and corresponding coronary
perfusion (common solid color, variant dashed color). LAD, left anterior descending; LCX, left circumflex; RCA, right
coronary arteries.

FIGURE 4.6 The left and the right coronary ostia in the two-dimensional aortic short-axis view (A) and with added
color flow Doppler (B). The left coronary ostium is visible in the middle of the left coronary cusp at the 1- to 2-o’clock Video 4.1A
positions. The right coronary ostium is visible in the middle of the right coronary cusp at the 6-o’clock position (see
Video 4.1B
Video 4.1A+B).
middle of the left coronary cusp at the 1- to 2-o’clock positions (Video 4.2) (2). The right coronary ostium Video 4.2
is visible in the middle of the right coronary cusp at the 6- to 7-o’clock positions.
Left coronary artery: The LAD is visualized by further rotation to ∼120 to 130 degrees and a slight turn
of the probe to the left (Video 4.3). To follow the LCX from the left main bifurcation ME AV SAX view, the Video 4.3
probe is turned leftward and advanced slightly while following the LCX on its way around the atrioven-
tricular groove (Fig. 4.7, Video 4.4) (3). Video 4.4
Right coronary artery: The proximal RCA can also be imaged from the ME AV SAX view supported by
slight anteflexion (Fig. 4.6, Video 4.1A+B) (2). In addition, the ostium and proximal parts of the RCA can be
imaged in a modified ME AV LAX view at 120 to 160 degrees (Fig. 4.8, Video 4.5). Video 4.5
Doppler Evaluation of Coronary Artery Blood Flow

For color flow Doppler assessment of coronary blood flow, it is recommended to initially set the Nyquist
limit to 50 cm/s for examination of the left coronary artery and to 20 cm/s for the RCA (4). Further
reduction in the Nyquist limit is often required to obtain an adequate signal (5). The angle of incidence
has to be taken into account when interpreting the results, as the angle may continuously change for
neighboring sections of the same vessel due to the curved course of the coronary arteries. Normal coro-
nary arterial blood flow shows a biphasic, laminar pattern with a short systolic wave of slower velocity
and a longer diastolic wave of higher velocity with a deceleration slope. This can be measured using
pulse wave Doppler (Fig. 4.9). Reported normal mean peak coronary flow velocities are in the range of
30 to 35 cm/s during systole and 70 to 75 cm/s during diastole for the left coronary artery, and approxi-
mately 25 cm/s during systole and 40 cm/s during diastole for the RCA (6). Visualization of the coronary
ostia and arteries, and of intracoronary flow may be of importance in situations with acute new seg-
mental wall motion abnormalities, for example, during separation from cardiopulmonary bypass (CPB)

Video 4.4 FIGURE 4.7 The left circumflex coronary artery (arrow) in long axis (see Video 4.4).
after mitral valve surgery (5,7), in patients with aortic dissection (8), or during transcatheter aortic valve
implantation (9).
Detection of Coronary Artery Pathology

Although echocardiographic diagnosis of coronary artery stenosis is not a daily practice, it can be clini-
cally valuable for assessing proximal vessel disease when coronary angiography is not practical (i.e., dur-
ing emergent cardiac surgery) (4,10). Indicators are increased echo density, suggesting calcification of the
vascular intima, and turbulent color Doppler flow signals. The following velocities have been published as
threshold for hemodynamically relevant stenosis (>50%): Left main coronary artery >140 cm/s, LAD >90
cm/s, LCX >110 cm/s (11). The percentage reduction in vessel diameter or diastolic velocity–time integral
Video 4.5 FIGURE 4.8 The right coronary ostium and proximal RCA (arrow) in a modified ME AV LAX view (see Video 4.5).

FIGURE 4.9 Pulsed wave Doppler recording of coronary flow. Normal coronary arterial blood flow shows a biphasic,
laminar pattern with a short systolic wave of slower velocity and a longer diastolic wave of higher velocity.
at the site of stenosis compared to the normal segment proximal to the stenosis correlates well with the
degree of stenosis diagnosed by coronary angiography.
PHYSIOLOGIC BASIS FOR THE DETECTION OF ISCHEMIA

Segmental endocardial motion and myocardial thickening are the foundations for echocardiographic detec-
tion of myocardial ischemia. As first observed by Tennant and Wiggers in 1937, occlusion of a coronary
artery results in severe regional wall motion abnormality (RWMA) in the corresponding myocardium (12).
Decades later, Pandian et al. established the value of echocardiography for detecting ischemic RWWAs
(13,14). Since then, multiple human studies have shown that RWCA (i.e., reductions in systolic wall motion
and/or thickening) detected by echocardiography are an earlier and more sensitive indicator of ischemia
than electrocardiography (ECG) (15–21).
The progression in wall dysfunction from hypokinesia to dyskinesia correlates to the progression
in degree of perfusion abnormalities which has been established in dog studies. Reductions in systolic
wall thickening reflect subendocardial ischemia, while akinesia reflects ischemia sparing the subepicar-
dial myocardial layer only, and dyskinesia plus acute wall thinning are seen in the setting of transmural
ischemia (22). An echocardiographic dog study has found that segmental contraction abnormalities are
induced only when myocardial perfusion is less than 25% of control (14). Although human data on the pos-
sible quantitative relationship between myocardial perfusion and segmental wall contraction are missing,
from a clinical point of view acute changes in segmental function are highly indicative of acute ischemia.
Prolonged reduction or cessation of coronary flow leads to infarction. By echocardiography, acutely
infarcted myocardium may look similar to acutely ischemic myocardium. In contrast, scar tissue presents
echocardiographically as a thin, dense, and permanently akinetic or dyskinetic wall.
Although reduced or absent wall thickening may be the most sensitive indicator of ischemia, reduced
endocardial motion may be the more conspicuous echocardiographic sign of severe ischemia. However,
adjacent nonischemic regions may pull the endocardium of an ischemic area inward; this points out the
importance of also considering wall thickening that will still indicate ischemia. Quite typically, unaffected,
nonischemic regions develop exaggerated inward movement (termed compensatory hyperkinesis) that par-
tially offsets the adverse effects of akinesis or dyskinesis in other regions on cardiac stroke volume. This is
the principal reason why hemodynamic instability is a late and ominous sign of ischemia and usually only
occurs with very severe regional or global ischemia.

TABLE 4.1 Characteristics, Echocardiographic Findings, and Clinical Implications of Myocardial Ischemia
Stunned Hibernating
Condition Acute ischemia myocardium myocardium Infarction
Definition Reversible Postreperfusion Chronic, ischemic Permanent ischemia
hypoperfusion contractile dysfunction with myocyte
dysfunction damage
Resting coronary flow Reduced Normal Slightly reduced Severely reduced
Regional wall motion Hypokinesia Hypokinesia Hypokinesia Akinesia–dyskinesia
Response to inotropes Worsens Biphasic Biphasic No change
Contractile Full Full to partial Full to partial None
recovery after
revascularization
Perioperative Urgent Common Revascularization Revascularization
implications pharmacologic following superior not indicated
or interventional CPB to medical
treatment management, may
indicated, show immediate
infarction if improvement
ongoing after CPB
CPB, cardiopulmonary bypass (23,24).
Clinical Syndromes of Myocardial Ischemia

The echocardiographer must be cognizant of the various presentations of ischemic tissue, including
myocardial stunning and hibernation, which complicate the echocardiographic assessment of myocardial
viability. Acute ischemia results from severe reductions in coronary blood flow and is associated reductions
in wall thickening and endocardial inward motion (14). Stunned myocardium occurs following an acute
episode of ischemia when a potentially reversible RWCA transiently persists despite full restoration of
blood flow. Hibernation is a chronic ischemic condition where RWCAs persist in viable myocardium with
marginal resting blood flow. LV function may improve markedly and mortality may be reduced following
successful coronary revascularization. The time course of recovery is variable.
The echocardiographic appearance of stunning and hibernation during resting conditions is similar to
acutely ischemic myocardium (Table 4.1) (25,26). Echocardiography and other imaging techniques can be
used in combination with clinical algorithms for differentiation of myocardial ischemia, hibernation, stun-
ning, and nonviable, infarcted tissue (27,28). Dobutamine stress echocardiography is used for the detec-
tion of viable hibernating myocardium. Viable myocardium shows improved regional contractile function
(inotropic reserve) in response to low dose dobutamine administration. For patients with ischemic heart
disease, dobutamine stress echocardiography predicts the likelihood of left ventricular functional recovery
following revascularization. In addition, in patients with left ventricular dysfunction, caused by myocar-
dial infarction, dobutamine stress echocardiography is useful for evaluating the presence of hibernating
myocardium due to a residual stenosis that warrants intervention. Patients with left ventricular dysfunc-
tion who demonstrate myocardial viability with dobutamine stress echocardiography have a better sur-
vival with revascularization than with medical therapy (29). A key message is that an RWCA is not always
caused by acute ischemia but may reflect stunning, hibernation, and/or nonviable infarcted tissue.
ECHOCARDIOGRAPHIC ASSESSMENT OF ISCHEMIA
Anatomic Localization of Ischemia: The 17-segment Model

The 17-segment model of LV topographical anatomy (30) (Fig. 4.2) provides a common nomenclature
across imaging specialties to define the LV segmental anatomy. Using the 17-segment model in the setting
of perioperative TEE has the advantage of applying the same topographical concept for describing regional
function of the LV as in transthoracic echocardiography, cardiovascular magnetic resonance imaging,
nuclear cardiology, and cardiac computed tomography (30). It also serves as the basis for correlating the
location of RWCA with coronary perfusion.

Echocardiographic Imaging of the 17 Myocardial Segments

The 17-segment model divides the LV along its longitudinal axis into three levels plus the apical cap
(Fig. 4.2). The basal and mid (midpapillary) levels are subdivided into six segments: The anteroseptal, ante-
rior, anterolateral, inferolateral (formerly “posterior”), inferior, and inferoseptal segments. The apical level
is subdivided into an anterior, lateral, inferior, and septal segment.
The three standard ME views (31) (ME four-chamber, ME two-chamber, and ME long-axis) (Figs. 4.3–4.5)
allow visualization of parts of all 17 segments. Although all the three views theoretically visualize the distant
apical slice (segment 17), often the echo imaging plane transects the ventricle above the true apex and the
TEE image is “foreshortened.” To obtain correct alignment of the imaging plane along the long axis of the LV,
the echocardiographer should focus on obtaining the maximum long-axis dimension in each view. Favorable
settings include a low ultrasound frequency (usually no higher than 6 MHz), because the apex is in the far
field of the TEE image; a focal zone placed in the area of the apex; and optimized gain settings in that field.
The transgastric (TG) short-axis views (basal, mid, and apical) allow visualizing the entire radius of
16 segments excluding the apical cap. The TG basal and midpapillary short-axis views are unique in that
myocardial territories perfused by all the three main coronary arteries are visualized (Fig. 4.2). Although
ischemia monitoring in TG midpapillary short-axis view is popular, using this view alone is inadequate,
because ischemia caused by stenosis in an artery more distal to this plane will be missed. Repeated assess-
ment of multiple views is essential as limiting the examination to the TG midpapillary SAX view alone will
miss the majority of RWCA (32). We advise comprehensive monitoring of all the 17 segments for ischemia
utilizing both ME and TG imaging planes.
Coronary Perfusion of LV Segments

The coronary perfusion to the 17 LV segments is shown in Figures 4.2–4.5. Many segments have a con-
sistent coronary artery perfusion. Recent imaging studies, however, have altered traditional concepts of
coronary perfusion zones as well as reveal the significant individual variation in coronary supply to the
myocardial segments. For example, the apical segments are now understood in the majority of cases to
be supplied by the LAD with the LCX and RCA seen in a minority of individuals. The greatest overlap
in coronary artery distribution occurs in the inferolateral region corresponding either to RCA or LCX
territories, as well as the inferoseptal region that may be supplied by the LAD artery, RCA, or even a left-
dominant LCX artery. Figure 4.2 incorporates these recent findings and emphasizes the large amount of
myocardium supplied by the LAD artery and potential for substantial infarct size with LAD occlusion (1).
In those segments with physiologic variability in coronary supply, the culprit coronary artery of an RWCA
can often be identified by examining neighboring segments whose coronary supply is known. For example,
the combination of ischemia in the anterolateral and inferolateral walls is consistent with a left dominant or
co-dominant LCX occlusive disease while the presence of anterolateral ischemia without inferolateral wall
ischemia is specific for a non-dominant LCX occlusion.
Assessment and Grading of Regional Wall Contraction Abnormalities

To grade the severity of ischemia, it is important to analyze both systolic myocardial thickening and endo-
cardial inward motion (“radial shortening”) (Table 4.2). The American Society of Echocardiography/Society
of Cardiovascular Anesthesiologists (ASE/SCA) guidelines for TEE examination classify systolic ventricu-
lar contraction in five grades (31): Normal contractility, mild hypokinesis, severe hypokinesis, akinesis, and
dyskinesis (Table 4.2). For systolic myocardial thickening, a 50% increase is regarded as normal, but given
TABLE 4.2 Five-grade Scale of Segmental Wall Contraction Abnormalities
Radial shortening Myocardial thickening

Grade 1 Normal contractility >30% +++ (30–50%)
Grade 2 Mild hypokinesis 10–30% ++
Grade 3 Severe hypokinesis <10% +
Grade 4 Akinesis 0 0
Grade 5 Dyskinesis Lengthening Thinning
Diagnostic of ischemia when contractility worsens by two grades (21,31).

FIGURE 4.10 Normal LV M-mode (motion mode) reading. Normal inward endocardial excursion and wall thickening
are illustrated on an M-mode image through the inferior (top) and anterior (bottom) walls in the transgastric short-axis
view (top inset). Systole starts at the onset of the QRS complex and ends near the end of the T wave (arrows). M-mode
echocardiographic imaging coupled with the electrocardiogram can on occasion provide helpful information regarding
the timing of wall motion.
substantial intersegment and intersubject variability, a value of 30% thickening has been defined as the
lower normal limit (33). Similarly, systolic radial shortening has been defined as normal if it exceeds 30%.
In clinical practice, two-dimensional (2D) visual assessment of systolic regional contraction is most
commonly used as it provides a quick, qualitative monitor for ischemia. Motion mode (M-mode) imaging
provides a quantitative assessment of systolic myocardial thickening and radial shortening (Fig. 4.10). The
high temporal resolution and better delineation of endocardial and epicardial borders are advantages with
M-mode. However, with TEE the ability to place the ultrasound beam perpendicular to the myocardial wall is
limited to the inferior and anterior walls. One alternative is provided by the free (anatomical) M-mode, where
a virtual ultrasound beam can be placed anywhere in the imaging sector. A limitation of this technique is that
the free M-mode image is calculated from the 2D image and, thus, lacks the high temporal and spatial resolu-
tion of the real M-mode. As a result, quantitative assessments are limited in clinical practice and the visual
assessment of regional myocardial contraction remains the method generally used in the operating room.
Wall function abnormalities can reflect acute or chronic ischemic conditions or nonischemic patholo-
gies (i.e., viral cardiomyopathy). Only when regional systolic contraction deteriorates by two grades (i.e.,
from normal contraction to severe hypokinesia) is the diagnosis of new onset myocardial ischemia confirmed
(21). Side-by-side comparison of corresponding digital cine loops acquired at different periods of the intra-
operative course greatly aids the comparative analysis of regional contraction. The defined requirement
of a temporal deterioration in regional systolic contraction implies that myocardial ischemia cannot be
diagnosed by a single echocardiographic examination alone.
Important Methodologic Aspects of Wall Contraction

Analysis and Potential Pitfalls
Considering endocardial motion alone may result in incorrect segmental grading in situations with rota-
Video 4.6 tional or translational movement of the heart (Fig. 4.11, Video 4.6), with bundle branch block or ventricu-
Video 4.7A lar pacing (Video 4.7A+B), or in ischemic segments where the endocardium is pulled inward by adjacent,
Video 4.7B normally contracting myocardium (“tethering”). Wall contraction analysis must also consider that the basal
septum is mainly membranous and physiologically does not thicken as much as it is more muscular brethren.
This segment is well-known to be read as falsely positive for RWCA by inexperienced echocardiographers.
Systolic translation and rotation of the heart (Fig. 4.11, Video 4.6) may complicate segmental wall contrac-
tion analysis (34). Translational and rotational movements are minimal at the midpapillary SAX levels (35).

A B
FIGURE 4.11 Effects of translational and rotational movements of the heart on analysis of segmental contraction. A: With
a fixed reference system not compensating for translation and rotation, segmental contraction looks severely impaired in
the anteroseptal segment and hyperkinetic in the inferolateral segment. B: With a floating reference system compensat-
ing for translation and rotation, segmental contraction is correctly diagnosed as normal in all segments (see Video 4.6). Video 4.6
During cardiac surgery, translational and rotational movements frequently increase after separation from
CPB and complicate analysis of segmental wall contraction (36). Application of fixed reference systems after
CPB (Fig. 4.11A) can result in the false-positive diagnoses of septal akinesis or dyskinesis and lateral hyper-
kinesis (36). In contrast, application of a floating reference system (Fig. 4.11B), which compensates for heart
movements, reduces the alleged septal RWMAs which occur post-CPB (36). To minimize diagnostic errors in
ischemia detection we encourage analysis of both wall motion and myocardial thickening and the choosing of a
floating reference system in cardiac surgical patients with significant translational cardiac motion.
Endocardial inward motion may markedly overestimate the area of hypoperfused ischemic myocar-
dium (37). One cause for this observation is the tethering effect of the hypokinetic segment on an adjacent
nonischemic myocardium. In clinical practice, this potential overestimation of ischemic area by impaired
endocardial motion may facilitate echocardiographic detection of ischemia, and the skillful echocardiog-
rapher will estimate the true extent of ischemic area more reliably by assessing myocardial thickening.
Correct alignment of the imaging plane with the axis of the ventricle is another important prerequisite
for obtaining correct echocardiographic information. Incorrect alignment in the long-axis views results
in foreshortening (i.e., an echocardiographic image that is shorter than the real structure). Foreshortening
is particularly problematic in the ME TEE views as the true apex is missed (Fig. 4.12, Video 4.8A+B). Video 4.8A
Incorrect alignment also results in nonperpendicular intersection of walls and consequently overestima- Video 4.8B
tion of diastolic wall thickness and pseudo thickening during systole (Fig. 4.13A–D). Pseudo thickening
may mimic normal wall contraction in segments with severe wall contraction abnormalities, as illustrated
in Figure 4.12 (Video 4.8A+B). Pseudo thickening with associated incorrect imaging of wall contraction
similarly occurs when systolic translation of the heart (Fig. 4.11, Video 4.6) displaces the imaging plane Video 4.6
away from the axis of the ventricle.
Limitations of Echocardiographic Detection of Myocardial Ischemia

Even if the echocardiographer copes well with all potential pitfalls, some methodologic limitations remain
and must be taken into account. The fact that a single echocardiographic examination alone cannot provide
definite evidence of myocardial ischemia is one limitation of echocardiography. Echocardiography is more
sensitive and specific for diagnosing ischemia than ECG when acute deterioration of regional wall contrac-
tion is observed (38–40). However, if an RWCA is detected during an initial echocardiographic exam-
ination, causes other than acute ischemia also must be taken into consideration. These causes include
stunning, hibernation, previous myocardial infarction, or nonischemic pathology such as myocarditis or
cardiomyopathy (Table 4.1).
A major limitation of regional wall contraction analysis is that it is not based on quantitative measure-
ments but relies on qualitative (“semiquantitative” at best) assessment. The qualitative character implies a

FIGURE 4.12 Foreshortening may mimic normal contraction in pathologic segments. A: Foreshortening mimicking
Video 4.8A normal contraction of the anteroapical segment. B: After correct alignment, it becomes clear that inward motion and
Video 4.8B thickening of the akinetic anteroapical segment was mimicked by foreshortening (see Video 4.8A+B).
degree of subjective bias that may impair the reliability of wall contraction readings. Automated, quantitative
analysis of regional and global LV function is offered by color kinesis based on real-time, spatiotemporal
analysis of endocardial motion (41). Despite its advantages, color kinesis has not become widely adopted
in the perioperative setting because it is time-consuming, and neither considers myocardial thickening nor
corrects for translational or rotational movement. In addition, color kinesis is limited by the requirement
of a clearly delineated endocardial border throughout the cardiac cycle.
In clinical practice, endocardial and epicardial borders are rarely perfectly delineated in each frame of
the cardiac cycle. Accordingly, we have adopted a practical approach in which we only grade a segment as
normal if at least 50% of endocardial and epicardial borders are visible and contracting normally. In con-
trast, a segment with a clearly detectable RWCA is graded as pathologic even if less than 50% of endocardial
and epicardial borders are visible (42).
Echo contrast agents improve delineation of endocardial borders in patients with suboptimal image
quality but are rarely used in the perioperative setting. One reason is that they do not improve assess-
ment of myocardial thickening. Another reason is the 2007 black box warning of the U.S. Food and Drug
Administration on the use of contrast agents in patients with acute coronary syndromes and unstable car-
diopulmonary conditions, which still has not been completely removed (43).
Another limitation is that echocardiographic monitoring for ischemia is time-consuming. It cannot be
performed in an automated fashion like electrocardiographic ST segment analysis but requires repeated
imaging and analysis of multiple cross-sectional views. Monitoring restricted to a single cross-sectional
view ignores major parts of the LV wall and results in missing a majority of RWCA, even if the view is visu-
alizing myocardium supplied by each of the three main coronary arteries like the TG SAX views (32,44).
The time needed for repeatedly analyzing multiple views may also explain the observation that echocardio-

A B
C D
FIGURE 4.13 X-plane transgastric short-axis and corresponding long-axis views illustrating correctly centered (A, B)
and foreshortened long-axis views (C, D), each during diastole (A, C) and systole (B, D). Foreshortening mimics inad-
equate wall thickness in diastole (C), excessive endocardial inward motion and myocardial thickening in systole (D), and
decreased diastolic and systolic diameters of the left ventricle (C, D).
graphic real-time detection of ischemia by busy anesthesiologists in the operating room was slightly less
reliable than off-line detection by readers who had no other concomitant duties (45). Finally, acute changes
in LV loading conditions have important impacts on regional LV contraction. Acute decreases in preload
can cause new RWCA in the absence of ischemia (42), and acute increases in afterload mimic RWCA in
postischemic myocardium (46).
Alternative Echocardiographic Methods for Detection of Ischemia

Acute Mitral Regurgitation: Acute ischemia frequently causes new or worsening mitral regurgitation. Isch-
emic mitral regurgitation occurs due to impaired contraction of the left ventricle, or ischemic dysfunction
of one or both papillary muscles resulting in restricted leaflet motion, or by acute annular enlargement
(Fig. 4.14, Video 4.9A+B). Progressive mitral regurgitation is a marker for the clinical severity of LV myo- Video 4.9A
cardial ischemia and, if it resolves, an indicator for effective therapy (see Chapter 8, Mitral Regurgitation). Video 4.9B
Doppler indicators: Diastolic function is impaired at an early stage of ischemia, and Doppler indices of
diastolic function can be monitored quickly and quantitatively (e.g., the E/A ratio of diastolic transmitral
inflow). Studies in awake patients have revealed that changes in transmitral inflow patterns are diagnostic
of myocardial ischemia. In anesthetized patients, however, the E/A ratio of diastolic transmitral flow failed
to reliably indicate ischemia induced by dobutamine stress testing or transient coronary occlusion during
off-pump CPB surgery (47,48). Explanations for the failure of the diastolic E/A ratio to detect myocardial
ischemia in anesthetized surgical patients include the confounding effects of general anesthesia and the
frequent changes in preload seen intraoperatively (48).
Three-dimensional (3D) echocardiography: Using semiautomated endocardial border detection soft-
ware, 3D TEE allows quantification of end-diastolic and end-systolic volumes, stroke volume, and ejec-
tion fraction. It also allows for quantitative analysis of endocardial motion of the 17 LV segments. Such
quantification should be a major advance compared to the qualitative regional wall contraction analysis

Normal mitral valve Mitral regurgitation
Apex Apex
Displacement of
the posteromedial Anterolateral
Anterolateral papillary muscle
papillary muscle
Posteromedial Left papillary muscle
papillary muscle Left
ventricle ventricle
Restricted
Area of leaflet closure
ischemic
Chordae Right distortion Right
ventricle ventricle
Aorta Aorta
Posterior
Mitral leaflet Left Mitral Left
atrium regurgitation atrium
valve Anterior
leaflet
A B
FIGURE 4.14 Ischemic mitral regurgitation. A normal mitral valve is shown in panel A. Ischemic mitral regurgitation, in
which the leaflets cannot close effectively, is shown in panel B. The orientation of the illustration is typical of transthoracic
Video 4.9 echocardiographic imaging (see Video 4.9).
(“eyeballing”) according to the established five-grade system. Unfortunately, 3D measurements are per-
formed off-line and require a time-consuming manual definition of key points of the endocardial border
at end-diastole and end-systole. It must also be noted that the lower frame rate with 3D echocardiography
may limit image quality and that the diagnostic accuracy of 3D measurements has not been assessed in the
perioperative setting. Accuracy of this approach is also limited as myocardial thickening is not considered.
This limitation becomes particularly important in cardiac surgical patients after CPB where confounding
factors such as translational and rotational movements (36) and ventricular pacing occur more frequently.
Tissue Doppler imaging: Tissue Doppler imaging of the mitral annulus and analysis of strain and strain
rate are additional, potentially useful techniques for quantitative assessment of regional ventricular func-
tion (49). However, these methods also have substantial limitations, and studies on their diagnostic value
in the operating room are lacking. Speckle tracking is another novel and promising method for quantitative
analysis of segmental myocardial function. Two-dimensional speckle tracking has become available for TEE,
but to date the more promising 3D speckle tracking technology has only been released for transthoracic use.
Right Ventricular Ischemia

The RV plays an important role in morbidity and mortality after cardiac surgery, and TEE is a crucial tool for
assessing its function (50,51). The anterior location of the RV in the chest and its thin walls make the RV more
susceptible than the LV to incomplete myocardial preservation during on-pump cardiac surgery. As the RCA
originates more anterior from the aorta in the supine patient, it is also at a higher risk of acute air lock than
the left main coronary artery in situations with incomplete de-airing after open heart surgery or air entrain-
ment from an assist device cannula (52). For these reasons, assessment of the RV should not be neglected (53).
Coronary perfusion of most RV walls originates from the RCA. Nevertheless, a more sophisticated
appreciation of RV coronary perfusion is clinically important (53). For example, the RV anteroseptal wall
and minor parts of the anterior wall receive blood supply from the LAD coronary artery, which also gives
origin to the moderator band artery. The latter may provide collateral blood supply in case of occlusion of

the RCA and, thus, influence the extent of RV infarction. In addition, a separate ostial origin of the conal
artery, which is found in 30% of subjects, may explain preserved myocardial function of the RV outflow
tract despite proximal occlusion of the RCA.
There are no established rules for detailed analysis of regional contraction of the RV similar to those
for the LV, or criteria for diagnosis of acute RV ischemia. Most of the knowledge on RV function is based
on studies performed by TTE in awake patients. Acute ischemia will result in acute diastolic and systolic
dysfunction with akinesis and, because RV walls are thin, in marked RV distension (Video 4.10). Marked Video 4.10
distension of the RV in the absence of a markedly elevated pulmonary artery pressure is a strong indicator
of RV ischemia. Only four of the standard views recommended in the comprehensive intraoperative TEE
examination focus on the RV (31). We find these insufficient in the case of suspected RV pathology and
utilize additional views to improve imaging of the RV apex (54).
COMPLICATIONS OF MYOCARDIAL ISCHEMIA

The immediate and obvious consequence of myocardial ischemia is the impairment of diastolic and systolic
myocardial function and consequently systemic hemodynamics (Table 4.3). Ischemic mitral or tricuspid
regurgitation, as discussed before, may further increase hemodynamic instability (55,56).
When ischemia progresses to infarction, more disastrous sequelae must be considered. Local inflamma-
tion can lead to pericarditis and subsequent pericardial effusion (Video 4.11) hindering ventricular filling and Video 4.11
performance. The infarcted, akinetic region of myocardium is a trigger for thrombus formation (Video 4.12). Video 4.12
If the infarcted area dilates during fibrous transformation, an aneurysm (Video 4.13) may develop, further Video 4.13
reducing cardiac performance and increasing the risk for thrombus formation. Recognition of thrombi is
important because intraoperative surgical manipulation of the heart can dislodge the thrombus, with poten-
tially fatal embolic consequences. Differentiation of intracardiac thrombus from artifacts (caused by near-field
echos, reverberations, marked trabeculation in hypertrophic LV, tendons, false chordae, etc.) may be difficult
(57). True thrombi are located in areas with severe RWCA and should be diagnosed using multiple views.
The most catastrophic complication of myocardial infarction is myocardial rupture. A rupture in the
cardiac free wall leads to massive pericardial tamponade (Video 4.14) and is usually a lethal complica- Video 4.14
tion. A rupture isolated to the interventricular septum causes a ventricular septal defect (VSD) with a left
to right shunt (Video 4.15) and ultimately if untreated, cardiac failure. Acute ischemic papillary muscle Video 4.15
rupture results in severe mitral regurgitation and requires immediate surgical treatment (Video 4.16). A Video 4.16
small, incomplete myocardial rupture can be contained, leading to a pseudoaneurysm that usually shows
thrombus formation (Video 4.17). Video 4.17
TABLE 4.3 Complications of Myocardial Infarction
Ischemic mitral or tricuspid regurgitation Ischemia causes diastolic stiffness, reduced

systolic ventricular contraction, and may
result in ventricular dilatation. Changes
in ventricular geometry lead to changes
in chord tension and direction, called
“tethering.” Annular dilatation will cause
valvular insufficiency as well. Additional
papillary muscle dysfunction will aggravate
the pathology.
Echo findings: Central insufficiency jet, vena
contracta as direct measurement for grade
of severity most helpful. Annular dilatation,
reduced area of coaptation, and increased
tethering distance and tethering area are
predictors.
Video 4.9A
(see loop 4.9A+B) Video 4.9B
(continued)

TABLE 4.3 Complications of Myocardial Infarction (continued)
Pericardial effusion–pericardial tamponade Pericardial effusion of serous fluid in pericarditis

or blood originating from postoperative
bleeding or myocardial rupture present as
black, echo-free space in the pericardium.
With clot formation, echo density similar
to thrombus develops. Signs of ventricular
compression start with impaired diastolic
expansion, followed by paradoxical septal
motion. Reduced systolic contraction
(beyond the initial impairment caused by the
infarction itself ) may follow. Because of low
pericardial compliance, even little amounts
of fluid (<2 cm in diameter) can be clinically
significant.
Cave: Tamponade is a clinical diagnosis!
Video 4.11 (see loops 4.11 and 4.14)

Video 4.14 LV thrombus Blood stasis in trabecular wall with RWCA favor
thrombus formation. No thrombus formation
without adjacent RWCA!
TEE has a high sensitivity and specificity for
detecting thrombi but special attention to a
possible apical thrombus is needed. Use deep
transgastric views.
Echo findings: Acute thrombi look similar to
myocardium, old thrombi may be more
echodense. Shape of thrombi is variable,
more frequently sessile and laminated than
pedunculated and mobile.
Cave: Differentiation from artifact! A thrombus
should be visible in ≥2 planes in an area with
severe RWCA.
Video 4.12 (see loop 4.12)

LV aneurysm LV aneurysm develops after transmural
infarction. Wall stress increases with LV
dilatation and thinning of the infarct zone,
causing stretching of the fibrous scar. It is
more common after infarction in the supply
area of the LAD (anterior wall). Most common
locations are the LV apex (90%) or the basal
inferior or inferolateral wall.
Echo features: Thin wall without systolic
thickening and dyskinetic motion, wide neck.
Frequently with thrombus formation.
Cave: If akinetic or dyskinetic wall is not thin:
Suspect thrombus!
Video 4.13 (see loop 4.13)

TABLE 4.3 Complications of Myocardial Infarction (continued)
Post infarction VSD Most likely in inferior infarction, usually 3–6

days post myocardial infarction, with single
or multiple defects. Left to right shunt causes
RV dilatation and decrease in function. The
LV seems hypercontractile through acute LV
afterload reduction by VSD. The VSD is often
difficult to locate. Use color flow Doppler for
locating, transgastric views are preferable
due to angle dependency in Doppler studies.
Use pulsed wave Doppler or continuous
wave Doppler to measure pressure gradients
between LV and RV; beware of angle
mismatch.
Interpretation: Larger defect → lower gradient
→ lower velocities measured (volume transfer
increases RV pressure and lowers LV pressure).
(see loop 4.15) Video 4.15

Papillary muscle rupture Rupture is more likely in posteromedial than
anterolateral papillary muscle (single vs. dual
artery supply).
t Complete rupture: Both leaflets involved, flail
leaflets and chords, often with attached piece
of the papillary muscle. Grade 3 insufficiency
with usually central jet, vena contracta
>6 mm, large PISA, pulmonary venous S
inversion.
t Incomplete rupture: Prolapse or partial flail
of one or both leaflets. Grade of insufficiency
varies, often asymmetric jet.
Other findings: RWCA in wall segments
adjacent to papillary muscle, but globally
hyperdynamic LV with acute mitral
regurgitation and retrograde LV “unloading.”
Pseudoaneurysm Pseudoaneurysm has the same pathology as
VSD. Most frequently in inferior wall, small
free rupture contained by pericardium. The
size of the tear in the myocardium determines
the flow of blood into the pericardial space
and, together with the speed of coagulation,
the amount and extent of pericardial blood
and pericardial tamponade.
Echo signs: Small neck, variable amount of
pericardial fluid and/or thrombus, varying
signs of tamponade.

SUMMARY
Detecting ischemia, grading its severity, and recognizing its complications are important priorities for the
intraoperative echocardiographer. Monitoring for ischemia is based on analysis of regional endocardial
motion and wall thickening according to established concepts and criteria (i.e., on the 17-segment model
and the five-grade scale of regional systolic contraction). In addition, the clinician needs to be aware of
limitations and potential pitfalls of regional wall contraction analysis in order to avoid misdiagnosis.
REFERENCES
1. Ortiz-Pérez JT, Rodriguez J, Meyers SH, et al. Correspondence between the 17-segment model and coronary arterial anatomy
using contrast-enhanced cardiac magnetic resonance imaging. J Am Coll Cardiol Cardiovasc Imaging. 2008;1:282–293.
2. Salerno P, Jackson A, Shaw M, et al. Transesophageal echocardiographic imaging of the branches of the aorta: A guide to
obtaining these images and their clinical utility. J Cardiothorac Vasc Anesth. 2009;23:694–701.
3. Ender J, Singh R, Nakahira J, et al. Echo didactic: Visualization of the circumflex artery in the perioperative setting with trans-
esophageal echocardiography. Anesth Analg. 2012;115:22–26.
4. Theunissen T, Coddens J, Foubert L, et al. Intraoperative severity assessment of coronary artery stenosis in patients at risk: The
role of transesophageal echocardiography. Anesth Analg. 2006;102:366–368.
5. Ender J, Selbach M, Borger MA, et al. Echocardiographic identification of iatrogenic injury of the circumflex artery during
minimally invasive mitral valve repair. Ann Thorac Surg. 2010;89:1866–1872.
6. Kasprzak JD, Drozdz J, Peruga JZ, et al. Definition of flow parameters in proximal nonstenotic coronary arteries using trans-
esophageal Doppler echocardiography. Echocardiography. 2000;17:141–150.
7. Ender J, Gummert J, Fassl J, et al. Ligation or distortion of the right circumflex artery during minimal invasive mitral valve
repair detected by transesophageal echocardiography. J Am Soc Echocardiogr. 2008;21:408 e4–e5.
8. Kyo S, Takamoto S, Omoto R, et al. Intraoperative echocardiography for diagnosis and treatment of aortic dissection. Utility
of color flow mapping for surgical decision making in acute stage. Herz. 1992;17:377–389.
9. Gurvitch R, Tay EL, Wijesinghe N, et al. Transcatheter aortic valve implantation: Lessons from the learning curve of the first
270 high-risk patients. Catheter Cardiovasc Interv. 2011;78:977–984.
10. Ahmari SA, Idris A, Amri HA, et al. Failure of multiple coronary angiographies to identify left main coronary artery disease in
a patient diagnosed by transesophageal echocardiography. Eur J Echocardiogr. 2005;6:308–310.
11. Vrublevsky AV, Boshchenko AA, Karpov RS. Diagnostics of main coronary artery stenoses and occlusions: Multiplane transo-
esophageal Doppler echocardiographic assessment. Eur J Echocardiogr. 2001;2:170–177.
12. Tennant R, Wiggers C. The effect of coronary occlusion on myocardial contraction. Am J Physiol. 1935;112:351–361.
13. Pandian NG, Kerber RE. Two-dimensional echocardiography in experimental coronary stenosis. I. Sensitivity and specificity
in detecting transient myocardial dyskinesis: Comparison with sonomicrometers. Circulation. 1982;66:597–602.
14. Pandian NG, Kieso RA, Kerber RE. Two-dimensional echocardiography in experimental coronary stenosis. II. Relationship
between systolic wall thinning and regional myocardial perfusion in severe coronary stenosis. Circulation. 1982;66:603–611.
15. Hauser AM, Gangadharan V, Ramos RG, et al. Sequence of mechanical, electrocardiographic and clinical effects of repeated
coronary artery occlusion in human beings: Echocardiographic observations during coronary angioplasty. J Am Coll Cardiol.
1985;5:193–197.
16. Wohlgelernter D, Cleman M, Highman HA, et al. Regional myocardial dysfunction during coronary angioplasty: Evaluation by
two-dimensional echocardiography and 12 lead electrocardiography. J Am Coll Cardiol. 1986;7:1245–1254.
17. Lambertz H, Kreis A, Trumper H, Hanrath P. Simultaneous transesophageal atrial pacing and transesophageal two-dimensional
echocardiography: A new method of stress echocardiography. J Am Coll Cardiol. 1990;16:1143–1153.
18. Agati L, Renzi M, Sciomer S, et al. Transesophageal dipyridamole echocardiography for diagnosis of coronary artery disease.
J Am Coll Cardiol. 1992;19:765–770.
19. Seeberger MD, Cahalan MK, Chu E, et al. Rapid atrial pacing for detecting provokable demand ischemia in anesthetized
patients. Anesth Analg. 1997;84:1180–1185.
20. Seeberger MD, Skarvan K, Buser P, et al. Dobutamine stress echocardiography to detect inducible demand ischemia in anes-
thetized patients with coronary artery disease. Anesthesiology. 1998;88:1233–1239.
21. Wang J, Filipovic M, Rudzitis A, et al. Transesophageal echocardiography for monitoring segmental wall motion during off-
pump coronary artery bypass surgery. Anesth Analg. 2004;99:965–973.
22. Gallagher KP, Kumada T, Koziol JA, et al. Significance of regional wall thickening abnormalities relative to transmural myocar-
dial perfusion in anesthetized dogs. Circulation. 1980;62:1266–1274.
23. Opie LH. The multifarious spectrum of ischemic left ventricular dysfunction: Relevance of new ischemic syndromes. J Mol
Cell Cardiol. 1996;28:2403–2414.
24. Nihoyannopoulos P, Vanoverschelde JL. Myocardial ischaemia and viability: The pivotal role of echocardiography. Eur Heart J.
2011;32:810–819.
25. Kloner RA, Jennings RB. Consequences of brief ischemia: Stunning, preconditioning, and their clinical implications: Part 2.
Circulation. 2001;104:3158–3167.
26. Kloner RA, Jennings RB. Consequences of brief ischemia: Stunning, preconditioning, and their clinical implications: Part 1.
Circulation. 2001;104:2981–2989.
27. Underwood SR, Bax JJ, vom Dahl J, et al. Imaging techniques for the assessment of myocardial hibernation. Report of a Study
Group of the European Society of Cardiology. Eur Heart J. 2004;25:815–836.

28. Chareonthaitawee P, Gersh BJ, Araoz PA, et al. Revascularization in severe left ventricular dysfunction: The role of viability
testing. J Am Coll Cardiol. 2005;46:567–574.
29. Colucci WS. Dobutamine stress echocardiography in the evaluation of hibernating myocardium. UpToDate 2012;http://www.
uptodate.com/contents/dobutamine-stress-echocardiography-in-the-evaluation-of-hibernating-myocardium?source=search_
result&search=Dobutamine+stress+echocardiography%2C+Colucci&selectedTitle=1~71: February 6, 2013.
30. Cerqueira MD, Weissman NJ, Dilsizian V, et al. Standardized myocardial segmentation and nomenclature for tomographic
imaging of the heart: A statement for healthcare professionals from the Cardiac Imaging Committee of the Council on Clinical
Cardiology of the American Heart Association. Circulation. 2002;105:539–542.
32. Rouine-Rapp K, Ionescu P, Balea M, et al. Detection of intraoperative segmental wall-motion abnormalities by transesophageal
echocardiography: The incremental value of additional cross sections in the transverse and longitudinal planes. Anesth Analg.
1996;83:1141–1148.
33. Pandian NG, Skorton DJ, Collins SM, et al. Heterogeneity of left ventricular segmental wall thickening and excursion in
2-dimensional echocardiograms of normal human subjects. Am J Cardiol. 1983;51:1667–1673.
34. Sengupta PP, Tajik AJ, Chandrasekaran K, et al. Twist mechanics of the left ventricle: Principles and application. JACC
Cardiovasc Imaging. 2008;1:366–376.
35. Schnittger I, Fitzgerald PJ, Gordon EP, et al. Computerized quantitative analysis of left ventricular wall motion by two-dimen-
sional echocardiography. Circulation. 1984;70:242–254.
36. Lehmann KG, Lee FA, McKenzie WB, et al. Onset of altered interventricular septal motion during cardiac surgery. Assessment
by continuous intraoperative transesophageal echocardiography. Circulation. 1990;82:1325–1334.
37. Buda AJ, Zotz RJ, Pace DP, et al. Comparison of two-dimensional echocardiographic wall motion and wall thickening abnor-
malities in relation to the myocardium at risk. Am Heart J. 1986;111:587–592.
38. Seeberger MD, Cahalan MK, Chu E, et al. Rapid atrial pacing for detecting provokable demand ischemia in anesthetized
patients. Anesth Analg. 1997;84:1180–1185.
39. Seeberger MD, Skarvan K, Buser P, et al. Dobutamine stress echocardiography to detect inducible demand ischemia in anes-
thetized patients with coronary artery disease. Anesthesiology. 1998;88:1233–1239.
pump coronary artery bypass surgery. Anesth Analg. 2004;99:965–973.
41. Mor-Avi V, Vignon P, Koch R, et al. Segmental analysis of color kinesis images: New method for quantification of the magni-
tude and timing of endocardial motion during left ventricular systole and diastole. Circulation. 1997;95:2082–2097.
42. Seeberger MD, Cahalan MK, Rouine-Rapp K, et al. Acute hypovolemia may cause segmental wall motion abnormalities in the
absence of myocardial ischemia. Anesth Analg. 1997;85:1252–1257.
43. Food and Drug Administration Center for Drug Evaluation and Research. Joint meeting of the cardiovascular and renal drugs advisory
committee and the drug safety and risk management advisory committee. http://www.fda.gov/downloads/AdvisoryCommittees/
CommitteesMeetingMaterials/Drugs/CardiovascularandRenalDrugsAdvisoryCommittee/UCM256586.pdf 2011; May 2.
44. Shah PM, Kyo S, Matsumura M, et al. Utility of biplane transesophageal echocardiography in left ventricular wall motion
analysis. J Cardiothorac Vasc Anesth. 1991;5:316–319.
45. Bergquist BD, Leung JM, Bellows WH. Transesophageal echocardiography in myocardial revascularization: I. Accuracy of
intraoperative real-time interpretation. Anesth Analg. 1996;82:1132–1138.
46. Buffington CW, Coyle RJ. Altered load dependence of postischemic myocardium. Anesthesiology. 1991;75:464–474.
47. Filipovic M, Seeberger MD, Rohlfs R, et al. Doppler indices of diastolic transmitral flow velocity are invalid indicators of myo-
cardial ischaemia during high-dose dobutamine infusion in anaesthetized patients. Eur J Anaesthesiol. 2002;19:789–795.
48. Wang J, Seeberger MD, Skarvan K, et al. Intra-operative myocardial ischaemia cannot be detected by analysis of transmitral
inflow patterns in patients undergoing off-pump coronary surgery. Eur J Anaesthesiol. 2008;25:1–7.
49. Liel-Cohen N, Tsadok Y, Beeri R, et al. A new tool for automatic assessment of segmental wall motion based on longitudinal
2D strain: A multicenter study by the Israeli Echocardiography Research Group. Circ Cardiovasc Imaging. 2010;3:47–53.
50. Davila-Roman VG, Waggoner AD, Hopkins WE, et al. Right ventricular dysfunction in low output syndrome after cardiac
operations: Assessment by transesophageal echocardiography. Ann Thorac Surg. 1995;60:1081–1086.
51. Maslow AD, Regan MM, Panzica P, et al. Precardiopulmonary bypass right ventricular function is associated with poor outcome
after coronary artery bypass grafting in patients with severe left ventricular systolic dysfunction. Anesth Analg. 2002;95:1507–1518.
52. Leyvi G, Rhew E, Crooke G, et al. Transient right ventricular failure and transient weakness: A TEE diagnosis. J Cardiothorac
Vasc Anesth. 2005;19:406–408.
53. Rudski LG, Lai WW, Afilalo J, et al. Guidelines for the echocardiographic assessment of the right heart in adults: A report from
the American Society of Echocardiography endorsed by the European Association of Echocardiography, a registered branch of
the European Society of Cardiology, and the Canadian Society of Echocardiography. J Am Soc Echocardiogr. 2010;23:685–713.
54. Kasper J, Bolliger D, Skarvan K, et al. Additional cross-sectional transesophageal echocardiography views improve periopera-
tive right heart assessment. Anesthesiology. 2012;117:726–734.
55. Glasson JR, Komeda M, Daughters GT, et al. Early systolic mitral leaflet “loitering” during acute ischemic mitral regurgitation.
J Thorac Cardiovasc Surg. 1998;116:193–205.
56. Kono T, Sabbah HN, Rosman H, et al. Mechanism of functional mitral regurgitation during acute myocardial ischemia. J Am
Coll Cardiol. 1992;19:1101–1105.
57. Stratton JR, Lighty GW Jr, Pearlman AS, et al. Detection of left ventricular thrombus by two-dimensional echocardiography:
Sensitivity, specificity, and causes of uncertainty. Circulation. 1982;66:156–166.

QUESTIONS
1. Which statement regarding coronary c. Incorrect alignment of the imaging plane
topographic anatomy is true? with the axis of the ventricle
a. The left main coronary artery runs in the d. The physiologic variability in myocardial
atrioventricular sulcus between the pulmo- perfusion of some segments depending on
nary trunk and the left atrial appendage the type of coronary distribution
b. In the midesophageal short-axis view of
6. Normal systolic contraction can be
the aortic valve, the right coronary ostium
diagnosed if:
is seen in the middle of the right coronary
a. Thickening of the myocardium is 20% or more
cusp at the 9-o’clock position
b. Radial shortening is more than 30%
c. The marginal branches of the left circumflex
c. Rotation and translation of the heart can be
coronary artery supply the interventricular
excluded
septum
d. All of the above apply
d. The coronary sinus runs along the anterior
atrioventricular groove and drains into the 7. Which statement is correct regarding
right atrium echocardiographic findings during acute
ischemia?
2. Which statement regarding coronary blood
a. The degree of ischemic mitral regurgitation
supply is true?
is typically independent of changes in pre-
a. The inferolateral segments of the LV are
load and afterload
always supplied by the right coronary artery
b. Coronary air embolism after open heart sur-
b. The anterolateral segments of the LV are
gery most frequently causes systolic wall con-
always supplied by the left circumflex
traction abnormalities of the anterior wall
coronary artery
c. Acute akinesia indicates myocardial isch-
c. The anterior segments of the LV are always
emia, acute dyskinesia myocardial infarction
supplied by the left anterior descending cor-
d. None of the above
onary artery
d. The anteroseptal wall of the RV is always 8. All of the following statements are true
supplied by the right coronary artery regarding myocardial perfusion EXCEPT:
a. Maintained contraction of the RVOT may
3. Acute occlusion of the left circumflex
be present despite ostial occlusion of the
coronary artery does not cause dysfunction
right coronary artery
of the:
b. Parts of the RV anterior wall may receive
a. Inferolateral segments of the LV
blood supply from the left anterior descend-
b. Anteroseptal segments of the LV
ing coronary artery
c. Anterolateral segments of the LV
c. The moderator band artery originates from
d. Apicolateral segment of the LV
the right coronary artery and may provide
4. Studies in humans have shown that: collateral blood supply in case of occlusion
a. Akinesia and dyskinesia are always indica- of the left circumflex coronary artery
tive of ischemia d. There are no established rules for detailed
b. The basal septum does not thicken as much analysis of regional contraction of the right
as the other parts of left ventricular walls ventricle
c. New dyskinesia is associated with a worse
9. Which of the following statements
outcome than new severe hypokinesia
regarding complications of ischemia is true?
d. Echocardiography of acutely infarcted myo-
a. Acute myocardial ischemia and acute myo-
cardium looks similar to scar tissue
cardial infarction cannot be differentiated
5. Echocardiographic detection of myocardial by echocardiography
ischemia may be complicated by all the b. Ischemic rupture in the septum causes a
following factors EXCEPT: ventricular septal defect with an interven-
a. Translational and rotational movements of tricular left to right shunt
the heart c. A pseudoaneurysm has the same pathology
b. Ventricular pacing as a ventricular septal defect
d. All of the above apply

10. Regarding complications of ischemia all c. In the absence of an ECG tracing, a capture
statements are true EXCEPT: of 1 second or more is required
a. Papillary muscle rupture is more likely in d. Ventricular systole is more difficult to
the posteromedial than the anterolateral determine with paced rhythms
papillary muscle
16. All 17 segments of the LV model adopted
b. Patients with papillary muscle rupture
by the ASE/SCA can be visualized by the
typically have a severely hypodynamic left
combination of:
ventricle
a. The ME four-chamber and LAX views and
c. Complete rupture of a papillary muscle
the TG mid-SAX view
affects both leaflets of the mitral valve
b. The TG mid-SAX, two-chamber, and LAX
d. Ventricular septal defects develop most fre-
views
quently after inferior myocardial infarction
c. The ME four-chamber, two-chamber, and
11. Regarding variations in coronary anatomy LAX views
it is true that: d. The TG basal SAX, mid-SAX, and apical
a. With a left dominant blood supply, the SAX views
interventricular septum is perfused only by
17. All of the following “tricks” are helpful in
the left coronary artery
attempting to visualize the LV apex EXCEPT:
b. About 80% of individuals have a balanced
a. Probe retroflexion at the level of the TG
coronary distribution type
SAX view
c. The posterolateral branch originates from
b. Optimizing far field gain and time gain
the RCA in the balanced distribution type
compensation settings
d. The posterior descending artery originates
c. Moving the focal zone over the apex
from the RCA in about 50% of individuals
d. Maximally increasing the frequency of the
12. Which of the following is not a transducer in the ME four-chamber view
complication of myocardial infarction?
18. The TG mid-SAX view is commonly used for
a. Pericardial tamponade
monitoring during CABG surgery because:
b. Papillary muscle rupture
a. Changes in intracavitary volume are easily
c. Membranous ventricular septal defect
determined
d. Ventricular thrombus
b. Territories of all three main coronary
13. TEE is useful in off-pump coronary artery arteries perfusing the LV are visualized
bypass (OPCAB) for: c. The papillary muscles serve as a useful
a. Evaluating the adequacy of the coronary reference point to ensure that the same
anastomosis territory is being evaluated
b. Evaluating the ability of the patient to toler- d. All of the above
ate vessel occlusion
19. Which of the following may be associated
c. Evaluating the hemodynamic consequences
with wall contraction abnormalities?
of cardiac displacement
a. Ventricular pacing
d. All of the above
b. Hypovolemia
14. The most sensitive TEE indicator of c. Hypertrophic cardiomyopathy
myocardial ischemia is: d. All of the above
a. A reduction of systolic wall thickening
20. Chronic ischemic mitral regurgitation
b. The presence of systolic wall thinning
is postulated to occur through all of the
c. A reduction in endocardial excursion
following mechanisms EXCEPT:
d. The presence of compensatory hyperkinesis
a. Ventricular dilatation with incomplete leaf-
15. All of the following statements are true let coaptation
regarding digital cine loops EXCEPT: b. Papillary muscle rupture
a. Electrocardiography (ECG) monitoring from c. Ischemic dysfunction of one or both papil-
the echocardiographic machine should be lary muscles
standard practice d. Hypokinesis of the ventricular segment
b. The cine loop captures off the P wave underlying a normal papillary muscle

II ESSENTIALS OF DOPPLER ECHO
5 Doppler Technology and Technique

TWO - DIMENSIONAL ECHOCARDIOGRAPHY PROVIDES remarkable high-resolution, full motion display

of cardiac structures. Yet despite the ability to reveal the most intricate anatomic detail, two-dimensional
imaging is unable to visualize blood flow. Blood flow in cardiac chambers and the great vessels is simply
presented in black on the two-dimensional display. Since the movement of blood is the raison d’être of the
cardiovascular system, this limitation presents a serious challenge to the diagnostic capability of echocar-
diography. Doppler ultrasonography overcomes this limitation in the assessment of blood flow. Its color
flow display affords the echocardiographer dramatic views of blood flow. In addition, spectral Doppler
provides the tools to quantify the magnitude and direction of flow. Since Doppler evaluation is quantitative,
it provides a means of grading the severity of disease in many cases in which two-dimensional echocardiog-
raphy merely demonstrates the presence of an abnormality. As such, mastery of Doppler examinations is a
critical element in the training of a perioperative echocardiographer.
DOPPLER FREQUENCY SHIFT

Doppler examinations are based on principles fundamentally different from those underlying two-dimensional
imaging. As is addressed in the sections that follow, these differences necessitate altered approaches and
techniques when Doppler examinations are performed. Many times, the required view and imaging fre-
quencies are contrary to those selected for two-dimensional imaging of the same anatomic region. To
obtain an optimal assessment of both the form and function of the desired cardiac structure, it is essential
to remain cognizant of the underlying physical principles of the two approaches and how they differ.
The Doppler Effect

As explained in Chapter 1, two-dimensional imaging is based on the intensity and time delay of reflected
ultrasound. To determine the velocity of blood flow, Doppler systems examine the change in frequency of
the ultrasound reflected from red blood cells. Our ability to use the movement of red blood cells to gauge
blood flow velocity dates back to the experiments of the Austrian physicist Christian Doppler. Trumpet-
ers on a high-speed locomotive played a tone at a specific pitch so that the effects of motion on sound
frequency could be examined. A second group of musicians stationed on a loading dock played the same
tone as the train passed by. As Doppler had predicted, the two tones were audibly different. The change in
pitch, known as the Doppler effect, occurs because the motion of an object causes the sound wave to be
compressed in the direction of the motion and expanded in the direction opposite to the motion.
Signal Frequency and Blood Flow

Red blood cells reflect ultrasound as they travel through the blood stream. By directing an ultrasound signal
at flowing blood and listening for the change in frequency produced by the red cell reflections, Doppler
echocardiography can assess the direction and speed of blood flow.
Figure 5.1 illustrates the principle of the Doppler effect for cardiac applications. When ultrasound
is transmitted to blood, it is scattered by the multitude of red blood cells, and a small portion of this
102

5. Doppler Technology and Technique 103
FT No flow
FR = FT
A FR
FT
FR > FT
B FR
FT
FR < FT
C FR
FIGURE 5.1 Detecting blood flow: Effects of red cell motion on ultrasound frequency. The motion of an object alters
the frequency of a reflected ultrasound signal. A: The reflected echoes from a stationary target are of the same frequency
as the transmitted signal. B: Objects such as red blood cells moving toward the transducer compress the sound signal,
and the reflected frequency is increased. C: When red cells travel away from the transducer, the frequency of the reflected
echoes is decreased. These modulations in the frequency of the reflected ultrasound are used to detect blood flow. FT ,
transmitted signal frequency; FR , reflected signal frequency.
scattering is reflected back toward the transducer. The strength of the echoes returning to the transducer
is related to the number of particles reflecting the ultrasound. If the hematocrit is increased, more inter-
faces are available for reflection and the ultrasound signal is stronger. However, this effect is self-limited
because at a hematocrit exceeding 30%, the reflected signal strength is weakened by destructive inter-
ference. Modern echocardiography systems are designed to detect Doppler signals over a wide range of
hematocrit values.
If the red cells are stationary, the signal is reflected at the same frequency as the transmitted signal. Since
no Doppler frequency shift occurs, the situation is similar to that of two-dimensional echocardiography.
When blood flows toward the ultrasound transducer, the reflected signal is compressed by the motion of
the red cells, and its frequency is higher than that of the transmitted signal. Conversely, when blood flows
away from the ultrasound transducer, the frequency of the reflected signal received by the transducer is
lower than that of the transmitted signal. The technical term for the alterations in the frequency of the
ultrasound signals caused by the Doppler effect is modulation. Through analysis of the modulated signal,
both the direction and speed of the red blood cells can be determined.
DOPPLER ANALYSIS
The Doppler Equation: Linking the Frequency Shift to Velocity

The Doppler equation describes the relationship between the alteration in ultrasound frequency and blood
flow velocity (Fig. 5.2):
Δf = v × cos θ × 2ft/c
where Δf is the difference between transmitted frequency ( ft) and received frequency, v is blood velocity,
c is the speed of sound in blood (1,540 m/s), and θ is the angle of incidence between the ultrasound beam
and blood flow.

104 II. Essentials of Doppler Echo
2 FT
ΔF = v cos θ u
C
θ ΔF u C
v=
cos θ 2 FT
FIGURE 5.2 Calculating blood flow velocity: The Doppler equation. The Doppler equation calculates blood flow veloc-
ity based on two variables: The Doppler frequency shift (ΔF) and the cosine of the angle of incidence between the ultra-
sound beam and the blood flow. The Doppler frequency shift is measured by the echocardiographic system, but cos θ is
unknown, and manual entry by the echocardiographer is required for its estimation. v, blood flow velocity; FT , transmit-
ted signal frequency; FR , reflected signal frequency; ΔF, difference between FR and FT ; c, speed of sound in tissue; θ, angle
of incidence between the orientation of the ultrasound beam and that of the blood flow.
Conceptually, the equation can be simplified based on the observation that the change in ultrasound
frequency is directly related to just two variables: Blood velocity and cos θ. The remaining factors in the
equation, the speed of sound in blood (c) and the transmitted frequency ( ft), are constants. The Doppler
signal is shifted only by the component of the blood velocity that is in the direction of the beam path (i.e.,
v cos θ). For example, when the direction of the ultrasound beam is parallel to the blood flow, the observed
Δf fully reflects total blood velocity (cos θ = 1). With nonparallel orientation of the ultrasound beam to
blood flow, Δf is reduced by the factor cos θ. As illustrated in Figure 5.3, when the beam angle divergence is
small, the effects on Δf are limited. However, with angles greater than 30 degrees, the value of cos θ decreases
1.0
0.87
0.75
cos θ
0.5
0.25
0
0 10 20 30 40 50 60 70 80 90
θ
FIGURE 5.3 Cosine relationship. Most devices default to a simplified Doppler equation in which cos θ is ignored, with
the assumption that the Doppler beam is nearly parallel to the blood flow so that the cos θ factor is negligible. However,
at angles between beam and blood flow greater than 30 degrees, a precipitous drop in the cosine curve results in a sub-
stantial underestimation of blood flow velocity. θ, angle of incidence between the orientation of the ultrasound beam
and that of the blood flow.

rapidly. When the direction of the beam is perpendicular to the blood flow (90 degrees, cos 90 = 0), the
movement of blood is no longer appreciated by the Doppler system (Δf = 0).
Implications of Beam Orientation

The effect of the beam angle on Doppler measurements has important clinical implications. In clinical
practice, the ultrasound system measures the frequency shift to calculate velocity. By rearranging the
Doppler equation, the calculated blood velocity is derived as follows:
v = Δf /cos θ × c/2ft
The angle of incidence between the beam and the blood flow is not easily determined. Although a two-
dimensional image of the blood vessel allows the echocardiographer to estimate the angle in the x- and
y-planes, the orientation in the z-plane remains indeterminate. Assessment of the interrogation angle is
further complicated by eccentrically directed blood flow, as in mitral regurgitation. Most Doppler systems
default to a value of cos θ of 1, with the assumption that the echocardiographer has directed the ultrasound
beam to be nearly parallel with the blood flow of interest. This approach has the advantages of stronger
Doppler signals and a lower rate of errors as a consequence of the plateau shape of the cosine curve at
angles of low incidence. Therefore, in clinical practice, the transducer should be positioned such that the
beam and blood flow are nearly parallel for accurate velocity calculations. Figure 5.3 illustrates the basis for
the clinical practice of requiring the beam angle to be within 30 degrees of the direction of blood flow, so
that the rate of angle-related errors remains less than 15%. The assumption that the orientation of the ultra-
sound beam is parallel to the blood flow leads to a common error in Doppler velocity calculations. Because
of the shape of the cosine curve, when the incident angle between the beam and the blood flow is greater than
30 degrees, the blood flow is markedly underestimated (Fig. 5.4). However, even the 30-degree standard may
not be acceptable in certain conditions. For example, when very high velocities are interrogated, as in aortic
stenosis, even a 15% underestimation will correspond to a large difference in velocity and may result in an
underestimation of the severity of aortic stenosis.
400
θ = 41 degrees cm/s
41 degrees
ΔF
A ~ (cos 41)v = 0.75 v
ΔF = 300 = 25% error
θ = 10 degrees 400
cm/s
V
10 degrees
ΔF
B ~ (cos 10)v = 0.98 v

ΔF = 392 = 88% error
FIGURE 5.4 Underestimation of blood flow velocity with nonparallel beam orientation. A: With an angle of 41 degrees, the
vector component of blood flow velocity in the direction of the ultrasound beam is only 75% of the total. Therefore, a velocity
estimation based on ΔF alone will lead to a clinically unacceptable underestimation of the true blood flow velocity of 25%.
B: With an angle of 10 degrees, the vector component of blood flow velocity in the direction of the ultrasound beam is
92%, and the practice of ignoring the cos θ leads to a clinically acceptable 8% underestimation of velocity. ΔF, difference
between FR and FT; v, blood flow velocity; θ, angle of incidence between the orientation of the ultrasound beam and that
of the blood flow.

A B
FIGURE 5.5 Comparison of views selected for two-dimensional imaging versus Doppler flow measurement. A: Two-
dimensional echocardiography from the midesophageal aortic valve short-axis view (top) provides high-fidelity images
of the valve leaflets and their excursion. Since the direction of blood flow is orthogonal to the ultrasound beam in this
view, the continuous wave Doppler measurement of blood flow velocity (bottom) will substantially underestimate
blood flow velocity. B: After repositioning of the probe to obtain the transgastric long-axis view (top), the direction of
the ultrasound beam is parallel to the left ventricular outflow tract and ascending aorta, providing excellent continuous
wave measurements of blood flow velocity (bottom).
Clinical Caveats in Transesophageal Echocardiographic Doppler Examinations

1. Positioning the transesophageal echocardiography (TEE) probe so that the orientation of the Doppler
beam is parallel to the blood flow is often a significant challenge. Unlike the position of a transthoracic
probe, which can be moved freely about the chest wall to achieve proper orientation, the position of the
TEE probe is limited to the confines of the esophagus and stomach.
2. The standard views used for two-dimensional imaging are often inadequate for Doppler assessments.
Optimal two-dimensional images are obtained by directing the beam perpendicular to the structure
of interest to obtain strong, mirror-like reflections. Paradoxically, Doppler measurements are best
obtained when the beam is parallel to the blood flow to avoid underestimates of blood flow velocity. The
view that provides the best two-dimensional image of a structure typically provides only limited flow
information and can result in a failure to detect abnormal flow. Figure 5.5 illustrates the application of
this principle in examining the aortic valve.
Isolating the Doppler Frequency Shift

For the Doppler system to determine the frequency shift caused by red blood cells, it must first distinguish
red cell–modulated echoes from all the other nonfrequency-shifted echoes created by reflections from tis-
sue (Fig. 5.6). This demodulation process is often accomplished by comparing the returning echoes with
internal reference signals that are in phase and 90 degrees out of phase with the transmitted signal, a process
known as quadrature demodulation. Once the Doppler signal has been isolated, its frequency content can
then be determined by means of the fast Fourier transform technique. This approach transforms the demod-
ulated Doppler signal into its individual frequency components. The process is analogous to identifying the
individual harmonics that comprise a musical chord. At each time point, the analysis provides the range of
frequencies (i.e., velocities) detected and their magnitude (i.e., the number of red cells moving at this speed).

Received composite signal
MHz
Demodulator
Extracted Doppler frequency shifts
KHz
Fast Fourier transformer
Isolated Doppler frequencies
KHz
Doppler equation
spectral display
Velocity
Time
FIGURE 5.6 Looking for a needle in a haystack. Extracting the low-frequency, low-amplitude Doppler signal for the
received composite signal is a technical challenge requiring several procedures, including demodulation and fast Fourier
transform. Once isolated, the Doppler frequencies can be analyzed and displayed.
PRESENTATION OF DOPPLER DATA
Audible Broadcast
Blood flow in the heart and great vessels creates a Doppler frequency shift in the kiloHertz range, with a
high-velocity aortic stenotic jet generating a Doppler frequency shift in the order of 20 kHz. Since these
frequencies are within the audible range, most echocardiography machines provide a sound system that
amplifies and broadcasts the signal to the operator. By listening to the loudness and pitch of the broadcast
Doppler frequencies, the echocardiographer can precisely position the Doppler beam to interrogate the desired
flow signal. Typically, the ideal location is identified when the signal reaches its highest frequency and greatest

loudness. Soft, low-decibel signals indicate that the Doppler beam is misdirected and is only glancing a
small part of the blood flow. In addition, the texture and pitch of the Doppler signal are useful in diagnosis.
For example, when transvalvular flow across the aortic valve is examined, a coarse, high-pitched signal
is diagnostic of a high-velocity, turbulent jet caused by aortic stenosis and contrasts markedly with the
smooth-sounding, low-pitched signals generated by the laminar flow in a normal aortic valve. The ability
to use the audible Doppler signal to guide beam positioning is a favored technique of experienced echocar-
diographers, and development of this skill remains a goal for all trainees.
Spectral Display
Presenting Doppler data as a time–velocity plot is known as a spectral display (Fig. 5.7). At each point in
time, the spectrum of velocities detected by the Fourier transformation is displayed. For blood flow mea-
surements, the low-velocity signals emanating from myocardial motion are filtered and not displayed (the
use of these “tissue Doppler” signals is presented in Chapters 3 and 7). Frequencies with greater ampli-
tude (loudness) are marked with brighter pixels. The excellent temporal resolution of the spectral display
allows beat-to-beat assessment of blood flow and is the basis for the quantitative calculations of cardiovas-
cular hemodynamics. Measurement of peak velocity, acceleration (Δv/Δt), and the time–velocity integral
(represented by the area under the velocity–time plot from a single cardiac cycle) are examples of the many
important measurements that are easily obtained from the spectral display (see Chapter 6 for a detailed
examination of the use of these measurements in clinical echocardiography).
Despite the ease with which velocity measurements are made from the spectral display, vigilance is
required on the part of the echocardiographer. The measurements will be accurate only when the underly-
ing principles of good Doppler technique have been followed. First, the Doppler beam must be properly
positioned to interrogate the targeted blood flow. For example, small alterations in beam position deter-
mine whether the displayed spectral velocities represent a targeted high-frequency jet of mitral stenosis or
the lower blood flow velocities found along its perimeter. Second, the direction of the Doppler beam must
be parallel to the path of the targeted blood flow. Errors in diagnosis are often related to failure to meet
these essential requirements.
FIGURE 5.7 Doppler spectral display. Blood flow through the left ventricular outflow tract and aorta is captured by
using continuous wave Doppler directed from the transgastric long-axis view. This time–velocity display shows the
Doppler-calculated velocities on the x-axis, with flow toward the transducer as positive deflections and flow away from
the transducer as negative deflections. Planimetry of the velocity waveform has been performed by the operator, and the
machine’s analysis package calculates the velocity–time integral and the mean and peak flow velocities.

A B
FIGURE 5.8 Hunting for the jet core. A: Despite high-quality two-dimensional imaging of the transgastric long-axis view,
Doppler interrogation of the transvalvular flow fails to detect the high-velocity flow of aortic stenosis. The wispy signal wave-
form provides no clear definition of peak velocities. B: After adjustment of the probe position to obtain the deep transgastric
long-axis view, the resulting Doppler interrogation detects a 400-cm/s high-velocity jet, revealing aortic stenosis. Note the
potential for misdiagnosis if the echocardiographer bases the diagnosis on the initial signal obtained in (A).
Poor ultrasound technique can often be detected by an examination of the spectral display. High-quality
signals result in a pattern commonly referred to as a clean envelope, denoted by a sharply demarcated
border, bright pixels, and clear peaks. When these features are lacking, the echocardiographer should be
reluctant to accept the data from the spectral display and improve the Doppler signal through alterations in
probe position or imaging view (Fig. 5.8). Inexplicably, seemingly minor alterations can resolve difficulties
in obtaining a flow signal. In this regard, there is no substitute for perseverance and experience.
DOPPLER TECHNIQUES
Two Doppler techniques, pulsed wave and continuous wave, are commonly used to evaluate blood flow. A
thorough understanding of the advantages and disadvantages of each technique is critical in selecting the
one most appropriate for the clinical setting at hand.
In clinical practice, pulsed wave and continuous wave Doppler are frequently used in conjunction with
two-dimensional imaging. The two-dimensional image is used to identify the area of interest and guide the
echocardiographer in precisely localizing the sampling volume in a pulsed wave study or in directing the
beam in a continuous wave study.
Pulsed Wave Doppler

The pulsed wave transducer uses a single crystal as both the emitter and the receiver of ultrasound waves.
Like the pulsed echo system described for two-dimensional imaging, the pulsed wave Doppler system
transmits a short burst of ultrasound toward the target and then switches to receive mode to interpret the
returning echoes. Since the speed of sound (c) in tissue is constant, the time delay for a signal to reach its
target and return to the transducer depends solely on the distance (d) to the target:
Time delay = 2d/c
Consequently, reflected signals from locations more distant from the transducer return after a greater
time interval. The electronic circuitry of the pulsed wave transducer interprets returning echoes only after
a predetermined time period has elapsed because the transmission of an ultrasound pulse. In this way, only

those signals associated with a specific depth or location are selected for evaluation, a process known as time
gating. It is important to remember that the transducer transmits a three-dimensional beam. Therefore, the
small portion of reflected sound accepted by the time-gating process corresponds to a volume of blood at
a specific location, called the sample volume. The pulse length, which equals the product of the wavelength
and the number of cycles contained in each sound pulse, determines the length of the sample volume. The
width and height of the sample volume are related to the transducer size, signal frequency, and beam focus.
Clinical Caveats for Pulsed Wave Doppler

Since red cells scatter the ultrasound signal, the reflected Doppler signal returning to the transducer
represents only a fraction of the transmitted signal. Therefore, the returning signal is much weaker than
the strong specular reflections from tissue interfaces. Accordingly, the clinician faces a trade-off between
good range resolution (i.e., a small sample length) and an accurate determination of velocity. In contrast
to the preferred settings in two-dimensional echocardiography, in which axial resolution is a priority and the
pulse length is kept very short, large Doppler sample volumes (length >10 mm) are preferred by most echocar-
diographers to improve the accuracy of the velocity measurement because they provide more wavelength for
demodulation. A more powerful Doppler signal is produced because the signal-to-noise ratio is increased.
In summary, pulsed wave Doppler allows the echocardiographer to select both the location and dimen-
sions of the sample volume to determine blood flow velocity at a discrete location. The ability to select a
sample volume from which to record blood velocities was a major advancement in the diagnostic capability
of echocardiography.
Pulsed Wave Doppler System Processing

The pulsed Doppler system uses a repeating pattern of ultrasound transmission and reception. After pro-
ducing a short burst of ultrasound, it waits for a period of time, proportional to the selected distance, to
receive the signal from the sample volume. The transducer then sends another burst of ultrasound, waits
and receives, and so on. The rate at which the device repeatedly generates sound bursts is known as the
pulse repetition frequency (PRF). The longer the pulsed wave system waits for the returning echoes, the
lower the PRF. Since the speed of sound through tissue is a constant, the PRF is directly related to the depth
of the sample volume. The PRF is analogous to the frame rate of a movie camera. Like the multiple frames
on a roll of movie film, each ultrasound pulse interacts with the blood flow for a brief period of time, and
just as a series of movie frames display motion, a series of pulsed cycles are consecutively analyzed to deter-
mine the blood flow. The demodulation process examines the returning echoes from a series of pulses to
determine the Doppler frequency shift and calculate blood flow velocity.
Limitations of Pulsed Wave Doppler

Since the Doppler data are collected intermittently, the maximal frequency and blood flow velocity that
can be accurately measured by pulsed wave Doppler are limited. The maximal frequency, which equals
one-half the PRF, is known as the Nyquist limit. Figure 5.9 illustrates the principle of the Nyquist limit with
the example of an orbiting comet. A similar effect is seen in movie animation, in which a rapidly spinning
wheel appears to spin backward because of the slow frame rate. At Doppler shifts above the Nyquist limit,
analysis of the returning signal becomes ambiguous, so that the velocity is indeterminate. This ambiguous
signal for frequencies above the Nyquist limit, known as aliasing, appears on the spectral display as a signal
on the other side of the baseline, often referred to as wraparound (Fig. 5.10). The intermittent sampling of
the pulsed system can resolve only frequencies that are less than half the pulse repetition rate.
Maximizing Pulsed Wave Velocity Measurements

The echocardiographer has several techniques available to maximize the velocity performance of a pulsed
wave system:
1. The first clinical principle is to select the view that places the transducer closest to the sample volume.
Lessening the target distance increases the PRF, thereby increasing the velocity that can be assessed.

Time (s)
FIGURE 5.9 Nyquist illusions. The Nyquist limit of one-half the pulse repetition frequency (PRF) applies to any system
based on intermittent observation. In this illustration, the position of the orbiting comet at each observation point is dis-
played. The orbiting velocity of the comet is progressively increased from the top to the bottom rows. At the low orbiting
velocity of one-fourth PRF, the serial observations properly portray the comet as moving in a clockwise direction. As the
speed of the comet is increased so that its orbiting velocity is three-fourth the PRF, it appears to be traveling counter-
clockwise. It appears to be moving not at all when its orbiting velocity equals the PRF. At five-fourth the PRF, it appears to
be orbiting at the same speed as when it was traveling at the much slower speed of one-fourth the PRF.
2. The second clinical principle is to select a low transmitted frequency. The lower transmitted frequency
has two major advantages:
a. The modulated echo ( fr) will be of a lower frequency for any given blood velocity because fr = ft +
Δf. Therefore, increased velocities can be measured without the aliasing that would be caused by a
Doppler signal with a higher transmitted frequency.
FIGURE 5.10 Alias artifact. Alias artifact appears once velocities exceed the Nyquist limit. In this example, the pulsed wave
Doppler sample volume is located in the left ventricular outflow tract, and when the peak velocities of the spectral signal
exceed 70 cm/s, aliasing occurs and they appear on the opposite side of the baseline, a condition known as wraparound.

11
10
9
8
Nyquist limit (cm/s)

7
6
5
4 2.5 MHz
3
2
5.0 MHz
1
0
0 2 4 6 8 10 12 14 16
Distance (cm)
FIGURE 5.11 Effect of distance and frequency on the Nyquist limit. Two important variables under the echocardiogra-
pher's control that can be used to minimize the potential for aliasing in Doppler signals are target distance and transmit-
ted frequency. As the transducer is moved closer to the target or the transmitted frequency is lowered, the pulsed wave
Nyquist limit rises substantially, allowing higher-velocity signals to be measured accurately.
b. Lower frequencies provide a stronger signal because they are less attenuated by tissue. This is important
because Doppler signals are much weaker than those used for imaging. Figure 5.11 illustrates the impor-
tance of target distance and transmitted frequency to the velocity performance of a Doppler system.
3. The third clinical principle is to set the baseline of the spectral display to provide the greatest range of
velocities in the direction of interest. Figure 5.12 illustrates the practical implications of baseline adjustment.
A B
FIGURE 5.12 Effect of baseline setting on pulsed wave Doppler aliasing. A: With the velocity baseline set in the midportion of
the display, the signal aliases at 50 cm/s. B: The baseline has been adjusted to the upper portion of the display, which increases
the Nyquist limit to more than 80 cm/s for flow away from the transducer and captures the spectral signal without aliasing.

Echocardiography technology has also tried to address the velocity limitation of pulsed wave Doppler
systems with the development of high-frequency pulsed Doppler. This approach sacrifices some of the
spatial resolution of the pulsed wave system in exchange for the ability to measure significantly faster
flows. The principle of high-frequency pulsed Doppler is to emit a second or third pulse signal before
the first signal has returned. In this way, the PRF is doubled or tripled, and it becomes possible to calcu-
late a greater maximal velocity. However, with high-frequency pulsed Doppler, the operator cannot be
sure that the reflected echoes have come from the intended target rather than from other targets located
more proximally.
Despite technologic advancements, the Nyquist limit remains a major impediment to the measurement
of high-velocity blood flows, such as those across stenotic valves and in congenital cardiac lesions, with
pulsed wave Doppler. This limitation has led to an alternative approach for the Doppler assessment of high-
velocity blood flows, which is continuous wave Doppler.
Continuous Wave Doppler

The continuous wave Doppler technique avoids the maximal velocity limitation of pulsed wave systems.
The transducer of a continuous wave system is composed of two crystals, one continuously transmit-
ting and the other continuously receiving the reflected ultrasound signal. With continuous reception
of the Doppler signal, the Nyquist limit is not applicable, and blood flows with very high velocities can
be recorded accurately. A continuous wave transducer can measure velocities in excess of 7 m/s and is
therefore useful in measuring the high-velocity flows associated with stenotic valvular disease. Other
differences between the pulsed wave and continuous wave techniques are important. Since the continu-
ous wave signal is not time-gated like the pulsed wave technique, the continuous wave mode receives
reflected signals from blood flow throughout its beam path. Unlike the clean envelope achieved with
pulsed wave Doppler, the spectral display of continuous wave Doppler is typically shaded with the mul-
titude of velocities recorded along the beam path (Fig. 5.13). Consequently, the use of continuous wave
Doppler is limited primarily to detecting the highest velocities along the beam path, represented by the
edge of the spectral envelope.
FIGURE 5.13 Continuous wave spectral signal. Whereas pulsed wave Doppler obtains targeted sample volume record-
ings, the continuous wave system detects blood flow along the entire beam path. Top: In this example, the Doppler
beam was positioned from the deep transgastric long-axis view. Bottom: The resulting spectral signal shows two distinct
peaks, a pattern often referred to as a double envelope. The major peak at 400 cm/s is the high-velocity jet caused by
aortic stenosis recorded from that portion of the beam in the aorta. The minor peak of 100 cm/s represents the blood
velocity in the left ventricular outflow tract.

Color Flow Mapping

Color flow mapping provides a dramatic display of both blood flow and cardiac anatomy. To achieve
these remarkable images, the technique combines two-dimensional ultrasonic imaging and pulsed wave
Doppler methods. The pulsed wave Doppler used for color flow mapping differs from that previously dis-
cussed in two important ways. First, instead of recording from a single, operator-selected sample volume,
color flow mapping performs multiple pulsed wave sample determinations of velocity along the depth
of each scan line. Multiple sample volume recordings are obtained along each scan line as the beam is
swept through the sector. This approach provides flow data matched with the structural data obtained
by two-dimensional imaging. The second difference is that the Doppler velocity data from each sample
volume are color-coded and superimposed on top of the gray scale two-dimensional image. In the most
widely accepted color code, red indicates flow toward the transducer and blue indicates flow away from the
transducer. In addition to flow direction, flow velocity alters the color map. Increasing flow velocities
are displayed by various hues; high-velocity flow toward the transducer is displayed as yellow, and high-
velocity flow away from the transducer is displayed as cyan. Flow with directional variance, as in areas of
turbulence, is displayed as green.
The ability to provide a real-time, integrated display of flow and structural information makes color
flow Doppler useful for assessing valvular function, aortic dissection, and congenital heart abnormalities.
However, several important caveats to its use in the clinical setting must be noted. Since it relies on pulsed
wave Doppler measurements, color flow mapping is susceptible to alias artifacts. In fact, color flow will alias
at a lower velocity than a conventional pulsed wave device because a part of the signal must be used for image
generation, and this effectively decreases the PRF. Aliasing in the color flow map is illustrated in Figure 5.14.
At the extreme of accurate velocity measurement (e.g., bright yellow for flow toward the transducer), pro-
gressively increasing flow rates appear cyan, then dark blue, and then dark red. In a high-velocity jet, several
cycles of color alias can occur, which appear as a tiger stripe pattern in hues of red and blue. Because of
the complex acquisition of multiple Doppler samples and the sharing of acquisition time with the imaging
processor, the velocities displayed by the color flow mapper lack the fidelity of a conventional pulsed wave
device. Color flow mapping neither measure blood flow velocity nor track alterations in velocity through
the cardiac cycle with the precision of a conventional Doppler device. Because of these limitations, the color
flow mapper is often used to identify a flow abnormality that is subsequently characterized by a conventional
Doppler approach.
FIGURE 5.14 Aliasing of color display. Blood flow through the mitral valve (midesophageal four-chamber view) during
early diastole results in aliasing in the color flow mapper. Flow velocity accelerates in the left atrium as blood is fun-
neled to the mitral valve orifice, shown as the color code of dark blue transitioning to light blue, and reaches 32 cm/s
(the Nyquist limit), as seen on the color bar. As a result, aliasing signals are coded bright yellow, then red, as the velocity
reaches a maximum at the level of the leaflet tips. Once in the left ventricle, the blood flow decelerates to fall below the
Nyquist limit and is again appropriately coded blue by the echocardiographic system.

SUMMARY
Doppler echocardiography has greatly expanded the diagnostic capabilities of clinical echocardiography.
Quantitative measurements of blood velocity derived from the spectral display of pulsed wave and con-
tinuous wave Doppler signals are widely used to characterize systolic and diastolic cardiac performance
and valve function. Color flow mapping allows the visualization of cardiac blood flow. The broad clinical
applications of Doppler echocardiography are described in detail in the next chapters. The clinician must
remain mindful of the underlying principles of good technique to obtain optimal Doppler signals and avoid
incorrect diagnoses related to erroneous measurements.
SUGGESTED READINGS
Hatle L, Angelsen B. Doppler Ultrasound in Cardiology. Philadelphia, PA: Lea & Febiger; 1985.
Nishimura RA, Miller FA, Callahan MJ, et al. Doppler echocardiography: Theory, instrumentation, technique, and application.
Mayo Clin Proc. 1985;60:321–343.
Quinones MA, Otto CM, Stoddard M, et al. Recommendations for quantification of Doppler echocardiography: A report
from the Doppler Quantification Task Force of the Nomenclature and Standards Committee of the American Society of
Echocardiography. J Am Soc Echocardiogr. 2002;15:167–184.
Weyman A. Principles and Practice of Echocardiography. Philadelphia, PA: Lea & Febiger; 1994.

QUESTIONS
1. Which of the following statements about 7. The Nyquist limit is directly related to:
Doppler echocardiography is true? a. Blood flow velocity
a. The received Doppler signal is stronger than b. Pressure gradient
the 2D signal c. Pulse repetition frequency
b. Christian Doppler was a Swedish echocar- d. Red cell mass
diographer
8. Which of the following statements about
c. Doppler velocity measurements are based
color flow Doppler is true?
on the change in the signal’s frequency
a. It is susceptible to aliasing
d. Doppler velocity measurements are based
b. It is a good choice for measuring high blood
on reflections from plasma
velocities
2. In clinical practice the Doppler frequency c. It is based on continuous wave technology
shift is: d. It provides nonquantitative information
a. Typically 2.5 to 7.5 MHz
9. Demodulation:
b. Less than 1 MHz
a. Filters out noise in the Doppler signal
c. Not relevant to the Nyquist limit
b. Identifies the Doppler shift
d. Negative for flow directed perpendicular to
c. Is not necessary for color flow Doppler
the ultrasound beam
d. Is not necessary for continuous wave Doppler
3. The Doppler frequency shift is affected by
10. A spectral display with sharp, dense edges:
all of the following except:
a. Is diagnostic of stenotic lesions
a. Transmitted frequency
b. Suggests echoes from a strong reflector such
b. Blood velocity
as a near-by calcified valve
c. Incident angle of the ultrasound beam
c. Assures that the beam is parallel to blood
d. Distance of the target from the transducer
flow
4. Fast Fourier analysis is applied to: d. Suggests proper interrogation of blood flow
a. Pulse wave but not continuous wave Doppler
11. Increasing distance will increase the
signals
Nyquist limit
b. Identify the Doppler frequency shift
a. True
c. Identify the component frequencies of the
b. False
Doppler frequency shift
d. Extract noise from weaker Doppler signals 12. Which of the following is likely in the
case of a double envelope spectral signal
5. All the following statements are true of
obtained from the TG LAX view with peak
pulsed wave Doppler except:
velocities of 115 cm/s?
a. Requires two separate crystals
a. Severe aortic stenosis is present
b. Is useful to identify blood flow in a particular
b. Fractional area change of 55%
area
c. Biscuspid aortic valvular disease is present
c. Has a limited maximum velocity that can be
d. Subaortic stenosis is present
measured
d. Is the basis for color flow Doppler 13. To increase accuracy in velocity
measurements of subpulmonic artery blood
6. Techniques useful to correct an alias signal
flow in a patient with pulmonic stenosis
include all the following except:
from the UE aortic arch SAX view?
a. Adjust baseline
a. The selected sample volume should have a
b. Position transducer closer to target
length greater than 10 mm
c. Increase transmitted frequency
b. Range resolution should be adjusted to high
d. Use high–frequency-pulsed Doppler
c. Continuous wave Doppler should be employed
d. The imaging array should be adjusted to 0
degrees to obtain the UE aortic arch LAX view

14. In obtaining blood velocity measurements 17. Time gating:

of the right ventricular outflow tract using a. Filters out low-frequency signals
PW Doppler the angle of incidence is b. Filters out high-frequency signals
70 degrees. The resulting measurement: c. Requires a fixed speed of sound
a. Will display blood flow in the opposite d. Selects a defined distance from the trans-
direction of true blood flow ducer face
b. Will underestimate blood flow by approxi-
18. Compared to pulsed wave Doppler,
mately 70%
continuous wave Doppler can more
c. Will underestimate blood flow by approxi-
accurately measure high blood flow
mately 30%
velocities because:
d. Will be more accurate using the color flow
a. It uses two transducers rather than one
Doppler setting
b. It uses M-mode technology
15. All the following are true concerning color c. It time gates the signal
flow Doppler except: d. It uses high signal frequency
a. High velocity flow away from the transducer
19. The color flow map is set at ±32 cm/s. Blood
can appear dark red
flow traveling away from the transducer at
b. Color flow Doppler displays B-mode acquired
77 cm/s will appear:
images
a. Green
c. Color flow Doppler uses pulse wave tech-
b. Blue
nology
c. Red
d. Turbulent flow is displayed as bands of red,
d. As banded colors
yellow, and blue
20. The color flow map is set at ±32 cm/s. Blood
16. As per the Doppler equation, the difference
traveling perpendicular to the probe at
between the reflected and received
77 cm/s will appear as:
frequency is inversely related to the cosine
a. Green
of the angle of incidence between the
b. Blue
ultrasound beam and blood flow.
c. Red
a. True
d. Black
b. False

6 Quantitative Doppler and Hemodynamics
When you can measure what you are speaking about, and express it in numbers, you know some-
thing about it; but when you cannot express it in numbers, your knowledge is of a meagre and
unsatisfactory kind.
—Lord Kelvin
H EMODYNAMICS IS THE STUDY OF blood flow and its associated forces. The objective of this chapter
is to describe the use of Doppler echocardiography for the quantitative assessment of hemodynamics.
Although two-dimensional echocardiography displays cardiac dimensions and motion, it does not read-
ily assess cardiac blood flow and pressures. Doppler echocardiography provides excellent assessments of
hemodynamics that compare favorably with more invasive measurements. Accordingly, a quantitative
Doppler assessment of blood flow, chamber pressures, valvular disease, pulmonary vascular resistance
(PVR), ventricular function (systolic and diastolic), and anatomic defects is an essential component of the
echocardiographic examination.
The accuracy of the Doppler evaluation depends on the ability to minimize interference from neighbor-
ing blood flows and align the ultrasound beam parallel to the blood flow of interest. Traditionally, trans-
thoracic echocardiography was a superior approach because it offered multiple windows and angles from
which blood flow could be interrogated. The introduction of multiplane transesophageal echocardiography
(TEE) has increased the number of imaging windows and angles from which the heart can be evaluated
with TEE and has greatly facilitated accurate hemodynamic evaluation.
VOLUMETRIC BLOOD FLOW CALCULATIONS

Doppler Measurements of Stroke Volume and Cardiac Output
Principles
In many instances, knowledge of the volume of blood flow is desired. Cardiac output (CO) and stroke
volume (SV) are familiar examples. It is important not to confuse blood flow velocity, which is the speed
at which blood flows (expressed in centimeters per second), with volumetric flow, which is the amount of
blood that flows (expressed in cubic centimeters per second). The volumetric flow (Q) at any point in time
equals the blood flow velocity (v) times the cross-sectional area (CSA) of the conduit.
Q = v × CSA
To determine the volumetric flow with echocardiography, a Doppler measurement of the instantaneous
blood flow velocities and a two-dimensional measurement of the CSA are required.
In the clinical setting, the volume of blood produced during each cardiac cycle, known as the SV, is
an important parameter of cardiac performance. To calculate the SV, the instantaneous velocities during
systole are traced from the spectral display, and the internal software package of the echocardiographic sys-
tem calculates the time–velocity integral (TVI), which is expressed in centimeters (Fig. 6.1). Conceptually,
the TVI represents the cumulative distance, commonly referred to as the stroke distance, that the red cells
have traveled during the systolic ejection phase. When the stroke distance is multiplied by the CSA (in
square centimeters) of the conduit (e.g., aorta, mitral valve [MV], pulmonary artery [PA]) through which
118

6. Quantitative Doppler and Hemodynamics 119
CSA
Stroke distance
V t
AoV close
Stroke distance (cm) = v × t = ∫vdt
AoV open
Stroke volume (mL) = Stroke distance × CSA
FIGURE 6.1 Determination of stroke volume. Volumetric flow can be determined from a combination of area and veloc-
ity measurements. In this example, flow through the ascending aorta is used to determine the stroke volume. Integrating
the Doppler-derived flow velocities over time (known as the time–velocity integral) during a single cardiac cycle calcu-
lates the stroke distance. The cross-sectional area measurement is obtained with two-dimensional echocardiography.
The product of these two measurements, conceptualized as a cylinder, is the stroke volume. CSA, cross-sectional area;
AoV, aortic valve.
the blood has traveled, the SV (in cubic centimeters) is obtained (1–7). CO, which expresses volumetric
flow in cubic centimeters per minute, is estimated from the product of the SV and the heart rate (HR).
Echocardiographic Technique for Doppler Measurements of Stroke Volume

The SV and CO are best measured with TEE at the left ventricular outflow tract (LVOT) or aortic valve
(AoV) (1–7). These locations offer several advantages to the clinical echocardiographer. First, the entire
ejected SV traverses these structures, whereas it does not in more distant vessels, so that the total SV can
be calculated. Second, Doppler interrogation typically assesses blood flow from only a small fraction of the
total CSA of the vessel, and therefore SV calculations assume that the measured velocity reflects the mean
flow velocity throughout the cross section of the vessel. This assumption is most accurate when blood flow
is laminar and has the same velocity across the entire vessel, a situation known as a blunt or flat flow profile
(Fig. 6.2). Since the blood is accelerated along the truncated LVOT during systole, the velocity profile has a
blunt, uniform pattern rather than the parabolic pattern seen in the ascending aorta or PA. Consequently,
the LVOT and AoV are attractive because the risk for sampling blood velocities that are not reflective of
the average blood flow velocity is reduced. Third, the LVOT and ascending aorta are more circular and the
CSA changes less during the cardiac cycle. Multiplane TEE offers excellent windows at these sites for both
Doppler blood flow measurements and two-dimensional echocardiographic measurements of the CSA.
Several clinical studies have confirmed that the CO measurements obtained by TEE compare favorably
with those obtained by thermodilution (1–3,5–7).
LVOT or transaortic valvular flows are most reliably obtained from the transgastric (TG) long-axis and
the deep TG long-axis views because the blood flow is nearly parallel to the ultrasound beam. It is critical

Parabolic profile
Turbulent profile
Flat profile
A B
FIGURE 6.2 Common flow profiles. A: The acceleration of the blood flow as it enters the truncated left ventricular
outflow tract leads to a “flat” profile in which velocities are uniform. As blood travels in the ascending aorta, the effects of
wall friction and a curved conduit result in an asymmetric and parabolic flow profile. B: When blood is forced through a
narrow opening, laminar flow is replaced with turbulence. In this illustration, aortic stenosis has created a narrow, high-
velocity jet encased by turbulent flow.
to interrogate blood flow carefully through minor alterations in the probe position and multiplane angle
to obtain the optimal Doppler spectral signal. The maximal velocity profile with a dense spectral signal is
sought.
Calculation of the left Ventricular Outflow tract Stroke Volume

1. The pulsed wave Doppler sample volume is positioned in the LVOT immediately proximal to the AoV
(TG long-axis and deep TG long-axis views).
2. The CSA for the LVOT is best obtained from the midesophageal (ME) LVOT view. The CSA is calculated
from a measurement of the LVOT diameter as follows:
CSA LVOT = π(diameter/2)2
Calculation of the Transaortic Valve Stroke Volume

1. The continuous wave Doppler beam is directed through the AoV orifice from the TG long-axis or deep
TG long-axis view (Fig. 6.3).
2. The CSA of the valve is best estimated by planimetry of the equilateral triangle-shaped orifice observed
in midsystole (6). The AoV is viewed in cross section from the ME AoV short-axis window, and frame-
by-frame review is used to capture the valve in midsystole. Planimetry of the triangle-shaped orifice
yields the effective CSA.
Calculation of the Stroke Volume of the Right Side of the Heart

Alternatively, right-sided flows and diameters can be analyzed from the main PA or the MV. Pulsed wave
or continuous wave Doppler analysis proceeds after the main PA is imaged from high esophageal windows
at the level of the superior mediastinal vessels (Fig. 6.4) or the right ventricular outflow tract (RVOT) is
imaged from TG windows at 110- to 150-degree rotation of the transducer and rightward turn of the TEE
probe (Fig. 6.5). In all cases, the maximal velocity profile is sought. Flow across the MV is measured by

A B
FIGURE 6.3 Stroke volume (SV) calculated from the left ventricular outflow tract (LVOT). The right panel demonstrates
measurement of the left ventricular outflow tract (LVOT) diameter (2.2 cm) from the midesophageal long-axis window.
The left panel shows pulse wave (PW) Doppler measurement of blood flow velocities across the LVOT (TVILVOT ) from the
deep transgastric left ventricular outflow tract window. The time–velocity integral (TVILVOT ) is 16 cm. The cross-sectional
area of the LVOT (CSALVOT ) is calculated from the measured diameter using the equation: π(D/2)2. The calculated area of
the LVOT (3.75 cm2) multiplied by the TVI (16 cm) yields a stroke volume of 60 mL/beat. When multiplied by the heart rate
(HR), the cardiac output is obtained.
placing the sample volume at the level of the mitral annulus to obtain the transmitral TVI, which is then
multiplied by the area of the MV annulus. Compared with the diameters of the LVOT and ascending aorta,
the diameters of the main PA and MV fluctuate more during the cardiac cycle, and these measurements are
less reliable than those from the LVOT and AoV (4). In addition, the MV orifice is not circular, and its size
changes during diastole.
FIGURE 6.4 Calculation of cardiac output from the main pulmonary artery (MPA) performed from the ME ascending
aortic SAX view seen in the right panel from which the MPA diameter (2.6 cm) can be measured. The MPA time–velocity
integral (TVI) is assessed by the pulsed wave Doppler beam being aligned with pulmonary artery blood flow and with
the sample volume placed at the same location (plane) where the MPA diameter was measured. The cross-sectional area
(CSA) of the pulmonary artery (π[D/2]2) is calculated as 5.3 cm2. Manual tracing of the spectral display of pulmonary
blood velocities shows a TVI of 9.92 cm. When multiplied by the CSA, the stroke volume is calculated as 53 mL/beat. Diam,
diameter; SV, stroke volume.

FIGURE 6.5 Stroke volume (SV) through the right ventricular outflow tract (RVOT) was calculated from the transgastric
right ventricular inflow/outflow window. The product of the RVOT area (4.5 cm2) and the RVOT time–velocity integral
(TVI; 15 cm) was used with RVOT area calculated from the RVOT diameter measurement (2.2 cm; area = π[D/2]2). PV, pul-
monary valve; RA, right atrium; RV, right ventricle; TVI, time–velocity integral; D, diameter.
Regurgitant Volume
Regurgitant volume is the quantity of blood that flows back through a regurgitant lesion in a single cardiac
cycle. The total SV traversing a regurgitant valve during systole is greater than that in a normal valve. For a
regurgitant valve, the total SV equals the regurgitant volume plus the SV delivered to the peripheral circula-
tion. The regurgitant volume can be calculated as the difference between the total forward flow through the
regurgitant valve and the total forward flow through a reference valve.
Regurgitant volume = forward flow through regurgitant valve − forward flow through reference valve
In the case of mitral regurgitation (MR) (in the absence of significant AoV disease), the SV across the
AoV can be used as the true SV.
Regurgitant volume MV = forward flow through MV − flow through AoV

RVMV (mL ) = SVMV − SVAoV
However, there is a significant potential for error in the mitral flow measurements because the MV
orifice is not circular (4), and its diameter changes during the cardiac cycle.
Similarly, the aortic regurgitant volume can be calculated as follows:
Regurgitant volume AV = forward flow through AoV − flow through MV
The regurgitant fraction is simply the ratio of the regurgitant volume to the total SV through the dis-
eased valve and is typically expressed as a percentage:
Regurgitant fraction (%) = regurgitant volume/forward flow
Alternative techniques to measure the severity of valvular regurgitation are discussed in Chapters 8
and 11.

Intracardiac Shunts
The ratio of pulmonic to systemic SV, Qp/Qs, is important in assessing the severity of shunts and in guiding
treatment. Intracardiac shunts are assessed by calculating the SV (8). By measuring the left-sided (LVOT or
AoV) and right-sided (PA or RVOT) SVs, one can determine Qp/Qs:
Qp/Qs = SVRight heart ( e.g. , PA , RVOT ) /SVLeft heart ( e.g., LVOT , AoV )
These measurements are often combined with two-dimensional and color Doppler data to provide a
complete assessment of congenital lesions.
Valve Area: The Continuity Equation

The principle of conservation of mass is the basis of the continuity equation, which is commonly used to
measure the AoV area (9) (Fig. 6.6B). The continuity equation simply states that the volume of blood pass-
ing through one site (e.g., the LVOT) is equal to the mass or volume of blood passing through another site
P2
v2
ΔP = 4v22
v1
P1
A
v2
A1 A2 A1 × v1 = A2 v2
A1 v1
v1 A2 =
v2
FIGURE 6.6 Calculating the pressure gradient and valve area. A: Bernoulli equation. The simplified Bernoulli equa-
tion states that the pressure drop (Ρ2 − Ρ1 = Δ 4P) across a stenotic orifice is four times the square of the velocity of the
high-velocity jet. P1, blood pressure proximal to stenosis; v1, flow velocity proximal to stenosis; P2, blood pressure distal
to stenosis; v2, flow velocity through stenosis. B: Continuity equation. The continuity equation is often described as the
principle of “what goes in must come out.” Accordingly, flow proximal to the stenosis (A1 × v1) should equal flow through
the stenosis (A2 × v2). A1, cross-sectional area proximal to stenosis; v1, flow velocity proximal to stenosis; A2, cross-sectional
area of stenosis; v2, flow velocity through stenosis.

(e.g., the AoV). Of course, there must be no intervening channels for this principle to apply. By using the
principle of volumetric flow, discussed earlier, the continuity equation can be applied clinically.
Volumetric flow1 = Volumetric flow2
CSA 1 × TVI1 = CSA 2 × TVI 2

CSA 1 = CSA 2 × TVI 2 /TVI1
To calculate the area of the aortic valve (AoV):
Area AoV = Area LVOT × (VLVOT /VAoV )

Area AoV = π( DLVOT /2)2 × (VLVOT /VAoV )
where Dlvot is the diameter of the LVOT and Vlvot is the velocity in the LVOT.
TEE assessments of LVOT and aortic flows and LVOT diameter were described earlier in the section
“Doppler Measurements of Stroke Volume and Cardiac Output.” The continuity equation is the basis for
assessments based on the proximal isovelocity surface area method (10–12), which is described in detail
in Chapter 9.
INTRACARDIAC PRESSURES AND PRESSURE GRADIENTS:

THE BERNOULLI EQUATION
Pressure gradients are used to estimate intracavitary pressures and to assess conditions such as valvu-
lar disease (e.g., aortic stenosis), septal defects, outflow tract abnormalities (e.g., LVOT obstruction), and
major vessel pathology (e.g., coarctation). As blood flows across a narrowed or stenotic orifice, blood flow
velocity increases. The increase in velocity is related to the degree of narrowing. The Bernoulli equation
describes the relation between the increases in blood flow velocity and the pressure gradient across the
narrowed orifice (13):
ΔP = 1/2ρ (v22 − v12 ) + ρ (dv /dt )d x + R(v )

Convection Flow Viscous
acceleration acceleration friction
where P is the pressure gradient across the area of interest (mm Hg), ρ is the density of blood (1.06 × 103 kg/
m3), v1 is the peak velocity of blood flow proximal to the area of interest (m/s), and v2 is the peak velocity of
blood flow across the area of interest (m/s).
In clinical practice, the Bernoulli equation is simplified by ignoring the effects of flow acceleration, viscous
friction, and the velocity proximal to the area of interest (v1) because of the following:
1. Peak flows are of interest in clinical measurements. During peak flow, the flow acceleration is virtually
nonexistent and thus can be ignored.
2. Viscous friction contributes significantly only in discrete orifices with an area of less than 0.25 cm2.
Blood flow is thought to be constant for orifices with an area greater than this, so that viscous friction is
also eliminated in the Bernoulli calculation.
3. For clinically significant lesions, v2 is substantially greater than v1, such that v22 − v12 is approximated by
just v22.
The elimination of these factors yields the simplified Bernoulli equation:
Simplified Bernoulli equation: ΔP = 4 v 22
Therefore, a pressure gradient is obtained in clinical echocardiography by the straightforward process of

measuring the peak velocity of blood flow across the lesion of interest (Fig. 6.6A). However, when v1 is

greater than 1.4 m/s then the Modified Bernoulli equation is considered to account for the higher proxi-
mal velocity:
Modified Bernoulli equation: ΔP = 4 v 22 − 4 v12 or 4(v22 − v12 )
To calculate the pressure gradient, the pulsed wave Doppler sample volume or continuous wave Doppler
beam is directed across the region of interest. The measured peak velocity is then entered into the simpli-
fied Bernoulli equation (ΔΡ = 4v22) to estimate the pressure gradient. When blood flow velocities are high
(≥1.4 m/s), continuous wave Doppler is preferred to avoid the aliasing that may occur with pulsed wave
Doppler. It is imperative that the Doppler beam be positioned so that it interrogates the jet with the highest
velocity; otherwise, the pressure gradient will be significantly underestimated. To obtain the highest veloc-
ity flow, interrogation from multiple windows is preferred. Also, accuracy is improved by assessing multiple
flow profiles (3 to 5 for a regular rhythm and 10 for an irregular rhythm) at end-expiration. The simplified
Bernoulli equation is the basis for most pressure gradient calculations in clinical echocardiography.
Assessment of Valvular Disease

The Bernoulli equation is most commonly used to measure the pressure gradient across a stenotic valve.
This application is illustrated in Figure 6.6A. The assessment of valvular stenosis is discussed extensively in
Chapters 9 and 12.
In addition, the rate of decline in the pressure gradient across the valve is related to the severity of
disease (14). The pressure half-time is the time required for the peak transvalvular pressure gradient to
decrease by 50%. Typically, a larger orifice has a shorter pressure half-time because pressure can equalize
more quickly. The assessment of mitral stenosis and aortic insufficiency (AI) can be aided by pressure half-
time measurements (see Chapters 9 and 12).
Measurement of Intracavitary Pressures

Intracavitary and pulmonary arterial pressures can be measured by combining a Doppler-derived pressure
gradient from a regurgitant jet and a known (or estimated) pressure either proximal or distal to the cham-
ber of interest (Table 6.1). Since accuracy depends on alignment of the ultrasound beam with the blood
flow, velocities of central regurgitant jets are more accurately assessed than those of eccentric jets.
Right Ventricular Systolic Pressure and Pulmonary Artery Systolic Pressure

With the simplified Bernoulli equation, the peak velocity of the tricuspid regurgitant (TR) jet is used to
calculate the pressure gradient between the right ventricle (RV) and right atrium (RA) (15). The peak TR
velocity is obtained by placing the continuous wave Doppler beam parallel to the regurgitant jet. By adding
a known or estimated right atrial pressure (RAP) or central venous pressure (CVP) to the RV–RA pres-
sure gradient, the right ventricular systolic pressure (RVSP) is estimated. In patients without significant
TABLE 6.1 Calculation of Cardiopulmonary Pressures
Pressure Equation
RVSP or PASP = 4(vTR2) + RAP
PAMP = 4(vearly PI)2 + RAP
PADP = 4(vlate PI)2 + RAP
LAP = SBP − 4(vMR)2
LVEDP = DBP − 4(vAI end)2
RVSP, right ventricular systolic pressure; PASP, pulmonary artery systolic pressure; v, peak velocity; TR, tricuspid regurgitation;
RAP, right atrial pressure; PAMP, pulmonary artery mean pressure; PI, pulmonic valve insufficiency; PADP, pulmonary artery
diastolic pressure; LAP, left atrial pressure; SBP, systolic blood pressure; MR, mitral regurgitation; LVEDP, left ventricular end-
diastolic pressure; DBP, diastolic blood pressure; AI, aortic insufficiency.

A B
C D
C D
FIGURE 6.7 The pulmonary artery systolic pressure (PASP) is estimated from the peak velocity of the tricuspid regurgi-
tant velocity profile (TR; V TR). In the figure shown, there are three midesophageal views of the color flow Doppler profile
of the TV. The valve should be interrogated from multiple angles to yield a velocity flow profile that is online with the
Doppler beam, shows minimal interference from other flows, and is associated with the highest velocity. The peak veloc-
ity was 3.76 m/s. The simplified Bernoulli equation was used to calculate the transtricuspid gradient, which when added
to a known central venous pressure of 20 mm Hg yielded a pulmonary artery systolic pressure of 76.6 mm Hg. LA, left
atrium; RA, right atrium; RV, right ventricle; CVP, central venous pressure; TRvel, peak tricuspid regurgitation velocity;
TRgrad, peak tricuspid regurgitation gradient.
pulmonic valve stenosis or RVOT obstruction, the RVSP and pulmonary artery systolic pressure (PASP)
are similar (Figs. 6.7 and 6.8).
RVSP or PASP mm Hg = 4 vTR

2
+ RAP mm Hg
The TEE examination is performed by using the ME RV inflow view with the transducer rotated
from 0 to 110 degrees. Interference from left atrial (LA) flows is minimized in many patients by advanc-
ing the probe to the level of the coronary sinus, so that the position of the Doppler beam is posterior
to the LA.
Pulmonary Artery Mean Pressure and Pulmonary Artery Diastolic Pressure

These pressures are determined from the pulmonic valve regurgitation (pulmonary insufficiency [PI]) flow
profile (15,16) (Fig. 6.9). After the continuous wave Doppler beam is placed parallel to the regurgitant jet,
the peak early diastolic velocity is obtained to measure the early diastolic gradient between the PA and RV.

A B
FIGURE 6.8 The pulmonary artery systolic pressure (PASP) is estimated from the peak velocity of the tricuspid regur-
gitant velocity profile (V TR) using the transgastric RV inflow–outflow view of the tricuspid valve. The peak velocity was
2.67 m/s. The simplified Bernoulli equation (4v2) was used to calculate the transtricuspid gradient. It was then added
to the catheter determined central venous pressure of 8 mm Hg. The estimated pulmonary artery systolic pressure was
36.5 mm Hg. TR, tricuspid regurgitation; RA, right atrium; RV, right ventricle; CVP, central venous pressure; TRvel, peak
tricuspid regurgitation velocity; TRgrad, peak tricuspid regurgitation gradient.
FIGURE 6.9 Pulmonary artery mean and diastolic pressures can be estimated from the early and late peak pulmonary
insufficiency velocities respectively. From the TG RV inflow–outflow view, the pulmonic valve regurgitation is interro-
gated and the lines shown mark the early and late peak velocities. In this case, the Doppler-measured early and late
pulmonary insufficiency gradients (13 and 8 mm Hg, respectively) were added to a catheter derived mean central venous
pressure of 10 mm Hg to yield a mean and diastolic pulmonary artery pressures of 23 and 18 mm Hg respectively. MPA,
main pulmonary artery; PV, pulmonic valve; RV, right ventricle; RA, right atrium; CVP, central venous pressure; mPAP,
mean pulmonary artery pressure; PADP, pulmonary artery diastolic pressure.

Using RA pressure as a substitute for RV pressure in early diastole, this gradient is added to a known or
estimated RA pressure to yield the pulmonary artery mean pressure (PAMP).
PAMP = 4(vearly PI )2 + CVP
The pulmonary artery diastolic pressure (PADP) can be estimated by using the late peak velocity from
the same flow profile.
PADP = 4(vlate PI )2 + CVP
The pulmonic valve regurgitant flow is interrogated by using gastric views with rotation of the trans-
Video 6.1 ducer from 110 to 150 degrees combined with rightward rotation of the TEE probe (Video 6.1).
Left Atrial and Left Ventricular Pressures

Left atrial pressure (LAP) can be derived by applying the Bernoulli equation or by examining the flow pat-
terns across the MV (17) (Fig. 6.10).
To measure the LAP, the peak velocity of the MR flow profile is obtained. The calculated pressure gradi-
ent is then subtracted from a known systemic systolic blood pressure (SBP), which is similar to left ven-
tricular (LV) systolic pressures in the absence of AoV disease or obstructive outflow tract pathologies.
LAP = SBP − 4(vMR )2
Most often, standard ME views provide the best alignment of the ultrasound beam and MR flow.
FIGURE 6.10 The left atrial pressure estimated by using the mitral regurgitation velocity profile. The peak ventricu-
loatrial (LV–LA) pressure gradient, calculated using the peak velocity of the mitral regurgitation profile (line: 4.5 m/s) and
the simplified Bernoulli equation (4v2) yields 81 mm Hg. This value is subtracted from the known systolic blood pressure
(100 mm Hg) to yield a Doppler-estimated left atrial pressure of 19 mm Hg. LAP, left atrial pressure; MR, mitral regurgita-
tion; vel, velocity; SBP, systolic blood pressure; VMR, peak velocity of the mitral regurgitant flow profile.

A B
FIGURE 6.11 Estimation of left ventricular end-diastolic pressure (LVEDP) from the end velocity of the aortic valve
regurgitant (AI) velocity profile. This represents the gradient between the aorta and the left ventricle (Ao-LV grad) during
diastole. The LVEDP was calculated using the modified Bernoulli equation (4v2). This value was then subtracted from the
measured systemic diastolic blood pressure (DPB) of 35 mm Hg. The AI velocity profile was obtained using continuous
wave Doppler from the deep transgastric left ventricular outflow tract window. LV, left ventricle; RV, right ventricle; Ao,
aorta; LA, left atrium.
Left Ventricular End-diastolic Pressure

The LV end-diastolic pressure (LVEDP) is assessed by using the AoV regurgitation (AI) velocity profile (18)
(Fig. 6.11). The end-diastolic velocity is obtained by placing the continuous wave Doppler beam parallel to
the regurgitant jet. The calculated aortic-ventricular gradient, measured from the peak end-diastolic veloc-
ity, is subtracted from the systemic diastolic pressure (DBP) to yield the LVEDP.
LVEDP = DBP − 4(v AI end )2
The AI flow profile is obtained by using TG windows of the AoV and LVOT, in particular the deep and
long-axis views.
LA and LV pressures can also be estimated from the transmitral and pulmonary venous velocity pat-
terns (19–25). This approach is discussed in detail in Chapter 7.
Vascular Resistance (Figs. 6.12 and 6.13)

Cardiac evaluation involves assessments of preload, contractility, and afterload, the latter being referred
to as resistance. This information can be obtained from the right and the left side of the heart. Although
the resistance to flow can be qualitatively determined from measurements of flow and pressures, this does
not replace a quantitative assessment. PVR and systemic vascular resistance (SVR) can be calculated (or
estimated) by comparing the atrioventricular valvular regurgitant jet velocity to the respective ventricular
outflow tract TVI.
Abbas et al. (26) determined that SVR could be assessed by comparing the ratio of the mitral regurgitant
peak velocity (Vmr m/s) to the Doppler flow profile of the LVOT (TVILVOT cm) (Fig. 6.12).
VMR /TVI LVOT

SVR Echo = 0.46 + 49.4(VMR /TVI LVOT )
VMR /TVI LVOT > 0.27 = SVR > 14 Wood units
VMR /TVI LVOT < 0.2 = SVR < 10 Wood units
When the Vmr/TVIlvot was greater than 0.27, the SVR was greater than 14 WU. This had a 70% and 77%
sensitivity and specificity. When the VMR/TVIlvot was less than 0.2, the SVR was less than 10 WU, which

FIGURE 6.12 Measurement of the systemic vascular resistance is demonstrated by comparing the mitral regurgitant
peak velocity (MRV; VMR) to the time–velocity integral of the left ventricular outflow tract (TVILVOT ). Although a specific
value can be obtained, the assessment may be simplified by applying cutoffs: MRV/TVILVOT > 0.27 = SVR > 14 Wood units
and MRV/TVILVOT < 0.2 = SVR < 10 Wood units. SVRECHO, systemic vascular resistance; MRV, VelMR and VMR, mitral regurgitant
peak velocity; TVILVOT, time–velocity integral of left ventricular outflow tract; WU = Wood unit.
carried a 92% and 88% sensitivity and specificity. The basis of these measures considers that the Vmr may
represent systemic velocity, whereas the TVILVOT represents forward flow. A number of variables may
reduce the accuracy of this measure, and include significant mitral and/or AoV disease.
PVR can also be estimated by a similar ratio as described above (27–29) (Fig. 6.13). The PVR may be
estimated by calculating the ratio of the tricuspid valve regurgitant peak velocity (Vtr) to the Doppler pro-
file of the RVOT (TVIrvot). The PVR can be obtained by the following equation (28,29):
PVR = (VTR /TVI RVOT ) × 10 + 0.16

PVR echo = 10(VTR /TVIRVOT ) + 0.16 Wood units
VTR /TVI RVOT > 0.175 (or > 0.2) = PVR > 2 Wood units
FIGURE 6.13 Measurement of the pulmonary vascular resistance is demonstrated by comparing the tricuspid regur-
gitant peak velocity (TRV; V TR) to the time–velocity integral of the right ventricular outflow tract (TVIRVOT ). Although
a specific value can be obtained, the assessment may be simplified by applying cutoffs: TVR/TVIRVOT > 0.27 = PVR >
14 Wood units and TVR/TVIRVOT < 0.2 = PVR < 10 Wood units. PVRECHO, pulmonary vascular resistance; TRV, TRVEL and V TR,
tricuspid regurgitant peak velocity; RVOT TVI and TVIRVOT, time–velocity integral of right ventricular outflow tract; WU =
Wood unit.

A value of 0.2 was found to be the cutoff for patients above or below 2 WU that is, less than 0.175 esti-
mated that the PVR was less than 2 WU.
Other methods to obtain the PVR include measuring components of the RVOT Doppler profile (30).
PVR = 0.156 + (1.54 × [(PEP/AcT )/TT ])
In this equation, the PVR is related to the durations of the pre-ejection period (PEP), the acceleration
time (AcT), and the total systolic time (TT) of the RVOT flow profile.
Ebeid et al. (27) compared a number of components of the main PA Doppler flow profile to measured
PA pressure and resistance. These included the AcT, right ventricular pre-ejection period (RVPEP), the
right ventricular ejection time (RVET), and the TVIrv. Analysis included comparisons of the individual
components and of a number of ratios (27).
RVPEP/RVET RVPEP/TVI RV
Significant correlations were found between these two ratios and PVR. The RVPEP/RVET was able to
discern between patients with normal PVR (RVPEP/RVET <0.3) and elevated PVR (RVPEP/RVET >0.4)
regardless of PA pressures. More accurate was the correlation between RVPEP/TVIrv and PVR. A value less
than 0.4 m/s selected patients with a PVR less than 3 WU. A value between 0.4 and 0.6 m/s correlated with
a PVR of 3 to 7.5 WU. A value equal to or greater than 0.6 m/s predicted a PVR equal to or greater than
7.5 WU. These data had greater than 90% accuracy.
Additional Imaging Techniques

Propagation velocity:
Heart chamber pressures can be assessed or estimated using the propagation velocity (VProp), which
combines color Doppler with m-mode imaging across the MV to yield a color Doppler profile of transmi-
tral flow from the mitral annular plane to approximately 4 cm into the ventricular cavity (31,32) (Fig. 6.14).
A VProp > 45 cm/s is considered normal, and <25 cm/s is consistent with restrictive physiology and elevated
left heart pressures (>15 mm Hg). When combined with conventional pulse wave Doppler data, an E/VProp
≥2 correlates with elevated LVEDP.
Shandas et al. (31) assessed PVR by measuring the propagation velocity of the RVOT (RVOT Vprop)
or PA outflow. A higher RVOT Vprop correlates with a lower PVR. An RVOT Vprop greater than 18 cm/s
A B
FIGURE 6.14 The propagation velocity is obtained by assessing flow across the mitral valve with simultaneous color
flow Doppler and M-mode imaging. The slope is measured from the early filling phase from the mitral annular plane
to approximately 4 cm toward the LV apex (yellow line). The slope reflects the composite of the pressure differential
between the left atrium (LA) and left ventricle (LV) and the differential chamber compliances. This value has been used to
calculate chamber pressures and to estimate diastolic function.

FIGURE 6.15 Tissue Doppler analysis measures the tissue velocity, which is the speed of motion of the myocardium
during the cardiac cycle. The velocity profile (right panel) reflects early diastole (E′; Em), late diastole (A′; Am), and systole
(S′; Sm). These data allow assessments of both diastolic and systolic functions, and chamber pressures.
correlated with a PVR less than 6 WU. In the in vitro model, this cutoff was found at a RVOT Vprop greater
than 15 cm/s. An RVOT Vprop greater than 20 cm/s was consistent with a PVR less than or equal to 2 WU.
Tissue Doppler Analysis

By filtering out high-velocity blood signals, tissue Doppler imaging (TDI) can analyze the low velocity sig-
Video 6.2 nals of myocardial motion (Fig. 6.15, Video 6.2). This information is then used to assess heart function and
assess chamber pressures (33–35).
For purposes of measuring global chamber function and pressures, myocardium at the level of the annu-
lar plane (septal and/or lateral regions) is sampled for motion in the direction of the apex (Fig. 6.15). Tissue
Doppler analysis focuses on systolic motion (Sm) where >7.5 cm/s correlates with a normal LVEF and
<6.0 cm/s predicts poor prognosis and the early diastolic (E′) motion where >8.0 cm/s correlates with
normal relaxation and E′ lateral wall ≤7 cm/s and E′ septal wall ≤6 cm/s suggest abnormal relaxation.
Compared to conventional PW Doppler data, the analogous TDI data often has the advantage of being less
sensitive to loading conditions.
Left heart filling and pulmonary capillary wedge pressure are assessed by combining pulse wave and
TDI measurements. The ratio of the early filling blood flow velocity (E) measured with PW Doppler to
the early diastolic tissue velocity (E′) measured with TDI is commonly chosen (34–36). This approach is
superior to using the E-wave velocities alone for PCWP estimation as the E-wave values are impacted by
both filling pressure and diastolic dysfunction. For example, a patient with impaired relaxation will have a
low E velocity despite normal filling pressures (see Chapter 7) and thus the E velocity underestimates filling
pressure in this setting. By dividing E by the E′ measurement in effect provides an adjustment for diastolic
disease and thereby a measure of preload that is more accurate in the presence of cardiac impairment. The
benefits of this approach have been born out with the E/E′ ratio correlating better with clinical symptom-
atology and PCWP than other individual velocities. PCWP is estimated as:
PCWP = 1.5(E / E′ ) + 1.5
Accordingly, values of E/E′ ≥10 are consistent with PCWP > 15 mm Hg.
Similarly, tissue Doppler of the right heart (tricuspid valve annular velocity) can estimate right-sided
pressures and outcomes (37). In the operating room setting for patients with reduced RV systolic function:
RAP = (E/E′ ) + 5

HEART RHYTHM
Pulsed wave Doppler echocardiography is valuable in assessing heart rhythm. In particular, Doppler analy-
sis of transmitral flow and flow in the LA appendage may be useful in assessing rate, rhythm, and atrial
function. As discussed in detail in Chapter 7, normal transmitral flow analysis demonstrates early (E wave)
and late (A wave) atrial contraction components. The latter describes the contribution of the atrial contrac-
tion to the ventricular preload. The presence of both waves indicates that a sinus or atrioventricular rhythm
is present. The velocity profile of the LA appendage may also help to diagnose an atrial dysrhythmia. The
normal LA appendage profile contains a single positive deflection during atrial contraction.
SUMMARY
Quantitative hemodynamic assessment with Doppler echocardiography offers a range of measurements:
Valve area, pressure gradients, chamber pressures, blood flow, resistances, and rate/rhythm. These mea-
surements are essential in assessing valvular disease. The echocardiographer should establish a systematic
approach to quantitative Doppler that is clinically useful and can be performed reliably and easily online.
In combination with the two-dimensional echocardiographic examination, these quantitative techniques
provide extensive information about cardiac performance.
REFERENCES
1. Savino JS, Troianos CA, Aukburg S, et al. Measurements of pulmonary blood flow with transesophageal two-dimensional and
Doppler echocardiography. Anesthesiology. 1991;75:445–451.
2. Gorcsan J III, Diana P, Ball BS, et al. Intraoperative determination of cardiac output by transesophageal continuous wave
Doppler. Am Heart J. 1992;123:171–176.
3. Maslow AD, Haering J, Comunale M, et al. Measurement of cardiac output by pulsed wave Doppler of the right ventricular
outflow tract. Anesth Analg. 1996;83:466–471.
4. Stewart WJ, Jiang L, Mich R, et al. Variable effects of changes in flow rate through the aortic, pulmonary, and mitral valves on
valve area and flow velocity: Impact on quantitative Doppler flow calculations. J Am Coll Cardiol. 1985;6:653–666.
5. Muhiuden IA, Kuecherer HF, Lee E, et al. Intraoperative estimation of cardiac output by transesophageal pulsed Doppler
echocardiography. Anesthesiology. 1991;74:9–14.
6. Darmon PL, Hillel Z, Mogtader A, et al. Cardiac output by transesophageal echocardiography using continuous-wave Doppler
across the aortic valve. Anesthesiology. 1994;80:796–805.
7. Perrino AC, Harris SN, Luther MA. Intraoperative determination of cardiac output using multiplane transesophageal echo-
cardiography: A comparison to thermodilution. Anesthesiology. 1998;89:350–357.
8. Valdes-Cruz LM, Horowitz S, Mesel E, et al. A pulsed Doppler echocardiographic method for calculating pulmonary and sys-
temic blood flow in atrial level shunts: Validation studies in animals and initial human experience. Circulation. 1984;69:80–86.
9. Blumberg FC, Pfeifer M, Holmer SR, et al. Quantification of aortic stenosis in mechanically ventilated patients using multi-
plane transesophageal Doppler echocardiography. Chest. 1998;114:94–97.
10. Bargiggia GS, Tronconi L, Sahn DJ, et al. A new method for quantitation of mitral regurgitation based on color flow Doppler
imaging of flow convergence proximal to regurgitant orifice. Circulation. 1991;84:1481–1489.
11. Rodriguez L, Thomas JD, Monterroso V, et al. Validation of the proximal flow convergence method: Calculation of orifice area
in patients with mitral stenosis. Circulation. 1993;88:1157–1165.
12. Rittoo D, Sutherland GR, Shaw TR. Quantification of left-to-right atrial shunting defect size after balloon mitral commis-
surotomy using biplane transesophageal echocardiography, color flow Doppler mapping, and the principle of proximal flow
convergence. Circulation. 1993;87:1591–1603.
13. Nishimura RA, Miller FA, Callahan MJ, et al. Doppler echocardiography: Theory, instrumentation, technique, and application.
Mayo Clin Proc. 1985;60:321–343.
14. Nakatani S, Masuyama T, Kodama K, et al. Value and limitations of Doppler echocardiography in the quantification of stenotic
mitral valve area: Comparison of the pressure half-time and the continuity equation methods. Circulation. 1988;77:78–85.
15. Come PC. Echocardiographic recognition of pulmonary arterial disease and determination of its cause. Am J Med. 1988;
84:384–393.
16. Lee RT, Lord CP, Plappert T, et al. Prospective Doppler echocardiographic evaluation of pulmonary artery diastolic pressure
in the medical intensive care unit. Am J Cardiol. 1989;64:1366–1377.
17. Gorcsan J III, Snow FR, Paulsen W, et al. Noninvasive estimation of left atrial pressure in patients with congestive heart failure
and mitral regurgitation by Doppler echocardiography. Am Heart J. 1991;11:858–863.
18. Nishimura RA, Tajik AJ. Determination of left-sided pressure gradients by utilizing Doppler aortic and mitral regurgitation
signals: Validation by simultaneous dual catheter and Doppler studies. J Am Coll Cardiol. 1988;11:317–331.
19. Oh JK, Appleton CP, Hatle LK, et al. The noninvasive assessment of left ventricular diastolic function with two-dimensional
and Doppler echocardiography. J Am Soc Echocardiogr. 1997;10:46–70.

20. Nishimura RA, Housmans PR, Hatle LK, et al. Assessment of diastolic function of the heart: Background and current applica-
tions of Doppler echocardiography. Part II Clinical Studies. Mayo Clin Proc. 1989;64:181–194.
21. Nagueh SF, Kopelen HA, Quinones MA. Assessment of left ventricular filling pressures by Doppler in the presence of atrial
fibrillation. Circulation. 1996;94:138–145.
22. Temporelli PL, Scapellato F, Corra U, et al. Estimation of pulmonary wedge pressure by transmitral Doppler in patients with
chronic heart failure and atrial fibrillation. Am J Cardiol. 1999;83:724–727.
23. Moller JE, Poulsen SH, Songderfaard E, et al. Preload dependence of color M-mode Doppler flow propagation velocity in
controls and in patients with left ventricular dysfunction. J Am Soc Echocardiogr. 2000;13:902–909.
24. Garcia MJ, Ares MA, Asher C, et al. An index of early left ventricular filling that combined with pulsed Doppler peak E velocity
may estimate capillary wedge pressure. J Am Coll Cardiol. 1997;9:448–454.
25. Gonzalez-Viachez F, Ares M, Ayuela J, et al. Combined use of pulsed and color M-mode Doppler echocardiography for the
estimation of pulmonary capillary wedge pressure: An empirical approach based on an analytical relation. J Am Coll Cardiol.
1999;34:515–553.
26. Abbas AE, Fortuin D, Patel B, et al. Noninvasive measurement of systemic vascular resistance using Doppler echocardiogra-
phy. J Am Soc Echocardiogr. 2004;17:834–838.
27. Ebeid MR, Ferrer PL, Robinson B, et al. Doppler echocardiographic evaluation of pulmonary vascular resistance in children
with congenital heart disease. J Am Soc Echocardiogr. 1996;9:822–831.
28. Abbas AE, Fortuin FD, Schiller NB, et al. A simple method for noninvasive estimation of pulmonary vascular resistance. J Am
Coll Cardiol. 2003;41:1021–1027.
29. Frazaneh R, McKeown BH, Dang D, et al. Accuracy of Doppler-estimated pulmonary vascular resistance in patients before
liver transplantation. Am J Cardiol. 2008;101:259–262.
30. Scapellato F, Temporelli PL, Eleuteri E, et al. Accurate noninvasive estimation of pulmonary vascular resistance by Doppler
echocardiography in patients with chronic heart failure.J Am Coll Cardiol. 2001;37:1813–1819.
31. Shandas R, Weinberg C, Ivy DD, et al. Development of a noninvasive ultrasound color M-mode means of estimating pul-
monary vascular resistance in pediatric pulmonary hypertension: Mathematical analysis, in vitro validation, and preliminary
clinical studies. Circulation. 2001;104:908–913.
32. Kidawa M, Coignard L, Drobinski G, et al. Comparative value of tissue Doppler imaging and m-mode color Doppler mitral
flow propagation velocity for the evaluation of left ventricular filling pressure. Chest. 2005;128:2544–2550.
33. Hasegawa H, Little WC, Ohno M, et al. Diastolic mitral annular velocity during the development of heart failure. J Am Coll
Cardiol. 2003;41:1590–1597.
34. Nagueh SF, Middleton KJ, Kopelen HA, et al. Doppler tissue imaging: A noninvasive technique for evaluation of left ventricular
relaxation and estimation of filling pressures. J Am Coll Cardiol. 1997;15:1527–1533.
35. Nagueh SF, Mikati I, Kopelen HA, et al. Doppler estimation of left ventricular filling pressure in sinus tachycardia. A new
application of tissue Doppler imaging. Circulation. 1998;98:1644–1650.
36. Nagueh SF, Lakkis NM, Middleton KJ, et al. Doppler estimation of left ventricular filling pressures in patients with hypertro-
phic cardiomyopathy. Circulation. 1999;99:254–261.
37. Sade LE, Gulmez O, Eroglu S, et al. Noninvasive estimation of right ventricular filling pressure by ratio of early tricuspid inflow
to annular diastolic velocity in patients with and without recent cardiac surgery. J Am Soc Echocardiogr. 2007;20:982–988.

QUESTIONS
C ASE 1 C ASE 2
70-year-old man having CABG surgery is being 48-year-old man is having CABG surgery. Monitoring
monitored with an A-line, CVP, and TE. includes an A-line, CVP, and TEE. The LV appears to
On echo, the AV appears to be sclerosed with restricted be dilated and hypocontractile. There is a central jet
leaflet motion and trace AR. of MR judged to be 2+ to 3+ in severity. The following
measurements are made:
The following measurements are made:
t 4ZTUFNJD#1 140/65 mm Hg
t Heart rate 80 bpm
t %JBNFUFS-705 2.5 cm
t Systemic BP 105/65 mm Hg
t 57*-705 15 cm
t CVP 12 mm Hg
t .JUSBMBOOVMBSEJBNFUFS 3.7 cm
t Diameter LVOT 2 cm t 57*NJUSBMBOOVMBSGMPX 12 cm
t TVI LVOT 20 cm t 1*4"SBEJVT 0.7 cm
t Peak velocity LVOT 1.2 m/s t 1*4"BMJBTWFMPDJUZ 45 cm/s
t TVI AV 65 cm t 1FBLWFMPDJUZ.3 445 cm/s
t 57*.3 180 cm
t Peak velocity AV 3.8 m/s
t Peak velocity TR 2.5 m/s 6. The stoke volume (mL) through the LVOT
is:
1. The calculated stroke volume is:
a. 94
a. 62 mL
b. 74
b. 31 mL
c. 30
c. 2,480 mL
d. 21
d. 1,240 mL
7. The stroke volume (mL) through the mitral
2. The calculated right ventricular systolic
valve is:
pressure in mm Hg is:
a. 188
a. 12
b. 144
b. 25
c. 130
c. 16
d. 94
d. 37
8. The mitral valve regurgitant volume (mL) is:
3. The calculated peak aortic valve gradient in
a. 130
mm Hg is:
b. 74
a. 14.4
c. 68
b. 58
d. 56
c. 104
d. consistent with mild aortic stenosis 9. The calculated left atrial pressure in mm Hg
is:
4. Based on the continuity equation the
a. 34
calculated aortic valve area in cm2 is:
b. 21
a. 0.7
c. 15
b. 1.0
d. 10
c. 1.4
d. 2.2
5. Based on the double envelope technique the
aortic stenosis is graded as severe.
a. True
b. False

C ASE 3 14. The calculated stroke volume (mL) using

LVOT measurements is:
60-year-old obese female s/p cardiac arrest following
total hip replacement. Emergent intraoperative TEE a. 64
suggests a pulmonary embolus. b. 74
Vital signs: c. 84
d. 94
Heart rate 100 bpm
Systemic BP 90/60 mm Hg 15. The patient’s examination demonstrates
CVP 20 mm Hg aortic insufficiency.
TEE data: a. True
Pulmonary artery diameter 2.2 cm b. False
Pulmonary artery TVI 8 cm 16. The regurgitant fraction across the aortic
Aortic valve TVI 14 cm valve is:
TR peak velocity 3.8 m/s a. Negligible
b. About one-fourth of ejected volume
10. The right heart stroke volume (mL) is:
c. About one-third of ejected volume
a. 20
d. About one-half of ejected volume
b. 30
c. 40 17. The calculated left ventricular end-diastolic
d. 60 pressure (mm Hg) is:
a. 12
11. The calculated cardiac output (L/min) is:
b. 24
a. 2.5
c. 36
b. 3
d. 48
c. 4
d. 5 C ASE 5
12. Calculated RV systolic pressure (mm Hg) is: 56-year-old man presents for AV surgery.
a. 18 Vital signs:
b. 38 Heart rate 84 bpm
c. 58 Systemic BP 90/70 mm Hg
d. 78 CVP 14 mm Hg
BSA 1.98 m2
13. The estimated aortic valve area (cm2) is:
a. not calculable by continuity equation TEE data:
b. 2.1 LVOT TVI 23 cm
c. consistent with moderate stenosis LVOT diameter 2.2 cm
d. consistent with severe stenosis Aortic valve mean 63 mm Hg
gradient
C ASE 4 Aortic valve TVI 122 cm
A 60-year-old, 84-kg male presents with acute aortic TR peak velocity 3.6 m/s
dissection.
Vital signs: 18. The pulmonary artery systolic pressure
Heart rate 80 bpm (mm Hg) is estimated as:
Systemic BP 120/60 mm Hg a. 28
TEE data:
b. 52
c. 66
LVOT diameter 2 cm
d. 74
LVOT TVI 30 cm
MV diameter 3 cm
MV TVI 10 cm
AI TVI 160 cm
AI end-diastolic velocity 3 m/s

C ASE 6 19. The calculated left atrial pressure (mm Hg)

is:
78-year-old man undergoing AAA surgery becomes
hypoxic and hypotensive with cross-clamping of the a. 12
abdominal aorta. TEE reveals 1–2+ MR, 1+ TR without b. 25
AS or AI. The following measurements are made: c. 36
Vital signs: d. 45
Heart rate 110 bpm 20. The calculated right ventricular systolic
Systemic BP 85/50 mm Hg pressure (mm Hg) is:
CVP 8 mm Hg a. 57
TEE data: b. 49
Aortic valve area midsystole 2.3 cm2 c. 37
Aortic valve area maximum 2.7 cm2 d. exceeds left ventricular systolic pressure
Aortic valve TVI 12 cm (pressure inversion)
Peak velocity MR 3.5 m/s
Peak velocity TR 3.5 m/s

7 A Practical Approach to the Echocardiographic
Evaluation of Ventricular Diastolic Function
Stanton K. Shernan
I N COMPARISON TO SYSTOLE, THE diastolic phase of the cardiac cycle has only recently acquired appro-
priate recognition as an important, independent component of overall cardiac performance. Diastole is
no longer perceived simply as a passive stage of ventricular filling interposed between each contraction.
Adequate ventricular filling is actually dependent upon a complex interaction between ventricular relax-
ation, compliance, and systolic function, in addition to an important late diastolic contribution from atrial
contraction.
Following the advent of cardiac catheterization in the 1960s, quantification of ventricular mechanics
and ventricular diastolic properties accelerated with the introduction of pulse wave Doppler echocar-
diography (PWD) in the early 1980s. The relative feasibility, safety, and practicality of echocardiography
has helped to delineate diastolic dysfunction over the last several decades, as a major pathophysiologic
component of several cardiac disorders including acute and chronic congestive heart failure (CHF) (1). In
addition, Doppler echocardiographic modalities have been used to predict functional class and prognosis
(2). Recent echocardiographic studies have also suggested that diastolic dysfunction may contribute to
perioperative hemodynamic instability and adverse outcomes following cardiac surgery (3). This chapter
presents a practical approach to understanding the importance and utility of traditional and newer echo-
cardiographic modalities in assessing ventricular filling and diastolic dysfunction.
BASICS OF DIASTOLIC PHYSIOLOGY

The diastolic phase of the cardiac cycle is defined as the period from aortic valve (AV) closure to mitral
valve (MV) closure (Fig. 7.1). Diastole can be further divided into an initial isovolumic relaxation period,
followed by early rapid left ventricular (LV) inflow responsible for 80% to 90% of diastolic filling, diastasis,
and finally, atrial systole (4). LV filling during diastole is dependent on a complex interaction of numerous
factors including ventricular relaxation, diastolic suction, viscoelastic forces of the myocardium, pericar-
dial restraint, ventricular interaction, MV dynamics, load heterogeneity, intrathoracic pressure, heart rate/
rhythm, and atrial function (5).
Diastolic dysfunction is often defined clinically as an impaired capacity of the ventricles to fill at low
pressure and usually involves an abnormality in ventricular relaxation and/or chamber compliance. LV
relaxation is associated with re-sequestration of calcium from the cytosol to the sarcoplasmic reticu-
lum, via a complex energy-dependent process that is required to deactivate the contractile elements
and subsequently allow the myofibrils return to their original, precontraction length (6). Ventricular
relaxation is classically evaluated with high-fidelity, manometer-tipped catheters that measure the rate
and duration of the LV pressure decrease after systolic contraction during isovolumic relaxation (Fig.
7.2A) (7). The time constant of relaxation (τ) is a clinically and experimentally acceptable technique
for assessing isovolumic relaxation, although limitations have been described (6). LV chamber compli-
ance is dependent upon the passive properties of the ventricle, and is determined from the exponential
relationship between the change in volume and the change in pressure during diastolic filling (dV/dP)
(Fig. 7.2B) (7).
The LA contribution to LV end-diastolic volume (LVEDV) can also be an important determinant of
filling. The LA serves not only as a blood reservoir and passive conduit, but also as an active pump during
contraction at end-diastole. The LA contribution to LV diastolic filling is usually <20% in young healthy
patients, yet may approach 50% in patients with decreased LV filling associated with early diastolic
138 dysfunction.

7. A Practical Approach to the Echocardiographic Evaluation of Ventricular Diastolic Function 139
LV
volume
1 2 3 4
AVO
Aorta AVC
LV
pressure
LA
MVC
MVO
FIGURE 7.1 Diastolic phase of the cardiac cycle. During isovolumic relaxation (1), left ventricular (LV) pressure falls
rapidly following aortic valve closure (AVC). When LV pressure decreases below left atrial (LA) pressure, the mitral valve
opens (MVO) initiating early, rapid LV filling (2). Equilibration of LV and LA pressures results in diminished transmitral
flow during diastasis (3) until atrial contraction (4) which normally contributes <20% of the total LV end-diastolic volume.
Diastole terminates with MV closure (MVC) prior to isovolumic contraction and the AV opening (AVO) which permits LV
ejection. (Reproduced with permission from Plotnick GD. Changes in diastolic function—Difficult to measure, harder to
interpret. Am Heart J. 1989;118:637–641.)
ECHOCARDIOGRAPHIC EVALUATION OF LEFT

VENTRICULAR DIASTOLIC FUNCTION
Conventional, direct assessment of diastolic function requires invasive measurements (high-fidelity,
intraventricular, micromanometer catheters) or sophisticated technology (three-dimensional sonomi-
crometry, cardiac magnetic resonance imaging, ultrafast computed tomography) (6). Pulmonary artery
catheterization can be useful for assessing global cardiac performance; however, evaluation of diastolic
function is limited by the inability to directly measure LV pressure, volume, or transmitral flow. In con-
trast, echocardiography provides a relatively safe, practical, and noninvasive means to evaluate diastolic
function.
Two-dimensional and M-mode Echocardiography

Indirect evidence of diastolic function can be obtained during a comprehensive two-dimensional (2D)
echocardiographic examination by assessing LV ejection fraction and LVEDV. Echocardiographic evidence
of LV hypertrophy without dilatation and with normal systolic function indicates the presence of diastolic
heart failure (DHF) in a symptomatic patient. LA enlargement (>4 cm) is often associated with elevated LV
filling pressures (8).
Doppler Echocardiographic Evaluation of LV Filling: Transmitral Inflow

The utilization of Doppler echocardiography to measure transmitral blood flow (TMDF) velocities pro-
vides valuable information toward the assessment of diastolic function. The PWD recording of TMDF

100
LV pressure
HCM Normal
Left ventricular pressure (mm Hg)
Peak b
Diastolic pressure
(−) dP/dt c
50
LV dP/dt (P =&e−t/τ)
MVO a
0 500 1000
A Time (s) Diastolic volume B
FIGURE 7.2 A: Left ventricular (LV) relaxation can be invasively evaluated by measuring the minimum value of the
first derivative of ventricular pressure with respect to time (−dp/dtmin) or preferably, by calculating the time constant (τ)
of isovolumic LV pressure decline according to the equation shown. An increase in τ (dashed line) generally indicates
impaired LV relaxation (myocardial ischemia, hypertrophic heart disease, negative inotropes) which can be associated
with decreased LV filling and diminished cardiac performance. P, LV pressure; A, LV pressure at −dp/dtmin; t, time after
−dp/dtmin; e, natural logarithm; MVO, mitral valve opening. B: LV pressure–volume (P–V) relationships. LV compliance
(dV/dP) is described by the tangent drawn to the P–V curve at a particular point. A decrease in LV compliance results in
an increase in LV filling pressure depicted as either a shift of the pressure–volume (P–V) curve upward and to the left
when myocardial stiffness increases (point a–c), or to a steeper portion of the curve when volume increases (point a–b).
(Reproduced with permission from Zile M, Smith V. Relaxation and diastolic properties of the heart. In: Fozzard H, Haber
E, Jennings R, Katz A, Morgan H, eds. The Heart and Cardiovascular System: Scientific Foundations, 2nd ed. New York, NY:
Raven; 1991:1353–1367.)
velocities is obtained by placing the sample volume at the MV leaflet tips (Fig. 7.3). A typical TMDF velocity
profile has a biphasic pattern. An initial peak flow velocity (E-wave) occurs during early diastolic filling and
a later peak flow velocity (A-wave) occurs during atrial systole. Blood flow during the interposed period
of diastasis is usually minimal, since little LV filling occurs during this phase. Several indices of diastolic
function have been derived from the TMDF profile and correlated with more classic measures of diastolic
function including angiography, radionucleotide techniques, and direct measures of intraventricular pres-
sures (Table 7.1) (6,9).
TMDF velocities are determined by the transmitral pressure gradient (TMPG) which is dependent upon
several variables including heart rate and rhythm, early filling loads, atrial contractility, MV disease, ven-
tricular septal interactions, the intrinsic LV lusitropic state, and ventricular compliance (10). With normal
aging, delayed LV relaxation at any given LV pressure, creates a lower initial TMPG, which results in pro-
portionally less early filling (lower peak E-wave velocity) and a greater, compensatory late filling (higher
peak A-wave velocity) accounting for 35% to 40% of LV diastolic inflow. Conversely, more efficient LV
relaxation and elastic recoil observed in young adults is associated with predominant early LV filling cor-
responding with a greater initial TMPG, and a smaller contribution (10% to 15%) from atrial contraction.
Alternatively, TMPG elevation in patients with decreased LV compliance is primarily due to a progres-
sively increasing LA pressure (LAP). Thus alterations in LV relaxation and compliance along with con-
sequential changes in LAP alter the TMPG and resulting TMDF profiles. The isovolumic relaxation time
(IVRT, the time from cessation of systolic ventricular outflow to the onset LV inflow) is also affected by

IVRT DT AWD
TVIE TVIA
Peak A
A wave
Peak E
B E wave
FIGURE 7.3 A: Transmitral Doppler flow velocity (TMDF) profile using transesophageal echocardiography. The TMDF
profile is obtained by placing a pulse wave Doppler sample volume (1 to 2 mm) at the tips of the mitral valve (MV).
The initial rapid phase of early left ventricular (LV) filling (E) is followed by a variable period of minimal flow (diastasis)
and finally late diastolic filling during atrial contraction (A). B: Schematic of TMDF profile depicting relevant indices of
diastolic function. Several indices of LV diastolic function can be obtained from the TMDF profile including the E- and
A-wave peak velocities and ratio, the E- and A-wave time velocity integrals (TVI, area under each Doppler envelope) and
corresponding E/A TVI ratio, the A-wave duration (AWD), the E-wave deceleration time (DT, the time interval from the
peak E-wave velocity to the zero baseline), and the isovolumic relaxation time (IVRT, the time from cessation of systolic
ventricular outflow to the onset of transmitral LV inflow).
alterations of diastolic function. A shortened IVRT (<60 milliseconds) indicates premature MV opening
and can be observed in patients with elevated LAP. Delayed MV opening (IVRT > 110 milliseconds) occurs
with impaired LV relaxation. The deceleration time (DT, the interval from the peak E-wave velocity to the
zero baseline) generally reflects the mean LAP and LV compliance (11). A relatively short DT (<140 mil-
liseconds) can be seen in patients with reduced LV compliance, whereas a prolonged DT is associated with
poor LV relaxation.
Changes in LV relaxation and compliance contribute to the spectrum of Doppler LV filling patterns
that are observed with progressive diastolic dysfunction. The initial abnormality of diastolic filling in most
disorders of cardiac physiology is impaired myocardial relaxation exceeding that expected with aging
alone. Impaired LV relaxation occurs with myocardial ischemia/infarction, LV hypertrophy, hypertro-
phic cardiomyopathy, and in the early stages of infiltrative disorders (12). The TMDF profile associated
with impaired relaxation is typically characterized by a prolonged IVRT and a decreased initial TMPG

TABLE 7.1 Left and Right Ventricular Doppler Echocardiographic Indices of Diastolic Function Filling
Dynamics in Normal Subjects
Age 21–49 y Age ≥ 50 y

Left ventricular inflow
Peak E (cm/s) 72 (44–100) 62 (34–90)
Peak A (cm/s) 40 (20–60) 59 (31–87)
E/A ratio 1.9 (0.7–3.1) 1.1 (0.5–1.7)
DT (ms) 179 (139–219) 210 (138–282)
IVRT (ms) 76 (54–98) 90 (56–124)
Pulmonary vein
Peak S (cm/s) 48 (30–66) 71 (53–89)
Peak D (cm/s) 50 (30–70) 38 (20–56)
S/D ratio 1 (0.5–1.5) 1.7 (0.8–2.6)
Peak A (cm/s) 19 (11–27) 23 (−5–51)
Right ventricular inflow
Peak E (cm/s) 51 (37–65) 41 (25–57)
Peak A (cm/s) 27 (11–43) 33 (17–49)
E/A 2 (1–3) 1.3 (0.5–2.1)
DT (cm/s) 188 (144–232) 198 (152–244)
Superior vena cava
Peak S (cm/s) 41 (23–59) 42 (18–66)
Peak D (cm/s) 22 (12–32) 22 (12–32)
Peak A (cm/s) 13 (7–19) 16 (10–22)
Normal reference values for Doppler echocardiographic indices of ventricular diastolic function in two age groups of normal
subjects. Data presented are mean values (confidence interval). A, late diastolic atrial flow velocity associated with atrial
contraction; D, diastolic flow velocity; DT, deceleration time; E, early diastolic flow velocity; IVRT, isovolumic relaxation time;
S, systolic flow velocity.
Reproduced with permission from Cohen G, Pietrolungo J, Thomas J, et al. A practical guide to assessment of ventricular
diastolic function using Doppler echocardiography. J Am Coll Cardiol. 1996;27: 1754.
(Fig. 7.4) (13). Consequently, the peak E-wave velocity decreases relative to the peak A-wave velocity
when LV relaxation is impaired (E/A < 1), since the MV tends to open before relaxation is complete. In
addition, the duration of LV relaxation is prolonged resulting in a prolonged DT (5) since the LA–LV pres-
sure gradient takes longer to equilibrate. There is a subsequent, compensatory flow increase during atrial
contraction accounting for the increased peak A-wave velocity, time velocity integral (TVI), and dura-
tion due to the relatively high atrial preload. Thus, the TMDF velocity profile with impaired relaxation
is characterized by “E/A reversal” (decreased peak E-wave velocity and increased peak A-wave velocity),
prolonged IVRT, and prolonged DT.
Diastolic dysfunction associated with markedly decreased LV compliance and severely increased LAP
is often described as a “restrictive” LV filling disorder (12). The TMDF profile associated with a restric-
tive pattern of LV diastolic dysfunction is characterized by an elevated peak E-wave velocity relative to
the A-wave velocity due to the elevated LAP (Fig. 7.4) (13). Even though impaired relaxation co-exists
with decreased compliance when diastolic dysfunction has progressed, the consequential increase in LV
end-diastolic pressure (LVEDP) results in a markedly elevated LAP and an elevated peak E-wave velocity,
consistent with very rapid filling during early diastole. The IVRT is shortened as the MV opens prematurely
due to the elevated LAP. The DT is also abnormally short, as early transmitral flow into the poorly com-
pliant LV results in rapid equilibration of LA and LV pressures that may even be associated with diastolic
mitral regurgitation (MR) (12). Finally, the peak A-wave velocity and duration tend to be compromised by
poor atrial contractility and the rapid increase in LV pressure, which can prematurely terminate late mitral
inflow. Thus, a restrictive TMDF velocity profile is characterized by an elevated peak E-wave velocity and
decreased peak A-wave velocity (E/A ratio > 2) along with a shortened IVRT and DT.

Impaired LV relaxation
Decrease in LV compliance
Young Middle age Older Poor relaxation Pseudonormal Restrictive

TMDF m/s
0
A
1 E IVRT
PVDF m/s
PVS
PVD
0.5
0
PVAR
A
2.0
1.5
E/A ratio
1.0
0.5
0
Best Worst
B Diastolic function
FIGURE 7.4 A: The impact of progressive left ventricular (LV) diastolic dysfunction on transmitral (TMDF) and pulmo-
nary venous Doppler flow (PVDF) velocity profiles. Note that all pulsed Doppler indices of the TMDF and PVDF profiles
present a parabolic distribution over the progression from normal to advanced diastolic dysfunction. The transmitral
pressure gradient is initially elevated in normal, young individuals due to vigorous LV relaxation and elastic recoil, before
diminishing when relaxation becomes impaired, and finally increasing again when left atrial pressure increases due
to an elevated LV end-diastolic pressure in the restrictive pattern of LV diastolic dysfunction. Respective changes are
noted in the PV profile. E, E-wave; A, A-wave; IVRT, LV isovolumic relaxation time; PVAR, late diastolic retrograde velocity;
PVS1, first systolic component; PVS2, second systolic component; PVD, diastolic component. (Modified with permission
from Appleton C, Hatle L. The natural history of left ventricular filling abnormalities: assessment by two-dimensional
and Doppler echocardiography. Echocardiography. 1992;9:437–457.) B: Parabolic distribution of transmitral E/A velocity
ratios associated with progressive diastolic dysfunction.
Typically there is a progression of diastolic dysfunction from impaired relaxation to restrictive

pathophysiology. During this transition, the TMDF profile may assume a pseudonormalized pattern that
resembles normal LV filling (Fig. 7.4A) (13). The pseudonormalized filling pattern represents a moderate
stage of diastolic dysfunction where a “normal” early TMPG is generated by the balance between compro-
mised LV relaxation and gradually increasing filling pressures as LV compliance decreases. Consequently,
for varying degrees of diastolic dysfunction, the spectrum of E/A velocity ratios assumes a parabolic shape
beginning with a vigorous LV relaxation pattern seen in young, athletic individuals and terminating with a
similar appearing restrictive pattern consistent with severe diastolic dysfunction (Fig. 7.4B). The intermedi-
ate, pseudonormalized stage of diastolic dysfunction is therefore characterized by normal values for peak
E-wave and A-wave velocities, IVRT, and DT. Reducing preload by utilizing reverse Trendelenburg posi-
tioning, partial cardiopulmonary bypass (CPB), a Valsalva maneuver (14), or by administering nitroglycerin

may also reveal underlying impaired LV relaxation in a patient with pseudonormalized transmitral inflow
(15). Normal individuals usually respond to preload reduction with a more proportional decrease in both
E- and A-wave velocities (12). Preload reduction may also be useful in grading the severity of diastolic
dysfunction (15). For example, a restrictive pattern is considered “irreversible, end-stage” if it does not
pseudonormalize in response to preload reduction (4).
Doppler Echocardiographic Evaluation of LA Filling: Pulmonary Venous Flow

The evaluation of LA filling can provide important insight into the assessment of LV diastolic function
especially when combined with data obtained from the TMDF. A typical pulmonary venous Doppler flow
(PVDF) profile consists of an antegrade systolic velocity which may appear monophasic, or biphasic espe-
cially in the presence of low LAP probably owing to temporal dissociation of atrial relaxation and mitral
annular motion (Fig. 7.5) (16). The first systolic component, PVS1, is dependent upon LA relaxation and the
ECG
PVs2 PVD
PVs1
PVAR
B PVAR dur
FIGURE 7.5 A: Pulmonary venous Doppler flow velocity (PVDF) profile. LA filling can be assessed by placing a PWD
sample volume (2 to 4 mm.) approximately 1 cm into a pulmonary vein (PV) orifice where it joins the left atrium (LA).
B: Schematic of PVDF profile depicting relevant indices of diastolic function. Indices of left ventricular (LV) diastolic
function obtained from the PVDF include the peak S/D velocity ratio, as well as the peak A-wave reversal veloc-
ity and duration. LAA, left atrial appendage; LUPV, left upper pulmonary vein; PVAR, late diastolic retrograde velocity;
PVAR dur, PVAR-wave duration; PVS1, first systolic component; PVS2, second systolic component; PVD, diastolic component;
SV, sample volume; LPV, left pulmonary vein.

subsequent decrease in pressure. The later peaking PVS2, reflects right ventricular (RV) stroke volume, LA
compliance, the effects of early ventricular systole on LAP and any concomitant MR. An additional, large
antegrade velocity occurs during diastole (PVD) following early transmitral inflow while the LA serves as an
open conduit between the PV and the LV. The late diastolic retrograde velocity, also known as pulmonary
venous atrial flow reversal (PVAR), occurs during LA systole and is dependent upon LA contractility, heart
rate, and compliance of the LA, PV, and LV (10).
Normally, the PV systolic peak amplitude and TVI are equal to or slightly greater than the correspond-
ing PVD values (Table 7.1) (9). A reduced systolic fraction (systolic TVI divided by the sum of systolic and
diastolic TVI) less than 40% has been correlated with increased mean LAP (17). In addition, the normal
PVAR (≈90 to 115 milliseconds) duration is the same or less than the transmitral A-wave duration (≈120
to 140 milliseconds) (11). In general, LA contraction should result in a greater net forward blood volume
and flow toward a normal, compliant LV compared with any retrograde flow back toward the PV. A PVAR
velocity that exceeds the mitral A-wave by >35 cm/s or PVAR duration >30 milliseconds longer than the
transmitral A-wave duration usually indicates an age-independent elevation in LVEDP (18).
The analysis of PVDF compliments the assessment of TMDF in the evaluation of various stages of
diastolic dysfunction (Fig. 7.4). The PVDF profile consistent with impaired LV relaxation is characterized
by a reduced PVD velocity that parallels the mitral E-wave velocity, and a compensatory increase in the
PVS velocity, resulting in a pattern of systolic predominance. Conversely, the systolic antegrade veloc-
ity is reduced when LV filling is restrictive, because of the elevated LAP and decreased LV compliance
resulting in a pattern of systolic blunting. A greater proportion of antegrade flow occurs during diastole,
although the PVD DT is usually shortened analogous to the rapid deceleration of the transmitral E-wave
velocity. The PVAR velocity and duration may be prolonged in the presence of restrictive pathophysiology
due to decreased LV compliance and associated increase in LAP, which can promote retrograde flow.
Alternatively, the PVAR velocity may be diminished in patients with severe, irreversible restrictive filling,
due to atrial mechanical failure (19). The pseudonormalized PV Doppler flow velocity profile is often
characterized by a pattern of relative systolic blunting and a prolonged PVAR duration and velocity com-
pared with the transmitral A-wave duration depending upon the LAP and degree of reduced LV compli-
ance (Fig. 7.4). In this scenario, the PVDF pattern may be helpful in distinguishing a pseudonormal from
normal TMDF profile. However, in normal young adults and athletes who do not rely on a significant LA
contribution for LV filling, the LA behaves more like a “passive conduit,” and PVs blunting may be com-
monly observed (19).
Influence of Physiologic Variables on LA and LV Doppler Flow Profiles

The TMDF and PVDF profiles are considered useful for evaluating LV diastolic function in both nonsur-
gical and surgical patient populations. The utility of these echocardiographic parameters throughout the
perioperative period is limited, however, by the unavoidable effects of changes in preload, afterload, heart
rate, and rhythm on peak velocities and proportions of early and late filling (20). Increases in preload will
often be associated with a more proportionate increase in the transmitral peak E-wave velocity, a short-
ened IVRT, and steeper DT. The opposite changes will occur with decreases in preload. MR may produce
a transmitral Doppler flow velocity profile with an increased E-wave velocity due to the elevated LAP and
increased volume flow rate across the MV. Isolated LV systolic dysfunction may be also be associated with
an increased transmitral peak E-wave velocity and reduced A-wave since diastolic filling occurs at a steeper
portion of the LV pressure–volume curve (21). Finally, the location of the PWD sample volume and respira-
tory pattern can also affect the TMDF profile (22).
Tachycardia causes fusion of the transmitral E- and A-wave velocities and a pseudo-increase in the
A-wave velocity and duration especially if the E- at A-wave velocity is greater than 20 cm/s (10). Dysrhythmias
and pacing may also be associated with unique alterations in the TMDF and PVDF profiles. For example,
atrial flutter may present with “flutter waves” in the TMDF profile. In patients with atrial fibrillation (AF),
the transmitral and PVAR-waves are absent and the E-wave peak velocity and DT vary with the length of the
cardiac cycle. AF may also be associated with a loss of PVS1, and a decreased PVS2 relative to the dominant
PVD (23). Peak acceleration rate of the E-wave velocity (24), transmitral E-wave DT shortening, and the
duration and initial deceleration slope time of PVD may still correlate with increased LV filling pressure in
the presence of AF (23).

Newer Echocardiographic Techniques for Assessing LV Diastolic

Function: Mitral Annular Doppler Tissue Imaging and Color
M-mode Transmitral Propagation Velocity
Mitral Annular Motion Assessed with Doppler Tissue Imaging
Recently, newer echocardiographic techniques for assessing LV diastolic function have been described
that reportedly are less vulnerable to the effects of acute changes in loading conditions. Mitral annular
motion is evaluated with Doppler tissue imaging (DTI), a technique which utilizes a low velocity, high
amplitude signal to eliminate high velocities associated with blood flow, and provides a signal with high
temporal and velocity range resolution (25). Initial studies describing the utilization of DTI to evaluate
mitral annular motion used transthoracic echocardiography and a four- or two-chamber apical acoustic
window. A midesophageal four-chamber view obtained with a TEE probe is also an appropriate window
to position a PWD sample volume (2.5 to 5 mm) on the lateral corner of the mitral annulus (Fig. 7.6).
Alternatively, the septal side of the mitral annulus can be evaluated although the tissue velocities tend
to be lower and blood flow velocities in the LV outflow tract may obscure the tissue Doppler profile (26).
The PWD Doppler beam should be aligned as parallel as possible to the longitudinal axial motion of the
LV. It is important to realize that these recorded velocities not only represent the rate of myocardial fiber
shortening and lengthening of a specifically selected segment at the level of the mitral annulus, but are
also influenced by velocities associated with translation and rotation of cardiac structures (27). The lowest
wall filter and minimal optimal gain should be used to eliminate blood flow velocity signals produced by
transmitral flow. Finally the Nyquist limit, sweep speed, and size of the Doppler profile should be adjusted
for optimal visualization.
The mitral annular DTI profile has a systolic component, which has been shown to correlate with
ejection fraction (26), and a biphasic diastolic component that appears as an exact mirror image of the
TMDF profile except that the tissue velocities are much lower in magnitude (8 to 15 cm/s). The initial,
early diastolic tissue velocity (E′) begins simultaneously with mitral inflow, yet its peak precedes the peak
transmitral E-wave velocity and ends before LV inflow termination (28). In the absence of gross geomet-
ric distortion and severe regional wall motion abnormalities, E′ reflects tissue velocities associated with
changes in LV volume and is primarily influenced by the rate of myocardial relaxation and elastic recoil. In
the normal patient, the peak E′ velocity is greater than the later diastolic tissue velocity (A′), which tends to
reflect LA systolic function (29).
FIGURE 7.6 Mitral annular motion assessed with Doppler tissue imaging (DTI). The PWD sample volume is positioned
at the level of the lateral mitral valve (MV) annulus to obtain the DTI profile. The mitral annular DTI profile has a bipha-
sic diastolic component that includes an initial early (E′) and a later (A′) diastolic tissue velocity. LA, left atrium; LV, left
ventricle.

Mitral flow
Mitral annulus velocity
Normal Poor relaxation Pseudonormal Restrictive
FIGURE 7.7 Patterns of mitral inflow (E, A) and mitral annular velocities (E′, A′) associated with progressive left ven-
tricular diastolic dysfunction. Although both E/A and E′/A′ decrease with delayed relaxation, the concordance is dis-
rupted with progressive patterns of diastolic dysfunction. E′/A′ remains reduced with the pseudonormalization and
restrictive patterns supporting the utility of E′ as a measure of LV relaxation, and its relative insensitivity to preload
compensation.
E′ has been demonstrated to correlate with τ, supporting its value as an index of LV relaxation (30). E′
and E′/A′ have also been shown to decline with age and are reduced in pathologic LV hypertrophy similar to
transmitral inflow velocities (26,27). The concordance between mitral annular motion assessed by DTI and
mitral inflow velocities, however, is disrupted with progressive diastolic dysfunction when poor relaxation
coexists with an elevated filling pressure. In patients with elevated LVEDP who present with a pseudo-
normal (27) or restrictive transmitral Doppler inflow velocity profile (28), E′ remains reduced suggesting
relative preload independence (Fig. 7.7). In fact, E′ has actually been shown to be the best discriminator
between normal and pseudonormal patients when compared to any single or combined index of TMDF or
PVDF profiles (25). Furthermore, neither peak E′ velocity nor E′/A′ velocity ratio change significantly after
preload alteration with a saline infusion or nitroglycerin (29). Thus, E′ is a relatively preload insensitive
measure of LV diastolic function that may be particularly useful in the perioperative period when loading
conditions can vary considerably.
Color M-mode Transmitral Propagation Velocity

The onset of active LV relaxation is asynchronous, initially starting in apical myocardial segments which
serve as a prominent source of recoil during early diastole (30). Early LV relaxation generates a suction
force that creates an intraventricular pressure gradient initiated at the level of the mitral orifice. This pres-
sure gradient is maintained in the mid-LV during early diastole and is responsible for accelerating flow and
promoting sequential filling toward the apex (30).
The propagation rate of LV peak inflow velocity that is driven by rapid ventricular relaxation, can be
evaluated using color M-mode Doppler echocardiography. While standard PWD permits only a temporal
distribution of blood flow velocities in a single spatial location, color M-mode Doppler echocardiography
provides a spatiotemporal distribution of these velocities, which can be used to delineate the slope of the
propagating wavefront (Vp) from the mitral orifice toward the LV apex (27). The velocity at which flow
propagates within the ventricle (Vp) can be determined from the slope of the color wavefront (Fig. 7.8).
A significant negative correlation between Vp and τ has been demonstrated and suggests that rapid LV
relaxation (short τ) promotes faster propagation of LV filling from the base to the apex (31). In addition,
patients with elevated LV minimal pressure and LVEDP have lower Vp (30). Thus Vp may represent a useful
technique for evaluating LV diastolic function.
The technique for obtaining color M-mode Doppler images of LV filling is often described using transtho-
racic, apical long-axis acoustic windows. A midesophageal, four-chamber TEE view also permits visualization

FIGURE 7.8 Transmitral color M-mode Doppler flow propagation velocity (Vp) is obtained by placing the M-mode
cursor through the center of the mitral inflow region in a transesophageal midesophageal four-chamber view, and mea-
suring the slope of the first aliasing velocity.
of Vp when an M-mode Doppler beam is aligned parallel to the color flow Doppler (CFD) display of trans-
mitral inflow (Fig. 7.8). Measurement of Vp can be obtained from the slope of the first aliasing velocity slope
beginning at the mitral annulus and ideally extending 3 to 4 cm into the LV toward the apex (27). Visualization
of the color wavefront can be optimized by shifting the baseline toward the direction of flow, maximizing
sweep speed, and adjusting the depth.
In young healthy individuals, color M-mode Vp has been reported between 55 and 100 cm/s (31).
Impaired LV relaxation results in a diminished ventricular minimal pressure, thereby compromising the
propagation of early filling (Fig. 7.9). In contrast to standard Doppler filling indices, Vp is relatively inde-
pendent of preload, yet responds to changes in lusitropic conditions (32) and systolic performance (33).
Consequently, while TMDF and PVDF tend to show a parabolic distribution from normal through progres-
sive diastolic dysfunction, Vp remains reduced with pseudonormal or restrictive LV filling. Furthermore,
altering preload by utilizing various techniques (partial CPB, inferior vena cava [IVC] occlusion, intrave-
nous nitroglycerin, amyl nitrate inhalation, Valsalva maneuver, Trendelenburg positioning, leg lifting) is
associated with changes in transmitral peak E-wave velocity, E/A-wave velocity and E-wave deceleration,
but has little affect on Vp (33–35). Interestingly, the ratio of peak E-wave velocity to propagation veloc-
ity (E/Vp) may be useful to predict LAP (33) and also relates directly with LV filling pressures in patients
with AF (24). Vp has also been shown to improve significantly after both on-pump and off-pump coronary
artery bypass graft surgery (36). Thus, like E′, Vp is a relatively preload insensitive measure of LV diastolic
function that may be particularly useful in the perioperative period when loading conditions can vary
considerably (37).

A B
80 cm/s 27 cm/s
Normal Impaired relaxation
FIGURE 7.9 In comparison to the normal patient (A), the transmitral color M-mode propagation velocity (Vp) is reduced
when left ventricular relaxation is impaired (B).
Strain and Strain Rate

Strain imaging is a relatively new echocardiographic modality derived from DTI, which uses low veloc-
ity and high amplitude signals to determine velocity gradients between two myocardial point locations
(38,39). Strain (S) is the deformation of tissue as a function of applied forces (stress), while strain rate (SR)
is a measure of the rate of tissue deformation. Diastolic strain rate (SR) measurements that comprise all
LV segments may be advantageous over myocardial velocity alone for assessing diastolic function. In 50
patients with simultaneous right heart catheterization and echocardiographic imaging, Wang et al. (40)
demonstrated that mitral early diastolic velocity (E)/SR ratio during the isovolumetric relaxation (IVR)
period correlated well with mean wedge pressure. E/SRIVR was most useful in patients with ratio of E to
mitral annulus early diastolic velocity (E/Ea ratio) of 8 to 15, and was more accurate than E/Ea in patients
with normal ejection fraction and regional dysfunction (both P < 0.01). Diastolic deformation of the LV
can also be analyzed with strain imaging and Vp to describe both early and late filling. Pixel velocity
values obtained by color DTI can be processed to velocity gradients as a measure of longitudinal strain
rate with a technique termed strain rate imaging (SRI), which can show the spatial–temporal relations
of the diastolic phases. The phases of early and late filling can be seen to consist of a stretch wave in the
myocardium, propagating from the base to the apex (Vp). Diastolic function is characterized by both peak
strain rate and propagation velocity of this wave (41) (Fig. 7.10). In a series of 26 patients with hyperten-
sion, normal systolic function and impaired diastolic function, Stoylen et al. (41) demonstrated that both
the peak diastolic SR and Vp are reduced. In addition, Hoffman et al. (42) demonstrated in patients with
ischemic LV dysfunction, that SR analysis can detect differences in diastolic function between viable and
nonviable myocardial segments. Both SR and S imaging are angle dependent. However, they are generally
used in long-axis views to measure longitudinal shortening (systolic function) or lengthening (diastolic
function) of the LV along the ultrasound beam. Consequently, unlike DTI, both S and SR are relatively
independent of translational or rotational movement. Thus strain imaging may have additional advan-
tages over conventional echocardiography techniques for evaluating diastolic function in the periopera-
tive period.
Right Ventricular Diastolic Function

Indirect evidence of RV diastolic function can be obtained from a comprehensive 2D echocardiographic
examination by examining RV mass or volume. A thorough assessment of RV diastolic function, however,
requires a Doppler echocardiographic evaluation of transtricuspid blood flow velocities (Fig. 7.11A). Trans-
tricuspid Doppler flow (TTDF) velocities are affected by the same physiologic variables that affect LV filling
although they tend to be lower due to the larger tricuspid valve (TV) annular size. Direct comparisons of
RV and LV inflow velocities also reveal differences in timing and reciprocal respiratory variation. During
spontaneous inspiration, negative intrapleural pressure results in an increase in right atrial (RA) volume

FIGURE 7.10 The phases of the heart cycle. A: The relation of the phases with different methods. Top: Longitudinal
M-mode image from the septum of a healthy subject. Center: The same M-mode image in color Doppler tissue imaging
(DTI). Bottom: The DTI and M-mode curves from the septal part of the mitral ring. Isovolumic contraction (IVC) is seen as
a brief, nearly simultaneous shortening, followed by a short recoil, an ejection as a phase of prolonged shortening, and
isovolumic relaxation (IVR) as a phase of lengthening, with a short recoil. The early filling phase (E), corresponding to the
E-wave of the mitral flow, is seen as a wave of stretching that propagates from the base to the apex, and this phase results
in the E-wave of the DTI curve of the mitral ring. The stretch wave is followed by short recoil, propagating from the apex
to the base, resulting in a small oscillation in the DTI curve. The phase of late filling during atrial systole (A) behaves like
the early filling phase. B: Longitudinal M-mode images from five different healthy subjects, showing the considerable
variation of the strain rate imaging pattern, especially in the isovolumic relaxation. The stretch waves can be seen to
return from the apex to the base in all five samples. (Reproduced with permission from Stoylen A, Slordahl S, Skjelvan G,
et al. Strain rate imaging in normal and reduced diastolic function: Comparison with pulse Doppler tissue imaging of the
mitral annulus. J Am Soc Echocardiogr. 2001;14:264–274.)
and subsequent greater RV diastolic filling velocities up to 20% compared to end-expiratory values (21). LA
and LV filling is actually reduced during spontaneous inspiration relative to end-expiration. These recipro-
cal patterns of respiratory variation become exaggerated in patients with diastolic dysfunction. Although
not thoroughly investigated, positive pressure ventilation (PPV) would presumably have an opposite effect
on TTDF velocity patterns in comparison to spontaneous ventilation.
The echocardiographic evaluation of RV diastolic function also includes an assessment of RA inflow
velocities including the hepatic venous (HV), IVC, and superior vena cava (SVC) Doppler profiles all of
which have similar contours and components. The HVs join the intrahepatic IVC tangentially, and can
be visualized by advancing and turning the TEE probe rightward from a midesophageal, bi-caval acoustic
view. The normal HV Doppler profile (Fig. 7.11B) is characterized by (i) a small reversal of flow following
atrial contraction (AR-wave), (ii) an antegrade systolic phase during atrial filling from the SVC and IVC

A B
FIGURE 7.11 A: Normal transtricuspid Doppler flow velocity profile. B: Normal hepatic venous Doppler flow velocity
profiles. C: Prominent hepatic flow reversal at end-systole (V) in a patient with decreased right ventricular compliance.
E, early diastolic velocity; A, late diastolic velocity; AR, atrial contraction flow reversal; S, antegrade early systolic flow;
D, antegrade flow during right ventricular filling; HV, hepatic vein; TV, tricuspid valve.
(S-wave) that is influenced by TV annular motion, RA relaxation, and tricuspid regurgitation (TR), (iii) a
second small flow reversal at end-systole (V-wave) that is influenced by RV and RA compliance, and (iv) a
second antegrade filling phase while the RA acts as a passive conduit during RV filling (D-wave) (21).
Diastolic RV dysfunction can manifest with the same relative changes in transtricuspid peak E- and
A-wave velocities, E/A-wave ratios, and DT that occur with TMDF profiles associated with alterations in
LV relaxation and compliance (43,44). The ratio of the total hepatic reverse flow integral to total forward
flow integral (TVIA + TVIV/TVIS + TVID) increases with either RV diastolic dysfunction or significant TR,
but appears to be more affected by the former (45). In addition, a marked shortening of the transtricuspid
DT and diastolic predominance of HV flow with prominent V- and A-wave reversals during spontane-
ous inspiration, indicates significant decreases in RV compliance and increased diastolic filling pressures
(Fig. 7.11C) (10). Changes in IVC diameter during spontaneous inspiration also reflect RA pressure (RAP).
In general, low RAP (0 to 5 mm Hg) is associated with a small IVC (<1.5-cm diameter) and a spontaneous
inspiratory collapse >50% of the original diameter. In contrast, significant increases in RAP (>20 mm Hg)
are associated with dilated IVC and HVs, with little respiratory variation (21). Diastolic RV dysfunction

(lower TV peak E-wave velocity, lower E/A ratios, and prolonged RV IVRT) has also been demonstrated in
patients with pulmonary hypertension (PHT) and in those with symptomatic CHF even in the absence of
PHT, suggesting a potential role for ventricular interdependence in impaired RV filling (46).
Pericardial Disease: Constrictive Pericarditis and Pericardial Tamponade

Pericardial pathology, including constrictive pericarditis (CP) and pericardial tamponade (PT) from effu-
sions can impede diastolic flow. Although chest radiography and magnetic resonance imaging may be help-
ful in diagnosing pericardial disease, echocardiography continues to be essential for delineating associated
pathophysiology. Two-dimensional echocardiography can be helpful in diagnosing CP by identifying a
thickened, fibrotic, and calcified echogenic pericardium together with abnormal ventricular septal motion,
flattening of the LV posterior wall during diastole, and a dilated IVC (47). Alternatively, 2D echocardio-
graphic identification of pericardial effusions usually reveals an echo-free space that may contain thrombi.
Although small (<25 mL), loculated effusions can be difficult to visualize, larger effusions associated with
PT pathophysiology are usually accompanied by additional 2D echocardiographic and M-mode features
including persistence of the effusion throughout the cardiac cycle, a characteristic “swinging motion” of
the heart, early diastolic RV collapse, late diastolic to early systolic RA inversion, and abnormal ventricular
septal motion (47).
The diagnosis of CP and PT includes identification of significant respiratory variation in atrial and
ventricular Doppler inflow profiles. Normally during spontaneous respiration, intrathoracic pressures are
transmitted equally to the pericardial space and intracardiac chambers. The transmission of intrathoracic
pressure, however, is shielded by the thickened noncompliant pericardium in patients with CP and by
significant pericardial effusions. Consequently, LA and LV filling pressure gradients are decreased during
spontaneous inspiration, resulting in diminished pulmonary venous forward diastolic velocities, delayed
MV opening, prolonged IVRT, and decreased mitral E-wave velocity (23,48). Similarly, relative increases
in LA and LV filling pressure gradients during spontaneous expiration are responsible for corresponding
increases in LA and LV Doppler inflow velocities. Exaggeration of ventricular interdependence with CP
and PT is responsible for reciprocal changes in right-sided intracardiac flows, resulting in increased tri-
cuspid E-wave velocities during spontaneous inspiration. In addition, HV forward velocities decrease and
reverse flows increase during expiration (49). Since intrathoracic pressure changes associated with PPV
are opposite in direction from those seen with spontaneous breathing, mechanical ventilation reverses the
respiratory variation pattern of LA and LV inflow velocities seen with CP (Fig. 7.12) (50). Thus, the demon-
stration of respiratory variation in atrial and ventricular Doppler inflow profiles can be a useful technique
to establish the diagnosis of hemodynamically significant pericardial pathology.
The distinction between restriction and constriction may be difficult to determine from LV and LA
Doppler inflow velocities alone because both disorders may present with profiles resembling restrictive
LV diastolic filling (48). However, discordant pressure changes between the LV and RV during respiration
are usually not observed with restrictive cardiomyopathy. Consequently, CP can be differentiated from
restrictive cardiomyopathy by demonstrating respiratory variation in TMDF and PVDF (51). Furthermore,
patients with CP and preserved systolic function compared to those with restrictive cardiomyopathy, have
more rapid Vp (52) and normal or elevated E′ (53).
CLINICAL RELEVANCE OF DIASTOLIC DYSFUNCTION

CHF is the most common diagnosis amongst inpatients in the United States and accounts for 720,000 hos-
pital admissions annually (54). Nearly half of the patients with CHF have diastolic dysfunction and normal
ejection fraction (55). Diastolic dysfunction increases with age, especially amongst elderly patients with
hypertensive heart disease (55). Although the prognosis for patients with DHF is more favorable than for
patients with systolic dysfunction, mortality is increased fourfold when compared with age- and gender-
matched normal subjects (10). Thus, diastolic dysfunction poses an important and clinically relevant chal-
lenge to the health care industry.
The relatively high prevalence of DHF in the community is also a concern for the perioperative inten-
sivist since many affected patients will present to the operating room for cardiovascular procedures.

Normal Impaired Relaxation Pseudonormal Restrictive
FIGURE 7.12 Doppler echocardiographic measures of diastolic function. TMDF, transmitral Doppler flow velocity;
MADTI, mitral annular Doppler tissue imaging; PVDF, pulmonary venous Doppler flow velocity; Vp, transmitral color
flow propagation velocity; E, peak early transmitral Doppler flow velocity; A, peak late transmitral Doppler flow velocity;
E′, early diastolic mitral annular tissue velocity; A′, late diastolic mitral annular tissue velocity; AR, pulmonary venous
atrial flow reversal; S, systolic pulmonary venous Doppler flow velocity, D, diastolic pulmonary venous Doppler flow
velocity.
Preoperative, asymptomatic diastolic filling abnormalities have been reported in over 60% of geriatric
and vascular surgical patients (56), and have been associated with short- and long-term adverse cardio-
vascular outcomes (57,58). Preoperative diastolic dysfunction has also been reported in 30% to 70% of
cardiac surgical patients and independently associated with difficult weaning from CPB, more frequent
inotropic support, and increased morbidity (3,37). Merello et al. (59) evaluated diastolic dysfunction in
191 CABG patients. Mortality and complications through 30 days postoperatively were compared with
that predicted by the EuroSCORE and Parsonnet score. Increasing degrees of diastolic dysfunction cor-
related well with survival. However, mortality was not predicted by either the EuroSCORE or Parsonnet
score suggesting the potential values adding a measure of diastolic dysfunction to these widely used risk
stratification schemes (59). While more complex algorithms for evaluating diastolic dysfunction may be
considered impractical to obtain in the perioperative period, simpler echocardiographic measures of dia-
stolic dysfunction including the tissue Doppler-derived surrogate for LV diastolic pressure E/e′, have also
been shown to be prognostic of adverse postoperative outcomes after cardiac surgery (60,61). Following
CPB, acute or progressive diastolic dysfunction associated with ischemia–reperfusion injury, hypother-
mia, metabolic disturbances or myocardial edema may develop and persist for several minutes to days
(62). Identifying high-risk patients preoperatively and monitoring diastolic function intraoperatively may
allow for the institution of prophylactic therapeutic strategies, including the administration of pharmaco-
logic agents with direct or indirect lusitropic properties (63) that could facilitate weaning from CPB and
reduce perioperative morbidity.

TABLE 7.2 Doppler Echocardiographic Values for Indices of Left Ventricular Diastolic Dysfunction
Normal Normal Impaired Pseudonormal Restrictive

(young) (adult) relaxation filling filling
E/A (cm/s) >1 >1 <1 1–2 >2
DT (ms) <220 <220 >220 150–200 <150
IVRT (ms) <100 <100 >100 60–100 <60
S/D <1 ≥1 ≥1 <1 <1
PVAR (cm/s) <35 <35 <35 ≥35a ≥25a
Vp (cm/s) >55 >45 <45 <45 <45
E′ (cm/s) >10 >8 <8 <8 <8
a
Unless atrial mechanical failure is present.
E/A, early-to-late left ventricular (LV) filling ratio; DT, early LV filling deceleration time; IVRT, isovolumic relaxation time; S/D,
systolic-to-diastolic pulmonary venous flow ratio; PVAR, pulmonary venous peak atrial contraction reversal velocity; Vp,
transmitral color M-mode propagation velocity; E′, peak early diastolic mitral annular velocity.
Reproduced with permission from Garcia M, Thomas J, Klein A. New Doppler echocardiographic applications for the study of
diastolic function. J Am Coll Cardiol. 1998;32:872.
SUMMARY
Normal diastolic function is required for optimal cardiac performance. Impaired ventricular filling and
increased chamber stiffness are responsible for a significant component of the pathophysiology associated
with CHF. Diastolic dysfunction is prevalent amongst cardiovascular surgical patients and may contribute
to perioperative morbidity. Echocardiography provides an effective, noninvasive means for diagnosing the
presence, extent, and etiology of diastolic dysfunction (64) (Fig. 7.12, Table 7.2). Although conventional
Doppler echocardiographic measurements of atrial and ventricular inflow velocities are still an important
component of a thorough examination, newer techniques including mitral annular DTI and color M-mode
transmitral Vp, may be less sensitive to changes in loading conditions. In the near future, the availability of
more sensitive, cost-effective echocardiographic techniques for diagnosing diastolic dysfunction will hope-
fully facilitate the development of perioperative therapeutic intervention.
REFERENCES
1. Grossman W. Diastolic dysfunction in congestive heart failure. N Engl J Med. 1991;22:1557–1564.
2. Pinamonti B, Lenarda A, Sinagra G, et al. Restrictive left ventricular filling pattern in dilated cardiomyopathy assessed by
Doppler echocardiography: Clinical, echocardiographic, and hemodynamic correlations and prognostic implications. J Am
Coll Cardiol. 1993;22:808–815.
3. Bernard F, Denault A, Babin D, et al. Diastolic dysfunction is predictive of difficult weaning from cardiopulmonary bypass.
Anesth Analg. 2001;92:291–298.
4. Plotnick GD. Changes in diastolic function—Difficult to measure, harder to interpret. Am J Heart J. 1989;118:637–641.
5. Nishimura R, Tajik A. Evaluation of diastolic filling of left ventricle in health and disease: Doppler echocardiography is the
clinician's Rosetta stone. J Am Coll Cardiol. 1997;30:8–18.
6. Pagel P, Grossman W, Haering J, et al. Left ventricular diastolic function in the normal and diseased heart: Perspectives for the
anesthesiologist. Anesthesiology. 1993;79:836–854.
7. Zile M, Smith V. Relaxation and diastolic properties of the heart. In: Fozzard H, Haber E, Jennings R, Katz A, Morgan H, eds.
The Heart and Cardiovascular System: Scientific Foundations. 2nd ed. New York, NY: Raven; 1991:1353–1367.
8. Appleton C, Galloway J, Gonzalez M, et al. Estimation of left ventricular filling pressures using two-dimensional and Doppler echo-
cardiography in adult patients with cardiac disease: Additional value of analyzing left atrial size, left atrial ejection fraction and the
difference in duration of pulmonary venous and mitral flow velocity at atrial contraction. J Am Coll Cardiol. 1993;22:1972–1982.
9. Cohen G, Pietrolungo J, Thomas J, et al. A practical guide to assessment of ventricular diastolic function using Doppler echo-
cardiography. J Am Coll Cardiol. 1996;27:1753–1760.
10. Appleton C, Firstenberg M, Garcia M, et al. The echo-Doppler evaluation of left ventricular diastolic function: A current per-
spective. In: Kovacs S, ed. Cardiology Clinics. Philadelphia, PA: W.B. Saunders Company; 2000:513–546.
11. Little W, Ohno M, Kitzman D, et al. Determination of left ventricular chamber stiffness from the time for deceleration of early
left ventricular filling. Circulation. 1995;92:1933–1939.
12. Oh J, Appleton C, Hatle L, et al. The noninvasive assessment of left ventricular diastolic function with two-dimensional and
Doppler echocardiography. J Am Soc Echocardiogr. 1997;10:246–270.

13. Appleton C, Hatle L. The natural history of left ventricular filling abnormalities: Assessment by two-dimensional and Doppler
echocardiography. Echocardiography. 1992;9:437–457.
14. Dumesnil J, Gaudreault G, Honos G, et al. Use of Valsalva maneuver to unmask left ventricular diastolic function abnor-
malities by Doppler echocardiography in patients with coronary artery disease or systemic hypertension. Am J Cardiol.
1991;68:515–519.
15. Hurrell D, Nishimura R, Ilstrup D, et al. Utility of preload alteration in assessment of left ventricular filling pressure by
Doppler echocardiography: A simultaneous catheterization and Doppler echocardiographic study. J Am Coll Cardiol. 1997;30:
459–467.
16. Nishimura R, Abel M, Hatle L, et al. Relation of pulmonary vein to mitral flow velocities by transesophageal Doppler echocar-
diography: Effect of different loading conditions. Circulation. 1990;81:488–497.
17. Kuecherer H, Muhiudeen I, Kusumoto F, et al. Estimation of mean left atrial pressure from transesophageal pulsed Doppler
echocardiography of pulmonary venous flow. Circulation. 1990;82:1127–1139.
18. Yamamoto K, Nishimura R, Burnett J, et al. Assessment of end-diastolic pressure by Doppler echocardiography: Contribution
of duration of pulmonary venous versus mitral flow velocity curves at atrial contraction. J Am Soc Echocardiogr. 1997;10:52–59.
19. Appleton C, Hatle L, Popp R. Relation of transmitral flow velocity patterns to left ventricular diastolic function: New insights
from a combined hemodynamic and Doppler echocardiographic study. J Am Coll Cardiol. 1988;12:426–440.
20. Nishimura R, Abel M, Hatle L, et al. Assessment of diastolic function of the heart: Background and current applications of
Doppler echocardiography: Part II. Clinical studies. Mayo Clin Proc. 1989;64:181–204.
21. Otto C. Echocardiographic evaluation of ventricular diastolic filling and function. Textbook of Clinical Echocardiography. 2nd
ed. Philadelphia, PA: W.B. Saunders Company; 2000:132–152.
22. Oka Y, Kato M, Strom J. Mitral valve. In: Oka Y, Goldinger P, eds. Transesophageal Echocardiography. Philadelphia, PA: J.B.
Lippincott Co.; 1992:99–151.
23. Oh J. Assessment of diastolic function. In: Oh J, ed. The Echo Manual. 2nd ed. Philadelphia, PA: Lippincott Williams & Wilkins;
1999:45–57.
24. Nagueh S, Kopelen H, Quinones M. Assessment of left ventricular filling pressures by Doppler in the presence of atrial fibril-
lation. Circulation. 1996;94:2138–2145.
25. Farias C, Rodriguez L, Garcia M, et al. Assessment of diastolic function by tissue Doppler echocardiography: Comparison with
standard transmitral and pulmonary venous flow. J Am Soc Echocardiogr. 1999;12:609–617.
26. Nagueh S, Middleton K, Kopelen H, et al. Doppler tissue imaging: A noninvasive technique for evaluation of left ventricular
relaxation and estimation of filling pressures. J Am Coll Cardiol. 1997;30:1527–1533.
27. Garcia M, Thomas J, Klein A. New Doppler echocardiographic applications for the study of diastolic function. J Am Coll
Cardiol. 1998;32:865–875.
28. Garcia M, Rodriguez L, Ares M, et al. Differentiation of constrictive pericarditis from restrictive cardiomyopathy:
Assessment of left ventricular diastolic velocities in longitudinal axis by Doppler tissue imaging. J Am Coll Cardiol. 1996;
27:108–114.
29. Sohn D, Chai I, Lee D, et al. Assessment of mitral annulus velocity by Doppler tissue imaging in the evaluation of left ventricu-
lar diastolic function. J Am Coll Cardiol. 1997;30:474–480.
30. Takatsuji H, Mikami T, Urasawa K, et al. A new approach for evaluation of left ventricular diastolic function: Spatial and
temporal analysis of left ventricular filling flow propagation by color M-mode Doppler echocardiography. J Am Coll Cardiol.
1996;27:363–371.
31. Brun P, Triboiulloy C, Duval A, et al. Left ventricular flow propagation velocity during early filling is related to wall relaxation:
A color M-mode Doppler analysis. J Am Coll Cardiol. 1992;20:420–432.
32. Garcia M, Smedira N, Greenberg N, et al. Color M-mode Doppler flow propagation velocity is a preload insensitive index of
left ventricular relaxation: Animal and human validation. J Am Coll Cardiol. 2000;35:201–208.
33. Garcia M, Ares M, Asher C, et al. An index of early left ventricular filling that combined with pulsed Doppler peak E velocity
may estimate capillary wedge pressure. J Am Coll Cardiol. 1997;29:448–454.
34. Moller J, Poulsen S, Sondergaard E, et al. Preload dependence of color M-mode Doppler flow propagation velocity in controls
and in patients with left ventricular dysfunction. J Am Soc Echocardiogr. 2000;13:902–909.
35. Garcia M, Palac R, Malenka D, et al. Color M-mode Doppler flow propagation velocity is a relatively preload-independent
index of left ventricular filling. J Am Soc Echocardiogr. 1999;12:129–137.
36. Ng K, Popovic Z, Troughton R, et al. Comparison of left ventricular diastolic function after on-pump versus off-pump coro-
nary artery bypass grafting. Am J Cardiol. 2005;95:647–650.
37. Djainani G, Ti L, Mackensen B, et al. Color M-mode propagation velocity identifies patients with diastolic dysfunction during
coronary bypass surgery. Anesth Anlag. 2001;92:SCA74.
38. Sutherland G, Di Salvo G, Claus P, et al. Strain and strain rate imaging: A new clinical approach to quantifying regional myo-
cardial function. J Am Soc Echocardiogr. 2004;17:788–802.
39. Gilman G, Khanderia B, Hagen M, et al. Strain and strain rate: A step-by-step approach to image and data acquisition. J Am
Soc Echocardiogr. 2004;17:1011–1020.
40. Wang J, Khoury D, Thohan V, et al. Global diastolic strain rate for the assessment of left ventricular relaxation and filling pres-
sures. Circulation. 2007;115:1376–1383.
41. Stoylen A, Slordahl S, Skjelvan G, et al. Strain rate imaging in normal and reduced diastolic function: Comparison with pulse
Doppler tissue imaging of the mitral annulus. J Am Soc Echocardiogr. 2001;14:264–274.
42. Hoffmann R, Altiok E, Nowak B, et al. Strain rate analysis allows detection of differences in diastolic function between viable
and nonviable myocardial segments. J Am Soc Echocardiogr. 2005;18:330–335.
43. Klein A, Hatle L, Burstow D, et al. Comprehensive Doppler assessment of right ventricular diastolic function in cardiac amy-
loidosis. J Am Coll Cardiol. 1990;15:99–108.

44. Spencer K, Weinert L, Lang R. Effect of age, heart rate and tricuspid regurgitation on the Doppler echocardiographic evalua-
tion of right ventricular diastolic function. Cardiology. 1999;92:59–64.
45. Nomura T, Lebowitz L, Koide Y, et al. Evaluation of hepatic venous flow using transesophageal echocardiography in coronary
artery bypass surgery: An index of right ventricular function. J Cardiothorac Vasc Anesth. 1995;9:9–17.
46. Yu C, Sanderson J, Chan S, et al. Right ventricular diastolic dysfunction in heart failure. Circulation. 1996;93:1509–1514.
47. Feigenbaum H. Pericardial disease. In: Feigenbaum H, ed. Echocardiography. 5th ed. Baltimore, MD: Williams & Wilkins;
1994:556–588.
48. Klein A, Cohen G, Pietrolungo J, et al. Differentiation of constrictive pericarditis from restrictive cardiomyopathy by Doppler
transesophageal echocardiographic measurements of respiratory variations in pulmonary venous flow. J Am Coll Cardiol.
1993;22:1935–1943.
49. Burstow D, Oh J, Bailey K, et al. Cardiac tamponade: Characteristic Doppler observations. Mayo Clin Proc. 1989;64:312–324.
50. Abdalla I, Murray D, Awad H, et al. Reversal of the pattern of respiratory variation of Doppler inflow velocities in constrictive
pericarditis during mechanical ventilation. J Am Soc Echocardiogr. 2000;13:827–831.
51. Schiavone W, Calafiore P, Salcedo E. Transesophageal Doppler echocardiographic demonstration of pulmonary venous flow
velocity in restrictive cardiomyopathy and constrictive pericarditis. Am J Cardiol. 1989;63:1286–1288.
52. Rodriguez L, Ares M, Vandervoort P, et al. Does color M-mode flow propagation differentiate between patients with restrictive
vs. constrictive physiology? [Abstract]. J Am Coll Cardiol. 1996;27:268A.
53. Rajagopalan N, Garcia M, Rodriguez L, et al. Comparison of Doppler echocardiographic methods to differentiate constrictive
pericarditis from restrictive cardiomyopathy [Abstract]. J Am Coll Cardiol. 1998;31:164A.
54. Yusef S, Thom T, Abbott RD. Changes in hypertension treatment and congestive heart failure mortality in the United States.
Hypertension. 1989;13(suppl):174–179.
55. Vasan R, Larson M, Benjamin E, et al. Congestive heart failure in subjects with normal versus reduced left ventricular ejection
fraction: Prevalence and mortality in a population-based cohort. J Am Coll Cardiol. 1999;33:1948–1955.
56. Philip B, Pastor D, Bellows W, et al. Prevalence of congestive diastolic filling abnormalities in geriatric surgical patients. Anesth
Analg. 2003;97:1214–1221.
57. Flu W, van Kuijik J, Hoeks S, et al. Prognostic implications of asymptomatic left ventricular dysfunction in patients undergoing
vascular surgery. Anesthesiology. 2010;112:1316–1324.
58. Matyal R, Hess P, Subramaniam B, et al. Perioperative diastolic dysfunction during vascular surgery and its association with
postoperative outcome. J Vasc Surg. 2009;50:70–76.
59. Merello L, Riesle E, Alburquerque J, et al. Risk scores do not predict high mortality after CABG in the presence of diastolic
dysfunction. Ann Thorac Surg. 2008;85:1247–1255.
60. Groban L, Sanders D, Houle T, et al. Prognostic value of tissue Doppler-derived E/e on early morbid events after cardiac sur-
gery. Echocardiography. 2010;27:131–138.
61. Swaminathan M, Nicoara A, Phillips-Bute B, et al. Utility of a simple algorithm to grade diastolic dysfunction and predict
outcome after coronary artery bypass graft surgery. Ann Thorac Surg. 2011;91:1844–1851.
62. De Hert S, Rodrigus I, Haenen L, et al. Recovery of systolic and diastolic left ventricular function early after cardiopulmonary
bypass. Anesthesiology. 1996;85:1063–1075.
63. Doolan L, Jones E, Kalman J, et al. A placebo-controlled trial verifying the efficacy of milrinone in weaning high-risk patients
from cardiopulmonary bypass. J Cardiothorac Vasc Anesth. 1997;11:37–41.
64. Nagueh S, Appleton C, Gillebert T, et al. Recommendations for the evaluation of left ventricular diastolic function by echocar-
diography. J Am Soc Echocardiogr. 2009;22:107–133.

QUESTIONS
1. Which one of the following patterns of left that is most related to which one of the
ventricular diastolic dysfunction occurs following cardiac cycle components?
most commonly in the early stages of a. Left atrial relaxation
infiltrative disorders? b. Left ventricular contraction
a. Restrictive c. Left atrial contraction
b. Pseudonormal d. Left ventricular compliance
c. Constrictive
6. A pulmonary venous Doppler flow velocity
d. Poor relaxation
profile with a biphasic systolic component,
2. During spontaneous inspiration, patients has a later peaking systolic antegrade
with pericardial tamponade will most likely velocity (PVS2) that is most related to which
demonstrate which one of the following of the following cardiac cycle components?
changes in the peak E-wave velocity of the a. Right ventricular stroke volume
transtricuspid and transmitral Doppler flow b. Left atrial compliance
profiles? c. Left ventricular contraction
d. Concomitant mitral regurgitation
Peak E-wave velocity
e. All of the above
Transtricuspid Transmitral
a. Increase Decrease 7. In comparison to normal adult values,
Decrease
the restrictive pattern of left ventricular
b. Decrease
diastolic function exhibits which one of
c. Decrease Increase
the following sets of relative changes in
d. Increase Increase Doppler echocardiographic velocities?
3. In comparison to the restrictive pattern Pulmonary Transmitral
of left ventricular diastolic dysfunction, vein S/D ratio Mitral annular DTI color M-mode
the impaired relaxation pattern is Velocity Peak E Propagation
characterized by which of the following ratio velocity (E¢) velocity (Vp)
changes in the transmitral Doppler flow a. Increased Increased Decreased
velocity isovolumic relaxation and E-wave b. Decreased Decreased Decreased
deceleration times? c. Increased Increased Increased
Transmitral Doppler flow velocity d. Decreased Decreased Increased
Isovolumic E-wave deceleration
relaxation time time 8. Which one of the following Doppler
a. Increase Increase echocardiographic measurements is the
Decrease
best predictor of increased left ventricular
b. Increase
filling pressure in patients with atrial
c. Decrease Increase
fibrillation?
d. Decrease Decrease a. Increased PVAR/MVA duration ratio
b. Decreased pulmonary venous diastolic flow
4. An increased pulmonary AR-wave/mitral
c. Increased transmitral peak E-wave velocity
A-wave duration ratio is consistent with
d. Decreased transmitral E-wave deceleration
which one of the following conditions?
time
a. Increased left atrial compliance
b. Decreased left atrial pressure 9. The use of a nitroglycerin will convert a
c. Increased left ventricular end-diastolic pseudonormalized left ventricular inflow
pressure pattern to which one of the following
d. Decreased pulmonary venous compliance transmitral Doppler flow velocity patterns?
a. Normal
5. A pulmonary venous Doppler flow velocity
b. Restrictive
profile with a biphasic systolic component,
c. Poor relaxation
has an initial antegrade velocity (PVS1)
d. Constrictive

10. The transmitral color M-mode propagation e. Ratio of early transmitral Doppler flow
velocity (Vp) is most likely to increase velocity to early mitral annular Doppler
during which one of the following tissue velocity (E/e′)
conditions?
16. In comparison to normal adult values,
a. Administration of milrinone
patients with hypertension, normal systolic
b. Reverse Trendelenburg positioning
function, and impaired diastolic function
c. Administration of nitroglycerin
are more likely to demonstrate which one of
d. Valsalva maneuver
the following sets of relative changes?
11. In comparison to other conventional
Peak diastolic strain Propagation
Doppler echocardiographic measures of
rate (SR) velocity (Vp)
diastolic function, which of the following
a. Increased Reduced
is most unique for strain imaging?
a. Angle dependence b. Reduced Increased
b. Independent of rotational and translational c. Increased Increased
movement of the heart d. Reduced Reduced
c. Uses measures of tissue velocity
d. Can also be used to evaluate systolic function 17. Perioperative diastolic dysfunction in
cardiac surgical patients is associated with
12. Which one of the following echocardio- which of the following adverse events?
graphic measurements made during a. Difficulty weaning from cardiopulmonary
spontaneous inspiration is most consistent bypass
with a diagnosis of decreased right b. More frequent inotrope support
ventricular compliance and increased c. Mortality
filling pressures? d. All of the above
a. Prolonged transtricuspid E-wave decelera-
tion time 18. Which of the following echocardiographic
b. Diastolic predominance of hepatic vein flow measures of diastolic function is least
c. Diminished hepatic AR-wave velocity time sensitive to changes in loading conditions?
integral a. Early mitral annular Doppler tissue
d. >50% inspiratory collapse of the IVC b. Late transmitral Doppler flow velocity
c. Diastolic pulmonary venous Doppler flow
13. Approximately what percentage of patients velocity
with congestive heart failure have diastolic d. Transmitral deceleration time
dysfunction and normal ejection fractions?
a. 10% 19. Left atrial contraction usually contributes
b. 30% what percentage of left ventricular filling in
c. 50% normal patients?
d. 70% a. <20%
e. 90% b. 20% to 40%
c. 40% to 60%
14. Preoperative diastolic dysfunction has been d. >60%
reported in approximately what percentage
of cardiac surgical patients? 20. Which of the following echocardiographic
a. <10% measures of diastolic function are observed
b. 10% to 30% in patients with a pseudonormal pattern?
c. 30% to 60% a. Increased early transmitral Doppler flow
d. 70% to 90% velocity (E)
e. >90% b. Decreased late transmitral Doppler flow
velocity (A)
15. Which of the following echocardiographic c. Increased early mitral annular Doppler
measures is the best surrogate of left tissue velocity
ventricular end-diastolic pressure? d. Decreased systolic pulmonary venous
a. Propagation velocity (Vp) Doppler flow velocity
b. Deceleration time (DT) e. Decreased diastolic pulmonary venous
c. Pulmonary venous systolic flow velocity (PVs) Doppler flow velocity
d. Isovolumic relaxation time (IVRT)

III VALVULAR DISEASE
8 Mitral Regurgitation
A. Stephane Lambert
TRANSESOPHAGEAL ECHOCARDIOGRAPHY (TEE) HAS BECOME a standard of care in the cardiac oper-
ating room, allowing the anesthesiologist to play an important part in the surgical decision-making pro-
cess. In that role, few areas are as challenging as the assessment of intraoperative mitral regurgitation (MR).
Yet few applications of intraoperative TEE have as much impact on the course of surgery and on patient
outcome as the evaluation of MR.
ANATOMY
The mitral valve is bicuspid and consists of a large anterior leaflet and a smaller posterior leaflet (Fig. 8.1).
The anterior leaflet covers about two-thirds of the surface area of the valve. The posterior leaflet is C-shaped
and wraps around the anterior leaflet accounting for about two-thirds of the circumference of the valve.
The leaflets join at the anterolateral and posteromedial commissures. The posterior leaflet is further divided
anatomically into three scallops, whereas the anterior leaflet does not have scallops per se. It is important
to keep in mind when considering the various TEE imaging planes of the mitral valve that coaptation of
the two leaflets forms a semicircular, not linear, path. The valve is encircled by a dynamic fibromuscular
ring, the mitral annulus. It is saddle shaped and plays an important role in proper valve closure by reduc-
ing its diameter in systole. In various disease states the mitral annulus dilates and tends to flatten, causing
increased stress on the mitral leaflets and impairs its function (1). The mitral valve attaches to two papil-
lary muscles, anterolateral and posteromedial, through chordae tendineae. Each papillary muscle sends
Pulmonary valve
Aortic valve
Mitral valve
Papillary muscle Tricuspid valve
FIGURE 8.1 Anatomy of the mitral valve.

159

160 III. Valvular Disease
off chordae tendineae to both mitral leaflets. In systole, the papillary muscles contract to keep the chordae
tendineae taut and prevent prolapse of the leaflets into the left atrium (2).
The blood supply to the papillary muscles is variable, but in the majority of patients, the anterolateral
papillary muscle receives blood supply from branches of two major coronary arteries, the left anterior
descending (LAD) and the left circumflex (LCx), while the posteromedial papillary muscle receives blood
supply from a single coronary artery, the right coronary artery (RCA). This is important clinically, because
the incidence of posterolateral papillary muscle infarction is much higher than that of anterolateral papil-
lary muscle infarction.
There are three types of chordae tendineae. First-order (or primary) chordae attach to the edge of the
leaflets, second-order (or secondary) chordae attach to the body of the leaflets, and third-order (or tertiary)
chordae attach to the base of the posterior leaflet. The anterior leaflet of the mitral valve shares the same
fibrous attachment as the aortic valve, an area sometimes referred to as the fibrous body or crux of the heart.
This relationship is important to consider and surgery to one valve can result in impaired function of the
other.
NOMENCLATURE
There exist three nomenclatures of the mitral valve in the literature. The classic anatomic nomenclature
refers to the three scallops of the posterior leaflet of the mitral valve as anterolateral, middle, and postero-
medial, according to their anatomic location (3). The anterolateral scallop is the closest to the left atrial
(LA) appendage. No specific description is given to any part of the anterior leaflet. The most commonly used
nomenclature amongst echocardiographers is attributed to Carpentier (4) and defines the three scallops
of the posterior leaflet as P1, P2, and P3, where P1 is closest to the LA appendage. It also defines three cor-
responding areas of the anterior leaflet as A1 (opposite P1), A2 (opposite P2), and A3 (opposite P3). This
nomenclature was adopted by the American Society of Echocardiography Council for Intraoperative Echo-
cardiography and the Society of Cardiovascular Anesthesiologists Task Force for Certification in Periop-
erative Transesophageal Echocardiography, in their published “Guidelines for performing a comprehensive
intraoperative multiplane transesophageal echocardiography examination” (5).
A third nomenclature, often called the Duran nomenclature (6), describes the mitral valve segments
according to their attachment to the papillary muscles. It refers to the three scallops of the posterior leaflet
as P1, PM (middle), and P2, where P1 is closest to the LA appendage. The PM scallop is further subdivided
into PM1 laterally and PM2 medially. Duran divides the anterior leaflet into two areas, A1 and A2, opposite
the corresponding scallops of the posterior leaflet. The two commissural areas of the valve are defined as
C1 (between A1 and P1) and C2 (between A2 and P2). The rationale for this nomenclature is that every part
of the mitral valve attached to the anterolateral papillary muscle is given the number one and every part
of the mitral valve attached to the posteromedial papillary muscle is given the number two. A schematic
representation of the three nomenclatures of the mitral valve is shown in Figure 8.2 (7).
Anterolateral
Middle Posteromedial
Classic anatomic Carpentier Duran
FIGURE 8.2 Schematic representation of the various nomenclatures of the mitral valve. The mitral valve is shown with
its relationship to the aortic valve, viewed from the left atrium. See text for details. (Adapted from Lambert AS, Miller JP,
Merrick SH, et al. Improved evaluation of the location and mechanism of mitral valve regurgitation with a systematic
transesophageal echocardiography examination. Anesth Analg. 1999;88:1205–1212, with permission.)

8. Mitral Regurgitation 161
Each institution or group of practitioners favors one nomenclature over another and it does not matter
which one is used, as long as every member of the team agrees on which terminology is used. The reader
is encouraged to have a basic understanding of all of them to avoid confusion. For example, P2 refers to a
different area of the valve in the Carpentier and Duran nomenclatures.
ETIOLOGY AND MECHANISM OF MITRAL REGURGITATION

MR can be classified according to its etiology (Table 8.1), or more simply, according to the pathophysiologic
mechanism leading to the regurgitation. Carpentier proposed the now widely used classification of MR
based on leaflet motion (8,9) (Fig. 8.3).
t In type 1 lesions, the leaflet motion is normal. In such cases, the MR jet tends to be central or slightly
off-center. Type 1 MR is usually the result of annular dilatation Fig. 8.3A, but less common mechanisms
include mitral valve clefts, aneurysms, perforation, or destruction, as a result of endocarditis Fig. 8.3B.
t In type 2 lesions, there is excessive mitral leaflet motion and the MR jet is typically directed away from the
diseased leaflet. The spectrum of severity of excessive leaflet motion is illustrated in Figure 8.4. Billowing
(or scalloping) refers to a situation where part of a mitral leaflet projects above the annulus in systole,
but the coaptation point remains below the plane of the mitral annulus. Prolapse is used to describe the
excursion of a leaflet tip above the level of the mitral annulus during systole, causing regurgitation. The
term flail is reserved for a situation where a leaflet edge is flowing freely into the left atrium in systole,
as a result of one or more ruptured chordae tendineae. The distinction between severe prolapse and flail
is sometimes difficult to make because the ruptured chordae may not be visible by echocardiogram. It is
also somewhat academic, as the hemodynamic consequences and the surgical treatment of the two are
often the same Fig. 8.3C, D.
t Type 3 lesions refer to restricted leaflet motion and are further subdivided into type 3a and 3b. In type 3a,
the restriction is “structural” (most often rheumatic) and the leaflet motion is affected in both systole and
diastole Fig. 8.3E. In type 3b, the restriction is “functional” and proper coaptation is prevented by systolic
tethering of the mitral leaflets as a result of a dilated left ventricle (LV) and/or displaced papillary muscles
Fig. 8.3F. Coronary artery disease is often the etiology of type 3b MR and is referred to as ischemic MR. In
type 3b, leaflet motion is normal in diastole. Usually in type 3 lesions, the regurgitant jet may be directed
towards the diseased leaflet if only one leaflet is affected, but the jet may also be central if both mitral
leaflets are equally affected by the disease process. This is often the case in type 3b abnormalities because
each papillary muscle supports both leaflets. Structural restriction of leaflet motion commonly coexists
with some degree of mitral stenosis. An ischemic (i.e., stiff ) papillary muscle may also temporarily
restrict leaflet motion, causing failure of coaptation.
TABLE 8.1 Causes of Mitral Regurgitation
Congenital
Endocardial cushion defect
Associated with other pathologies (e.g., corrected transposition)
Myxomatous degeneration
Rheumatic (often accompanied by mitral stenosis)
Endocarditis
Bacterial, viral, etc.
Cardiomyopathy
Dilated (ischemic, idiopathic, ethanol, drug related)
Hypertrophic
Other
Systemic lupus
Rheumatoid arthritis
Ankylosing spondylitis

A B
C D
E F
FIGURE 8.3 Carpentier′s classification of mitral regurgitation (MR) based on leaflet motion. In type 1, the leaflet motion
is normal and the MR jet tends to be central (A,B). In type 2, there is excessive leaflet motion and the MR jet is typically
directed away from the diseased leaflet (C,D). In type 3 lesions, the leaflet motion is restricted and is further subdivided
into type 3a (structural) (E) and type 3b (functional) (F). In type 3 lesions, the regurgitant jet may be directed towards
the diseased leaflet if only one leaflet is affected, or it may be central if both mitral leaflets are equally affected. (Courtesy
Dr. Gregory M. Hirsch.)

A B C
FIGURE 8.4 Excessive leaflet motion. A: Billowing (or scalloping) refers to a situation where part of a mitral leaflet (arrow)
projects above the plane of the annulus in systole, but the coaptation point remains below the mitral annulus. B: Prolapse
is used to describe the excursion of a leaflet tip above the level of the mitral annulus during systole, causing regurgita-
tion. C: The term flail is reserved for a situation where a leaflet edge (arrow) is flowing freely into the left atrium in systole.
APPROACH TO THE TRANSESOPHAGEAL ECHOCARDIOGRAPHY

EVALUATION OF MITRAL REGURGITATION
In the setting of mitral valve surgery, the intraoperative TEE evaluation of MR requires one to answer three
basic questions: (a) How severe is the MR? (b) What is the mechanism of the MR and where on the mitral
valve is the lesion? (c) Can the valve be surgically repaired?
How Severe is the Mitral Regurgitation?

The severity of MR is classified as trivial, mild, moderate, or severe. This corresponds to 1+, 2+, 3+, and 4+ by
angiography. The basic two-dimensional (2D) examination (see Chapter 2 on basic examination) of the heart
often provides clues that significant MR may be present. Such clues may be direct, like a large coaptation
defect or a structural anomaly of a leaflet, or indirect indicators such as the hemodynamic sequelae of severe
MR, like volume overload of the left ventricle and left atrium, or signs of pulmonary hypertension (dilated and
hypertrophied right ventricle, septal flattening, dilated pulmonary arteries). A detailed 2D examination of
the mitral valve is extremely valuable for precise localization of lesions and is discussed in the following text.
Color Doppler remains the easiest and best method to screen for MR because of its high sensitivity and
specificity. It also provides a semi-quantitative assessment of the severity of MR. The general appearance (size
and depth of penetration) of the regurgitant jet offers a rough index of the severity of regurgitation, but that
appearance is highly dependent on machine settings as well as pressures in the receiving chamber and may
lead to confusion. The “experienced eyeball method” tends to work only in mild or severe cases. The ratio of
the regurgitant jet area (RJA) over the total left atrial area (LAA) has been reported to correlate better with the
severity of MR on cardiac catheterization in almost 94% of a group of 82 patients (10). An RJA/LAA greater than
40% was found in patients with severe MR on cardiac catheterization. However, there are also important limita-
tions to this sign (11–13) and the severity of MR should not be determined only by the size of the Doppler jet.
The narrowest portion of the jet, known as the vena contracta, can be measured and diameters of
5.5 mm or more correlate with severe MR on cardiac catheterization (14) (Fig. 8.5). The use of 7 mm as
the cutoff point for severe MR is useful as it provides more specificity but not surprisingly at the cost of
decreased sensitivity (15). Note that, in order to be relevant, this measurement should be taken in the
midesophageal long-axis (ME-LAX) view.
The direction of the MR jet is also important, not only as a clue to its etiology, but also as a sign of its
severity. While central jets may be functional in nature (i.e., they may result from annular dilatation or
ventricular dysfunction), eccentric jets (Fig. 8.6, Video 8.1) are almost always due to a structural abnormal- Video 8.1
ity of the mitral apparatus itself and they are unlikely to improve after revascularization. Furthermore,
wall-hugging jets always warrant a close examination: First, jets that have enough energy to “hug the wall”
of the atrium for some distance should be considered hemodynamically significant until proven otherwise

FIGURE 8.5 Measurement of the vena contracta. This is a color Doppler scan of the mitral valve in the midesophageal
four-chamber view. The diameter of the base of the mitral regurgitation (MR) jet correlates with the severity of regurgitation.
(16). Second, wall-hugging jets are subjected to the “Coanda effect.” This is a physical principle by which
a fluid jet will get “sucked” against the wall, making it appear smaller by color Doppler than it actually is.
Consequently, a wall-hugging jet should be considered severe until proven otherwise.
As mentioned in the preceding text, it is important to remember that any quantitative assessment made
by color Doppler is highly dependent on the settings of the echo machine (aliasing velocity, pulse repetition
frequency, frame rate, etc.). This is further discussed in the chapter on color Doppler.
FIGURE 8.6 Eccentric mitral regurgitation (MR) jet. This is a color Doppler scan of the mitral valve in the midesophageal
four-chamber view. Note the severe MR jet which “hugs” the medial wall of the left atrium. Wall-hugging jets should be
considered severe until proven otherwise.

Spectral Doppler adds to the semi-quantitative assessment of the valve. While the peak velocity of the
regurgitant jet is mostly a function of the systolic gradient between the LV and the LA, the density of the
MR signal by continuous wave (CW) Doppler is proportional to the number of blood cells detected by
the Doppler beam (see Chapter 5 on Doppler). A dense MR jet with a sharp envelope on CW Doppler
suggests that a large fraction of the left ventricular (LV) output is going backward into the left atrium.
Conversely, a weaker signal with an incomplete envelope suggests a smaller regurgitant fraction (RF).
The evaluation of pulmonary venous flow by pulsed wave (PW) Doppler is also very important and
should be a routine part of any assessment of MR. The normal PW Doppler pattern of pulmonary venous
flow is forward in systole and in diastole. Significant regurgitation of the LV stroke volume in systole
causes blunting or reversal of the systolic component of pulmonary vein flow and this sign is a reliable
indicator of hemodynamically significant MR (Fig. 8.7) (17). However, it is important to remember that
although pulmonary venous flow reversal is specific, it is not a particularly sensitive method to detect MR.
The absence of systolic pulmonary venous flow blunting or reversal does not rule out severe MR, espe-
cially in chronic cases where a large and compliant left atrium may dissipate the energy from the regurgi-
tant jet. Table 8.2 summarizes the Doppler parameters typically found in mild, moderate, and severe MR.
Finally, it is important to remember that none of the signs described in the preceding text are enough
by themselves to make a diagnosis of severe MR, but taken as a group, they provide much better diagnostic
accuracy. Zoghbi et al. (15) provide an excellent review on the use of multiple techniques for assessing MR
severity.
More precise quantitative assessments of MR require the use of mathematical calculations, which are
described in a later section of this chapter.
FIGURE 8.7 Pulsed wave Doppler of the pulmonary vein flow. The top panel shows the normal pattern, forward in
systole and diastole. The middle panel shows blunting of the systolic flow, associated with increasing degrees of mitral
regurgitation. The bottom panel shows the typical pattern of systolic reversal seen in severe MR. Note the nonlaminar
aspect of the flow in the reversed S wave, caused by severe MR.

TABLE 8.2 Doppler and Quantitative Values Typically Found in Mild, Moderate, and Severe Mitral Regurgitation
Mild Moderate Severe

■ Doppler parameters
Jet area/LA area <4 cm2 or <20% of LA area — >10 cm2 or >40% of LA area
Density of CW Incomplete or faint Usually dense Dense complete envelope
Pulmonary venous flow Systolic dominance Systolic bluntinga Systolic reversala
■ Quantitative parameters
Vena contracta (mm) <3 3–6.9 ≥7
Regurgitant volume (mL) <30 30–59 ≥60
Regurgitant fraction (%) <30 30–49 ≥50
EROA <0.20 0.20–0.39 ≥0.40
a
Systolic blunting and reversal are specific but not sensitive signs. See text for details.
LA, left atrial; CW, continuous wave; EROA, effective regurgitant orifice area.
ME four chamber ME commissural
Atrial View (surgeon’s view)
Anteroflex
P1 A1 A1
Neutral P1
A2
A2
P2
A3 P2 A3
Retroflex P3 P3
AP view
Ventricular View A1
P1
AP view
Aorta A1 P1
Aorta A1 P1
A2
P2
A3
A2
P2
P3
A3 A2 P2 60 degrees
P3
P3 A2 P1
A3 P3
FIGURE 8.8 A: Sequential examination of the mitral valve from midesophageal windows, Midesophageal Four-
Chamber and Commissural views: The top of the figure displays the mitral valve from the atrial side, which is similar
to direct intraoperative visualization. The bottom of the figure displays the valve from the ventricular side, which
corresponds more closely to the TEE cross-sections.

Atrial View (surgeon’s view)

ME two chamber ME long axis
Probe turned to right
Probe neutral
Probe
P1 A1 P1 A1
turned
A2 A2
to left P2 A3 P2 A3
P3 P3
Ventricular View
AP View AP View
P3
P2
P1 P1 P1
Aorta Aorta
A1 A1
A2
A2
A3 A3 P2
P2 135 degrees
P3 P3 P3
A2 A1
A2
P2
P3
A3 A2
FIGURE 8.8 (continued) B: Sequential examination of the mitral valve from midesophageal windows, Long Axis Views:
Again, the valve is depicted from the atrial side at the top, which is similar to direct intraoperative visualization, and
from the ventricular side at the bottom, which corresponds more closely to the TEE cross-sections. ME = midesophageal;
AP = anteroposterior.
What is the Mechanism of Mitral Regurgitation and Where

on the Mitral Valve is the Lesion?
Systematic Two-dimensional Examination of the Mitral Valve
Once it has been established that there is significant MR, the next step is to determine the mechanism
of the MR and the precise location of the lesion, so that an appropriate surgical plan can be formulated.
The various mechanisms of MR were discussed in the preceding text. The precise localization of lesions
involves a systematic 2D echo examination of the mitral valve.
The systematic examination of the mitral valve combines techniques described in several publications
(5,7,18) and aims at obtaining multiple redundant views of all parts of the valve and to identify each
mitral segment using internal, recognizable cardiac landmarks. Accordingly, the sequence described in
the following text and illustrated in Figure 8.8 is recommended:
1. Begin the examination in the midesophageal (ME) four-chamber view at 0 degrees of transducer
rotation, with the mitral valve in the center of the screen. The anterior mitral leaflet is medial, adjacent to

the aortic valve and the posterior leaflet is lateral. Slight withdrawal (18) or anteflexion (7) of the probe
brings the left ventricular outflow tract (LVOT) into the plane of the scan, which demonstrates the
anterior segments of the valve (A1/A2, P1/P2). Conversely, with slight insertion (18) or retroflexion
(7) of the probe, the LVOT disappears from the scanning plane, allowing the examination of the
posterior segments of the valve (A2/A3, P2/P3). The entire mitral valve can therefore be seen at
0 degrees of transducer rotation, by gently anteflexing or retroflexing the probe. A note of caution:
Because of anatomic variations, this author does not believe that the average echocardiographer
can consistently discriminate between P1 and P2, or between P2 and P3 using only 0-degree views.
2. Obtain a ME mitral commissural view by rotating the imaging array to obtain the best possible
cut through the commissures. This is usually achieved between 60 and 90 degrees (5). This cross
section typically demonstrates P1 laterally, P3 medially, and variable amounts of anterior leaflet in
the middle. The apparent double orifice stems from the semicircular coaptation between the leaflets
of the mitral valve. The presence and severity of disease at the level of the commissures can be
evaluated here.
3. Next, the ME two-chamber view is obtained by rotating the transducer forward to approximately 80 to
100 degrees. In addition, by turning the shaft of the probe leftward and rightward, three reproducible
cross sections can be obtained, allowing further identification of the valve segments (7,18).
4. Then, the ME long-axis view is obtained by rotating the transducer to approximately 130 to 150 degrees.
This provides a cut through the center of each mitral valve leaflet, which allows reliable identification of
A2 and P2 (5). As this view cuts across the saddle-shaped annular plane at its most superior aspect, it
is a preferred view for assessing mitral valve prolapse because it avoids the false positives which occur
using the ME four-chamber view.
5. Finally, the probe is advanced into the stomach and the TG basal short-axis view of the mitral valve
is obtained (5,7) (Fig. 2.18). This cross section is useful to diagnose clefts and perforations and color
Doppler provides additional information on the origin of the regurgitant jet(s).
Technically, it is extremely important to remember that the classic imaging planes described in the
preceding text are obtained only when the echo scan crosses through the center of the mitral valve.
Indeed, turning of the probe shaft from the ME commissural or ME long-axis views will provide a lot of
additional three-dimensional (3D) information from transitional images, but it may be misleading to the
novice eye. For example, gently turning the probe to the right in the commissural view will reveal more of
the anterior leaflet, showing not only A2 but also extending toward A1 and A3. Turning the probe to the
left will reveal more of P2, not only P1 and P3 on either side as expected. Likewise in the long-axis view, a
well-centered scan usually demonstrates A2 and P2, but slight rotation of the probe to the right will move
the scan toward A3/P3 and slight rotation to the left will move the scan toward A1/P1. In addition, 3D
echocardiography has revealed that these relationships do not always hold true, especially when there is
rotation or distortion of the heart by chronic disease.
The whole detailed examination can be done very quickly when one becomes familiar with it. The
recommended sequence of views mentioned in the preceding text provides sufficient redundancy in the
segment identification that in the author’s experience results in high accuracy and consistent reliability.
Whatever the sequence of views, the examination should be consistent and systematic. As in other aspects
of echocardiography, repetition is important and by learning to recognize the variants of normal and the
wide spectrum of pathologies are better appreciated.
QUANTITATIVE EVALUATION OF THE MITRAL VALVE

Regurgitant volume (RV), regurgitant fraction (RF), and regurgitant orifice area (ROA) can be calcu-
lated using the continuity principle. For a detailed discussion of this principle, please see Chapter 6
on hemodynamic assessment.
t RV is the difference between the amount of blood that enters the left ventricle in diastole and the
amount of blood that exits through the aortic valve in systole. It is typically obtained by calculating
the stroke volume across the LVOT (VTILVOT × AreaLVOT) and subtracting it from the forward
stroke volume which crosses the mitral valve in diastole (VTIMV × AreaMV ). An alternative site

such as the pulmonary artery can also be used. Calculation of RV is limited by the fact that the mitral
valve opening is oval, not round, and its surface area changes throughout diastole. One can also use the
proximal isovelocity surface area (PISA) method to calculate the RV, as described in the following text.
t The RF (the percentage of LV blood that flows backward into the left atrium in systole) is the ratio of the
RV over the volume that flows forward across the mitral valve in diastole (i.e., the total stroke volume).
t Calculation of the effective regurgitant orifice area (EROA) is achieved by the PISA method, which
can also be used in the evaluation of mitral stenosis and it is described in detail in Chapter 9. PISA was
popular some years ago (19), but because of numerous limitations associated with the technique, it is
falling out of fashion. In brief, PISA takes advantage of the flow dynamics of blood as it is forced into
the regurgitant orifice. Approaching the orifice, the blood cells accelerate along a series of concentric
hemispheres which can be visualized by color Doppler. At the aliasing velocity (Nyquist limit) the color
turns from red to blue (Fig. 8.9). This point provides both the velocity and the radius of the hemisphere.
By knowing the velocity and radius of the hemisphere, one can calculate the volumetric flow at that
radius (= area × velocity = 2πr 2 × Nyquist limit). Then one measures the peak velocity of the MR jet by
CW Doppler to calculate the EROA.
2πr 2 × Nyquist limit
EROA =
MR velocity
The PISA method is based on a number of assumptions, which create important limitations (20):
First it assumes that the orifice is round, which may not be the case. Also, this method’s estimation of
cross-sectional area as 2πr2 assumes that the PISA “shells” are true hemispheres, not cones or flattened
shells. Utsunomiya et al. (21) established that PISA shells are closest to being true hemispheres when their
radius is approximately 11 to 15 mm. The Nyquist limit and the color baseline should be adjusted accord-
ingly to minimize error. Also, for eccentric jets, an angle correction must be used, as described in Chapter
9 on mitral stenosis.
Finally, when certain clinical conditions are met, a simplified PISA formula can be used. Indeed, when
the Nyquist limit is set at 40 cm/s and the gradient across the MR jet is 100 mm Hg, the whole formula
simplifies down to:
r2
EROA =
2
Note that if the r 2 value is greater than 1, it is reasonable to assume that the MR is severe.
0.45
−0.45
FIGURE 8.9 Estimated regurgitant orifice area by the proximal isovelocity surface area (PISA) method. The radius of the
hemisphere where the cells reach the aliasing velocity is measured and used in the PISA equation.

RV, RF, and regurgitant area are time-consuming measurements and may not always be practical in
the busy setting of the operating room. As such, they may not always be required in mild or severe cases.
However, they are the only true quantitative measurements of MR that we have and they are important
in borderline cases. They are also important research tools.
Table 8.2 summarizes the quantitative values typically found in mild, moderate, and severe
MR (15).
PITFALLS IN THE EVALUATION OF MITRAL REGURGITATION

Patients with mitral valve disease often have dilated hearts and distorted cardiac anatomy. This can
make the TEE examination challenging because it changes the appearance of the various TEE cross
sections of the mitral valve. Changes in preload, afterload, myocardial contractility, and compliance
can have a profound impact on the appearance of MR. In the operating room, all of these are affected
by general anesthesia (GA). Several authors have documented that the severity of MR decreases by at
least one grade following induction of anesthesia (22–24). The difference seemed least pronounced
in flail mitral valves and most significant in patients with functional MR (23). Gisbert et al. (24)
reported that the effect of GA can be reversed in most cases with the administration of phenyleph-
rine. Changing the condition of other valves may also affect MR. For example, in patients with MR in
the presence of significant aortic stenosis, the severity of MR usually improves following aortic valve
replacement (AVR) due to lower intraventricular pressures. Finally, any of these factors can change
acutely many times during the course of an operation. For these reasons, the echocardiographer must
remain cognizant of the clinical conditions present at the time of the examination when assessing the
severity of MR.
FUNCTIONAL MITRAL REGURGITATION

MR can also be seen in the absence of structural abnormality of the mitral leaflets. Termed functional MR,
it typically occurs in the setting of chronic LV dysfunction. Most cases of functional MR fall into the Car-
pentier type 3b category, although some annular dilatation can also be present as part of the mechanism.
The most common cause of functional MR is ischemic cardiomyopathy, usually following inferoposterior
myocardial infarction. Functional MR can also be the result of other forms of dilated cardiomyopathies as
well. In the context of coronary artery bypass surgery, the clinical importance of functional MR resides in
the fact that it is associated with a worse overall prognosis for the patient. The mechanism of functional MR
is multifactorial, but at the source, functional MR is a ventricular disease and the patient’s prognosis after
surgery will depend on the progression or regression of LV dysfunction. Some of the factors that contribute
to functional MR include the following:
1. Regional wall motion abnormalities and dilatation (sometimes frank aneurysm) affecting the inferior
and posterior walls of the LV. The LV geometry is modified and there is increased sphericity of the
ventricle.
2. Distortion in the relationship between the LV and the mitral apparatus can result in increased
interpapillary distance and changes in papillary muscle orientation relative to the leaflets.
3. Eventually, this results in tethering of the mitral leaflets, which ultimately leads to failure of coaptation
and regurgitation.
4. Annular dilatation may also occur, developing mostly in the anteroposterior (AP) diameter.
5. Finally, if ventricular function is depressed, decreased closing forces on the mitral valve during systole
may also play some role in the failure of coaptation.
Two patterns of tethering have been recognized (25): Symmetric tethering where both mitral leaflets
coapt at the same level, but lower than usual; and asymmetric tethering where the tethering vector is

directed more posteriorly, creating more restriction of one leaflet than the other and creating an appear-
ance of “pseudoprolapse.” Note that this is not a true leaflet prolapse because the coaptation point is well
below the mitral annulus.
The best time to assess functional MR is preoperatively. This is because functional MR is particularly
sensitive to loading conditions. As mentioned in the preceding text, GA affects loading conditions and MR
is typically underestimated under anesthesia. In a case of structural MR, the jet may look less severe under
anesthesia, but the structural abnormality of the mitral valve will still be present. In functional MR, where
little structural abnormality in the mitral valve is present other than tethering of the leaflets, the reduced
loading conditions may mislead the clinician not to correct the pathology, which could be detrimental to
the patient.
When faced with having to assess functional MR in the operating room, the same general principles
apply:
t Anatomy, anatomy, anatomy: Rule out structural causes of MR, for example, leaflet prolapse.
t Carefully look at the mitral leaflets for tethering (leaflets not returning to the annular plane during
systole) or other restriction to valve closure, mitral annulus diameter, papillary muscles location, and wall
motion in areas supporting the papillary muscles. As noted above, this tethering could be symmetrical or
asymmetrical.
t Look at overall LV size and shape.
t Measure the “tethering distance” and the “tethering surface area” (also known as tenting distance and
tenting surface area) can be measured as an index of the severity of tethering. Clinically, this may not
correlate with the degree of MR.
The surgical approach to functional MR is controversial and is discussed at length in Chapter 10 on

mitral repair.
Three-dimensional Echocardiography
Three-dimensional echocardiography has been available for almost two decades, but until recently,
images consisted of computer-generated reconstructions of multiple, ECG-gated 2D scans, collected over
a fairly long period of time. The process was complex and time-consuming, and the images were of mar-
ginal quality. Recently, matrix technology has made it possible to fit a 3D transducer in the tip of a TEE
probe and to generate real-time 3D TEE images of the heart and its various structures. The mitral valve
is particularly well suited to 3D imaging because of its proximity to the base of the heart, and because
the central axis of the valve is perfectly aligned with the ultrasound beam. Of all the applications of 3D
TEE, the intraoperative imaging of structural mitral valve disease is arguably one of the most useful. Not
surprisingly, the body of literature devoted to 3D echo of the mitral valve has outpaced that of all other
cardiac structures.
Three-dimensional echocardiography has several advantages over 2D imaging. In many cases, 3D
images are more intuitively obvious than 2D images and they may facilitate communication with the sur-
gical team. Images can also be manipulated on the screen, allowing an infinite number of perspectives.
Moreover, 3D can provide information that is unavailable with 2D echo.
But like most technologic advances, 3D echocardiography also has its limitations. First, 3D ultrasound
remains ultrasound, and it is subjected to the same laws of physics. As a result, good 2D images usually
mean good 3D images, but 3D rarely makes up for poor 2D images. Second, 3D requires the processing
of huge amounts of information by the computer, leading to lower frame rates. The resulting images can
be “jerky” making interpretation of the images difficult. Next, 3D echo introduces a new set of artifacts
and pitfalls, which operators must become familiar with. Finally, pretty pictures do not guarantee a more
accurate diagnosis.
In 3D modes, a cone of information is acquired, which can then be sliced and looked at from any
number of different perspectives. Three-dimensional “en face” views of the mitral valve arguably
win the prize for the prettiest images in all of echocardiography. When the quality is good, these

FIGURE 8.10 Three-dimensional zoom of the mitral valve from the left atrial perspective. The various mitral valve seg-
ments are labeled, P1, P2, and P3 and A1 and A3, according to the Carpentier nomenclature. By convention, the left atrial
view of valve is displayed in the “surgeon’s view,” with the A2 segment (and the aortic valve) in the 12 o’clock position. The
large arrow points to a flail P2 scallop. Note the ruptured piece of chordae tendineae attached to the flail scallop (also note
that A2 is not labeled because it is behind the flail P2 scallop).
images can provide even the novice observer with an instantaneous appreciation of a number of
Video 8.2 mitral pathologies (Fig. 8.10, Video 8.2). This is especially true for mitral leaflet prolapse or flail
(Carpentier, type 2). However, MR due to leaflet restriction (Carpentier, type 3a), as well as func-
tional MR (type 3b), tends to be much more tricky to diagnose with 3D zoom alone, because of
depth perception and other technical considerations. En face views can be obtained from the LA
perspective—the surgeon’s view—or from the LV perspective—analogous to a computerized tomog-
raphy image. While the LA view shows the surgeon exactly what to expect at the time of atriotomy,
the LV perspective provides a rare opportunity to show the surgeon a vantage point that cannot be
obtained with the heart open.
Another 3D modality, called multiplane reconstruction (MPR), allows the simultaneous visualiza-
tion of three 2D orthogonal planes of the mitral valve, which can all be adjusted at will (Fig. 8.11, Video
Video 8.3 8.3). While this is an off-line modality, it can quickly be obtained in the operating room. In effect,
it provides a deconstruction of the mitral valve into three adjustable 2D planes, and allows accurate
recognition of any part of the valve, by confirming the position of any scanning plane in the other two
axes. This makes for very accurate localization of pathology. Note that this does not replace a thorough
understanding of 2D mitral valve scanning planes, but rather supplements it. In fact, once well under-
stood, all the views contained in the systematic 2D examination of the mitral valve can be obtained
off-line, with a full-volume data set and MPR. If a good 2D-TEE diagnosis rests in the hands of the
one manipulating the probe, a good 3D-TEE diagnosis rests in the hands of the one manipulating the
mouse!
Color flow Doppler can also be applied to 3D echocardiography. Because of its close proximity to the
echo transducer in the left atrium, en face views from the LA perspective readily demonstrate MR, allowing
precise 3D determination of the location, size, and direction of a mitral regurgitant jet.

FIGURE 8.11 Multiplane reconstruction of the mitral valve. As its name implies, this 3D modality displays multiple
adjustable 2D planes simultaneously. The top-left box displays a ME four-chamber view of the valve. Note the obvi-
ous P2 prolapse (white arrow). The top-right box displays a ME commissural view, again showing the same P2 prolapse
(yellow arrow). The bottom-left box displays a short-axis view of the mitral valve. Note that these planes can be adjusted,
providing a cross-reference for each view in multiple planes. See text for details.
Finally, MPR of 3D color flow Doppler images allows one to analyze an MR jet like any other 3D
structure. The jet can be cut in any axis, allowing volumetric measurements. A recent study suggests
that 3D TEE can estimate mitral RV within 1.2% of the gold standard cardiac MRI (26). Moreover,
MPR provides another opportunity for a quantitative analysis of MR. By aligning the color MR jet in
two planes, one can obtain a perfect cross-sectional view of the base of the jet in the third axis—the
vena contracta—allowing planimetry of its surface area (Fig. 8.12). Although not fully validated yet,
the surface area of the vena contracta promises a better diagnostic reliability than the unidimensional
diameter.
Mitral valve 3D analysis software provides a detailed structural analysis of the mitral valve anatomy and
pathology and their use may become widespread in the future. These techniques are relatively complex to
learn and they take time to perform. This makes their use impractical in the operating room, and they will
not be discussed any further.

FIGURE 8.12 Multiplane reconstruction of the mitral valve, with color flow Doppler: This image is similar to Figure 8.11,
except that color Doppler is applied. Note that in this case the MR is functional and the MR jet is central. Note the multiple
orthogonal views of the MR jet, allowing a good qualitative assessment of the origin, size, and direction of the jet. Also,
when the scanning planes are aligned with the MR jet in the top two boxes, the third box (bottom left) displays a perfect
short axis of the valve, allowing accurate planimetry of the vena contracta.
CONCLUSION
Intraoperative TEE has become an integral part of the surgical decision-making process in mitral valve
surgery, and a standard of care in the evaluation of MR. A thorough and systematic approach to the
examination of the mitral valve allows one to define the pathology and to pinpoint its precise location
on the valve.
Following the surgical procedure, the immediate results can be determined and further interventions
can be undertaken immediately if necessary. This will be discussed in Chapter 10 on mitral repair.
Three-dimensional echocardiography is becoming an important tool in the arsenal of the intraoperative
echocardiographer. At this time, it remains an adjunct to 2D echo, but it promises to play an ever-increasing
role in the intraoperative evaluation of mitral valve pathology.
REFERENCES
1. Salgo IS, Gorman JH III, Gorman RC, et al. Effect of annular shape on leaflet curvature in reducing mitral leaflet stress.
Circulation. 2002;106(6):711–717.
2. Joudinaud TM, Kegel CL, Flecher EM, et al. The papillary muscles as shock absorbers of the mitral valve complex. An experi-
mental study. Eur J Cardiothorac Surg. 2007;32(1):96–101.

3. Cheitlin MD, Finkbeiner WE. Cardiac anatomy. In: Chatterjee K, Cheitlin MD, Karliner J, et al., eds. Cardiology, an Illustrated
Text. Philadelphia, PA: JB Lippincott Co; 1991:1.9–1.10.
4. Carpentier AF, Lessana A, Relland JY, et al. The “physio-ring”: An advanced concept in mitral valve annuloplasty. Ann Thorac
Surg. 1995;60:1177–1185.
6. Kumar N, Kumar M, Duran CM. A revised terminology for recording surgical findings of the mitral valve. J Heart Valve Dis.
1995;4:70–75.
7. Lambert AS, Miller JP, Merrick SH, et al. Improved evaluation of the location and mechanism of mitral valve regurgitation
with a systematic transesophageal echocardiography examination. Anesth Analg. 1999;88:1205–1212.
8. Carpentier A. Cardiac valve surgery–the “French correction.” J Thorac Cardiovasc Surg. 1983;86:323–327.
9. Stewart WJ, Currie PJ, Salcedo EE, et al. Evaluation of mitral leaflet motion by echocardiography and jet direction by Doppler
color flow mapping to determine the mechanisms of mitral regurgitation. J Am Coll Cardiol. 1992;20:1353–1361.
10. Helmcke F, Nanda NC, Hsiung MC, et al. Color Doppler assessment of mitral regurgitation with orthogonal planes. Circulation.
1987;75:175–183.
11. Cape EG, Yoganathan AP, Weyman AE, et al. Adjacent solid boundaries alter the size of regurgitant jets on Doppler color flow
maps. J Am Coll Cardiol. 1991;17:1094–1102.
12. Simpson IA, Valdes-Cruz LM, Sahn DJ, et al. Doppler color flow mapping of simulated in vitro regurgitant jets: Evaluation of
the effects of orifice size and hemodynamic variables. J Am Coll Cardiol. 1989;13:1195–1207.
13. Stevenson J. Two-dimensional color Doppler estimation of the severity of atrioventricular valve regurgitation: Important
effects of instrument gain setting, pulse repetition frequency and carrier frequency. J Am Soc Echocardiogr. 1989;2:1–10.
14. Tribouilloy C, Shen WF, Quere JP, et al. Assessment of severity of mitral regurgitation by measuring regurgitant jet width at its
origin with transesophageal Doppler color flow imaging. Circulation. 1992;85:1248–1253.
15. Zoghbi WA, Enriquez-Sarano M, American Society of Echocardiography, et al. Recommendations for evaluation of the sever-
ity of native valvular regurgitation with two-dimensional and Doppler echocardiography. J Am Soc Echocardiogr. 2003;16(7):
777–802.
16. Schiller NB, Foster E, Redberg RF. Transesophageal echocardiography in the evaluation of mitral regurgitation. The twenty-
four signs of severe mitral regurgitation. Cardiol Clin. 1993;11:399–408.
17. Pu M, Griffin BP, Vandervoort PM, et al. The value of assessing pulmonary venous flow velocity for predicting severity of mitral
regurgitation: A quantitative assessment integrating left ventricular function. J Am Soc Echocardiogr. 1999;12:736–743.
18. Foster GP, Isselbacher EM, Rose GA, et al. Accurate localization of mitral regurgitant defects using multiplane transesophageal
echocardiography. Ann Thorac Surg. 1998;65:1025–1031.
19. Lambert AS. Proximal isovelocity surface area should be routinely measured in evaluating mitral regurgitation: A core review.
Anesth Analg. 2007;105(4):940–943.
20. Simpson IA, Shiota T, Gharib M, et al. Current status of flow convergence for clinical applications: Is it a leaning tower of
“PISA”? J Am Coll Cardiol. 1996;27(2):504–509.
21. Utsunomiya T, Doshi R, Patel D, et al. Calculation of volume flow rate by the proximal isovelocity surface area method:
Simplified approach using color Doppler zero baseline shift. J Am Coll Cardiol. 1993;22(1):277–282.
22. Grewal KS, Malkowski MJ, Piracha AR, et al. Effect of general anesthesia on the severity of mitral regurgitation by trans-
esophageal echocardiography. Am J Cardiol. 2000;85(2):199–203.
23. Bach DS, Deeb GM, Bolling SF. Accuracy of intraoperative transesophageal echocardiography for estimating the severity of
functional mitral regurgitation. Am J Cardiol. 1995;76(7):508–512.
24. Gisbert A, Souliere V, Denault AY, et al. Dynamic quantitative echocardiographic evaluation of mitral regurgitation in the
operating department. J Am Soc Echocardiogr. 2006;19(2):140–146.
25. Lee AP, Acker M, Kubo SH, et al. Mechanisms of recurrent functional mitral regurgitation after mitral valve repair in nonisch-
emic dilated cardiomyopathy: Importance of distal anterior leaflet tethering. Circulation. 2009;119:2606–2614.
26. Shanks M, Siebelink HM, Delgado V, et al. Quantitative assessment of mitral regurgitation: Comparison between three-dimensional
transesophageal echocardiography and magnetic resonance imaging. Circ Cardiovasc Imaging. 2010;3(6):694–700.

QUESTIONS
1. Which of the following types of mitral 6. Which of the following statements is false
regurgitation is typically not associated about the WFOBDPOUSBDUB?
with a “structural” defect of the mitral a. It represents the narrowest point of the MR
leaflets? jet
a. Type 1 b. It should be measured in the ME-
b. Type 2 commissural view
c. Type 3a c. A diameter of 7 mm or more is associated
d. Type 3b with severe MR
e. None of the above d. Like all other color Doppler measurements,
it may be affected by gain and Nyquist limit
2. Which of the following statements is false
regarding the mitral annulus?
a. It is saddle shaped 7. Which of the following echocardiographic
b. Its diameter decreases in systole signs is typically not associated with severe
c. In disease states, it tends to dilate, but main- MR?
tains its saddle shape a. A large mitral coaptation defect on 2D echo
d. When dilated, it may contribute to mitral b. A wall-hugging MR jet
regurgitation c. A vena contracta of 8 mm
e. None of the above statements is false d. A large color Doppler MR jet, which fills
two-thirds of the left atrial area
3. In the Carpentier nomenclature, which
e. All the above signs are associated with
mitral valve segment coapts with P3?
severe MR
a. A1
b. A2 8. A patient is stable in the coronary care
c. A3 unit, after a late-presentation inferior ST
d. None of the above elevation myocardial infarct. Suddenly, he
becomes severely dyspneic and requires
4. Assuming all measurements are taken
intubation. On auscultation, you hear a
appropriately, which of the following
new loud holosystolic murmur. In this
signs DPVMECFTFFO with severe mitral
clinical context, what is the most likely
regurgitation?
diagnosis and what do you expect to find on
a. Forward systolic pulmonary venous flow
echocardiography?
b. Vena contracta of 3 mm
a. Acute severe type 3b (functional) MR from
c. Regurgitant volume 15 mL
tethering of the mitral valve
d. Jet area/left atrial area 20%
b. Severe RV dilatation from acute pulmonary
embolism
5. A TEE report states that “the mechanism of c. Severe type 2 MR from a ruptured posterior
MR is type 2, with a central MR jet.” What papillary muscle
conclusion will you draw from this report? d. Acute endocarditis with a torn anterior
a. This is expected: The MR jet in type 2 dis- mitral leaflet
ease is usually central e. None of the above is very likely
b. This is impossible: The TEE report must be
9. Pick the CFTU answer among the following
wrong
choices: Mitral annular dilatation typically
c. This is expected, but only in cases of A2
occurs in which of the following situations?
prolapse
a. Chronic type 1 MR
d. This could happen if there is bileaflet pro-
b. Chronic type 2 MR
lapse
c. Chronic type 3b MR
d. It can occur in any of the above situations
e. None of the above is true

10. A patient presents to your operating room 14. Which of the following 3D modalities
for mitral valve repair. The preoperative allows simultaneous visualization of
evaluation showed severe (4+) MR. After multiple orthogonal 2D-echo planes?
induction of anesthesia, your examination a. 3D full-volume view
demonstrates only mild MR. Your course of b. Multiplane reconstruction (MPR)
action would include which of the following? c. 3D zoom
a. Obtain a second opinion from a colleague d. Live 3D
b. Administer vasopressors (e.g., phenyleph- e. None of the above
rine, ephedrine, or norepinephrine) to raise
15. Which of the following statements are USVF
the blood pressure
concerning 3D echo of the mitral valve?
c. Perform a comprehensive mitral valve
a. The images must be processed off-line and
examination to determine the anatomy and
cannot be used in the operating room
pathophysiology of the MR
b. It eliminates the need for novice echocar-
d. Review the preoperative images and contact
diographers to understand 2D images
the cardiologist, if possible
c. It allows imaging of the ventricular surface
e. All of the above are appropriate actions
of the mitral valve
11. During coronary artery bypass surgery, you d. It does not lend itself to quantitative mea-
perform a comprehensive TEE examination surements of the mitral valve
after induction of anesthesia, and you find e. None of the above
trace (1+) MR. Half an hour later, (without
16. Which of the following statements is
any change to the settings on the echo
GBMTF regarding the currently available
machine) you repeat the mitral valve images
quantitative 3D mitral valve analysis
and you find moderate to severe (3+) central
software packages?
MR! All of the following factors could
a. It can be used in the operating room
DPODFJWBCMZ contribute this sudden increase
b. It provides a detailed structural analysis of
in MR, EXCEPT:
the mitral valve
a. An acute ischemic event
c. It usually will not show mitral annular calci-
b. The surgeon opened the pericardium
fication
c. The patient received a large fluid bolus
d. It has many research applications
d. Surgical stimulation has caused a rise in
e. All the above statements are true
blood pressure
e. None of the above 17. Which of the following conditions is most
MJLFMZ to be associated with functional
12. Which of the following mechanisms are
(type 3b) MR?
believed to play a role in functional mitral
a. Alcoholic cardiomyopathy
regurgitation (type 3b)?
b. Myxomatous mitral valve disease
a. Posterior and apical papillary muscle dis-
c. Rheumatic mitral valve disease
placement
d. Acute bacterial mitral valve endocarditis
b. Mitral annular dilatation
e. Fibroelastic mitral valve disease
c. Tethering of the mitral valve leaflets
d. All of the above factors 18. If a patient ruptures his/her posteromedial
e. None of the above factors papillary muscle, all of the following mitral
segments (Carpentier nomenclature) are
13. Which of the following statements about
likely to be affected, EXCEPT:
3D TEE of the mitral valve is TRUE?
a. A2
a. 3D technology has only been available since
b. P2
2008
c. A3
b. 3D is not associated with any significant
d. P1
artifacts
e. P3
c. 3D technology often makes up for poor 2D
images quality
d. 3D technology eliminated the problem of
low frame rates
e. None of the above statements is true

19. Which of the following is not an example of 20. All of the following factors have an impact
UZQF mitral valve disease? on the surgeon’s ability to repair the mitral
a. Restricted P2 segment valve, EXCEPT:
b. Prolapsed A3/P3 segments a. The location of the pathology
c. Flail P2 segment b. The severity of the MR
d. Billowing A2 segment c. The mechanism of the MR
e. None of the above d. The degree of mitral annular calcification
e. The surgeon’s experience

9 Mitral Valve Stenosis
Colleen G. Koch
T HE 19 TH CENTURY PHYSICIAN J EAN Nicholas Corvisart established the diagnostic value of percus-
sion in the physical diagnosis of cardiac disorders. He described the diastolic thrill of mitral stenosis (MS)
as “a peculiar rushing like water, difficult to be described, sensible to the hand applied over the precor-
dial region, a rushing which proceeds apparently from the embarrassment which the blood undergoes
in passing through an opening which is no longer proportioned to the quantity of fluid which it ought to
discharge” (1). As early as 1898, D. W. Samways discussed the potential for performing cardiac surgery in
the most severe cases of MS in an article entitled “Cardiac Peristalsis: Its Nature and Effects,” published
in The Lancet (2). In the modern era of heart disease, cardiac catheterization has provided hemodynamic
information and assessed the severity of MS. Popovic et al. (3) investigated time-related trends in the use
of preoperative invasive hemodynamic measurements in 1,985 patients with isolated valvular stenosis.
During an 8-year study period, cardiac catheterization before valve surgery remained a common practice;
however, it was performed primarily to ascertain coronary anatomy. The need for invasive hemodynamic
measurements acquired during catheterization dramatically decreased, superseded by noninvasive hemo-
dynamic measurements obtained with echocardiography (3). Currently, two-dimensional (2D) and Doppler
echocardiography have supplanted cardiac catheterization in providing a complete evaluation of patients
with MS (4).
MITRAL VALVE ANATOMY

Morphologically, the mitral valve (MV) apparatus is composed of the left atrial wall, mitral annulus, ante-
rior and posterior MV leaflets, chordal tendons, anterolateral and posteromedial papillary muscles, and left
ventricular myocardium (5,6). The valvular tissue can be divided into two commissural regions, the antero-
lateral commissure and the posteromedial commissure, and two leaflet areas, the anterior and posterior
MV leaflets. The anterior mitral leaflet is somewhat triangular in shape, with an attachment to approxi-
mately one-third of the circumference of the mitral annulus. It is attached to the fibrous skeleton of the
heart, as are the left coronary cusp and half of the noncoronary cusp of the aortic valve. The attachment of
the posterior mitral leaflet to the mitral annulus is lengthier than that of the anterior mitral leaflet. Clefts
along the free margin of the posterior leaflet allow the identification of individual scallops (5). Although
the anterior mitral leaflet base-to-margin dimension is longer than that of the posterior mitral leaflet, and
although the basal attachments are different for each leaflet, the two leaflets are nearly identical in overall
surface area. Chordal tendons from each papillary muscle attach to both of the MV leaflets. On average,
120 chordal tendons attach to the undersurface of the MV leaflets. The chordal tendons subdivide as they
project from the papillary muscles toward the MV leaflets. The spaces between the chordae serve as sec-
ondary orifices between the left atrium (LA) and left ventricle (LV) (6).
The normal MV orifice area is approximately 4 to 6 cm2. An orifice area in the range of 2 cm2 causes a
minimal elevation in the transvalvular pressure gradient, whereas a valve area of less than 1.4 cm2 is associ-
ated with a significant transvalvular pressure gradient and the clinical presentation of MS (7–9).
ETIOLOGY OF MITRAL STENOSIS

The causes of MS include the following: Rheumatic heart disease, LA myxoma, severe mitral annular calci-
fication, thrombus formation, parachute MV deformity, congenital MS, supravalvular mitral ring, and cor
triatriatum (6,10). Figures 9.1 and 9.2 depict a large LA myxoma obstructing mitral inflow. 179

FIGURE 9.1 A transesophageal echocardiographic midesophageal four-chamber image displays a 3- × 6-cm left atrial
myxoma causing symptomatic mitral stenosis. The atrial myxoma is visualized prolapsed through the mitral valve into
the left ventricular cavity during diastole.
The most common cause of MS in adult patients is still rheumatic heart disease (3,6,9). Pathologic fea-
tures of rheumatic MS include fusion of the commissures; contracture, scarring, and diffuse thickening of
the leaflet tissue and subvalvular apparatus; and calcium deposition within the mitral leaflets. This process
results in a diminished size of the effective valvular orifice, in addition to valve rigidity as a consequence of
the leaflet fibrosis and calcification. As the valve area becomes more restricted, increases in the transval-
vular pressure gradient and LA pressure may lead to pulmonary hypertension with tricuspid regurgitation
and right ventricular dysfunction (6,8–10).
TRANSESOPHAGEAL ECHOCARDIOGRAPHIC
EVALUATION OF MITRAL STENOSIS
A discussion of the complete diagnostic evaluation follows, and the chapter concludes with a concise sum-
mary of the recommended approach to an accurate diagnosis of MS.
FIGURE 9.2 An atrial myxoma displayed from a transgastric basal short-axis imaging plane occupies a large portion of
the mitral orifice. The mitral valve orifice measures 1.86 cm2 in diastole.

9. Mitral Valve Stenosis 181
The anatomy of MS can be defined more clearly from multiple imaging planes of 2D transesophageal echo-
cardiography (TEE) than by any other diagnostic modality. On the basis of the pathophysiologic features of
rheumatic MS, key features that must be identified echocardiographically include the following: Degree of
leaflet thickening, amount of calcium deposition, extent of subvalvular involvement, decrement in leaflet
mobility, and overall changes in chamber dimensions and function (11). Related issues, such as involvement
of other valve structures and pulmonary hypertension, can also be assessed.
Mitral leaflet tissue can display varying degrees of thickening and calcium deposition that cause the MV
leaflets to appear “enhanced,” or echo-bright. The “shadow” cast by calcium may obstruct the view of the
distal anatomy; one of the strengths of TEE in this circumstance is the ability to view the structures from
another plane, so that the operator can see beyond the “shadow.” The standard midesophageal (ME) views
(four-chamber, commissural, two-chamber, and long-axis) assist in evaluating the extent of disease. The
chordal tendons can display varying degrees of thickening and contracture. The transgastric (TG) long-
axis imaging plane provides the best information with regard to the extent of subvalvular involvement in
the rheumatic process. The characteristic 2D echocardiographic findings associated with rheumatic MS
are represented in Figure 9.3 and Videos 9.1 to 9.3. Rheumatic heart disease results in varying degrees of Video 9.1
restricted mitral leaflet motion. In 2D TEE, restricted leaflet motion is characterized by decreased leaflet Video 9.2
excursion and by diastolic “doming” of the anterior mitral leaflet. The appearance of “doming” is the result Video 9.3
of fusion of the anterior and posterior leaflets along the medial and lateral commissures. The leaflets are
restricted or abnormally stenotic at the tips. The maximal amplitude of motion occurs in the mobile mid-
section, giving the anterior mitral leaflet an arched appearance, convex toward the LV outflow tract in dias-
tole (12,13). Figure 9.3 and Video 9.1 demonstrate the characteristic “doming” or “hockey stick” deformity
of the anterior mitral leaflet in diastole.
Echocardiographic Scoring System

In 1988, Wilkins et al. (11) developed an echocardiographic scoring system to assess MV morphology and
its relationship to the success of percutaneous balloon dilation of the MV. Each of the four components
of the scoring system is graded on a scale of 0 to 4, such that total scores range from 0 to 16. The four
components of the scoring system assess the MV for the pathologic changes characteristically associated
with rheumatic heart disease: Reduced leaflet mobility, leaflet thickening, subvalvular thickening, and cal-
cification. These investigators reported that a high echocardiographic score (>11), which is representative
FIGURE 9.3 A midesophageal AV long-axis view of rheumatic mitral stenosis displays the characteristic diastolic
“doming” of the anterior mitral leaflet in diastole and an enlarged left atrium. The mitral leaflets are thickened,
particularly at their margins, and appear echo-bright secondary to calcium deposition.

TABLE 9.1 Echocardiographic Scoring System
Grade Mobility Subvalvular thickening Thickening Calcification

1 Highly mobile valve Minimal thickening just below Leaflets nearly normal in Single area of increased
with only leaflet the mitral leaflets thickness (4–5 mm) echo-brightness
tips restricted
2 Leaflet mid and base Thickening of chordal Mid leaflets normal, Scattered areas of
portions have structures extending up to considerable brightness confined
normal mobility one-third of chordal length thickening of margins to leaflet margins
(5–8 mm)
3 Valve continues to Thickening extending to the Thickening extending Brightness extending
move forward in distal third of chords through the entire into midportion of
diastole, mainly leaflet (5–8 mm) the leaflets
from base
4 No or minimal forward Extensive thickening and Considerable thickening Extensive brightness
movement of the shortening of all chordal of all leaflet tissue throughout much
leaflets in diastole structures extending down (>8–10 mm) of the leaflet tissue
to papillary muscles
From: Wilkins G, Weyman A, Abascal V, et al. Percutaneous balloon dilatation of the mitral valve: An analysis of echocardiographic
variables related to outcome and the mechanism of dilatation. Br Heart J. 1988;60:299–308, with permission.
of advanced leaflet deformity, was associated with a suboptimal outcome after balloon dilation of the MV.
A low echocardiographic score (<9) was associated with an optimal outcome (11). Table 9.1 presents the
scoring system and describes what each grade on the scale represents for each of the four components.
Although this scoring system was developed for patients undergoing mitral balloon dilation, it can serve as
a useful guide during the TEE examination of patients with rheumatic MS.
Standard chamber dimensions can be altered depending on the duration and degree of MS. Typically,
an increase in the LA area is associated with chronic volume and pressure overload. Because of the low-
flow state, LA spontaneous echo contrast or thrombus formation may be present. Daniel et al. (14) char-
acterized LA spontaneous echo contrast as “dynamic clouds of echoes curling up slowly in a circular or
spiral shape within the left atrium.” They found that LA spontaneous echo contrast is useful in identifying
those patients with MS who are at increased risk for thromboembolic events. TEE is more sensitive than
transthoracic echocardiography in detecting LA spontaneous echo contrast. Since LA spontaneous echo
contrast indicates blood stasis and may be a warning of thrombus formation, it is critical to scan the LA
completely to exclude thrombus formation (14,15). Figure 9.4 displays an ME view of the LA with a throm-
bus in the LA appendage.
FIGURE 9.4 A left atrial appendage thrombus is visualized from a short-axis imaging plane of the left atrium.

Diastolic properties of the LV are also affected in rheumatic MS. In patients with severe isolated rheu-
matic MS, Liu et al. (16) demonstrated reduced LV diastolic compliance. The reduction in compliance
appeared to be related to a functional restriction resulting from chordal tethering to a rigid valve appara-
tus, a finding that was immediately reversed after balloon mitral valvuloplasty. LV systolic performance in
patients with severe isolated MS was nearly identical to that in age-matched controls. Chronic elevation in
LA pressure can cause structural alterations in the pulmonary vasculature, leading to pulmonary hyper-
tension and ultimately right-sided heart failure (8,9). TEE evaluation of the right side of the heart may
demonstrate varying degrees of right ventricular dysfunction and tricuspid regurgitation. A comprehensive
2D and Doppler TEE examination of the heart should be performed to exclude these associated findings and
other valvular pathology.
Physiologic Assessments
Determination of the Pressure Gradient
Normal flow velocity across the MV is less than 1.3 m/s. The pressure drop across a stenotic valve can be
calculated from the instantaneous flow velocity by means of the simplified Bernoulli equation (17,18):
Pressure gradient (mm Hg) = 4v 2

where v represents the instantaneous velocity.
The equation is modified from the original in that the terms that account for viscous friction and flow
acceleration have been eliminated. Since the velocity distal to the obstruction is significantly greater than
the velocity proximal to the obstruction, the proximal velocity term can be ignored (17,18). Continuous
wave Doppler interrogation of the inflow velocities across the valve is performed with the use of the ME
four-chamber, two-chamber, or long-axis view. Following manual tracing of the diastolic spectral profile,
the echocardiographic machine software provides a mean gradient in millimeters of mercury. Figure 9.5
displays a mean gradient measurement across the MV in a patient with MS obtained with continuous wave
Doppler and the ME four-chamber view. It is important to note that an increase in forward flow through
the mitral orifice, such as occurs in severe mitral valvular regurgitation, can result in a high transmitral
gradient although the valve is only mildly stenotic. One therefore must be aware that the degree of MS can be
overestimated in the face of significant mitral regurgitation (4). Pressure gradients are underestimated if the
angle between the sampling beam and the flow vector is large (>20 degrees) (17,19). Visualizing the inflow
jet with color Doppler and aligning the sample beam with the color inflow can help minimize this problem
(19). In general, a mean gradient of more than 10 mm Hg across a stenotic valve is considered to indicate
severe stenosis (20) (Table 9.2).
FIGURE 9.5 A diastolic spectral profile of mitral inflow has been obtained with continuous wave Doppler in this patient
with mitral stenosis. The profile has been traced out, and a mean pressure gradient of 13 mm Hg has been calculated with
the software available within the machine. Note that the inflow velocities are close to 2 m/s.

TABLE 9.2 Grading Severity of Mitral Stenosis
Grade
Specific findings:
MVA (cm2) >1.5 1–1.5 <1
Supportive findings:
Mean gradient (mm Hg)a <5 5–10 >10
Pulmonary artery pressure (mm Hg) <30 30–50 >50
a
Patients in normal sinus rhythm with a heart rate between 60 and 80 bpm.
MVA, mitral valve area.
Adapted from: Baumgartner H, Hung J, Bermejo J, et al. Echocardiographic assessment of valve stenosis: EAE/ASE
recommendations for clinical practice. J Am Soc Echo. 2009;22:1–23.
Calculations of Valve Area

The severity of MS is also estimated by determining the reduction in MV area. This can be done with the
use of 2D and Doppler echocardiographic techniques.
Planimetry Valve Area

Planimetry is a conceptually simple 2D technique used to calculate the MV area. It involves directly visu-
alizing the MV orifice in diastole from a TG basal short-axis imaging plane and tracing the orifice mar-
gins to acquire a valve area measurement in square centimeters (Fig. 9.6). The results obtained with this
technique have been shown to correlate well with valve area measurements acquired invasively (3,12,21).
Figure 9.6 demonstrates the use of planimetry in calculating the MV area from the TG basal short-axis
imaging plane in a patient with rheumatic MS. A number of operator “pitfalls” should be recognized when
this technique is used to optimize its accuracy. Instrumentation factors are critical in obtaining adequate
images for planimetry. For example, if the receiver gain settings are too low, the edges of the valve may be
obscured, resulting in “echo dropout,” and the valve area will be overestimated (12). The opposite occurs
FIGURE 9.6 The mitral valve orifice assumes a “fish mouth” appearance in a transgastric basal short-axis imaging plane
in a patient with rheumatic mitral stenosis. Tracing of the orifice margins of the mitral valve during diastole resulted in a
mitral valve area measurement of 1.25 cm2.

FIGURE 9.7 A diastolic spectral profile of mitral inflow obtained with continuous wave Doppler. Severe mitral stenosis
is confirmed by a pressure half-time measurement of 307 milliseconds.
when the gain settings are set too high, with resultant image saturation and a falsely narrowed valve orifice
(22). Inadequate imaging plane orientation is another important measurement error with this technique.
The stenotic MV looks like a funnel in diastole, the narrowest part being the commissural tip of the valve.
It is critical to scan the MV orifice superiorly to inferiorly to acquire the smallest orifice area. Measuring
too superiorly, in the body of the leaflets, can overestimate the valve area (21–23). In patients who have
undergone mitral valvuloplasty, the valve area may be underestimated because of the inability to measure
the extent of the commissural fractures with planimetry.
Pressure Half-time
The pressure half-time describes the pressure difference between the LA and LV and can be quantitatively
related to the degree of MS. As MS becomes more severe, the rate of pressure decline between the LA and
LV is proportionally slower, and consequently the gradient between the LA and LV is maintained for a lon-
ger period of time. The pressure half-time is the time required for the atrioventricular pressure difference to
decrease from the maximum to one-half of that value. To calculate the pressure half-time, the peak trans-
mitral flow velocity is measured by Doppler, and the time it takes to decrease by a factor of the square root
of 2 is traced and measured (3,20,24). Figure 9.7 displays the pressure half-time measurement in a patient
with MS. The signal is acquired by aligning the continuous wave Doppler beam with the mitral inflow and
acquiring a transmitral flow velocity signal. The machine software automatically calculates the pressure
half-time after the operator labels the maximal and minimal velocities. The pressure half-time increases
as the severity of MS increases (20,24–26). In a normal MV, the pressure half-time is generally less than
60 milliseconds. In mild MS, the average pressure half-time is approximately 100 milliseconds; in moderate
MS, it is approximately 200 milliseconds; and in severe MS, the average pressure half-time measurement is
more than 300 milliseconds (3,24,25) (Table 9.3).
TABLE 9.3 Methods of Determining Mitral Valve Area
Planimetry Trace frozen short-axis view in diastole

Pressure half-time (PHT, ms) MVA = 220/PHT
Deceleration time (DT, ms) MVA = 759/DT
Continuity equation MVA = (LVOT area × LVOT TVI)/(MV TVI)
PISA MVA = 2πr 2 × α/180 × va /vp
ms, milliseconds; MVA, mitral valve area (cm2); α, funnel angle; va, aliasing velocity; vp, peak transmitral velocity; LVOT, left
ventricular outflow tract; TVI, time–velocity integral; PISA, proximal isovelocity surface area.

Pressure Half-time Mitral Valve Area

The MV area can be calculated from the pressure half-time measurement by using the following formula,
originally described by Hatle and Angelsen (27):
MV area (cm2) = 220/pressure half-time (ms)
They noted that the rate of pressure decline across a stenotic MV depends on the cross-sectional area
of the valvular orifice. Hence, the tighter the orifice (smaller cross-sectional area), the slower the rate of
pressure decline.
The measurements obtained with the pressure half-time method are influenced by hemodynamic
factors and depend on the compliance of the LA and LV. These factors must be taken into consid-
eration when the pressure half-time method is applied to a stenotic MV. For example, decreased
LV compliance and severe aortic regurgitation can cause a rapid rise in the LV diastolic pressure,
with a resultant shortening of the pressure half-time measurement and an overestimation of the MV
area (28,29). Braverman et al. (28) demonstrated the dependence of the pressure half-time method
for calculating the MV area on hemodynamic variables such as peak transmitral gradient and
atrioventricular compliance. Conditions such as previous mitral valvuloplasty, atrial septal defect,
atrial tachycardia, and restrictive cardiomyopathy also affect the accuracy of the pressure half-time
method (20,30–32).
Deceleration Time
The deceleration time is another simple means of evaluating the MV area, in which decay of the mitral
inflow profile through a stenotic MV is examined. The following formula describes the relationship of the
deceleration time to the MV area (19):
MV area (cm2) = 759/deceleration time (ms)
The deceleration time is the interval between the peak velocity and the time at which the extrapo-
lated inflow velocity reaches baseline. Figure 9.8 graphically displays the measurement of deceleration
time. For profiles in which the decay is linear, the pressure half-time is equal to 29% of the deceleration
time (20,26).
Time (ms)
a b
Velocity (m/s)
FIGURE 9.8 The deceleration time is the interval between the peak velocity (a) and the time at which the extrapolated
inflow velocity reaches baseline (b). E, early wave; A, atrial wave.

Advanced Concepts that May be Helpful in Difficult Cases

Continuity Equation
The continuity equation for calculating the area of a valve is based on the law of conservation of mass in
hydrodynamics. In the absence of valvular regurgitation or shunts, flow volume at the MV should equal
that at another valve according to the following equation (26,29):
Volumetric flow = area1 × time–velocity integral1 = area2 × time–velocity integral2
Therefore,
Area2 = (area1 × time–velocity integral1)/(time–velocity integral2)
Flow through the MV can be calculated based on the measurements made by Doppler echocardiog-
raphy as the product of the valve orifice area and the time–velocity integral of the mitral inflow. Area1 ×
time–velocity integral1 represents volumetric flow through the reference valve. The reference area (area1) is
a cross-sectional area measurement that assumes the geometric model of a circle: πr2. The LV outflow tract
or pulmonary artery is commonly used for the reference area and time–velocity integral measurements.
The equation is rearranged to solve for the MS area, area2, as previously discussed. The continuity equation
is theoretically independent of transvalvular pressure gradients, LV compliance, and changing hemodynamic
conditions, such as the increased forward flow that occurs during exercise (3,28,29). The continuity equation
does not apply in circumstances of regurgitation in the reference valve or the MV because the forward volu-
metric flows are not equal, so that significant error is introduced (29,33).
Proximal Isovelocity Surface Area Method

The proximal isovelocity surface area (PISA) method, or flow convergence method, applies the continuity
principle to color flow Doppler mapping in the region of the MV orifice where flow is converging from the
LA. Figure 9.9 and Video 9.4 display a color flow Doppler example of proximal flow convergence in a patient Video 9.4
with rheumatic MS. When blood flow converges on an orifice that is small relative to the proximal chamber,
it may be considered to form isovelocity “shells” with the shape of a hemisphere. The velocity of blood flow
increases as blood approaches the small orifice, resulting in aliasing of the color flow signal and the creation
of a large proximal flow convergence region or shell. As blood approaches the orifice, its increasing velocity
is pictured by color flow imaging as progressively smaller shells. The radius of the first aliasing velocity shell
FIGURE 9.9 Color Doppler imaging from this midesophageal four-chamber view of the mitral valve demonstrates
proximal isovelocity surface area or flow convergence on the left atrial side of the mitral valve.

RA LA
First alias
Angle α
r
Mitral
leaflets
RV LV
α va
MVA = 2πr2 × degrees ×
180 vp
FIGURE 9.10 Midesophageal four-chamber view of the mitral valve demonstrates the measurements needed to calcu-
late the mitral valve area by the proximal isovelocity surface area method. α/180 degrees, angle correction factor; va, alias-
ing velocity; vp, peak transmitral inflow velocity; RA, right atrium; RV, right ventricle; LA, left atrium; LV, left ventricle; MVA,
mitral valve area. (Adapted from Rodriguez L, Thomas JD, Monterroso V, et al. Validation of the proximal flow convergence
method: Calculation of orifice area in patients with mitral stenosis. Circulation. 1993;88:1157–1165, with permission.)
is measured from the tips of the MV leaflets to the aliasing boundary (19,34–37) (Fig. 9.10). The volumetric
flow rate can be calculated as the product of the surface area of the hemisphere of flow and the aliasing
velocity. The mitral inflow velocity profile (at the orifice) is obtained with continuous wave Doppler. The
basic elements of the continuity equation can therefore be identified by this straightforward color mapping,
but the calculation of a valve area requires a correction for the true shape of the mitral orifice. Truly hemi-
spheric shells would occur if the surface of the valve were flat with the leaflets apposed at 180 degrees. The
angle α subtended by the mitral leaflets creates a funnel-shaped surface; an angle correction factor (α/180
degrees) adjusts the hemispheric surface area pictured by color flow mapping to calculate the volumetric
flow rate more accurately. The instantaneous volumetric flow rate (Q) in this region can be calculated as the
product of the surface area of a hemisphere (2πr 2) and the aliasing velocity at the shell (va):
Q = 2πr 2 × α/180 degrees × va
Flow through this region should equal flow through the restricted orifice based on the continuity prin-
ciple (34–36). Once the flow rate (Q) is calculated, the MV area can be obtained with the use of the conti-
nuity equation:
MV area (cm2) = Q/vp (cm/s)
where Q is the volumetric flow rate and vp is the peak transmitral inflow velocity.
Figure 9.10 illustrates the use of the flow convergence method in the calculation of MV area.
The MV area can be measured accurately with this method in the presence of mitral insufficiency.
Several investigators have validated the use of the flow convergence method in the calculation of MV area
by direct comparisons with anatomic and calculated measurements of orifice size (34,36,38,39). Calculation
of MV area by the flow convergence method can be time-consuming; however, its accuracy is not influ-
enced by associated mitral or aortic regurgitation. This method of calculating MV area may be best under
the circumstances in which 2D planimetry is technically limited, when the continuity equation cannot be
applied with the use of a reference volumetric flow, and when the pressure half-time method is affected by
hemodynamic changes (35).
A PRACTICAL APPROACH TO THE EVALUATION OF MITRAL STENOSIS

Step 1. A 2D evaluation of the MV is performed with a focus on answering the following questions: What
is the appearance of the valve—that is, is the valve disfigured? Are the leaflets of normal thickness and

mobility? If not, further assessment of the valve is needed to determine whether it is stenotic or regurgitant
(see Chapter 8). Planimetry of the MV in the TG basal short-axis view is initially performed to obtain a
rough estimate of the MV area.
Step 2. After completion of the 2D examination, MV inflow interrogation with continuous wave Doppler
is performed. The diastolic mitral inflow velocity profile is traced (Fig. 9.5), and the mean pressure gradient
is determined with the internal software of the echocardiography machine. In addition, the pressure half-
time method is used to calculate the MV area (Fig. 9.7). Most TEE machines also extrapolate the flow decay
and calculate the deceleration time.
If the measurements are in agreement according to Table 9.2, no further evaluation is required.
Step 3. The advanced methods (continuity equation and PISA) are reserved for those patients for whom the
pressure half-time method is unreliable or unavailable.
Three-dimensional Echocardiographic Evaluation of Mitral Stenosis

Three-dimensional (3D) echocardiography has demonstrated accuracy for measuring MV area both
for calcific (40) and rheumatic MS (41). Messika-Zeitoun et al. (42) examined the use of real-time 3D
echocardiography in the setting of percutaneous mitral commissurotomy. Three-dimensional echocar-
diography provided accurate and reproducible MV area measurements that were similar to 2D echocar-
diography. Of note, the authors found that 3D improved the “description” of valve anatomy and provided
an advantage for less experienced operators as a method for MV area measurements; experienced opera-
tors reported similar results to 2D echocardiography findings. In patients with rheumatic MS, Zamorano
et al. (41) reported real-time 3D was not only accurate and reproducible for measurement of MV area, but
also the most accurate when compared to (Gold standard) invasive methods. Others have described the
accuracy and reproducibility of MV area measurements with the use of real-time 3D echocardiography
(43) (Fig. 9.11).
Interestingly, Anwar et al. validated a new echocardiographic scoring system with the use of real-time
3D echocardiography for patients with MS. The concept of the new scoring system is similar to that of the
Wilkins score, yet makes use of real-time 3D echocardiography in the evaluation. The authors’ new scoring
system reportedly provides improved morphologic evaluation of specific aspects of the MV apparatus that
relate to calcium and commissural splitting. Similar to Wilkins score, the real-time 3D score involves an over-
all composite score based on the extent of valve calcification, thickening, mobility, and subvalvular involve-
ment, with higher scores representing more advanced valve pathology. However, the 3D assessment also
involves division of each leaflet into three scallops and scoring them separately for thickness, calcification,
FIGURE 9.11 Three-dimensional image of a patient with rheumatic mitral stenosis.

TABLE 9.4 Mitral Valve Score Based on Real-time Three-dimensional Echocardiography
Anterior leaflet Posterior leaflet

A1 A2 A3 P1 P2 P3
Thickness (0–6) (0 = normal, 0–1 0–1 0–1 0–1 0–1 0–1
1 = thickened)a
Mobility (0–6) (0 = normal, 0–1 0–1 0–1 0–1 0–1 0–1
1 = limited)a
Calcification (0–10) (0 = no, 0–2 0–1 0–2 0–2 0–1 0–2
1–2 = calcified)b
Subvalvular apparatusb
Proximal third Middle third Distal third
Thickness (0–3) (0 = normal, 0–1 0–1 0–1
1 = thickened)
Separation (0–6) (0 = normal, 0,1,2 0,1,2 0,1,2
1 = partial, 2 = no)
a
Normal = 0, mild = 1 to 2, moderate = 3 to 4, severe ≥5.
b
Normal = 0, mild = 1 to 2, moderate = 3 to 5, severe ≥6.
Reused from: Anwar A, Attia W, Nosir Y, et al. Validation of a new score for the assessment of mitral stenosis using real-time three-
dimensional echocardiography. J Am Soc Echocardiogr. 2010;23:13–22, with permission.
and mobility; the subvalvular apparatus is graded at three levels for extent of chordal thickness and separa-
tion (44,45) (Table 9.4).
SUMMARY
Table 9.3 summarizes the techniques used to calculate the MV area, and Table 9.2 presents the scores for
the various degrees of MS obtained with each of these techniques. In general, an MV area of greater than
1.5 cm2 is considered to indicate mild MS, 1.0 to 1.5 cm2 moderate MS, and less than 1.0 cm2 severe MS
(20). Each technique has its limitations. Agreement between the various methods of evaluating the valve
together with clinical correlation will enhance accuracy and overall judgment.
REFERENCES
1. Acierno LJ. Physical examination. In: The History of Cardiology. London: Parthenon Publishing Group; 1994:461–462.
2. Acierno LJ. Surgical modalities. In: The History of Cardiology. London: Parthenon Publishing Group; 1994:627.
3. Popovic AD, Thomas JD, Neskovic A, et al. Time-related trends in the preoperative evaluation of patients with valvular steno-
sis. Am J Cardiol. 1997;80:1464–1468.
4. Bruce CJ, Nishimura RA. Clinical assessment and management of mitral stenosis, valvular heart disease. Cardiol Clin.
1998;16:375–403.
5. Ranganathan N, Lam JH, Wigle ED, et al. Morphology of the human mitral valve: The valve leaflets. Circulation. 1970;41:459–
467.
6. Roberts WC, Perloff JK. Mitral valvular disease: A clinicopathologic survey of the conditions causing the mitral valve to func-
tion abnormally. Ann Intern Med. 1972;77:939–974.
7. Kennedy JW, Yarnall SR, Murray JA, et al. Quantitative angiocardiography. IV. Relationships of left atrial and ventricular pres-
sure and volume in mitral valve disease. Circulation. 1970;41:817–824.
8. Schlant RC, Alexander RW, O’Rourke RA, et al, eds. Mitral valve disease. In: Hurst's the Heart. 8th ed. New York, NY: McGraw-
Hill; 1994:1483–1518.
9. Selzer A, Cohn K. Natural history of mitral stenosis: A review. Circulation. 1972;45:878–890.
10. Olson LJ, Subramanian R, Ackermann DM, et al. Surgical pathology of the mitral valve: A study of 712 cases spanning 21 years.
Mayo Clin Proc. 1987;62:22–34.
11. Wilkins G, Weyman A, Abascal V, et al. Percutaneous balloon dilatation of the mitral valve: An analysis of echocardiographic
variables related to outcome and the mechanism of dilatation. Br Heart J. 1988;60:299–308.
12. Otto C, ed. Valvular stenosis: Diagnosis, quantitation, and clinical approach. In: Textbook of Clinical Echocardiography. 2nd ed.
Philadelphia, PA: WB Saunders; 2000:229–264.
13. Nichol PM, Gilbert BW, Kisslo JA. Two-dimensional echocardiographic assessment of mitral stenosis. Circulation. 1977;
55:120–128.

14. Daniel W, Nellessen U, Schroder E, et al. Left atrial spontaneous echo contrast in mitral valve disease: An indicator for an
increased thromboembolic risk. J Am Coll Cardiol. 1988;11:1204–1211.
15. Chen YT, Kan MN, Chen JS, et al. Contributing factors to the formation of left atrial spontaneous echo contrast in mitral
valvular disease.J Ultrasound Med. 1990;9:151–155.
16. Liu CP, Ting CT, Yang TM, et al. Reduced left ventricular compliance in human mitral stenosis: Role of reversible internal
constraint. Circulation. 1992;85:1447–1456.
17. Hatle L, Brubakk A, Tromsdal A, et al. Noninvasive assessment of pressure drop in mitral stenosis by Doppler ultrasound.
Br Heart J. 1978;40:131–140.
18. Oh JK, Seward JB, Tajik AJ. Hemodynamic assessment. In: The Echo Manual. 2nd ed. Philadelphia, PA: Lippincott Williams &
Wilkins; 1999:59–71.
19. Weyman AE, ed. Left ventricular inflow tract I: The mitral valve. In: Principles and Practice of Echocardiography. 2nd ed.
Philadelphia, PA: Lea & Febiger; 1994:391–497.
20. Baumgartner H, Hung J, Bermejo J, et al. Echocardiographic assessment of valve stenosis: EAE/ASE recommendations for
clinical practice. J Am Soc Echo. 2009;22:1–23.
21. Henry WL, Griffith JM, Michaelis LL, et al. Measurement of mitral orifice area in patients with mitral valve disease by real-
time, two-dimensional echocardiography. Circulation. 1975;51:827–831.
22. Martin RP, Rakowski H, Kleiman JH, et al. Reliability and reproducibility of two-dimensional echocardiographic measurement
of the stenotic mitral valve orifice area. Am J Cardiol. 1979;43:560–568.
23. Wann LS, Weyman AE, Feigenbaum H, et al. Determination of mitral valve area by cross-sectional echocardiography. Ann
Intern Med. 1978;88:337–341.
24. Libanoff AJ, Rodbard S. Atrioventricular pressure half-time: Measure of mitral valve orifice area. Circulation. 1968;38:144–
150.
25. Hatle L, Angelsen B, Tromsdal A. Noninvasive assessment of atrioventricular pressure half-time by Doppler ultrasound.
Circulation. 1979;60:1096–1104.
26. Bruce C, Nishimura R. Newer advances in the diagnosis and treatment of mitral stenosis. Curr Probl Cardiol. 1998;23:127–
184.
27. Hatle L, Angelsen B, eds. Pulsed and continuous wave Doppler in the diagnosis and assessment of various heart lesions. In:
Doppler Ultrasound in Cardiology: Physical Principles and Clinical Applications. Philadelphia, PA: Lea & Febiger; 1982:76–89.
28. Braverman AC, Thomas JD, Lee R. Doppler echocardiographic estimation of mitral valve area during changing hemodynamic
conditions. Am J Cardiol. 1991;68:1485–1490.
29. Nakatani S, Masuyama T, Kodama K, et al. Value and limitations of Doppler echocardiography in the quantification of stenotic
mitral valve area: Comparison of the pressure half-time and the continuity equation methods. Circulation. 1988;77:78–85.
30. Thomas JD, Wilkins G, Choong CYP, et al. Inaccuracy of mitral pressure half-time immediately after percutaneous mitral
valvotomy: Dependence on transmitral gradient and left atrial and ventricular compliance. Circulation. 1988;78:980–993.
31. Thomas JD, Weyman AE. Doppler mitral pressure half-time: A clinical tool in search of theoretical justification. J Am Coll
Cardiol. 1987;10:923–929.
32. Wranne B, Msee PA, Loyd D. Analysis of different methods of assessing the stenotic mitral valve area with emphasis on the
pressure gradient half-time concept. Am J Cardiol. 1990;66:614–620.
33. Karp K, Teien D, Eriksson P. Doppler echocardiographic assessment on the valve area in patients with atrioventricular valve
stenosis by application of the continuity equation. J Intern Med. 1989;225:261–266.
34. Rodriguez L, Thomas JD, Monterroso V, et al. Validation of the proximal flow convergence method: Calculation of orifice area
in patients with mitral stenosis. Circulation. 1993;88:1157–1165.
35. Deng Y, Matsumoto M, Wang X, et al. Estimation of mitral valve area in patients with mitral stenosis by the flow convergence
region method: Selection of aliasing velocity. J Am Coll Cardiol. 1994;24:683–689.
36. Rifkin R, Harper K, Tighe D. Comparison of proximal isovelocity surface area method with pressure half-time and planimetry
in the evaluation of mitral stenosis. J Am Coll Cardiol. 1995;26:458–465.
37. Vandervoort PM, Rivera M, Mele D, et al. Application of color Doppler flow mapping to calculate effective regurgitant orifice
area: An in vitro study and initial clinical observations. Circulation. 1993;88:1150–1156.
38. Degertekin M, Basaran Y, Gencbay M, et al. Validation of flow convergence region method in assessing mitral valve area in the
course of transthoracic and transesophageal echocardiographic studies. Am Heart J. 1998;135:207–214.
39. Faletra F, Pezzano A, Fusco R, et al. Measurement of mitral valve area in mitral stenosis: Four echocardiographic methods
compared with direct measurement of anatomic orifices. J Am Coll Cardiol. 1996;28:1190–1197.
40. Chu J, Levine R, Chua S, et al. Assessing mitral valve area and orifice geometry in calcific mitral stenosis: A new solution by
real-time three-dimensional echocardiography. J Am Soc Echocardiogr. 2008;21:1006–1009.
41. Zamorano J, Cordeiro P, Sugeng L, et al. Real-time three-dimensional echocardiography for rheumatic mitral valve stenosis
evaluation: An accurate and novel approach. J Am Coll Cardiol. 2004;43:2091–2096.
42. Messika-Zeitoun D, Brochet E, Holmin C, et al. Three-dimensional evaluation of the mitral valve area and commissural open-
ing before and after percutaneous mitral commissurotomy in patients with mitral stenosis. Eur Heart J. 2007;28:72–79.
43. Binder T, Rosenhek R, Porenta G, et al. Improved assessment of mitral valve stenosis by volumetric real-time three-dimensional
echocardiography. J Am Coll Cardiol. 2000;36:1355–1361.
44. Soliman O, Anwar A, Metawei A, et al. New scores for the assessment of mitral stenosis using real-time three-dimensional
echocardiography. Curr Cardiovasc Imaging Rep. 2011;4:370–377.
45. Anwar A, Attia W, Nosir Y, et al. Validation of a new score for the assessment of mitral stenosis using real-time three-
dimensional echocardiography. J Am Soc Echocardiogr. 2010;23:13–22.

QUESTIONS
1. Which among the following statements is when using the mean pressure gradient
correct concerning mitral valve anatomy? estimates.
a. The anterior mitral leaflet base-to-margin d. None of the above statements are correct.
dimension is longer than that of the pos-
6. Which among the following may introduce
terior mitral leaflet, yet the two leaflets are
error to mitral valve area measurements
nearly identical in overall surface area.
when using planimetry to calculate mitral
b. A normal mitral valve area is 4 to 6 cm2.
valve area?
c. The anterior mitral leaflet has an attach-
a. Instrumentation factors such as gain set-
ment of approximately one-third of the cir-
tings set too high or too low
cumference of the mitral annulus.
b. Inadequate imaging plane orientation
d. All of the above are correct.
c. Postmitral valvuloplasty
2. The “Hockey stick” deformity of the d. All of the above
anterior mitral leaflet is reflective of which
7. A mitral valve pressure half-time of 280
of the following findings in rheumatic
milliseconds from a Doppler spectral
mitral disease?
profile would yield a calculated mitral
a. Concomitant severe mitral regurgitation
valve area of:
b. Severe aortic insufficiency
a. 1.5 cm2
c. Restriction to mitral valve diastolic flow
b. 2 cm2
d. Pulmonary hypertension
c. 0.78 cm2
3. Two-dimensional features of long-standing d. 1.2 cm2
mitral stenosis include:
8. Which among the following mean pressure
a. Left atrial enlargement
gradient parameters are most consistent
b. Presence of spontaneous echo contrast in
with severe mitral stenosis?
the left atrium
a. 3 mm Hg
c. Thickened and relatively immobile mitral
b. 5 to 6 mm Hg
valve leaflets
c. >12 mm Hg
d. All of the above
d. 8 mm Hg
4. Severe mitral stenosis would be most
9. When using the pressure half-time to
consistent with which of the following
calculate mitral valve area, which among
pressure half-time measurements?
the following statements can lead to the
a. 60 milliseconds
introduction of measurement errors?
b. 120 milliseconds
a. Patients with mild aortic insufficiency
c. 180 milliseconds
b. Moderate pulmonary hypertension
d. >300 milliseconds
c. Severe aortic insufficiency
5. Which among the following statements d. Mild left ventricular compliance changes
is correct concerning the use of mean
10. The continuity equation can be used to
pressure gradient to assess severity of
calculate mitral valve area. Which among
mitral valve stenosis?
the following statements is true?
a. Presence of severe mitral regurgitation can
a. Concomitant regurgitation of the mitral
lead to an overestimation of mitral ste-
valve or reference valve may introduce error
nosis when using mean pressure gradient
b. Presence of pulmonary hypertension will
estimates due to an increase forward flow
limit accuracy
across the mitral valve.
c. Continuity equation is not theoretically
b. Mean pressure gradients across the mitral
independent of left ventricular compliance
valve are independent of degree of forward
d. Presence of shunt flow will not interfere
flow.
with the accuracy
c. Pulmonary hypertension can lead to an
underestimation of degree of mitral stenosis

11. One of the benefits to the use of the PISA 15. Given a deceleration time of 800
method to calculate mitral valve area is: milliseconds from a Doppler spectral
a. Presence of mitral regurgitation invalidates profile, the calculated mitral valve area
the PISA method in the calculation of mitral would be:
valve area a. <1.0 cm2
b. Aortic insufficiency introduces inaccuracies b. 1.5 cm2
when using PISA method to calculate mitral c. 2.8 cm2
valve area d. 2.0 cm2
c. PISA method accuracy is not influenced by
16. Which among the following statements
concomitant mitral or aortic regurgitation
concerning the echocardiographic finding
d. PISA method is not as quantitative a
of spontaneous echo contrast is correct?
method to calculate mitral valve area when
a. It is indicative of a high-flow state
compared to the use of planimetry.
b. May represent a warning sign for increased
12. PISA is most useful in the following patient risk for thrombosis
circumstances: c. Is present in the left atrium in patients with
a. When there are technical limitations to the severe mitral regurgitation
use of planimetry d. Is less common in patients with atrial fibril-
b. When continuity equation cannot be used lation
due to lack of reference valve forward flow
17. Long-standing mitral stenosis with chronic
c. When pressure half-time is affected by
elevation in left atrial pressure can result in:
hemodynamic changes
a. Structural alterations in the pulmonary vas-
d. All of the above
culature
13. Use of PISA for mitral valve area b. Right-sided heart failure
calculation requires the addition of which c. Pulmonary hypertension
of the following in order to improve d. All of the above
accuracy?
18. Which among the following mitral valve
a. Exclusion of peak flow rate
area measurements is most consistent with
b. Introduction of an angle correction factor:
severe mitral valve stenosis?
α/180 degrees
a. 2 cm2
c. Consideration of concomitant mitral regur-
b. <1 cm2
gitation
c. 1.5 cm2
d. A correction factor for presence of diastolic
d. 1.5 to 1.8 cm2
dysfunction
19. Pathologic features of rheumatic mitral
14. Which among the following statements
stenosis include which among the
regarding the newly proposed real-time
following?
three-dimensional score system for
a. Leaflet thickening
rheumatic mitral stenosis differentiates it
b. Calcium deposition
from the Wilkins criteria?
c. Restricted leaflet mobility
a. Does not include a measure of extent of
d. All of the above
subvalvular involvement
b. Provides a more detailed assessment of leaf- 20. Which among the following conditions can
let involvement by subdividing each leaflet lead to the development of mitral stenosis?
into three segments a. Rheumatic heart disease
c. Excludes extent of leaflet calcification b. Parachute mitral valve deformity
d. Does not include extent of leaflet thickening c. Cor triatriatum
d. All of the above

10 Mitral Valve Repair
Maurice Hogan and Jörg Ender
INDICATIONS
Mitral valve (MV) regurgitation is the most prevalent isolated heart valve disease (1), and valve repair or
replacement remains the only effective treatment for chronic severe disease (2,3).
MV regurgitation results from either structural or functional disorder (2,3). Structural (or primary)
MV regurgitation is most commonly caused by degenerative MV disease and implies pathology of the
architecture of the MV apparatus, that is, the valve leaflets, chordae tendineae, or papillary muscles.
Functional (or secondary) MV regurgitation implies that the mitral apparatus itself is structurally nor-
mal, and regurgitation is then typically caused by ischemic or dilated cardiomyopathy. In these cases of
functional mitral disease, regurgitation results from displacement of the papillary muscles consequent to
left ventricular (LV) dilatation often in combination with mitral annular dilatation. The displacement of
the papillary muscles causes tethering of the valve leaflets and restricts their motion, thereby preventing
coaptation (4).
MV repair improves long-term survival if patients are operated on early and in centers which have both
low operative mortality (<1%) and high rates of repair (80% to 90%), as opposed to valve replacement (5,6).
Patients who undergo MV repair rather than valve replacement clearly demonstrate lower operative mor-
tality, better recovery of left ventricular ejection fraction (LVEF), and better long-term survival (7,8). This
improvement in outcome for patients treated with repair versus replacement is intuitive considering that
they have lower rates of endocarditis, fewer thromboembolic events, and do not require long-term antico-
agulation (unless otherwise indicated).
Chronic severe mitral regurgitation (MR) ultimately leads to LV dilatation. To maintain forward
stroke volume in the face of significant regurgitant fraction, the LV chamber necessarily becomes more
compliant and develops eccentric cardiac hypertrophy. Pulmonary congestion then decreases also, as
the now dilated left atrium and ventricle can accommodate the regurgitant volume at lower filling pres-
sure. These early responses are therefore adaptive and during this phase the patient may remain asymp-
tomatic. Over time, however, the progressive LV enlargement and increasing LV end-diastolic pressures
lead to a reduction in LVEF. With progressive left atrial dilatation, the onset of atrial fibrillation and/or
pulmonary hypertension can develop, and their occurrence in patients with chronic severe MR consti-
tutes an indication for surgery, even in patients with preserved LVEF and LV end-systolic diameter less
than 40 mm (2,3).
The recommendations for the timing of surgery in patients with chronic severe MR rely on patient
symptoms and also on echocardiographic evaluation of LV function and size (Fig. 10.1) (2,3). It is notewor-
thy that patients with chronic severe MR, who are symptom free, have normal LV dimensions and function,
and do not have atrial fibrillation or pulmonary hypertension, are only recommended to undergo valve
surgery if it is likely that the valve can be repaired rather than replaced. The current recommendations also
suggest medical therapy for symptomatic patients who have depressed LV function and/or LV dilatation,
in whom chordal preservation is unlikely with conventional surgery; the option of percutaneous repair is
not yet considered in these guidelines. Although the percutaneous mitral clip procedure is less effective in
reducing MR than conventional repair surgery, it is associated with fewer major adverse events than con-
ventional repair and does improve patients’ clinical condition (9). Long-term results are not yet available
for the percutaneous mitral clip procedure but it may prove to be a valid alternative to medical therapy for
this cohort.
194

10. Mitral Valve Repair 195
Chronic severe mitral regurgitation
Clinical evaluation + Echo

Reevaluation
Symptoms?
No Yes
LV function? LV function?
Normal LV function LV dysfunction

EF ≤ 0.60 EF > 0.30 EF < 0.30 and/or
EF > 0.60 and/or ESD ≤ 55 mm ESD > 55 mm
ESD < 40 mm ESD ≥ 40 mm
Class I Class I
New onset AF? Chordal preservation

Pulmonary HT? likely?
MV repair
Yes Yes
Class IIa if not possible, Class IIa
MVR
No No
MV repair Medical therapy

likely?*
Yes*
Class IIa MV repair
No
Clinical eval
every
6 mo
Echo every
6 mo
FIGURE 10.1 Guidelines for the management of patients with chronic severe mitral regurgitation. *Mitral valve (MV)
repair may be performed in asymptomatic patients with normal left ventricular (LV) function if performed by an expe-
rienced surgical team and if the likelihood of successful repair is greater than 90%. AF indicates atrial fibrillation; echo,
echocardiography; EF, ejection fraction; ESD, end-systolic dimension; eval, evaluation; HT, hypertension; and MVR, mitral
valve replacement. Adapted from: Circulation. 2008;118:e523–e661.
ECHOCARDIOGRAPHIC EVALUATION
Intraoperative transesophageal echocardiography (TEE) is a class I indication for patients undergoing MV
repair (10), meaning that its use improves patient outcome. The role of intraoperative echocardiography
can be considered as two components: Pre- and postrepair.
THE PREREPAIR EVALUATION

The prerepair examination should evaluate the following:
1. Structure of the MV apparatus
2. Function of the MV leaflets according to the Carpentier classification

3. Severity of the MV regurgitation

4. Circumflex artery and its relationship to the MV annulus
5. Cardiac structures for secondary or coexisting abnormalities
This information is then summarized and the likelihood of successful repair discussed with the surgical
team so to be of use in planning the surgical procedure.
1. Evaluation of the Structure of the Mitral Valve Apparatus

The MV apparatus consists of the MV annulus, the MV leaflets (anterior and posterior), chordae tendineae,
papillary muscles, and left ventricle. The nomenclature proposed by Carpentier to describe the segments
of the mitral leaflets (11) is the most commonly used and is widely accepted as standard (Fig. 10.2). The
FIGURE 10.2 Mitral valve leaflet segments using the Carpentier leaflet nomenclature. A: Echocardiographic short-axis
or “fish mouth” view. B: Surgeon’s view through open left atrium from the patient’s right side. The echocardiographic
view is rotated 90 degrees counterclockwise relative to the surgeon (tilting one’s head to the left).

FIGURE 10.3 ME four-chamber view, with in this case A2 and P2 segments labeled. Although the typical ME four cham-
ber most often cuts through these segments, it is possible to view A1, P1 by slight probe withdrawal, or A3, P3 by slight
probe advancement (see Fig. 10.4).
anatomy of the mitral apparatus is detailed in Chapter 8, Mitral Regurgitation. To visualize all the struc-
tures of the MV apparatus and to elucidate fully the mechanism of MR and any associated pathology,
several views are necessary (12).
Midesophageal (ME) four-chamber view: Normally shows the A2 and P2 segments of the MV (Fig. 10.3).
From there, slight withdrawal of the probe will show the A1 and P1 segments, whereas slight advancement
of the probe will show the A3 and P3 segments (Fig. 10.4). LV systolic function can also be assessed in this
view by measuring LVEF. Interpretation of LVEF must take account of the patient’s loading conditions,
and patients with MR who have normal LV function demonstrate LVEF greater than or equal to 60% (3).
Probe advanced
Probe withdrawn
FIGURE 10.4 Three-dimensional full volume en face view of the mitral valve from the left atrium, with the aortic
valve located at approximately 12 o’clock. The middle line (4 Ch) shows how the typical ME four-chamber view cuts
through A2, P2 segments. Probe withdrawal means the 2D probe now would cut through A1, P1, and in the corre-
sponding 2D view, more of the aortic valve/LVOT enters the image. Probe advancement moves the 2D scan plane over
A3, P3 segments.

FIGURE 10.5 ME commissural view which typically shows the P3, A2, P1 segments.
Patients with reduced LVEF preoperatively also have reduced postoperative LVEF, higher perioperative
mortality, and poorer long-term survival (13,14).
ME mitral commissural view: From the ME four-chamber view, the MV should also be scanned by for-
ward rotation to show the P3, A2, and P1 segments (Fig. 10.5). Continued forward rotation produces the
ME two-chamber view with P3, A3, A2, and A1 segments (Fig. 10.6) and ME LAX views with the P2 and
A2 segments (Fig. 10.7).
From the ME position, the probe is advanced into the stomach to obtain the transgastric (TG) views.
TG mid-SAX view: Regional wall motion abnormalities as well as global LV function can be assessed by
measuring fractional shortening or fractional area change. This view serves as the reference view for pos-
sible new regional wall motion abnormalities which may arise due to complications of the MV repair in the
postrepair examination (see postrepair examination).
FIGURE 10.6 ME two-chamber view. Forward rotation from the ME commissural view to approximately 90 to 100
degrees reveals P3, A3, A2, A1 segments.

FIGURE 10.7 ME LAX view. The left atrium, left ventricle, left ventricular outflow tract, and aortic valve are viewed.
When there is no foreshortening, the mitral valve segments viewed are A2, P2.
TG two-chamber view: The ultrasound beam travels perpendicular to both the papillary muscles and
chordae so that these two structures are often very clearly visualized (Fig. 10.8). LV diameters are measured
in this view (15).
TG basal SAX view: Shows all segments of the MV leaflets together with both commissures (Fig. 10.9).
This view allows for planimetric measurement of the MV orifice area. An existing cleft pathology in one
of the leaflets can often be diagnosed in this view during diastole (Video 10.1, cleft anterior mitral leaflet). Video 10.1
The use of color flow Doppler (CFD) helps to confirm the diagnosis (Video 10.2, CFD cleft anterior mitral Video 10.2
leaflet), and with real-time (RT) 3D TEE the cleft can often be better elucidated (Video 10.3, cleft posterior Video 10.3
mitral leaflet).
Three-dimensional assessment of the MV: The additional value of RT 3D TEE for the evaluation of
MV pathology is still a matter of debate (16,17). There is a high level of consistency between RT 3D TEE
assessment of MV pathology and the findings of macroscopic surgical inspection (18). The most important
potential advantages of RT 3D TEE are that it is capable of providing several unique views and images
FIGURE 10.8 TG two-chamber view. This view is particularly helpful in demonstrating structural pathology of the
subvalvular apparatus, as the beam travels perpendicular to these structures, enhancing their visualization.

FIGURE 10.9 TG basal SAX. This view can be difficult to optimize, in its true form it reveals the basal left ventricle in
short axis, allowing basal wall motion abnormalities to be identified. In this figure the posteromedial commissure (PC)
and anterolateral commissure (AC) are visible. All six segments of the mitral valve are also identified. Mitral valve opening
area can be measured by planimetry. Applying CFD can often help to localize regurgitant jets.
which are intuitively more understandable. RT 3D TEE is probably the method of choice when available as
it can complement the standard 2D examination (19).
The guidelines for image acquisition and display using 3D echocardiography (20) recommend that the
MV be displayed with the aortic valve placed superiorly, regardless if the MV is oriented as viewed from the
left atrium or left ventricle. This brings the advantage that the anterior leaflet is readily identifiable inferior
to the aortic valve; the posterior leaflet must then be further inferior in this view. Viewed from the atrial
side, then the valve segments are named 1, 2, and 3, from left to right (Fig. 10.10). The view from the left
atrium is the most intuitively understandable and helpful 3D view of the MV (also referred to as the “en
face” or “surgical” view). This view is often particularly helpful in translating the TEE findings to the sur-
geon, as in this single view all segments of the MV can be seen and pathology can often be clearly localized,
FIGURE 10.10 Three-dimensional view of the mitral valve from the left atrial perspective. The aortic valve (AV) is
positioned superiorly, the left atrial appendage (LAA) is also visible. This view is also referred to as the “en face view”
or “surgeon’s view” of the mitral valve. All leaflet segments are simultaneously visible and are labeled here.

FIGURE 10.11 Three-dimensional view of the mitral valve viewed from the left atrial perspective, with the aortic valve
positioned superiorly. The left atrial appendage is also identified. The image is taken in systole, and a flail P2 segment
with ruptured chords is clearly recognizable.
especially in cases of excessive leaflet motion (Fig. 10.11, Video 10. 4). Cleft defects, indentations, or leaflet Video 10.4
perforations are often distinctly better viewed in this view compared to standard 2D images.
In examining the structure of the mitral apparatus it is important to identify and quantify the presence
and severity of calcification of the mitral apparatus, especially on the annulus and leaflets. Calcification
has a characteristic echodense appearance on echo and is not difficult to identify (Fig. 10.12). Because of
shadowing artifacts, however, it may impede visualization of other structures.
Quantitative measurements: In the preoperative structural assessment of the mitral apparatus, a
number of echocardiographic measurements should be made, as these are important firstly in assess-
ing whether the valve is amenable to repair and secondly in helping to determine the correct repair
technique.
FIGURE 10.12 Calcification. This ME LAX view shows a calcified segment of the posterior leaflet, and this echodense
and thickened segment of calcification creates a shadow artifact underneath which impedes visualization of underlying
structures.

FIGURE 10.13 ME LAX view through A2, P2, ensure that a true ME LAX view is achieved, that is, no foreshortening, and
avoiding an oblique slice through the aortic valve and left ventricular outflow tract. Measurements are made in diastole,
annulus (D1), length of anterior leaflet (D2), and posterior leaflet length (D3).
Size of Mitral Annulus

The normal mitral annulus is not round, rather it is described as saddle-shaped, and the ratio between
the transverse and anteroposterior diameters is approximately 4:3. When the annulus dilates, however,
it expands predominantly in the anteroposterior direction, thus reducing the normal 4:3 ratio, as its
fibroelastic skeleton is weakest around the posterior annulus. To assess for mitral annular dilatation
the annulus is therefore measured in its anteroposterior diameter between the base of the A2 and
P2 segments at the level of the mitral annulus. This is done in diastole using the ME LAX view (21),
(Fig. 10.13).
Length of Anterior Mitral Leaflet

This is a particularly important measurement to make in the setting of mitral repair and is used to deter-
mine the size of the annuloplasty ring to be implanted. The length is best measured during diastole using
the ME LAX view with the measurement made from the base of the anterior leaflet (at the annulus) to its
leaflet tip (21), (Fig. 10.13). Because of the semicircular shape of the anterior leaflet, the measurement along
the A2 segment in this image plane will be the longest. Care should be taken not to include the primary
chordae in the measurement, which attach to the tip of the leaflet.
Length of Posterior Mitral Leaflet

This can be measured using the same ME LAX image used for the annulus and anterior leaflet (21),
(Fig. 10.13). Measurement is made from the base of the leaflet at the annulus to the tip of the posterior
leaflet. The main significance of this measurement is in predicting the likelihood of systolic anterior motion
(SAM) of the anterior leaflet occurring postoperatively, as discussed later.
C-sept Distance
The distance from the coaptation point of the mitral leaflets to the septum is also useful in the risk assess-
ment for SAM postrepair. This measurement should be made again in the ME LAX view, this time in sys-
tole, so that the leaflets have coapted. The shortest direct distance from the coaptation point to the septum
is measured (Fig. 10.14).

AL PL
C-sept
LVID
FIGURE 10.14 Schematic demonstrating the transesophageal echocardiographic measurements used before repair
to assess the risk for systolic anterior motion. AL, anterior leaflet length; PL, posterior leaflet length; C-sept, distance
from the coaptation point to the septum; LVID, left ventricular internal diameter in systole. (Adapted from Maslow AD,
Regan MM, Haering JM, et al. Echocardiographic predictors of left ventricular outflow tract obstruction and systolic
anterior motion of the mitral valve after mitral valve reconstruction for myxomatous valve disease. J Am Coll Cardiol.
1999;34:2096–2104.)
Left Ventricular End-systolic Internal Diameter

This is best measured using the TG two-chamber view, with systole timed according to MV closure. The
long axis of the LV should be horizontal in the image and measurement is made at the level of the chordae
from endocardial edge to endocardial edge (Fig. 10.15). For improved accuracy an average measurement
FIGURE 10.15 Left ventricular end-systolic internal diameter. Here measured in the TG two-chamber view, the ME
two-chamber view is also suitable. The measurement is made in end systole, at the level of the chordae tendinae, from
endocardial edge to endocardial edge, that is, the red line in this figure.

from a number of cardiac cycles should be obtained, especially in the case of arrhythmia. A measurement
greater than 40 mm defines LV dilatation. The ME two-chamber view can also be used (15).
Left Ventricular End-diastolic Internal Diameter:

Left ventricular end-diastolic internal diameter can also be measured using either the TG or ME two-
chamber view, this time at end-diastole. Measurements are made at the level of the chordae, and greater
than 55 mm represents LV dilatation (15).
Tenting Height
Also referred to as coaptation depth, this is a very important measurement to make, as a preoperative tent-
ing height of 11 mm or higher is associated with poor repair results, and so is usually taken as an indication
for MV replacement rather than repair (22,23). This usually occurs in the setting of Carpentier type IIIb
pathology, where the left ventricle is dilated and the consequent restriction of the MV leaflets in systole
means that they coapt below the level of the mitral annulus. The measurement should be made in the ME
LAX or ME four-chamber views in systole. Using the zoom function over the MV or reducing the image
depth reduces the percentage error of the measurement. To make this measurement, the level of the mitral
annulus is first identified by marking the annular plane. The tenting height is the perpendicular distance
from this line marking the annulus level to the coaptation point (Fig. 10.16).
Tenting Area
Similar to tenting height this is measured using the ME LAX view in systole. Tenting area is that area which
is enclosed by the line drawn between anterior and posterior annulus and the valve leaflets (Fig. 10.17). An
area of >2.5 cm2 is unfavorable for MV repair in functional MR (19).
Coaptation Length
This represents the extent to which both leaflets come to oppose each other during systole. It is measured
at end systole in ME LAX views (Fig. 10.18). It is perhaps more important to measure postrepair, as it is one
of the fundamental goals of repair, and good coaptation length is associated with better repair durability
and long-term results. Usually the coaptation length is longer following implantation of artificial chords as
compared to leaflet resection (24).
FIGURE 10.16 Tenting height. Useful in helping to determine whether a valve is repairable in functional disease.
Measure in late systole using the ME LAX when the leaflets have coapted. Identify the plane of the mitral annulus (white
line); the tenting height is the perpendicular distance from the coaptation point to this line (red arrow).

FIGURE 10.17 Tenting area. Using the same view as for tenting height, measure the area enclosed by the line along the
annular plane and the atrial sides of both valve leaflets (red triangle).
2. Carpentier Classification System

Functional classification of the leaflets has implications in determining the likelihood of valve repair as will
be discussed later. The functional classification of the MV is based on leaflet motion. In type I dysfunction Video 10.5
the motion of the leaflets is normal, in type II it is excessive, and in type III it is restrictive (Fig. 10.19). Type Video 10.6
III is further subclassified as type IIIa (structural) with restricted motion during both systole and diastole
Video 10.7
due to leaflet damage (calcification or rheumatic disease) and type IIIb (functional) where the restriction is
Video 10.8
limited to systole and is due to tethering of the leaflets (ischemic or dilated cardiomyopathy).
Application of CFD is helpful in determining the functional classification. In type I the regurgitant jet Video 10.9
is usually central. In type II with one leaflet involved the regurgitant jet is eccentric and directed over the Video 10.10
noninvolved leaflet (Fig. 10.20, Videos 10.5–10.11). However, if both leaflets are involved the regurgitant Video 10.11
jet can be central. In type III dysfunction, usually, the regurgitant jet is central because most often both
leaflets are affected (Videos 10.12–10.16). With only one leaflet involved the regurgitant jet is eccentric and Video 10.12
Video 10.13
Video 10.14
Video 10.15
Video 10.16
FIGURE 10.18 Coaptation length (shown as red line). Using either the ME LAX or ME four-chamber views, measure the
length of apposition between the anterior and posterior leaflets in end systole.

A B
C D
E F
FIGURE 10.19 Carpentier’s classification of mitral regurgitation (MR) based on leaflet motion. In type I, the leaflet
motion is normal and the MR jet tends to be central (A,B). In type II, there is excessive leaflet motion and the MR jet is typi-
cally directed away from the diseased leaflet (C,D). In type III lesions, the leaflet motion is restricted leaflet motion and is
further subdivided into type IIIa (structural) (E) and type IIIb (functional) (F). In type III lesions, the regurgitant jet may be
directed towards the diseased leaflet if only one leaflet is affected, or it may be central if both mitral leaflets are equally
affected. (Courtesy Dr. Gregory M. Hirsch.)

FIGURE 10.20 Color flow Doppler of type II regurgitation, caused by excessive leaflet motion, in this case prolapse affect-
ing the P2 segment. The resulting jet is eccentric and blood is directed over the corresponding, nonaffected (A2) leaflet.
directed over the affected leaflet (Fig. 10.21). In addition, in type II dysfunction, one has to discriminate
between billowing, prolapse, and flail (19,21).
1. Billowing is defined as motion of the body of the leaflets above the mitral annulus plane (Fig. 10.22).
To some degree it is a normal finding. It is abnormal when >2 mm in ME LAX view or >5 mm in ME
four-chamber view. It is generally associated with excessive tissue, chordal elongation, and possibly later Video 10.17
occurrence of leaflet prolapse (Videos 10.17, 10.18). Video 10.18
2. Prolapse describes displacement of one or both leaflet edges above the plane of the mitral annulus
where the free margin is directed to the LV (Fig. 10.23). It is often associated with chordal elongation
but can also be associated with chordal rupture (Videos 10.5–10.11). The regurgitant jet seen with Video 10.5
CFD is always directed over the noninvolved segments in patients with type II dysfunction (Fig. 10.20, Video 10.6
Videos 10.6, 10.7, 10.9). Video 10.7
Video 10.8
Video 10.9
Video 10.10
Video 10.11
FIGURE 10.21 Color flow Doppler of regurgitation caused by restrictive leaflet motion. The posterior leaflet in this case
is restricted and does not move to coapt normally. The resulting jet is eccentric and directed over the affected posterior
leaflet.

FIGURE 10.22 ME four-chamber view (left) and 3D en face view of the mitral valve from the left atrium (right) both
showing extensive billowing of the anterior mitral leaflet. The body of the leaflet, but not its free edge, is pushed over
the level of the mitral annulus.
Video 10.19 3. Flail is defined as displacement of the free edge of one or both leaflets above the mitral annular plane,
Video 10.20 where the free edge of the leaflet is also directed into the left atrium (Fig. 10.24, Videos 10.19–10.21). It is
Video 10.21 often associated with chordal rupture but can also be associated with extreme elongation of the chords.
3. Assessment of the Severity of the Mitral Valve Regurgitation

The severity of the MV regurgitation is practically best assessed using the vena contracta width, the flow
convergence (or PISA) method, and the pattern of pulmonary venous flow, as described in Chapter 8,
Mitral Regurgitation.
FIGURE 10.23 Two-dimensional ME images: four-chamber (top left), commissural (top right), LAX (bottom left), and
3D en face view of the mitral valve from the left atrium, showing prolapse of the P2 segment. The P1 segment is not vis-
ible in this 3D view.

FIGURE 10.24 Two-dimensional ME commissural view (above left) and with color Doppler (above right), and 3D en
face view of the mitral valve from the left atrium, showing a flail P1 segment. The reason for the flail is chordal rupture;
the remaining segments of chordae attached to the segment also flail over the level of the mitral annulus and point up
in the direction of the left atrium.
4. Visualization of the Circumflex Coronary Artery and its Relationship

to the Mitral Valve Annulus
Damage or distortion of the circumflex coronary artery caused by the annuloplasty ring or prosthetic
valve sutures is a well recognized and potentially devastating complication which occurs in up to 1.8% of
patients undergoing MV surgery (25–27). Visualization of the circumflex coronary artery by TEE can be
accomplished in most patients by starting from the ME LAX view of the aortic valve and gradually turn-
ing the probe to the left (28). From the origin of the left main coronary artery, one can follow the course
to the bifurcation into the left anterior descending artery and the circumflex coronary artery by turning
the probe to the patient’s left. Further turning of the probe will visualize the course of the circumflex
along the mitral annulus (Fig. 10.25, Video 10.22). The circumflex coronary artery must be distinguished Video 10.22
from the coronary sinus, a venous structure that runs in a parallel direction to it, and noting that the
circumflex coronary artery decreases in diameter along its course from its point of origin, while the coro-
nary sinus increases in diameter, will help to differentiate the two (29). The distance of the circumflex
coronary artery from the mitral annulus can also be measured and this information may directly help
the surgeon. The preoperative visualization of the circumflex coronary artery acts as a reference for the
postrepair visualization.
5. Define Secondary and Coexisting Abnormalities of Other Cardiac Structures

It is recommended that a comprehensive TEE examination be performed both pre- and post bypass in
patients undergoing MV repair. In addition to defining the pathology and severity of the MV regurgitation,
it is important to examine for echocardiographic evidence of secondary features of MR and also to identify
any other coexisting cardiac pathology.
Assessment of LV global and regional systolic function and chamber size has been discussed already
and is important to quantify prebypass as a reference for the postoperative examination. Attention should
also be paid to the aorta, specifically looking for the presence of atherosclerotic plaque which, if pres-
ent, increases the risk of postoperative cerebrovascular events. Ascending aortic plaque or calcification
increases the risk of complications arising from aortic cannulation and cross-clamping, and if present,
these may warrant alteration of surgical technique (30). Plaque in the descending aorta becomes more rel-
evant if a retrograde perfusion technique is used, as in some minimally invasive techniques.

FIGURE 10.25 Visualization of the circumflex artery. LA, left atrium; LMCA, left main coronary artery; AML, ante-
rior mitral leaflet; Ao, aortic sinus; PA, pulmonary artery; Cx, circumflex artery; LAD, left anterior descending; CS,
coronary sinus. (Adapted from Ender J, Singh R, Nakahira J, et al. Echo didactic: Visualization of the circumflex
artery in the perioperative setting with transesophageal echocardiography. Anesth Analg. 2012;115(1):22–26, with
permission.)
The structure and function of the right-sided chambers should also be assessed. Tricuspid regurgita-
tion in patients with MV disease is associated with worse outcome and predicts poorer survival, heart
failure, and reduced functional capacity (31). Heart failure patients with moderate-to-severe MR and
reduced right ventricular function (tricuspid annular plane systolic excursion [TAPSE] < 14 mm) had
an absolute 2-year mortality that was 27% higher than similar patients who had a TAPSE > 14 mm (32).
Patients undergoing MV surgery, who also have severe tricuspid regurgitation, benefit from concur-
rent tricuspid valve repair, and tricuspid annuloplasty may be considered for less than severe tricuspid
regurgitation in patients undergoing MV repair, when there is either tricuspid annular dilatation or
pulmonary hypertension (3).
Help in Planning the Surgical Procedure

Based on the TEE assessment of valve structure and function and on the expertise of the surgeon, one
can estimate the likelihood of repair. Table 10.1 describes the likelihood of successful repair based on
the underlying pathology and echocardiographic features. MV prolapse is the most common cause
of MR in developed countries. With an isolated prolapse of the posterior leaflet, especially in the P2
segment, the success rate for repair is more than 92% (33), making this defect the most amenable to
repair. But more complex lesions can also be repaired with a high success rate, especially in high volume
centers (34).
Degenerative valve disease is the most common cause of type II MR and is further subclassified
as either Barlow’s disease or as fibroelastic deficiency. Typical echocardiographic features of Barlow’s
disease, also called diffuse myxomatous degeneration, are excessive leaflet motion, affecting usually
multiple (sometimes all) leaflet segments, with thickening of the valve leaflets, chordal elongation or
rupture, and annular dilatation. In addition, a posterior displacement of the posterior mitral annulus
Video 10.23 can be observed (Fig. 10.26, Video 10.23). Characteristically, there is an abundance of leaflet tissue,
leading to excessive motion and ultimately regurgitation. Patients with fibroelastic deficiency of their
MV tend to be older than Barlow’s disease patients, and typically only a single segment of the leaflet is

TABLE 10.1 Probability of Successful Mitral Valve Repair in Organic Mitral Regurgitation Based on Echo Findings
Mitral annulus Probability

Etiology Dysfunction Calcification dilation of repair
Degenerative II: Localized prolapse (P2 and/or A2) No/localized Mild/moderate Feasible
Ischemic/functional I or IIIb No Moderate Feasible
Barlow II: Extensive prolapse (≥3 scallops, Localized (annulus) Moderate Difficult
posterior commissure)
Rheumatic IIIa: but pliable anterior leaflet Localized Moderate Difficult
Severe Barlow II: Extensive prolapse (≥3 scallops, Extensive (annulus Severe Unlikely
anterior commissure) + leaflets)
Endocarditis II: Prolapse but destructive lesions No No/mild Unlikely
Rheumatic IIIa: Stiff anterior leaflet Extensive (annulus Moderate/severe Unlikely
+ leaflets)
Ischemic/functional IIIb: Severe valvular deformation No No or severe Unlikely
Adapted from: Lancellotti P, Moura L, Pierard LA, et al. European Association of Echocardiography recommendations for the
assessment of valvular regurgitation. Part 2: mitral and tricuspid regurgitation (native valve disease). Eur J Echocardiogr.
2010;11:307–332.
involved. The affected segment may be locally thickened, although this is less likely than for Barlow’s
disease, and chordal elongation or rupture of this segment is usually evident. Valve repair of patients
with Barlow’s disease is more challenging than for those with fibroelastic deficiency, but is still the
treatment of choice.
Endocarditis is not an automatic indication for valve replacement and valve repair may be feasible.
Although the presence and degree of annular and leaflet calcification can be assessed easily echocardio-
graphically, the decision to replace the valve in patients with mitral annular calcification relies also on mac-
roscopic inspection, as it may be possible to surgically remove some of the calcification. In all such cases it
is important to fully assess the structure and function of the mitral apparatus as outlined above in order to
best determine the optimum surgical strategy.
SAM of the anterior MV leaflet is a well-recognized potential complication of MV repair. Predictors
of SAM after MV repair in the preoperative TEE examination are a decreased distance from mitral
leaflet coaptation point to the septum (C-sept distance), a ratio of anterior to posterior mitral leaflet
height of <1.4, and an absolute height of the posterior leaflet of >1.5 cm (35,36) (Fig. 10.14, Videos 10.24, Video 10.24
10.25). This scenario is most likely to be seen in patients with Barlow’s disease, where the excess leaflet Video 10.25
tissue often predisposes to SAM. Septal wall hypertrophy is also associated with an increased likelihood
of SAM.
FIGURE 10.26 Typical echocardiographic appearance of a Barlow’s valve. Note that both leaflets are thickened and
the valve seems to have a lot of extra tissue (left). In late systole (right) the anterior leaflet prolapses and the posterior
annulus is markedly displaced posteriorly.

MITRAL VALVE REPAIR TECHNIQUES

The fundamental goals of MV repair are as follows (37):
1. Preserve or restore full leaflet motion
2. Create a large leaflet coaptation area
3. Remodel and stabilize the MV annulus
Various surgical techniques have been described, the most common of which are as follows:
1. Annuloplasty ring implantation
2. Artificial chordae implantation
3. Chordal transfer
4. Chordal shortening or papillary muscle shortening
5. Resection of valve leaflets
6. Edge-to-edge technique (Alfieri repair)
7. Repair technique of type I valve dysfunction
8. Repair technique of type III valve dysfunction
The particular surgical technique applied and the success of MV repair depend on the particular valve
pathology causing the regurgitation and the expertise and skill of the surgeon (2,3,19).
Annuloplasty
In almost all cases of open MV repair, an annuloplasty ring is implanted, and the principle behind this is to
try and stabilize the annulus and restore or maintain the normal 4:3 ratio of transverse to anteroposterior
distances of the MV in systole. As discussed previously, the mitral annulus dilates predominately in the
anteroposterior direction because the posterior annulus is structurally the weakest point, so offers least
resistance to enlargement. Annuloplasty ring insertion normalizes the geometry of the annulus and facili-
tates greater coaptation between the leaflets and thereby improves greatly the durability and long-term
success of the repair (38).
Most important of the many variables distinguishing the commercially available annuloplasty ring mod-
els is to select the correct size. Generally the optimum ring size corresponds to the length of the anterior
mitral leaflet (11), however, for some type II conditions (especially Barlow’s disease) the ring should tend
to be oversized in order to accommodate the excessive leaflet tissue, thus allowing for good coaptation
while reducing the likelihood of postoperative SAM. In cases of restrictive MV disease, the ring should be
downsized again to facilitate good coaptation between the leaflets. The surgeon will also verify the appro-
priateness of the ring size using a surgical sizer. More recently, strong correlation between annuloplasty size
determined using a combination of 3D TEE imaging with superimposed computer-aided design modeling
and surgically determined ring sizes has been demonstrated (39), and this approach may play a greater role
in future.
Implantation of Artificial Chordae

Video 10.26 Implantation of artificial chordae involves the attachment of polytetrafluoroethylene (PTFE) chordae to
Video 10.27 the corresponding papillary muscle (Video 10.26), then to the free margin of the involved mitral leaflet seg-
Video 10.28 ment (Video 10.27) and finally, the implantation of an annuloplasty ring (Video 10.28). Originally applied
to repair type II defects of the anterior leaflet, this technique is now also well established for the repair of
posterior and bileaflet defects (34,40).
The most challenging aspect of this technique is ensuring that the length of the new artificial chordae is
correct to facilitate good coaptation and normal leaflet motion. A variety of techniques have been described
in order to achieve this (41), some involving the use of TEE-derived measurements (42). Prebypass TEE-
derived measurements have the potential advantage that they can be made with the heart in systole, while
the surgeon is limited to measuring the heart while it is arrested in diastole (33,43). The advantages of
this method of repair are that it provides excellent results, can be applied to most cases of type II disease

irrespective of the state of the native chordae, tissue resection can usually be avoided, and it is considered
a highly reproducible technique.
Chordal Transfer
A second technique commonly applied to repair type II defects of the anterior leaflet is chordal transfer.
This involves taking normal chordae with a strip of leaflet tissue from the posterior leaflet and transferring
it to the free edge of the unsupported anterior leaflet; the defect in the posterior leaflet can then be repaired
normally by quadrangular resection (44). Another option is to transfer functioning secondary chordae from
the anterior leaflet to its prolapsing free edge or to fix the free edge of the anterior leaflet back onto second-
ary chordae with sutures. An advantage of this technique is that sizing and measurement of the transferred
chordae is not required; a disadvantage is that the technique is not always applicable as it usually requires
the posterior leaflet to be normal, which is not always the case.
Chordal Shortening, Papillary Muscle Shortening

This technique, originally described by Feldman (9), has been most often applied to cases of anterior leaflet
prolapse, caused by severe chordal elongation. An incision is made into the papillary muscle and the excess
chord is wrapped in a pericardial pledget placed within the muscle, which is then oversewn, capturing the
chord, and thereby effectively shortening it. In this type of repair an annuloplasty ring is mandatory to
reduce the tension on the chordae and help prevent later chordal rupture. However, the long-term results
of this technique have been found to be inferior to chordal transfer, mainly due to later chordal rupture.
Shortening the papillary muscle by removing a wedge-shaped section is another option aimed at correcting
type II anterior leaflet prolapse.
Leaflet Resection
The majority of MV pathologies in type II disease are ruptured and elongated chords from the middle
segment of the posterior leaflet. The technique of valve repair utilizing tissue resection consists of surgical
inspection of the MV in cardioplegic arrest (Video 10.29), resection (so called “triangular” or “quadran- Video 10.29
gular” resection depending on the shape of the excised section) of the involved segment (Video 10.30), Video 10.30
reconstruction of the leaflets (Video 10.31), and then implantation of an annuloplasty ring (Video 10.32). Video 10.31
This is the technique traditionally applied to isolated segmental prolapse of the posterior leaflet and has Video 10.32
provided excellent results; however, insertion of artificial chordae is usually a valid alternative, and in one
retrospective study, the coaptation length was found to be better following repair with artificial chordae
than for repair by resection in patients with type II posterior leaflet dysfunction (33). Isolated segmental
type II disease of the posterior leaflet is considered the defect most amenable to repair, and repair rates
for this condition should be of the order of 90% in any center offering mitral surgery. As far as possible,
resection of anterior leaflet tissue should be avoided, and if performed, should not involve more than 10% of
the leaflet surface area.
Edge-to-Edge (Alfieri Stitch) Repair

This technique involves suturing the anterior and posterior leaflets together at the coaptation surfaces,
classically between A2 and P2 segments, although other segments may also be sutured together. It is
especially applied in cases of anterior leaflet prolapse and also in cases of excess anterior leaflet tis-
sue typical of Barlow’s disease, where it functions both to reduce the likelihood of postrepair leaflet
prolapse and also to reduce the likelihood of postoperative SAM. The Alfieri stitch presents unique
challenges to the perioperative echocardiographer, in that, coaptation between A2 and P2 is fixed as
they are sutured together, which implies that leaflet motion in these segments is restricted, especially
in diastole, and that a so-called double orifice valve is created. The total opening area of the valve will
thereby be reduced, so the presence or absence of postrepair mitral stenosis must be evaluated on the
postoperative examination (Fig. 10.27).

FIGURE 10.27 Offline 3D analysis of the opening area of the mitral valve in a patient postrepair—in this case an Alfieri
stitch between A2 and P2, and insertion of an annuloplasty ring (right image). The opening area of each orifice is mea-
sured individually and the sum of both represents the total effective opening area (A1 + A2) (left image). Here the total
opening area is 0.82 cm2 (0.23 cm2 + 0.59 cm2), representing significant stenosis and a poor result.
Repair Technique for Type I Valve Dysfunction

Type I MV dysfunction encompasses pathologies such as mitral annular dilatation, cleft MV, leaflet inden-
tations, or leaflet perforation (trauma, endocarditis). Cleft MV is a congenital abnormality whereby a defect
is seen which extends from the leaflet tip to the annulus and is better identified in diastole. Almost exclu-
Video 10.1 sively, this is found to affect only the anterior leaflet (Video 10.1), and then usually in the region of A2
Video 10.3 segment, very rarely however the posterior leaflet may be affected (Video 10.3). Indentations are usually
Video 10.33 benign divisions found between the scallops of the posterior leaflet (Video 10.33). They do not normally
extend to the annulus and are identifiable normally during diastole, as they tend to close over during systole
and so do not cause regurgitation and are therefore not normally pathologic. Identification and differentia-
tion of mitral cleft and indentations is one area where the use of RT 3D TEE is especially helpful. With a
simple en face view of the MV, cleft or indentations can be directly visualized, whereas distinction of these
features using standard 2D TEE is much less obvious.
Another feature of mitral cleft is that it is often found in association with other congenital cardiac
defects such as endocardial cushion defects, atrial septal defect, ventricular septal defect, or transposi-
tion of the great arteries (45). In cases of cleft MV, the TEE examination should aim to identify or exclude
these defects. The repair of cleft defects or pathologic indentations is usually straightforward and can be
successfully accomplished by direct closure without the need for tissue resection and with placement of an
annuloplasty ring if annular dilatation or other indication exists.
Repair of Type III Valve Dysfunction

In type IIIa dysfunction, the MV leaflets are restricted during both systole and diastole. The most common
cause worldwide is rheumatic heart disease, and in the developed world, is valvular calcification. Although
balloon valvuloplasty is the treatment of choice for noncalcified rheumatic mitral stenosis, many patients
require open surgery for severe MR secondary to rheumatic heart disease. Calcium may be sometimes
surgically removed in an attempt to improve leaflet mobility and to facilitate suturing of the annuloplasty
ring. The presence of mitral annular calcification makes repair more difficult, and increases the postopera-
tive risk of paraannular leak and also of ventricular rupture. In cases of repair of stenotic mitral lesions
secondary to rheumatic heart disease, commissurotomy should be performed, as the characteristic feature
of this disease process is stenosis spreading inward from the commissures. The commissurotomy incision
should not extend to closer than 5 mm from the annulus to avoid postoperative commissural leakage, and
an annuloplasty ring will be required in the case of a dilated annulus. If the annulus is not dilated and only
a commissurotomy is performed, then an annuloplasty ring is often not required.

In type IIIb dysfunction where regurgitation results from leaflet restriction in systole, TEE plays an
important role in determining if a repair is even feasible. Preoperatively, it is important to determine the
size of the annulus and also the tenting height (see prerepair section). The principle is to “downsize” the
ring in order to bring the leaflets together for better coaptation. However, the length of the anterior mitral
leaflet is still measured as a reference.
Postrepair TEE Examination

The postrepair TEE examination consists of two distinct phases: The first is a shorter examination per-
formed before final weaning from cardiopulmonary bypass, and is focused specifically on identifying the
circumflex coronary artery and on ensuring complete deairing of the heart chambers, and the second phase
consists of a comprehensive TEE examination performed after weaning from bypass, focused on evaluation
of the MV repair and on identifying any other postoperative complications.
Postrepair, Prebypass Weaning TEE Examination

1. Identification of the circumflex coronary artery and its continued perfusion
2. Checking for complete deairing of the left ventricle
Postrepair, Postbypass TEE Examination

3. Localize and quantify any residual MR, either transvalvular or para-annular
4. Examine for mitral stenosis secondary to the MV repair
5. Screen for potential complications:
a. Global and regional ventricular functions
b. SAM of the anterior MV leaflet with consecutive LV outflow obstruction tract
c. New aortic valve regurgitation due to capture of the noncoronary cusp of the aortic valve with ring
sutures, aortic dissection, or ventricular rupture
Identification of the Circumflex Coronary Artery Perfusion

Postoperative examination for the circumflex coronary artery using combined 2D and CFD should be
carried out as described earlier in the preoperative assessment section. As a practical tip, it is often easier
to visualize while the patient is still on bypass, once the aortic cross clamp has been removed. Identifica-
tion of a patent circumflex coronary artery with good flow along its course at this stage is reassuring and
allows the rest of the postoperative examination to focus on identifying other potential complications. If
the course of the circumflex coronary artery cannot be visualized (Video 10.34), having been identifiable Video 10.34
preoperatively, then focus should switch to looking for LV regional wall motion abnormalities, especially
along the inferolateral and/or anterolateral wall, between the 2 and 5 o’clock positions on the TG mid-
SAX view and the surgeon should be informed (Video 10.35). Video 10.35
Checking for Complete Deairing of the Left Ventricle

During open repair of the MV, air enters the left-sided heart chambers. If this is not vented before com-
ing off bypass, it will embolize into the systemic circulation and be particularly problematic if it enters
either the cerebral or coronary circulation. Given its more anterior origin, air will preferentially enter
the right coronary artery of a supine patient (Video 10.36), and then manifest as an inferior wall or a Video 10.36
right ventricular wall motion abnormality (46). For minimally invasive MV repairs, where exposure and
access to the heart are limited, TEE assessment of intracavity air (Video 10.37) and identification of new Video 10.37
regional wall motion abnormalities are even more important. TEE assessment of intracardiac air is best
performed using the ME views (four-chamber, commissural, two-chamber, LAX), being careful to avoid
foreshortening or shadows from the mitral annuloplasty ring, and paying particular attention to the LV
apex, left atrial appendage, and left atrium, where air typically collects and appears as an echodense
bubble. As ventricular function improves, this air can be seen to dissipate on TEE and can be removed
through surgical vents.

Residual Mitral Regurgitation

Immediate postrepair assessment looks at the remodeled structure of the mitral apparatus, then examines
whether or not it is functionally competent, and finally checks for any new associated complications. It
is important to be aware of the particular surgical technique performed in order to be able to evaluate it
properly.
Focus is firstly directed at the motion of the MV leaflets. The anterior leaflet in particular should move
freely in both systole and diastole, and depending on the particular type of repair, motion of the posterior
leaflet is more likely to be limited, as in most repairs the posterior leaflet will have been pulled down
somewhat to provide for a large coaptation area, one of the fundamental goals of MV repair. In normal
MVs, the length of coaptation approximates 7 to 9 mm between A2 and P2 and decreases as the commis-
sures are approached. Coaptation length postrepair should aim to be at least 5 mm, measured between A2
and P2 segments, ideally more (Fig. 10.18) (24).
Another fundamental goal of MV repair, that is, restoration of normal leaflet motion, means particularly
that excursion of the leaflets during systole should not exceed the annular plane, that is, no billowing, pro-
lapse, or flail, and in general neither should motion of the leaflets be restricted. This does however depend
on the type of repair performed, for example, if the repair involves an Alfieri stitch (47), then P2 and A2
Video 10.38 segments will have been sutured together to create a double orifice MV (Fig. 10.27, Video 10.38). For this
reason exact details of the surgical repair must be known. Importantly, the annular plane is not now defined
by the margins of the annuloplasty ring, which will have been sutured on top of the annulus from the atrial
side, but rather by the anatomical mitral annulus.
The next step in the postrepair assessment is analysis of flow through the mitral apparatus using
CFD. To assess for postoperative MR cardiopulmonary bypass must be completely ended. The significance
of regurgitant jets identified in patients still under mechanical circulatory support cannot be accurately
interpreted, and the temptation to assess the repair while on bypass must be avoided. For accurate assess-
ment it is also imperative that the Nyquist limit be set appropriately (50 to 60 cm/s), and that the patients’
preload, afterload, and myocardial contractility are optimized. Blood flow will always follow the path of
least resistance, so if systemic blood pressure and afterload are low at the time of CFD assessment, then
any degree of MR can be underestimated, especially in the case of functional regurgitation. Baseline shift
of the Nyquist limit from 50 to 37.5 cm/s leads to better intra- and interobserver variability for vena con-
tracta measurements as well as for effective regurgitant orifice area (EROA) using PISA (48). Starting again
with the ME four-chamber view, the sector scan should be rotated through 180 degrees, this time with the
CFD sector placed over the MV, left atrium, and proximal subvalvular apparatus. Once regurgitant jets are
identified, they must be quantified and localized. Using RT 3D echo with CFD more precise localization of
residual MR is possible.
Quantification is most reliably performed by measuring the width of the vena contracta jet and PISA
method. In difficult cases, measurement of PISA may help to determine whether or not returning to bypass
and attempting to rerepair the valve is indicated. In general transvalvular jets of mild severity do not war-
rant a return to bypass, especially if the duration of the regurgitant jet is limited to early systole. However,
patients who had residual mild or moderate MR at the end of their surgery compared to those without,
showed a trend toward more often requiring later reoperation, although no increased morbidity or mortal-
ity was seen (49).
Postoperative 3D assessment is particularly valuable in localizing any residual regurgitant jets and in
Video 10.39 distinguishing para-annular (Fig. 10.28, Video 10.39) from transvalvular regurgitation (Fig. 10.29, Video
Video 10.40 10.40). In cases where regurgitation postrepair warrants a return to bypass and rerepair, it is extremely
helpful to be able to identify the exact location of the leak, and of course its pathology, as this will determine
the repair strategy and means the surgeon knows exactly where to look for the defect.
Three-dimensional images also provide a distinct advantage over standard 2D images in the planimetric
quantification of the residual orifice opening area after an Alfieri or mitral clip repair. Using 2D imaging
it can be difficult to obtain a clear TG basal SAX view of the MV and also to be certain that it is cut at the
correct level. Using 3D offline analysis, it is possible to crop the image in multiple planes so that the true
orifice area is identified and measured (Fig. 10.27).
Moderate or severe MR postrepair is unsatisfactory and depending on the underlying mechanism, and
other patient-specific factors should lead to attempted rerepair or even replacement. Improvement in the

FIGURE 10.28 Three-dimensional CFD showing a segment of the mitral valve (in this case postvalve replacement) with
a clear paravalvular leak. Note also that the left atrial appendage is identified, and serves as a reference for orientation.
pattern of pulmonary vein flow compared with preop suggests that the significance of the regurgitation has
been reduced for the patient. Ultimately the decision to return to bypass and attempt rerepair in cases of
residual regurgitation is patient-specific and should be made in collaboration between the surgeon and the
echocardiographer. For younger, otherwise healthy patients, a return to bypass in order to improve even
mild residual leak may ultimately benefit the patient, if a repairable defect is identified.
In the case of para-annular regurgitant jets, these should also be quantified in severity, and in general
there is a lower threshold for revising the repair for anything other than very mild jets, compared to transval-
vular jets. Most small para-annular jets seen directly postbypass are insignificant and often disappear after
protamine administration; however, persistent or larger jets may progress and lead to valvular dehiscence,
hemodynamic instability, or hemolysis if not corrected.
FIGURE 10.29 Three-dimensional CFD from a patient postannuloplasty and valve repair, demonstrating residual
insufficiency, which is localized to both commissures. Note the limitation on spatial resolution as the entire mitral valve
cannot be simultaneously viewed.

Postrepair Mitral Stenosis

Mitral stenosis is a rare complication of MV repair, occurring in less than 2% of patients (50). A mean trans-
mitral pressure gradient of ≥7 mm Hg as measured using continuous wave Doppler immediately follow-
ing cardiopulmonary bypass is suggested as being associated with clinically significant mitral stenosis (50).
The use of pressure half-time in quantifying mitral stenosis is not reliable in the early postoperative period
because of changes in left atrial and LV compliance and diastolic function. Care should be taken in inter-
preting pressure gradients measured by continuous wave Doppler in this setting. Particular difficulty may
arise following an Alfieri repair. Planimetry of the MV orifice area should be performed with 2D echo in
the TG basal SAX view or using 3D echo. The total valve opening area is the sum of both individual orifices
(Fig. 10.26). Aside from these attempts to quantify mitral stenosis, it is often helpful to eyeball the MV opening
during diastole. A valve that opens freely and facilitates a clear conduit between the left atrium and ventricle
is very unlikely to be associated with clinically significant stenosis. Planimetry of the MV area in the TG basal
SAX view during diastole is recommended to grade the severity of mitral stenosis whenever it is feasible (51).
Screening for Potential Complications

Global/Regional Ventricular Dysfunction
Apart from interrupted circumflex coronary artery perfusion, other potential causes of new regional
wall motion abnormalities include intracoronary air embolus, usually affecting the right coronary artery,
myocardial stunning, hibernation, or ischemia postbypass, or an effect of external cardiac pacing. The TG
midpapillary SAX view, TG basal SAX view, and ME four-chamber, two-chamber, and LAX views allow for
localization of any regional wall motion abnormalities. Right ventricular function should be quantified by
measuring fractional area change and TAPSE. Pulmonary artery systolic pressure also should be estimated.
Exclusion of Systolic Anterior Motion/Dynamic Left Ventricular Outflow Obstruction

The risk factors for the development of SAM of the anterior mitral leaflet and consequent dynamic LV
outflow tract obstruction have been discussed in the preoperative section. When these factors are identi-
fied preoperatively, the surgical repair can be tailored to minimize the risk of postoperative SAM, most
commonly by using a sliding leaflet plasty with P2 resection, thereby moving the coaptation point more
posteriorly, or by using short artificial chords to pull the posterior leaflet straight down, or alternatively by
inserting an Alfieri stitch and an annuloplasty ring which is as large as possible. If septal hypertrophy is
present, then a partial septal resection can also be considered. Diagnosis of SAM and dynamic LV outflow
tract obstruction is made echocardiographically. The fundamental problem is that blood being compressed
by the left ventricle during systole directs the anterior mitral leaflet not toward the left atrium as it should
normally, but anteriorly in the direction of the left ventricular outflow tract. This results in two prob-
lems, mitral incompetence and dynamic LV outflow tract obstruction. The situation is exacerbated by some
hemodynamic factors: hypovolemia, hyperdynamic circulation, tachycardia, and low afterload conditions,
all of which may arise after termination of bypass.
TEE diagnosis of SAM is best appreciated using the ME LAX and five-chamber views. The anterior
Video 10.23 leaflet can be seen to be pushed in the direction of the left ventricular outflow tract in systole (Video 10.23).
Video 10.24 CFD usually shows a regurgitant jet of MR and left ventricular outflow tract turbulence (Video 10.24).
Continuous wave Doppler profile through the left ventricular outflow tract shows a characteristic dagger
shape (Fig. 10.30) as the obstruction and consequently the pressure gradient peaks in late systole, unlike the
parabolic-shaped curve of aortic stenosis, where the pressure gradient peaks in midsystole. Dynamic LV
outflow tract obstruction causes turbulent flow through the aortic valve and may cause the aortic leaflets
to flutter in systole, and this can be demonstrated well using M-mode echocardiography with the beam
directed across the aortic valve.
Once SAM with or without dynamic LV outflow tract obstruction has been diagnosed, the next step
is to optimize the patient’s hemodynamics by ensuring adequate intravascular volume, avoiding tachycar-
dia, increasing afterload with vasoconstrictors, and if possible eliminating inotropes. Once this has been
achieved, the patient should be re-evaluated for SAM, MR, and dynamic LV outflow tract obstruction.
Only rarely then may it be necessary to return to bypass and rerepair or replace the valve. The decision as

FIGURE 10.30 Continuous wave Doppler through the left ventricular outflow tract and aortic valve of a patient who
developed systolic anterior motion after mitral repair. The shape of the Doppler profile is described as “dagger shaped,”
as the peak pressure occurs in late systole.
to whether or not to return to bypass and attempt to improve the repair should be patient-specific. SAM
and dynamic LV outflow tract obstruction are mixed structural and functional pathologies, so that patients
predisposed to develop SAM by the structure of their mitral apparatus will likely have symptoms precipi-
tated by functional demand, for example, with tachycardia and possibly dehydration during exercise. This
must be borne in mind in evaluating the risk to benefit profile of returning to bypass for a particular patient.
Aortic Insufficiency/Ventricular Rupture/Aortic Dissection

New aortic valve insufficiency can occur after MV repair, particularly if the annuloplasty suture has
captured either the left or noncoronary cusps of the aortic valve (Videos 10.41, 10.42). Ventricular rupture Video 10.41
is potentially life-threatening though extremely rare potential complication of MV surgery (52). Patients Video 10.42
with heavily calcified mitral annulus are most at risk. Aortic dissection, likewise, is a rare but potentially
devastating complication (53). It is recommended that the comprehensive intraoperative TEE examination
be repeated at the end of surgery to screen for these pathologies.
SUMMARY
Successful MV repair surgery relies on applying the appropriate surgical technique to the patient’s particu-
lar pathology (54). Accordingly, TEE plays an integral role in success by providing an accurate diagnosis of
the presence of regurgitation, classification of its pathophysiology and severity, estimation of the likelihood
of valve reparability, and postoperative evaluation of the surgical result.
REFERENCES
1. Klein AL, Burstow DJ, Tajik AJ, et al. Age-related prevalence of valvular regurgitation in normal subjects: A comprehensive
color flow examination of 118 volunteers. J Am Soc Echocardiogr. 1990;3:54–63.
2. Bonow RO, Carabello BA, Kanu C, et al. ACC/AHA 2006 guidelines for the management of patients with valvular heart
disease: A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines
(writing committee to revise the 1998 Guidelines for the Management of Patients With Valvular Heart Disease): Developed in
collaboration with the Society of Cardiovascular Anesthesiologists: Endorsed by the Society for Cardiovascular Angiography
and Interventions and the Society of Thoracic Surgeons. Circulation. 2006;114:e84–e231.
3. Bonow RO, Carabello BA, Chatterjee K, et al. 2008 Focused update incorporated into the ACC/AHA 2006 guidelines for
the management of patients with valvular heart disease: A report of the American College of Cardiology/American Heart

Association Task Force on Practice Guidelines (Writing Committee to Revise the 1998 Guidelines for the Management of
Patients With Valvular Heart Disease): Endorsed by the Society of Cardiovascular Anesthesiologists, Society for Cardiovascular
Angiography and Interventions, and Society of Thoracic Surgeons. Circulation. 2008;118:e523–e661.
4. Borger MA, Alam A, Murphy PM, et al. Chronic ischemic mitral regurgitation: Repair, replace or rethink? Ann Thorac Surg.
2006;81:1153–1161.
5. Enriquez-Sarano M, Akins CW, Vahanian A. Mitral regurgitation. Lancet. 2009;373:1382–1394.
6. Enriquez-Sarano M, Sundt TM 3rd. Early surgery is recommended for mitral regurgitation. Circulation. 2010;121:804–811.
7. Enriquez-Sarano M, Schaff HV, Orszulak TA, et al. Valve repair improves the outcome of surgery for mitral regurgitation. A
multivariate analysis. Circulation. 1995;91:1022–1028.
8. Chikwe J, Goldstone AB, Passage J, et al. A propensity score-adjusted retrospective comparison of early and mid-term results
of mitral valve repair versus replacement in octogenarians. Eur Heart J. 2011;32:618–626.
9. Feldman T, Foster E, Glower DD, et al. Percutaneous repair or surgery for mitral regurgitation. N Engl J Med. 2011;364:1395–
1406.
10. Thys D, Abel M, Bollen BA, et al. Practice guidelines for perioperative transesophageal echocardiography. A report by the
American Society of Anesthesiologists and the Society of Cardiovascular Anesthesiologists Task Force on Transesophageal
11. Carpentier AF, Lessana A, Relland JY, et al. The “physio-ring”: An advanced concept in mitral valve annuloplasty. Ann Thorac
Surg. 1995;60:1177–1185.
13. Enriquez-Sarano M, Tajik AJ, Schaff HV, et al. Echocardiographic prediction of survival after surgical correction of organic
mitral regurgitation. Circulation. 1994;90:830–837.
14. Tribouilloy CM, Enriquez-Sarano M, Schaff HV, et al. Impact of preoperative symptoms on survival after surgical correction
of organic mitral regurgitation: Rationale for optimizing surgical indications. Circulation. 1999;99:400–405.
Echocardiogr. 2005;18:1440–1463.
16. Grewal J, Mankad S, Freeman WK, et al. Real-time three-dimensional transesophageal echocardiography in the intraoperative
assessment of mitral valve disease. J Am Soc Echocardiogr. 2009;22:34–41.
17. Mukherjee C, Tschernich H, Kaisers UX, et al. Real-time three-dimensional echocardiographic assessment of mitral valve: Is
it really superior to 2D transesophageal echocardiography? Ann Card Anaesth. 2011;14:91–96.
18. Moustafa SE, Chandrasekaran K, Khandheria B, et al. Real-time three-dimensional transesophageal echocardiography assess-
ment of the mitral valve: Perioperative advantages and game-changing findings. J Heart Valve Dis. 2011;20:114–122.
19. Lancellotti P, Moura L, Pierard LA, et al. European Association of Echocardiography recommendations for the assessment of
valvular regurgitation. Part 2: Mitral and tricuspid regurgitation (native valve disease). Eur J Echocardiogr. 2010;11:307–332.
20. Lang RM, Badano LP, Tsang W, et al. EAE/ASE recommendations for image acquisition and display using three-dimensional
echocardiography. Eur Heart J Cardiovasc Imaging. 2012;13:1–46.
21. Shah PM. Current concepts in mitral valve prolapse–diagnosis and management. J Cardiol. 2010;56:125–133.
22. Calafiore AM, Gallina S, Di Mauro M, et al. Mitral valve procedure in dilated cardiomyopathy: Repair or replacement? Ann
Thorac Surg. 2001;71:1146–1152.
23. Kuwahara E, Otsuji Y, Iguro Y, et al. Mechanism of recurrent/persistent ischemic/functional mitral regurgitation in the chronic
phase after surgical annuloplasty: Importance of augmented posterior leaflet tethering. Circulation. 2006;114:I529–I534.
24. Falk V, Seeburger J, Czesla M, et al. How does the use of polytetrafluoroethylene neochordae for posterior mitral valve prolapse
(loop technique) compare with leaflet resection? A prospective randomized trial. J Thorac Cardiovasc Surg. 2008;136:1205–
1206.
25. Aybek T, Risteski P, Miskovic A, et al. Seven years’ experience with suture annuloplasty for mitral valve repair. J Thorac
Cardiovasc Surg. 2006;131:99–106.
26. Tavilla G, Pacini D. Damage to the circumflex coronary artery during mitral valve repair with sliding leaflet technique. Ann
Thorac Surg. 1998;66:2091–2093.
27. Pessa CJN, Gomes WJ, Catani R, et al. Anatomical relationship between the posterior mitral valve annulus and the coronary
arteries. Implications to operative treatment. Braz J Cardiovasc Surg. 2004;19(4):372–377.
28. Ender J, Selbach M, Borger MA, et al. Echocardiographic identification of iatrogenic injury of the circumflex artery during
minimally invasive mitral valve repair. Ann Thorac Surg. 2010;89:1866–1872.
30. Konstadt SN, Reich DL, Kahn R, et al. Transesophageal echocardiography can be used to screen for ascending aortic athero-
sclerosis. Anesth Analg. 1995;81:225–228.
31. Shiran A, Sagie A. Tricuspid regurgitation in mitral valve disease incidence, prognostic implications, mechanism, and manage-
ment. J Am Coll Cardiol. 2009;53:401–408.
32. Dini FL, Conti U, Fontanive P, et al. Right ventricular dysfunction is a major predictor of outcome in patients with moderate to
severe mitral regurgitation and left ventricular dysfunction. Am Heart J. 2007;154:172–179.
33. Seeburger J, Falk V, Borger MA, et al. Chordae replacement versus resection for repair of isolated posterior mitral leaflet pro-
lapse: A egalite. Ann Thorac Surg. 2009;87:1715–1720.

34. Seeburger J, Borger MA, Doll N, et al. Comparison of outcomes of minimally invasive mitral valve surgery for posterior, ante-
rior and bileaflet prolapse. Eur J Cardiothorac Surg. 2009;36:532–538.
35. Maslow AD, Regan MM, Haering JM, et al. Echocardiographic predictors of left ventricular outflow tract obstruction and
systolic anterior motion of the mitral valve after mitral valve reconstruction for myxomatous valve disease. J Am Coll Cardiol.
1999;34:2096–2104.
36. Gillinov AM, Cosgrove DM 3rd. Modified sliding leaflet technique for repair of the mitral valve. Ann Thorac Surg.
1999;68:2356–2357.
37. Carpentier A. Cardiac valve surgery–the “French correction”. J Thorac Cardiovasc Surg. 1983;86:323–337.
38. Johnston DR, Gillinov AM, Blackstone EH, et al. Surgical repair of posterior mitral valve prolapse: Implications for guidelines
and percutaneous repair. Ann Thorac Surg. 2010;89:1385–1394.
39. Ender J, Eibel S, Mukherjee C, et al. Prediction of the annuloplasty ring size in patients undergoing mitral valve repair using
real-time three-dimensional transoesophageal echocardiography. Eur J Echocardiogr. 2011;12:445–453.
40. Kuntze T, Borger MA, Falk V, et al. Early and mid-term results of mitral valve repair using premeasured Gore-Tex loops (‘loop
technique’). Eur J Cardiothorac Surg. 2008;33:566–572.
41. Duran CM, Pekar F. Techniques for ensuring the correct length of new mitral chords. J Heart Valve Dis. 2003;12:156–161.
42. Calafiore AM. Choice of artificial chordae length according to echocardiographic criteria. Ann Thorac Surg. 2006;81:375–377.
43. David TE. Outcomes of mitral valve repair for mitral regurgitation due to degenerative disease. Semin Thorac Cardiovasc Surg.
2007;19:116–120.
44. Gillinov AM, Cosgrove DM. Chordal transfer for repair of anterior leaflet prolapse. Semin Thorac Cardiovasc Surg.
2004;16:169–173.
45. Kondur A, Pitta S, Afonso L. Incremental utility of real-time three-dimensional echocardiography in the diagnosis and preop-
erative assessment of cleft mitral valve in adults. Eur J Echocardiogr. 2008;9:586–588.
46. Secknus MA, Asher CR, Scalia GM, et al. Intraoperative transesophageal echocardiography in minimally invasive cardiac
valve surgery. J Am Soc Echocardiogr. 1999;12:231–236.
47. Alfieri O, Maisano F, De Bonis M, et al. The double-orifice technique in mitral valve repair: A simple solution for complex
problems. J Thorac Cardiovasc Surg. 2001;122:674–681.
48. Hess H, Eibel S, Mukherjee C, et al. Quantification of mitral valve regurgitation with color flow Doppler using baseline shift.
Int J Cardiovasc Imaging. 2013;29:267–274.
49. Fix J, Isada L, Cosgrove D, et al. Do patients with less than ‘echo-perfect’ results from mitral valve repair by intraoperative
echocardiography have a different outcome? Circulation. 1993;88:II39–II48.
50. Riegel AK, Busch R, Segal S, et al. Evaluation of transmitral pressure gradients in the intraoperative echocardiographic diag-
nosis of mitral stenosis after mitral valve repair. PLoS One. 2011;6:e26559.
clinical practice. Eur J Echocardiogr. 2009;10:1–25.
52. Deniz H, Sokullu O, Sanioglu S, et al. Risk factors for posterior ventricular rupture after mitral valve replacement: Results of
2560 patients. Eur J Cardiothorac Surg. 2008;34:780–784.
53. Williams ML, Sheng S, Gammie JS, et al. Richard E. Clark Award. Aortic dissection as a complication of cardiac surgery:
Report from the Society of Thoracic Surgeons database. Ann Thorac Surg. 2010;90:1812–1816.
54. Adams DH, Rosenhek R, Falk V. Degenerative mitral valve regurgitation: Best practice revolution. Eur Heart J. 2010;31:
1958–1966.

QUESTIONS
1. Which of the following is true? c. Systolic flow reversal in a pulmonary vein
a. Chronic severe mitral regurgitation is a indicates severe mitral regurgitation
contraindication for surgery and should be d. Regurgitant jet vena contracta is best mea-
treated medically sured in the midesophageal four-chamber
b. Mitral regurgitation secondary to dilative and long-axis views
cardiomyopathy is typically a functional
6. All of the following are true regarding
rather than structural pathology
the functional classification for mitral
c. Patient outcome after mitral valve repair is
regurgitation EXCEPT:
independent of surgical skill level
a. In type IIIb regurgitation leaflet restriction
d. Successful repair should lead to restriction
is limited to systole
of the range of mitral valve leaflet motion
b. Cleft defect of a mitral leaflet is an example
2. Secondary cardiac pathophysiology of a type I pathology
associated with mitral regurgitation c. Type II regurgitation results from excessive
includes all of the following, EXCEPT: leaflet motion
a. Left ventricular dilatation d. Chordal rupture typically results in type III
b. Left atrial dilatation regurgitation
c. Lipomatous hypertrophy of the interatrial
7. When assessing the severity of mitral
septum
regurgitation, which of the following is true:
d. Eccentric cardiac hypertrophy
a. Vena contracta of the regurgitant jet should
3. Regarding mitral valve anatomy, the be measured at the narrowest part of the jet,
following are true EXCEPT: just proximal to the regurgitant orifice
a. The anterior mitral leaflet is divided ana- b. For multiple regurgitant jets, the sum of the
tomically into three segments by the pres- individual vena contractae represents the
ence of two indentations true severity of the regurgitation
b. The surface area of the posterior mitral leaflet c. When using the PISA method to quantify the
is less than that of the anterior mitral leaflet severity of mitral regurgitation, the Nyquist
c. Primary chordae tendineae attach to the limit should be set between 50 and 60 cm/s
free edge of the mitral leaflets d. Regurgitant jet area is not recommended for
d. The mitral valve has two commissures, one assessment of mitral regurgitation severity
anterolateral commissure and one postero-
8. Regarding the circumflex artery, the
medial commissure
following are true EXCEPT:
4. Regarding mitral valve anatomy, the a. The artery can be visualized using TEE
following are true EXCEPT: whilst the patient is on bypass, unless the
a. The mitral annulus normally has a saddle- aorta is cross-clamped
shaped profile b. Increasing the Nyquist limit for color flow
b. When the mitral annulus dilates, it does so in a Doppler will improve the sensitivity for
predominantly anterior to posterior direction detection of flow within the vessel
c. The length of the posterior leaflet is greater c. The incidence of circumflex artery occlu-
than the length of the anterior leaflet sion occurring following mitral valve sur-
d. The papillary muscles are each connected to gery is approximately 1% to 2%
both mitral leaflets by chordae tendineae d. Decreasing gain improves visualization of
the vessel
5. All of the following are true regarding
the assessment of the severity of mitral 9. Which of the following scenarios is most
regurgitation EXCEPT: compatible with successful mitral repair:
a. In patients under general anesthesia, the a. The mitral annulus is calcified
severity of mitral regurgitation is usually b. The dysfunction is localized prolapse (e.g.,
overestimated P2 segment)
b. The Nyquist limit for color flow Doppler c. The dysfunction is classified as type IIIa
assessment of the regurgitant jet should be d. The mitral annulus is severely dilated
set between 50 and 60 cm/s

10. Factors which help to predict the likelihood 15. Regarding excessive leaflet motion, which
of postoperative systolic anterior motion of the following is true?
(SAM) of the anterior mitral leaflet a. Billowing always progresses to prolapse and
occurring after mitral valve repair include then to flail
the following, EXCEPT: b. Billowing leaflets always result in a regurgi-
a. Decreased distance from the septum to tant jet
mitral leaflet coaptation point (C-sept) c. The regurgitant jet flows over the non-
b. An absolute height of the posterior leaflet of affected segment in patients with type II
more than 1.5 cm dysfunction
c. A ratio of anterior leaflet height to posterior d. Chordal rupture always results in flail leaflet
leaflet height of <1.4
16. New regional left ventricular wall
d. Presence of mitral annular calcification
motion abnormalities in the inferolateral
11. Regarding the management of postrepair or anterolateral segments occurring
SAM, which of the following is true? postbypass for mitral valve repair should
a. Presence of postoperative SAM almost prompt particular concern about:
always requires a return to bypass and fur- a. Iatrogenic circumflex coronary artery damage
ther surgical correction b. Coronary artery air embolus
b. Increasing heart rate and decreasing after- c. Myocardial stunning
load will reduce the severity of the SAM d. Hyperkalemia
c. Epinephrine is the drug of choice in the
17. Which of the following is not a benefit of
management of postoperative SAM
mitral valve repair versus replacement?
d. Left ventricular outflow tract obstruction is
a. Preservation of left ventricular function
usually also evident in patients with SAM
b. Fewer thromboembolic events
12. Regarding the assessment of immediate c. Better early and late survival rates
postrepair mitral stenosis, which of the d. Shorter operative time
following methods is most helpful if
18. Fundamental goals of mitral valve repair do
available?
not include:
a. Pressure half-time of mitral inflow
a. Restoration of full leaflet motion
b. Pulse wave Doppler assessment of the mean
b. Decreasing the size of the mitral valve ori-
gradient across the mitral valve
fice with an annuloplasty ring
c. Continuous wave Doppler assessment of
c. Stabilization and remodeling of the mitral
the peak gradient across the mitral valve
valve annulus
d. Planimetry of the mitral valve opening area
d. Creation of a large coaptation area
13. The A2/P2 segments of the mitral valve can
19. Common techniques for repair of mitral
usually be seen in the following TEE views,
valves include the following EXCEPT:
EXCEPT:
a. Chordal transfer
a. Midesophageal two-chamber
b. Implantation of an annuloplasty ring
b. Transgastric basal short-axis
c. Isolated chordal release
c. Midesophageal four-chamber
d. Implantation of synthetic chordae
d. Midesophageal long-axis
20. Regarding TEE for mitral valve repair, all of
14. The following statements regarding the
the following are true EXCEPT:
Alfieri stitch repair technique are true
a. TEE is a level I indication for mitral valve
EXCEPT:
repair
a. It involves suturing A2 and P2 segments
b. A problem-focused TEE should be used
together
preoperatively rather than a comprehensive
b. It leads to the creation of a triple orifice valve
exam
c. The effective opening area of the valve is equal
c. TEE evaluation of the mitral valve is gener-
to the sum of the individual orifice areas
ally superior to transthoracic echocardio-
d. Mitral stenosis is a recognized potential
graphy
complication
d. If TEE is contraindicated in a particular
patient, epicardiac echocardiography can
be used

11 Aortic Regurgitation
Ira S. Cohen
T HE EXQUISITE SENSITIVITY OF TRANSESOPHAGEAL echocardiography (TEE) in identifying aortic

regurgitation (AR) is manifested by its ability to detect the minute regurgitant jets engineered into the
design of the St. Jude prosthetic valve to flush platelet aggregates off the valve surface. Few studies have
been performed investigating the assessment of AR primarily using TEE because of its relatively invasive
nature. Most assessments of the severity of AR are based on the assumption that transthoracic echocardio-
graphic (TTE) approaches should be equally applicable to TEE.
MECHANISMS OF AORTIC REGURGITATION

The physiologic functioning of the aortic valve in diastole is dependent on the interplay of several com-
ponents forming a complex that includes the aortic annulus, sinuses of Valsalva, and the sinotubular
junction (Fig. 11.1). The annular basal insertions of the leaflets are into the muscle of the left ventricular
outflow tract (LVOT) and the fibrosa of the anterior mitral leaflet. The peripheral leaflet insertions then
extend as semilunar structures along the sinuses of Valsalva to end at the sinotubular junction where the
commissures are formed and whose diameter is normally 10% to 15% smaller than the diameter of the
annulus (1). This relationship can be visualized when the edges of the leaflets are caught obliquely in a
midesophageal long-axis view. A delineation of the mechanism of AR is of increasing clinical importance
FIGURE 11.1 ME AV LAX view demonstrating appropriate locations for measuring the aortic annulus (a), sinus of
Valsalva (b), sinotubular junction (c), and proximal ascending aorta (d). Ao, aorta; LA, left atrium; LVOT, left ventricular
outflow tract; RVOT, right ventricular outflow tract.
224

11. Aortic Regurgitation 225
as the mechanism impacts on the approach to surgical repair and valve sparing may be an option. A pro-
posed classification has been advanced that involves three functional mechanisms (2,3):
Type 1: Enlargement of any components of the aortic root (aortic annulus, sinuses of Valsalva, and sinotu-
bular junction) with normal cusps, seen in idiopathic annuloaortic ectasia, ascending aortic aneurysm,
Marfan’s syndrome, dissection, aortitis, and Ehlers–Danlos syndrome. This results in displacement of
the commissures outward so that the leaflet edges cannot coapt in diastole generally resulting in a cen-
tral regurgitant jet.
Type 2: Excessive cusp motion including whole, partial, or flail prolapse resulting in noncoaptation below
the annular plane (e.g., membranous [ventricular septal defect]VSD, congenitally elongated cusp)
or free edge perforation (with an otherwise normal cusp), often with an eccentric regurgitant jet
(Video 11.1). Video 11.1
Type 3: Primary cusp tissue damage, where one or more cusps do not reach the opposing cusps due to
restricted motion caused by fibrosis, calcification (sclerodegenerative, bicuspid, or rheumatic), or fenes-
tration (due to endocarditis) with an eccentric regurgitant jet (Video 11.2). Video 11.2
In general, Types 1 and 2 may be amenable to repair while Type 3 generally requires valve replacement.
TEE evaluation has been shown to correlate very highly with surgical findings and assessment of the sizes
of the components of this complex should be part of a routine TEE assessment (3). Recent studies have
shown that an intraoperative postrepair assessment can identify patients at significant risk for recurrent
regurgitation who require revision and possible valve replacement at the time of the initial procedure. Key
factors predicting a high risk of recurrence are the level of coaptation relative to the aortic annulus (lower
is worse), the presence or absence of residual AR (more is worse), and a coaptation length of the leaflets
(<4 mm is worse) (4).
Type 3 regurgitation due to sclerodegenerative or bicuspid aortic valve disease is the most common type
of regurgitation necessitating aortic valve replacement.
HEMODYNAMICS OF AORTIC REGURGITATION

AR represents both an increase in preload and afterload to the left ventricle (LV). The increase in preload is
a result of the increased end-diastolic volume resulting from the added regurgitant volume. The increase in
afterload is a function of the increased radius of the ventricle. Increase in the end-diastolic radius of a ven-
tricle at any wall thickness increases the wall stress and the force needed to eject blood (law of Laplace). The
general response of the ventricle to chronic AR is to dilate and become more compliant to accommodate
the extra volume and to hypertrophy to reduce wall stress. The hypertrophy occurs both longitudinally as
the heart enlarges—so-called eccentric hypertrophy—and concentrically, as evidenced by its maintaining
a “normal” wall thickness as it enlarges. Accordingly, the size of the ventricle is an index of the severity and
duration of the regurgitation and should be factored into the assessment of the severity of the lesion.
Acute AR, most commonly due to a tear in the valve secondary to endocarditis, to deceleration injury
in a motor vehicle accident, or to stretching of the annulus secondary to an acute dissection, offers a con-
trasting clinical presentation. Acute aortic insufficiency is one of the least well-tolerated valvular lesions
because of the limited ability of the heart to compensate for an acute increase in volume load by the mecha-
nisms discussed above. Consequently, the LV diastolic pressure rises rapidly and is transmitted to the lungs
resulting in severe pulmonary congestion. Therefore, in acute AR, the chamber is often normal in size but
with catastrophic hemodynamic consequences. Diagnosis of significant AR in the setting of heart failure is
essential as intra-aortic balloon counterpulsation is contraindicated because diastolic pressure augmenta-
tion worsens the regurgitation.
The assessment of the severity of valvular insufficiency is complicated by the potentially dramatic effects
of even transient changes in loading conditions and peripheral vascular resistance on Doppler indices of AR
severity. Since the operating room environment is the one in which a multitude of factors affect both the
preload and afterload of the ventricle, the potential impact of these changes must be borne in mind when
the severity of a valvular lesion is evaluated. Acute increases in peripheral vascular resistance (e.g., follow-
ing surgical stimulation or the administration of vasopressors) can increase the apparent degree of valvu-
lar insufficiency by increasing systemic vascular resistance and impeding peripheral runoff. Conversely,

vasodilators (e.g., volatile anesthetics, angiotensin-converting enzyme inhibitors and receptor blockers,
calcium channel blockers) reduce peripheral vascular resistance and decrease the apparent degree of insuf-
ficiency, both clinically and by Doppler interrogation. The physical properties (e.g., distensibility, elasticity,
compliance) of the source (aorta) and recipient (LV) of regurgitant flow, in addition to the size of the regur-
gitant orifice and the physical properties of the involved valve, are other dynamic variables that further
complicate intraoperative assessment. In fact, most clinicians feel it is not possible to definitively assess
regurgitant lesions in the operating room environment. As a result of the multitude of factors influencing
any assessment of the severity of AR, the estimate should be based on an integration of the results of all
Doppler approaches providing technically adequate data in any given patient.
ECHOCARDIOGRAPHIC EVALUATION OF THE AORTIC VALVE

The aortic valve can be evaluated by motion mode (M-mode), two-dimensional (2D), Doppler and three-
dimensional (3D) echocardiographic techniques. The primary approaches utilize 2D imaging and both
pulse wave (PW) and continuous wave (CW) Doppler to assess valve morphology and severity of disease.
Transesophageal 2D echocardiographic imaging of the aortic valve is generally superior to transthoracic
imaging because of the improved resolution of the higher-frequency TEE probe. Three-dimensional imag-
ing shares the limits inherent to all ultrasound techniques determined by the interrelation of sector size,
frame rate, and depth on image resolution. Both types of TEE imaging are best obtained from the mid-
esophageal short- and long-axis views. The ultimate role of 3D TEE in the assessment of AR remains under
investigation but reference is made to preliminary observations utilizing 3D imaging for measurement of
the vena contracta in the following discussion.
Methods for assessing the severity of AR have evolved along with advances in Doppler technology since
Ward et al. (5) first described the use of pulsed Doppler in conjunction with M-mode echocardiography and
auscultation to detect aortic insufficiency. The general approaches to assessing the severity of AR with TEE
will be presented in the order of their relative clinical applicability. Color mapping of the LVOT has tradition-
ally been regarded as the most accurate echocardiographic assessment (6–11). Measurement of the width
of the vena contracta, the narrowest cross-sectional area of the regurgitant jet as it traverses the valve plane,
is emerging as an attractive approach (12). It appears to be less dependent on loading conditions although
its efficacy is not as thoroughly documented (8,10). Most studies of this method have been done either in
vitro or in the OR with aortic flow probes. The proximity of the TEE probe to the aortic root and LVOT and
the ability to interrogate these structures with the higher-frequency TEE signal technically make it possible
to delineate the size of these regurgitant jets more accurately than can be done with TTE techniques. The
American Society of Echocardiography has published its recommendations for assessment of regurgitant
valvular lesions (13) with a more recent update by the European Association of Echocardiography (14).
RECOMMENDED VIEWS
In contrast to stenotic lesions, where the velocity of a jet is a critical factor in the assessment of the lesion,
AR interrogation of the leak both parallel and perpendicular to the regurgitant jet is critical because its
area of distribution in the LVOT is one of the major variables used in the assessment of severity. The most
useful views are generally obtained by starting from the standard ME four-chamber view and changing
the angle of interrogation to approximately 120 degrees to visualize the LVOT and proximal aorta in an
ME AV LAX view (Fig. 11.1). Withdrawal from this position and, occasionally, slight rotation are used to
optimize the view and allow inspection of the proximal ascending aorta. This view is optimal for measur-
ing the components of the aortic root for assessment of the mechanism of regurgitation. The ME AV SAX
view at approximately 45 to 60 degrees allows excellent resolution of the individual cusps of the aortic valve
Video 11.3 (Videos 11.3, 11.4). This too can be obtained from the four-chamber view by centering the atrioventricular
Video 11.4 (AV) groove and changing the angle to approximately 45 to 60 degrees. Occasionally the probe will need
to be withdrawn a few centimeters because the aortic valve is at a slightly higher plane than the AV groove.
Alternatively, but less frequently, reasonable views can be obtained from a deep transgastric (TG) posi-
tion at an angle close to 0 degrees or greater, subject to individual variation, or from a standard midpapillary

TG view at an angle of approximately 120 degrees (TG LAX view). These approaches have the advantage
of aligning the ultrasound beam nearly parallel to the direction of blood flow in some patients, while in
others orientation parallel to flow requires a deep TG view (Video 11.5). Parallel orientation is essential for Video 11.5
accurate quantitative Doppler analysis of both the slope of decay of the regurgitant jet and cardiac output.
Conversely, this beam orientation and the greater distances traveled reduce spatial resolution making them
a poor choice for visualizing the height or cross-sectional area of an AR jet immediately below the valve
plane. However, they may be the only means of assessing the LVOT in the presence of a prosthetic mitral
valve (MV), which frequently causes acoustic shadowing of the aortic annulus in more standard views, and
occasionally, of an aortic prosthesis when its ring obscures the LVOT image by acoustic shadowing.
The pressure gradient between the regurgitant and recipient chambers in regurgitant valvular lesions is
always high and in AR corresponds to the diastolic gradient between the aortic root (diastolic blood pres-
sure) and the LV. By the simplified Bernoulli equation, the gradient equals four times the square of the peak
jet velocity. Again, aligning a Doppler beam parallel to the flow is best accomplished in the TG views in the
view that is most parallel to flow. In aortic regurgitant lesions, it is the rate of change in pressure gradients
that provides clinically useful information unlike the peak velocity measurement used to assess stenotic
lesions. Fortunately, color flow Doppler (CFD) techniques for the assessment of AR lesions provide useful
information that is, to a significant degree, independent of the angle of the beam to the regurgitant flow.
When CFD is used, the appropriate gain setting for mapping is obtained by first setting the gain high
enough so that random color pixels appear within or outside the blood pool (on tissue). Gain is then decreased
until these random color pixels disappear. Failure to standardize the color examination in this manner leads
to invalid data and is the source of the so-called “dial-a-jet” phenomenon, in which overgaining the Doppler
signal can expand the apparent size of the jet. Similarly, using a standard color velocity scale is also impor-
tant because a change in the scale can markedly change the appearance of a jet and its distribution.
APPROACHES TO THE QUANTITATIVE ASSESSMENT

OF AORTIC REGURGITATION
COLOR FLOW MAPPING
In the initial efforts at quantifying AR, pulsed wave Doppler (PWD) was used to map the depth of penetra-
tion of the regurgitant jet into the LV cavity. This approach entailed several problems related to the effects
of a high-pressure gradient crossing a narrow regurgitant orifice (see later discussion). A better approach
was developed in which jet mapping from the then newly introduced CFD technique was used (7,15). Two
techniques for color flow mapping are recommended.
Ratio of Jet Height to Left Ventricular Outflow Diameter

Long-axis imaging of the LVOT is used to measure the height of the regurgitant jet immediately below
(within 1 cm of ) the aortic valve plane, which is then compared with the diameter of the LVOT at that
same point (7,15). The optimal views are the ME aortic valve long-axis view and, less frequently, the ME
five-chamber view (Fig. 11.2, Video 11.6). The long-axis view that shows the maximal height of the color jet Video 11.6
is selected for analysis. The maximal height during diastole is identified during slow motion freeze-frame
review. The analysis is performed using the software analysis package of the ultrasound machine. Alterna-
tively, an M-mode cursor can be placed perpendicular to the outflow tract at the point approximately where
the maximal LVOT dimension occurs (usually within 1 to 2 cm below the valve plane). If color flow map-
ping is then activated, the regurgitant jet will appear in color in the M-mode view of the outflow tract, and
the relative dimensions can be measured from this display by using the caliper function of the ultrasound
machine (Fig. 11.3). This is generally the easier of the two color methods of analysis to perform (Table 11.1)
and has been shown to be effective despite major changes in loading conditions in vitro (15). The need
for proximity of this measurement to a point close to its origin is readily observed with color flow map-
ping. The presence of a high-velocity jet (representing the aortic diastolic to LV diastolic pressure gradient)
causes rapid entrainment of blood in the ventricle within a few centimeters of this plane and a splaying out
of the color jet so that the jet rapidly enlarges below this plane. Imaging of this jet from planes deeper in the
ventricle graphically displays this phenomenon and obviates their utility in this measurement.

FIGURE 11.2 Midesophageal aortic valve long-axis view demonstrating calculation of the ratio of aortic insufficiency
height to left ventricular outflow tract diameter. The internal caliper on the echocardiography system is used to make
these measurements. In this example, the ratio is 31%, indicating mild aortic insufficiency.
Ratio of Jet Area to Left Ventricular Outflow Tract Area

In the second color flow mapping technique, the short-axis area of the regurgitant jet in the LVOT is
compared with the area of the LVOT at that same level (Fig. 11.4). The preferred view for this approach is
the ME AV SAX view, but with the probe advanced to immediately below the valve plane. Again, diastole
is evaluated by slow motion freeze-frame review, and the maximal jet area is traced and compared with
the area of the LVOT. The process is simplified by using the software analysis package of the ultrasound
machine. This method is slightly more accurate than the height–diameter ratio method but is technically
more difficult to perform.
FIGURE 11.3 Color M-mode assessment of aortic regurgitation. From the midesophageal aortic valve long-axis view,
the M-mode cursor is positioned perpendicular to the aortic root as close to the origin of the regurgitant jet as possible.
The jet and the outflow tract are well delineated in the color M-mode display. Caliper measurement of the jet height is
compared to that of the root and the resulting ratio of 60% corresponds to moderate aortic regurgitation (Table 11.1).

TABLE 11.1 Aortic Regurgitation
Parameter Caveats Mild Moderate Severe

2D imaging of LV at end Enlarged in other conditions Normal Variable Dilated (chronic)
diastole:
(Normal <5.6 cm or 3.2 cm/M2) Normal in acute AR
2D aortic leaflets Inaccurate Variable Variable Possible flail, coaptation
defect, variable
a
Color Doppler:
Jet height/LVOT height % Inaccurate with eccentric jets <25% 25–64% ≥65%
% jet diameter in LVOT/ Inaccurate with eccentric jets <5% 5–20% (mild to 21–59% (mod to severe);
Area of LVOT moderate) >59% severe
a
Vena contracta width (cm) Accuracy with multiple jets <0.3 cm 0.3–0.6 cm >0.6 cm
Diastolic flow reversal in Stiff aorta, brief is normal Brief, early Holodiastolic, Holodiastolic, increased
descending aorta (Nl) variable amplitude
height
Slope of the regurgitant jet Onset velocity ⬃ to diastolic/ Slow ≥2 m/s ≥3 m/s
LV by 4V2
Pressure half-time of Effected by aorta and LV >500 ms 200–500 ms <200 ms
regurgitant jet compliance
Regurgitant volume Maximum <30 mL 30–44 mL 45–59 mL (mod to
(mL/beat) (mild to severe); ≥60 mL
moderate) severe
Regurgitant fraction (%) Maximum <30% 30–39% 40–49% (mod to
(mild to severe); ≥50 mL
moderate) severe
EROA (cm2) Maximum; good with <0.10 cm2 0.10–0.29 cm2 ≥0.30 cm2
eccentric jets
CW Doppler spectral density Qualitative; mod to severe Faint Variable Dense
overlap
a
Aliasing velocity set at 50–60 cm/s.
LV, left ventricle; AR, aortic regurgitation; LVOT, left ventricular outflow tract; Mod, moderate; EROA, effective regurgitant orifice
area; CW, continuous wave.
FIGURE 11.4 Midesophageal aortic valve short-axis view demonstrating the jet area/left ventricular outflow tract area
method. The ratio of the areas is 51%, indicating moderate to severe aortic regurgitation.

A B
C D
FIGURE 11.5 Pseudosevere AR. A: Color M-mode of the LV outflow tract. The regurgitant jet fills most of the out-
flow tract in this plane. B: Vena contracta measurement of 0.6 cm consistent with moderate to borderline severe AR.
C: Left panel: Deep TG interrogation of the AR jet showing a slow decay with a prolonged pressure half-time. Right panel:
Interrogation of the proximal descending aorta showing a normal diastolic flow pattern. Both findings suggest mild AR.
D: Short-axis image of the regurgitant jet (arrows) which is along the coaptation line of the noncoronary cusp (NCC) and
left cusp (LCC). Right cusp is RCC. In the perpendicular long-axis views (A and B) the severity of the leak is exaggerated.
Caveats
In practice, these approaches provide reliable estimates of severity and have consequently become widely
regarded as among the best and most easily applied methods of Doppler assessment (16). They do, however,
require technically adequate views and color flow images that cannot always be obtained (Table 11.1).
Regurgitant jets have three dimensions. If a jet results from the lack of adequate alignment between two
aortic cusps along their line of coaptation (short-axis view), then interrogation at right angles to that jet
(long-axis view) may happen to orient perpendicularly to that line. A relatively narrow regurgitant orifice can
then appear to be causing regurgitant flow that fills the outflow tract resulting in an overestimation of the
severity of the leak. A cursory review of the outflow tract short-axis view of the jet will clarify this (Fig. 11.5).
Eccentric jets that are angled to the plane of the aortic valve are not adequately assessed by either
of these techniques. One approach is the use of a technique similar to that utilized for quantitative assess-
ment of mitral regurgitation based on an application of the conservation of mass using the continuity equa-
tion. The technique analyzes the proximal isovelocity surface area (PISA) defining the entrance of the jet
into its regurgitant orifice and analysis of the volume of flow into the LV to derive the regurgitant orifice.
Practical and theoretical problems with this technique are discussed below. The use of measurement of the
vena contracta can be helpful in analyzing eccentric jets and is a more practical approach intraoperatively
because TEE allows higher resolution definition of this than TTE.
MAPPING THE VENA CONTRACTA

The vena contracta is the narrowest portion of the jet immediately after crossing the valve plane and can
be identified by first visualizing the convergence zone of color flow (PISA) as it approaches and traverses
the valve plane. To optimize visualization, the echo sector is narrowed and the depth decreased to maxi-
mize the LVOT size and frame rate. Subtle adjustments of angulation and rotation from this point may be
needed to identify the vena contracta (Fig. 11.6). In some patients, particularly with very eccentric jets,
visualization is not possible. Long- and short-axis views are then obtained from the ME AV LAX and SAX
views respectively, as outlined earlier. The width of the vena contracta is measured as it passes through and
defines the regurgitant orifice as it exits the valve plane (10,17). The largest diameter of the vena contracta

Lens temperature <37.5°C
FIGURE 11.6 Midesophageal long-axis view. Arrows indicate the vena contracta. This often reaches its true (narrowest)
dimension slightly below the valve plane at the flow convergence zone. The latter is the point at which flow from the
central aorta reaches its narrowest dimension after it is “focused” by entering the regurgitant orifice on the aortic side of
the valve. LA, left atrium; Ao, aorta; LV, left ventricle.
during any portion of diastole is measured in the long-axis plane of the jet, or planimetry of its area is
performed in the short-axis view at the valve plane. In a small series of patients undergoing TEE, a vena
contracta width of more than 6 mm2 or an area of more than 7.5 mm2 predicted severe AR (10). A vena
contracta width of 3 to 6 mm2 defines moderate valvular insufficiency. When less than 3 mm2 the insuf-
ficiency is mild (Table 11.1). More importantly, and in contrast to observations made during assessments
of the severity of mitral regurgitation with this technique (18), changes in afterload obtained with phenyl-
ephrine or volume loading do not change the size of the vena contracta, suggesting this measurement to
be relatively load independent (16,19,20). This approach has become the method of choice for intraopera-
tive assessment because of its relative ease of acquisition and apparent load independence. It should be
emphasized again that regurgitant jets are 3D and as a consequence multiple views should be obtained and
analysis made of the best defined area of the vena contracta. The process is simplified by using the software
analysis package of the ultrasound machine. This method is slightly more accurate than the height–diam-
eter ratio method but is technically more difficult to perform.
Probably the major potential advantage of 3D imaging in the assessment of AR lies in its potential for
imaging of the vena contracta en face, particularly in patients with eccentric jets (Types 2 and 3). The alter-
native technique is to apply the continuity equation using PISA to calculate an effective regurgitant orifice.
However, obtaining a well-defined PISA is difficult, and frequently not possible, using 2D color flow imag-
ing in patients with AR. In addition, because of the proximity of adjacent structures, a correction factor
is necessary in a substantial number of cases to address the fact that the PISA is not truly hemispheric.
Further, with the onset of 3D imaging, it has become apparent that many regurgitant orifices have a complex
geometry and not the presumed circular configuration assumed present in the application of this technique.
Early experimental work using a sheep model showed an outstanding correlation of color 3D planimetry of
the vena contracta to electromagnetic flow measurements of the severity of regurgitation and to calculated
[effective regurgitant orifice] ERO size (21). The pyramidal data set acquired using either transthoracic or
transesophageal 3D technology can be cropped at any angle and the plane aligned parallel to the vena con-
tracta in the short axis by sequential cropping, from either the aortic or ventricular surface, to the minimal
cross-sectional area of the jet. Furthermore, planimetry of the regurgitant jets’ velocity–time integral (VTI)
multiplied by the measured vena contracta will provide an estimate of regurgitant volume.
In a series of 56 consecutive patients, Fang et al. (22), demonstrated an excellent correlation of the size
of the vena contracta determined by 3D transthoracic echo to angiographic grade (r = 0.95, p < 0.001) with
almost no overlap between grades. The technique was equally effective for both central and eccentric jets.
Although statistically 2D vena contracta determinations showed an excellent correlation, there was overlap
between grades. Interobserver and intraobserver variability of 3D measurement was low. They proposed
3D vena contracta area estimates of <0.2 cm2, 0.2 to 0.4 cm2, 0.4 to 0.6 cm2, and >0.6 cm2 correlating to

angiographic grades of I, II, III, and IV respectively. Other investigators have reported comparable results
using transthoracic 3D imaging (23).
To date there is no published literature on the use of this technique using TEE 3D imaging. Although
the superior resolution of transesophageal imaging would suggest comparable or superior utility, the rela-
tively more anterior anatomic position of the aortic valve suggests that in this case transthoracic tech-
niques might be more applicable. The role of vena contracta measurement using 3D TEE remains to be
established.
AORTIC DIASTOLIC FLOW REVERSAL

Another early index of the severity of aortic insufficiency was based on the demonstration of retrograde
diastolic flow in the ascending or, more preferably, the descending aorta or the aortic arch (24). Retrograde
flow is best assessed by interrogating the aorta in a plane near the arch (upper esophageal aortic arch
long-axis view), as demonstrated in Figure 11.7. This view is obtained by withdrawing the probe from the
ME position and rotating it posteriorly to visualize the descending aorta at 0 degrees in circular cross sec-
tion. In patients with a tortuous aorta, the angle necessary for a short-axis view may vary considerably. As
the probe is withdrawn into the upper esophagus, the plane elongates as the arch is cut tangentially at a
point slightly deeper than 20 cm from the incisors. Angulation with firm retroflexion from this position
generally allows interrogation of the high arch. Images of the ascending and descending portions of the
aorta are typically acquired only with significant obliquity and are, therefore, not generally used in clinical
spectral Doppler examinations. However, because the flow abnormality is assessed as the ratio of diastolic
to systolic flow as opposed to the absolute flow velocities, the inability to assess true flow velocities is not a
limitation. If quantitation is desired, the systolic and diastolic flow occurs are traced, and a ratio of diastolic
to systolic VTIs can be calculated. However, this is not usually quantitated other than to say that the closer
the diastolic VTI is to the systolic VTI, the greater the severity of the leak.
Normally, a minor retrograde flow pattern can be detected in the ascending aorta and proximal descend-
ing aorta related to runoff into the great vessels and coronary bed. As aortic insufficiency becomes more
severe, the degree of apparent retrograde aortic flow relative to antegrade aortic flow increases (25). In gen-
eral, the further distally in the aorta holodiastolic retrograde flow is detected (e.g., descending or abdominal
aorta) the more severe the AR. This assessment remains a useful adjunct for confirming the severity of AR
but is less accurate in the presence of coexisting aortic stenosis (11,24,26). Importantly, the usefulness of
the descending aortic diastolic reversal of flow as an index of severe AR intraoperatively has been confirmed
in patients in whom the LVOT cannot be adequately imaged on TEE for technical reasons (e.g., interposed
FIGURE 11.7 Upper esophageal aortic arch long-axis view demonstrating severe aortic regurgitation, evidenced by
flow reversal in the ascending aortic arch during diastole. Note flow away from the probe, below the baseline, through-
out diastole (holodiastolic flow).

MV prosthesis creating an acoustic shadow that obscures the LVOT). In these patients, CFD mapping of the
regurgitant jet is not possible (9).
SLOPE OF AORTIC REGURGITANT JET DECAY

Analysis of a continuous wave Doppler waveform of aortic insufficiency from the TG LAX or deep TG LAX
view is used because the Doppler beam is aligned parallel to the regurgitant jet flow. Basal esophageal views
of the LVOT are generally obtained at too great an angle to the flow for an accurate jet to be acquired. It is
essential that a smooth waveform with an intact envelope be recorded for analysis to be meaningful.
The principle of this analysis is that the velocity of the regurgitant jet is directly related to the pressure
gradient between the aortic root and the LV in diastole, in accordance with the Bernoulli equation. When
a large defect in the competence of the valve is present, the pressures equalize more rapidly because more
blood leaks through the valve per unit of time. Therefore, the pressure gradient between the aorta and the
LV decreases more rapidly in severe regurgitation and, as a result, the velocity of the jet also diminishes
more rapidly. The slope of the rate of decay of the velocity is, therefore, a measure of the rate of dissipa-
tion of the gradient and of the severity of regurgitation. A slope of AR velocity decay of 2 to 3 m/s suggests
moderately severe or severe (grades 3+ to 4+) AR. Rapid equalization of the pressure gradient can result in
premature closure of the MV before the onset of ventricular systole, indicative of severe AR, or in extreme
cases, premature opening of the aortic valve in diastole (27,28). These latter findings are generally seen only
with the acute onset of severe regurgitation. For an analysis of the slope of the AR jet on continuous wave
Doppler, the following two technical criteria must be met:
1. A smooth velocity envelope must be defined by continuous wave Doppler.
2. It must be confirmed that the core of the regurgitant jet has been interrogated. With appropriate
interrogation, the peak regurgitant jet velocity at the onset of the jet should approximate a value calculated
with the Bernoulli equation (4v2) as a reasonable estimate of the gradient between the measured arterial
diastolic pressure and an estimate of the LV diastolic pressure.
Typically jet velocities are high (>4 m/s) in lesser degrees of regurgitation because the initial diastolic
pressure gradient between the aorta and LV is generally 60 to 80 mm Hg. The exception is in severe acute
AR, in which the aortic and LV diastolic pressures may be similar. With the exception of the latter case, lower
peak velocities on the spectral display suggest that the true regurgitant jet is not being interrogated directly.
PRESSURE HALFTIME MEASUREMENT

Alternatively, a pressure half-time can be calculated. This is defined as the interval between the time when
the transvalvular AR pressure gradient is maximal and the time when the pressure gradient is half the maxi-
mum. The computer analysis package determines the pressure half-time from the slope of the AR jet decay
(Fig. 11.8). A pressure half-time of less than 200 milliseconds suggests severe AR (28). Factors related to LV
and aortic compliance and the presence of high LV diastolic pressures (heart failure, restrictive physiology,
diastolic dysfunction), all potentially cause the gradient to dissipate more rapidly and artifactually worsen
the apparent severity of the lesion by this and slope of regurgitant jet technique approaches. Accordingly,
these two methods of analysis of the decay curve should be used mainly to confirm the color flow findings.
CALCULATION OF REGURGITANT VOLUME

The AR volume can be calculated from the difference between the LV stroke volume and the right ven-
tricular (RV) stroke volume in the absence of other regurgitant lesions (e.g., mitral). The LV stroke volume
is calculated by multiplying the cross-sectional area of the LVOT by the VTI of LVOT flow. The RV stroke
volume is then estimated from the pulmonary outflow tract diameter and VTI calculated in a similar fash-
ion. Multiplication of the resultant stroke volumes by the heart rate gives the cardiac output for each circuit
and allows the quantitative calculation of the regurgitant volume as the difference between the two outputs.

FIGURE 11.8 Transgastric long-axis view with nearly parallel Doppler beam alignment demonstrating the aortic regur-
gitant jet velocity profile. The pressure half-time is 218 m/s, with a slope of 3.94 m/s indicating moderate-to-severe aortic
regurgitation.
However, obtaining accurate measurements of the necessary parameters in an intraoperative situation is

time-consuming and technically challenging, so that this approach may be impractical in a given patient.
Recent data based on 3D measurements of the LVOT show that it is frequently oval in shape and 2D diam-
eters may not be representative of the true outflow tract area, limiting the accuracy of these measurements.
COLOR FLOW MAPPING OF THE DEPTH OF THE REGURGITANT JET

This approach is included for completeness and is no longer used clinically except to screen for the presence
of AR.
Technique
In the first Doppler approach to quantification of the severity of AR, PWD was used to map the depth to
which the regurgitant jet extended into the LV cavity (25,29,30) (Table 11.1). Color Doppler has supplanted
this approach. The maximal depth below the 2D aortic valve plane at which the jet can be detected by color
Doppler imaging determines the equivalent angiographic grade of insufficiency. The size of the heart varies
with body surface area, so the scale is based on anatomic landmarks instead of depth below the valve plane.
Depth is recorded in relation to MV structures because more than 90% of regurgitant jets are oriented
toward the anterior mitral leaflet as a result of both the Coanda effect and the presence of either a Type 1 or
Type 2 lesion. In the less common situation in which the jet is oriented along the interventricular septum,
the depth at which it can be detected along the septum is compared with a corresponding depth in relation
to MV structures to estimate angiographic severity.
Limitations
As in any form of valvular insufficiency, a large pressure gradient exists between the two chambers where
the leak is occurring. Depending on the location, a pressure head of 60 to 110 mm Hg or greater drives the
regurgitant jet through a small orifice. Accordingly, a small regurgitant jet frequently extends far into the
recipient chamber despite a leak that is hemodynamically insignificant. In vitro analysis of models of AR
suggests that the depth is more an index of the gradient between the aorta and LV than of the angiographic
grade of severity (15,31).
Use of the color flow map of regurgitant flow as an index of severity is further complicated by the
entrainment of blood from a high-velocity jet entering a low-pressure chamber. This leads to color Doppler

overestimation of the apparent depth of the regurgitant jet. The same phenomena makes the area of the jet
in the LV appear larger from the apical view (deep TG TEE view). Measurements of the apparent depth are
much more likely to be affected by these phenomena than are measurements of jet height, which are made
close to the aortic valve plane.
ANCILLARY FINDINGS: ROLE OF THE DOPPLER SIGNAL

CHARACTERISTICS IN THE ASSESSMENT OF AORTIC REGURGITATION
Since the blood flow velocity is directly related to the pressure differential, the diastolic velocity is always
high (4 to 5 m/s) in comparison with the systolic velocities of 1 to 1.7 m/s across normal valves. The to-and-
fro systolic and diastolic Doppler signal is easily detected as abnormal by even an untrained ear when heard
through the audio system of the ultrasound machine. The sound becomes louder and its tone purer as the
alignment of the probe becomes more closely parallel to the core of the jet. High-velocity jets do not neces-
sarily mean severe regurgitation is present but rather that the gradient between aorta and LV is higher. If
the gain settings are constant, the intensity of the spectral Doppler signal is directly related to the severity
of the leak. This is because the larger the regurgitant flow, the greater the number of red blood cells con-
tained therein to reflect the ultrasound beam. Consequently, the more severe the regurgitation the more
intense the Doppler signals.
In more severe lesions, the velocity of the antegrade flow through the regurgitant valve may be increased
in comparison with that in normal subjects. This is a consequence of the increased stroke volume that
develops because the heart must eject both the regurgitant and the normal stroke volume through the
aortic annulus, which is a fairly rigid structure. The velocity of systolic flow in the LVOT increases with sig-
nificant insufficiency, and outflow tract velocities equal to or above 1.5 m/s suggest stenosis of the outflow
tract relative to the volume of blood flowing through it and support a diagnosis of significant regurgitation.
The clinical corollary of this phenomenon is the development of a functional systolic ejection murmur of
relative aortic stenosis, heard during auscultation of the heart in addition to the diastolic murmur of aortic
insufficiency. However, this technique can be misleading in patients with a hyperdynamic state, who can
also present with outflow tract flow velocities between 1.5 and 2 m/s.
ADDITIONAL USES OF TRANSESOPHAGEAL

ECHOCARDIOGRAPHY INTRAOPERATIVELY
The etiology of aortic insufficiency was discussed above and provides important information as whether
the valve may be successfully repaired instead of replaced. TEE can help delineate potential problems both
pre- and postoperatively. The mechanism of AR in cases of aortic dissection can be assessed and used to
guide surgery (32–37). For example, the efficacy of resuspension, as opposed to replacement, of a prolapsed
aortic valve to correct AR resulting from a Stanford type. A dissection is proportional to the percentage
of the annulus dissected and, to a lesser extent, the initial diameter of the aortic root (35). The superior
resolution of TEE is particularly helpful in defining the anatomic location of regurgitant lesions related to
prosthetic heart valves and the suture line of insertion of the valve.
The anatomic continuity of the anterior mitral leaflet with the posterior aortic root creates potential
problems in the mitral and aortic valves associated with the debridement of calcification in either annulus
or the placement of “overbiting” sutures when a prosthesis is inserted. The potential for poor seating of
the valve and paravalvular leaks as well as other complications of surgery can be analyzed with TEE and
resolved while the patient is still in the operating room.
The detection of paravalvular leaks is also another valuable screen. The annulus is generally best visual-
ized in the ME AV SAX view. In addition, seating of the prosthesis can be assessed in the ME AV LAX view
with CFD imaging. Here, shadowing by the prosthetic ring can hide small leaks. If neither of these views is
acceptable an attempt should be made to check for regurgitation from with a regular deep TG LAX view.
Generally small leaks will seal after heparin effect is reversed with protamine. The role of TEE in predicting
failure of a repair is discussed above.

SUMMARY
The intraoperative assessment of AR with TEE is generally best accomplished by measuring the width of
the vena contracta because this measurement is less load dependent than others. The next most useful is
jet height in the LVOT just below the aortic valve plane. The assessment of diastolic flow reversal in the
aorta itself remains an important and useful approach that has been reconfirmed. The other approaches
discussed in this chapter play an ancillary role, reinforcing the practitioner’s confidence in making a defini-
tive assessment. Information derived from imaging and analysis of the entire proximal aortic complex can
help guide the surgical approach.
REFERENCES
1. Underwood MJ, El Khoury G, Deronck D, et al. The aortic root: Structure, function, and surgical reconstruction. Heart.
2000;83(4):376–380.
2. El Khoury G, Glineur D, Rubay J, et al. Functional classification of aortic root/valve abnormalities and their correlation with
etiologies and surgical procedures. Curr Opin Cardiol. 2005;20(2):115–121.
3. le Polain de Waroux JB, Pouleur AC, Goffinet C, et al. Functional anatomy of aortic regurgitation: Accuracy, prediction of sur-
gical repairability, and outcome implications of transesophageal echocardiography. Circulation. 2007;116(11 suppl):I264–I269.
4. le Polain de Waroux JB, Pouleur AC, Robert A, et al. Mechanisms of recurrent aortic regurgitation after aortic valve repair:
Predictive value of intraoperative transesophageal echocardiography. JACC Cardiovasc Imaging. 2009;2(8):931–939.
5. Ward JM, Baker DW, Rubenstein SA, et al. Detection of aortic insufficiency by pulse Doppler echocardiography. J Clin
Ultrasound. 1977;5(1):5–10.
6. Meyerowitz CB, Jacobs LE, Kotler MN, et al. Assessment of aortic regurgitation by transesophageal echocardiography:
Correlation with angiographic determination. Echocardiography. 1993;10:269–278.
7. Rafferty T, Durkin MA, Sittig D, et al. Transesophageal color flow Doppler imaging for aortic insufficiency in patients having
cardiac operations. J Thorac Cardiovasc Surg. 1992;104(2):521–525.
8. Sato Y, Kawazoe K, Kamata J, et al. Clinical usefulness of the effective regurgitant orifice area determined by transesophageal
echocardiography in patients with eccentric aortic regurgitation. J Heart Valve Dis. 1997;6(6):580–586.
9. Sutton DC, Kluger R, Ahmed SU, et al. Flow reversal in the descending aorta: A guide to intraoperative assessment of aortic
regurgitation with transesophageal echocardiography. J Thorac Cardiovasc Surg. 1994;108(3):576–582.
10. Willett DL, Hall SA, Jessen ME, et al. Assessment of aortic regurgitation by transesophageal color Doppler imaging of the vena
contracta: Validation against an intraoperative aortic flow probe. J Am Coll Cardiol. 2001;37(5):1450–1455.
11. Zarauza J, Ares M, Vílchez FG, et al. An integrated approach to the quantification of aortic regurgitation by Doppler echocar-
diography. Am Heart J. 1998;136(6):1030–1041.
12. Yoganathan AP, Cape EG, Sung HW, et al. Review of hydrodynamic principles for the cardiologist: Applications to the study
of blood flow and jets by imaging techniques. J Am Coll Cardiol. 1988;12(5):1344–1353.
13. Zoghbi WA, Enriquez-Sarano M, American Society of Echocardiography, et al. Recommendations for evaluation of the
severity of native valvular regurgitation with two-dimensional and Doppler echocardiography. J Am Soc Echocardiogr. 2003;
16(7):777–802.
14. Lancellotti P, Tribouilloy C, European Association of Echocardiography, et al. European Association of Echocardiography rec-
ommendations for the assessment of valvular regurgitation. Part 1: Aortic and pulmonary regurgitation (native valve disease).
Eur J Echocardiogr. 2010;11(3):223–244.
15. Switzer DF, Yoganathan AP, Nanda NC, et al. Calibration of color Doppler flow mapping during extreme hemodynamic
conditions in vitro: A foundation for a reliable quantitative grading system for aortic incompetence. Circulation. 1987;
75(4):837–846.
16. Perry GJ, Helmcke F, Nanda NC, et al. Evaluation of aortic insufficiency by Doppler color flow mapping. J Am Coll Cardiol.
1987;9(4):952–959.
17. Tribouilloy CM, Enriquez-Sarano M, Bailey KR, et al. Assessment of severity of aortic regurgitation using the width of the vena
contracta: A clinical color Doppler imaging study. Circulation. 2000;102(5):558–564.
18. Kizilbash AM, Willett DL, Brickner ME, et al. Effects of afterload reduction on vena contracta width in mitral regurgitation.
J Am Coll Cardiol. 1998;32(2):427–431.
19. Ishii M, Jones M, Shiota T, et al. Evaluation of eccentric aortic regurgitation by color Doppler jet and color Doppler-imaged
vena contracta measurements: An animal study of quantified aortic regurgitation. Am Heart J. 1996;132(4):796–804.
20. Ishii M, Jones M, Shiota T, et al. Quantifying aortic regurgitation by using the color Doppler-imaged vena contracta: A chronic
animal model study. Circulation. 1997;96(6):2009–2015.
21. Mori Y, Shiota T, Jones M, et al. Three-dimensional reconstruction of the color Doppler-imaged vena contracta for quantifying
aortic regurgitation: Studies in a chronic animal model. Circulation. 1999;99(12):1611–1617.
22. Fang L, Hsiung MC, Miller AP, et al. Assessment of aortic regurgitation by live three-dimensional transthoracic echocardio-
graphic measurements of vena contracta area: Usefulness and validation. Echocardiography. 2005;22(9):775–781.
23. Chin CH, Chen CH, Lo HS. The correlation between three-dimensional vena contracta area and aortic regurgitation index in
patients with aortic regurgitation. Echocardiography. 2010;27(2):161–166.
24. Diebold B, Peronneau P, Blanchard D, et al. Non-invasive quantification of aortic regurgitation by Doppler echocardiography.
Br Heart J. 1983;49(2):167–173.

25. Quinones MA, Young JB, Waggoner AD, et al. Assessment of pulsed Doppler echocardiography in detection and quantifica-
tion of aortic and mitral regurgitation. Br Heart J. 1980;44(6):612–620.
26. Reimold SC, Maier SE, Aggarwal K, et al. Aortic flow velocity patterns in chronic aortic regurgitation: Implications for Doppler
echocardiography. J Am Soc Echocardiogr. 1996;9(5):675–683.
27. Cohen IS, Wharton TP Jr, Neill WA. Pathophysiologic observations on premature opening of the aortic valve utilizing a tech-
nique for multiplane echocardiographic analysis. Am Heart J. 1979;97(6):766–772.
28. Labovitz AJ, Ferrara RP, Kern MJ, et al. Quantitative evaluation of aortic insufficiency by continuous wave Doppler echocar-
diography. J Am Coll Cardiol. 1986;8(6):1341–1347.
29. Ciobanu M, Abbasi AS, Allen M, et al. Pulsed Doppler echocardiography in the diagnosis and estimation of severity of aortic
insufficiency. Am J Cardiol. 1982;49(2):339–343.
30. Toguchi M, Ichimiya S, Yokoi K, et al. Clinical investigation of aortic insufficiency by means of pulsed Doppler echocardiogra-
phy. Jpn Heart J. 1981;22(4):537–550.
31. Taylor AL, Eichhorn EJ, Brickner ME, et al. Aortic valve morphology: An important in vitro determinant of proximal regurgi-
tant jet width by Doppler color flow mapping. J Am Coll Cardiol. 1990;16(2):405–412.
32. Adam MC, Tribouilloy C, Mirode A, et al. [Contribution of transesophageal and transthoracic echography in the evaluation
of the mechanism and quantification of regurgitation in mitral and aortic bioprosthetic valves]. Arch Mal Coeur Vaiss. 1993;
86(9):1345–1350.
33. Brandstatt P, Carlioz R, Fontaine B, et al. [Acute post-traumatic aortic insufficiency: Transesophageal echocardiography in the
diagnosis and therapy of the lesions]. Ann Cardiol Angeiol (Paris). 1998;47(8):563–567.
34. Hioki J, Shibutani T, Naito T, et al. [Aortic valve insufficiency caused by nonpenetrating chest trauma difficult to distinguish
from infective endocarditis with transesophageal echocardiography: A case report]. J Cardiol. 1997;29 suppl 2:143–149.
35. Keane MG, Wiegers SE, Yang E, et al. Structural determinants of aortic regurgitation in type A dissection and the role of val-
vular resuspension as determined by intraoperative transesophageal echocardiography. Am J Cardiol. 2000;85(5):604–610.
36. Movsowitz HD, Levine RA, Hilgenberg AD, et al. Transesophageal echocardiographic description of the mechanisms of aortic
regurgitation in acute type A aortic dissection: Implications for aortic valve repair. J Am Coll Cardiol. 2000;36(3):884–890.
37. Oda H, Tanaka T, Yamazaki Y, et al. A case of nonpenetrating traumatic aortic regurgitation detected by transesophageal
echocardiography. Tohoku J Exp Med. 1997;182(1):93–101.

QUESTIONS
1. Which of the following factors can affect d. AR end-diastolic velocity profiles in the
the degree of AR during an operative descending aorta correlate better with AR
examination? severity than those in the ascending aorta
a. Administration of vasopressors
7. Which statement about continuous wave
b. Presence of volatile anesthetics
Doppler analysis of AR is true?
c. Patient’s volume status
a. Parallel alignment with the regurgitant jet is
d. All of the above
essential
2. Which TEE view is most helpful in b. The deep TG long-axis and TG long-axis
evaluating the aortic valve in a patient views are preferred
with a St. Jude mitral valve? c. ME views are seldom adequate because of
a. ME four-chamber view poor beam alignment
b. ME aortic valve long-axis view d. A smooth waveform with an intact enve-
c. ME aortic valve short-axis view lope is necessary
d. TG long-axis view e. All of the above
3. Which view allows for optimal Doppler 8. Which principle is not important in an
beam alignment in a patient with AR? evaluation of the slope of AR jet decay
a. ME four-chamber view with Doppler?
b. ME aortic valve long-axis view a. Pulsed wave Doppler is preferred because
c. ME aortic valve short-axis view of “cleaner” envelopes
d. TG short-axis view b. The velocity of the regurgitant jet is directly
e. Deep TG long-axis view proportional to the pressure gradient between
the aorta and the LV in diastole
4. When the ratio of the AR jet height to the
c. A severe regurgitant lesion will equalize the
LVOT diameter is used to quantify the
pressure gradient between the aorta and the
degree of AR, the following is true:
LV more quickly
a. One must optimize the color gain setting
d. The velocity of the AR jet diminishes more
b. The ME aortic valve long-axis view is pre-
quickly as the severity of AR increases
ferred
c. The ratio for AR with a grade of 4 + is more 9. Which of the following observations
than 65% is useful to remember in an attempt to
d. All of the above optimize the Doppler beam alignment
in a patient with AR?
5. When the pressure half-time method is
a. The velocity should be high (4 to 5 m/s)
used to quantify the severity of AR, which
b. AR has a loud and pure audio tone as the jet
of the following will NOT artificially
is entered
worsen the apparent severity of the AR?
c. The intensity (darkness) of the spectral
a. Congestive heart failure
Doppler signal is proportional to the sever-
b. Restrictive physiology
ity of the leak
c. Diastolic dysfunction
d. Patients with significant AR frequently have
d. Acute myocardial infarction
LVOT systolic velocities greater than 1.5 m/s
e. Acute hemorrhage
e. All of the above
6. Obtaining diastolic aortic flow reversal in
10. All of the following indicate severe AR
a patient with AR with TEE is difficult. The
EXCEPT:
following statements regarding techniques
a. Pressure half-time of less than 500 millisec-
are true EXCEPT:
onds
a. The upper esophageal aortic arch long-axis
b. Ratio of height of the AR jet in the LVOT to
view is useful
the diameter of the LVOT above 65%
b. Obtaining accurate flow velocities is essen-
c. Ratio of area of AR jet in LVOT to area of
tial
LVOT above 60%
c. Holodiastolic flow in the distal aorta indi-
d. Diastolic flow reversal in the descending
cates severe AR
aorta

For the following questions match each question 16. The superior insertion point of the
with the appropriate item(s) from the following commissures of the aortic leaflets is
choices: approximately at:
a. Midesophageal long-axis view a. The level of the sinotubular junction
b. Midesophageal short-axis view b. The level of the aortic annulus
c. Transgastric long-axis view c. The sinuses of Valsalva
d. Deep transgastric view d. The level of the takeoff of the right and left
coronary arteries
11. The mechanism and etiology of aortic
insufficiency is best assessed by which 17. Which of the following Type(s) of aortic
view(s)? regurgitation are most likely to require
aortic valve replacement?
12. The most clinically accurate assessment of
a. Type I
the severity of aortic regurgitation by color
b. Type II
Doppler utilizes which view(s)?
c. Type III
13. The optimal alignment for determining d. All of the above
the rate of decline of the diastolic gradient
18. The peripheral blood pressure in a patient
across the aortic valve utilizes which
with aortic regurgitation is 175/75 mm
view(s)?
Hg. The peak velocity at the onset of an
14. The least accurate color flow Doppler appropriately interrogated regurgitant
view for assessment of the severity of jet is approximately:
regurgitation is which view? a. 2 m/s
b. 3 m/s
15. Three-dimensional imaging of an eccentric c. 4 m/s
jet in the LV outflow tract: d. 5 m/s
a. May allow alignment with the vena con-
tracta in three planes, increasing accuracy 19. Following aortic valve repair for
of its measurement regurgitation, the following risk factors
b. Is readily obtained in all patients because of predict a high recurrence rate for
the large number of elements available in a significant AR EXCEPT:
3D TEE probe (approximately 3,000) a. High level of coaptation relative to the
c. May be difficult to obtain because of the annulus
relative depth of aortic valve from the probe b. Coaptation length <4 mm
tip c. Restrictive leaflet motion
d. Is not effected by aortic valve calcification d. Residual AR postrepair
e. All of the above
20. 3D TEE for AR is most useful for
f. a and c
calculation of the following:
g. b and d
a. Regurgitant volume
b. Effective regurgitant orifice area
c. Vena contracta
d. Not useful secondary to anterior location of
AV

12 Aortic Stenosis
Ira S. Cohen
INTRODUCTION
With the exception of coronary artery bypass grafting procedures, aortic valve replacement (AVR) for critical
aortic stenosis (AS) is the most common indication for cardiac surgery in patients past the age of 65 years.
The newly approved transcutaneous aortic valve replacement (TAVR) by either transfemoral or a combined
surgical catheter–based technique, assisted by three-dimensional (3D) transesophageal echocardiography,
will increase the number of patients who are candidates for valve replacement. The overwhelming majority
of patients in this age group have atherosclerotic degenerative changes of a tricuspid valve as their patho-
physiologic substrate. In contrast, most patients undergoing AVR for AS in the 35- to 55-year-old age groups
have a bicuspid aortic valve (AV), which typically calcifies early and may be associated with dilation of the
ascending aorta. AV involvement by rheumatic disease occurs much less frequently than in the preantibiotic
era, typically causes commissural fusion, and is almost invariably associated with mitral valve (MV) disease.
In general, critical AS is diagnosed preoperatively. Symptoms of hemodynamically significant AS indi-
cating a clinical need for AVR are congestive heart failure (often starting as exertional dyspnea), syncope,
and angina. Provided other potential causes of these symptoms have been excluded, their presence is of
paramount clinical significance because failure to operate at the onset of symptoms is associated with a
poor prognosis. This is so even if the estimated valve areas are less than “critical.” Calculated AV areas are
estimates based on assumptions that apply hydraulic principles to a physiologic system and on gradient
measurements dependent, to an important degree, on the cardiac output (CO) at the time of measurement.
The rate of progression of stenosis can be fairly rapid and tends to be linear for a given individual, but
it is not predictable based on the initial echocardiographic findings (1,2). The issue of whether to replace a
noncritically stenotic valve prophylactically during other cardiac surgery is increasingly important. Current
clinical guidelines support AVR at the time of primary coronary artery bypass surgery in patients with at
least moderate AS, even if asymptomatic, in view of the generally progressive nature of this disorder (3).
Accordingly, the intraoperative echocardiographer must be adept with the techniques used to assess the
severity of AS (Table 12.1).
PATHOPHYSIOLOGY
AS presents a slowly progressive increase in afterload on the ventricle developing over the course of years
as the degree of stenosis progresses. The resulting increase in wall stress (force/unit area) induces a vari-
able degree of a concentric hypertrophic response that tends to normalize wall stress. Ultimately this
TABLE 12.1 Grading Severity of Aortic Stenosis
Aortic sclerosis Mild Moderate Severe

Aortic jet velocity (m/s) ≤2.5 m/s 2.6–2.9 3–4 >4
Mean gradient (mm Hg) — <20 20–40 >40
AVA (cm2) — >1.5 1–1.5 <1
Indexed AVA (cm2/m2) — >0.85 0.60–0.85 <0.6
Velocity ratio — >0.50 0.25–0.50 <0.25
recommendations for clinical practice. J Am Soc Echocardiogr. 2009;22:1–23.
240

12. Aortic Stenosis 241
compensatory mechanism fails and typical symptoms develop. The hypertrophied chamber becomes less
compliant because of both the stiffness of hypertrophied muscle and concomitant collagen deposition. This
results in diastolic dysfunction and increasing preload dependence of the ventricle. Atrial contraction (the
“a” kick) can increase from the normal of 3 to 4 mm Hg to levels as high as 30 to 40 mm Hg to stretch the
hypertrophied ventricle before each contraction. Loss of atrial contraction by the development of atrial fibril-
lation can result in the development of acute pulmonary edema. The need for a relatively high preload (filling
pressures) in these noncompliant ventricles is an important key to effective postoperative management.
AS can cause angina in the absence of significant epicardial coronary artery disease. Prevailing theory
as to the mechanism of this has been that the tissue turgor of the hypertrophic wall compromises coronary
flow reserve by restricting the dilatory capacity of penetrating coronary vessels. Recent data have shown
that AV pressure gradients, left ventricular (LV) mass, female sex, LV filling pressure (septal E/e΄), and
myocardial fibrosis have univariate association with reduced myocardial perfusion reserve. Of these, LV
mass index (a determinant of O2 demand) and late gadolinium enhancement on MRI (a marker of fibro-
sis) appear to be the most important (4). Cardiac catheterization is therefore required to exclude critical
coronary artery disease (which coexists in approximately 50% of cases) in patients both with and without
angina as silent coronary disease is potentiated by the physical limitation on activity caused by the steno-
sis. Syncope is a consequence of the inability to increase CO in response to the peripheral vasodilation
associated with exercise, to arrhythmia, or to acute heart failure. Pulmonary congestion results from the
increasingly high preload (left atrial pressure) required for adequate function in a noncompliant ventricle
with diastolic dysfunction and the shortening of the diastolic filling period by exercise-induced tachycardia.
ECHOCARDIOGRAPHIC EVALUATION OF THE AORTIC VALVE

The AV can be evaluated by M-mode, two-dimensional (2D), Doppler, and 3D echocardiographic tech-
niques. The primary approaches utilize 2D imaging and both pulsed wave Doppler (PWD) and continu-
ous wave Doppler (CWD) to assess valve morphology and severity of disease. TEE 2D echocardiographic
imaging of the AV is generally superior to TTE imaging because of the improved resolution of the higher
frequency TEE probe. Three-dimensional imaging shares the limits inherent to all ultrasound techniques
determined by the interrelation of sector size, frame rate, and depth on image resolution. In some patients
the AV may be better visualized from the 3D TTE approach rather than 3D TEE because the valve is a more
anterior structure. The reduced temporal resolution of 3D imaging frequently results in dropout of the thin
leaflets of a normal AV (Videos 12.1, 12.2). With the thickening and calcification of the leaflets seen with Video 12.1
the development of valvular stenosis, 3D imaging is often better but may also be impaired by the associ- Video 12.2
ated acoustic shadowing. Preliminary data suggest that optimal images in 3D are obtained in a minority
of patients, but when obtainable add valuable additional information. Both types of TEE imaging are best
obtained from the ME SAX and LAX views. The ultimate role of 3D TEE in the assessment of AS remains
under investigation but reference is made to preliminary observations in the following discussions. Guide-
lines for the approach to the assessment of AS have recently been published (5). The following discussion
follows the recommended priority of methods for evaluation outlined therein.
Quantitative Doppler Assessment of Aortic Stenosis

The severity of AS is assessed quantitatively with Doppler echocardiography in two ways: Measuring the
gradient across the valve with the modified Bernoulli equation and estimating the AV area with the conti-
nuity equation. Both techniques require that the ultrasound beam be as parallel to the transvalvular blood
flow as possible.
Transesophageal Echocardiographic Doppler Views for Assessing Aortic Stenosis

In AS, aligning the TEE transducer parallel to the left ventricular outflow tract (LVOT) and AV can be
challenging. The deep transgastric (TG) and TG LAX views are commonly used depending on which one
offers the optimal window for interrogation parallel to the stenotic jet. Advancing the probe from a TG
short-axis view with continued anteflexion may allow acquisition of the deep TG long-axis view from near

the LV apex. Occasionally, counterclockwise rotation of the probe and varying the angle of interrogation
over a wide range may facilitate this. The TG long-axis view is obtained with the probe at the midpapillary
level or slightly above and the imaging plane angle of interrogation increased to 120 to 140 degrees where
the LVOT, AV, and ascending aorta come into view. Both techniques offer an excellent approach to AV
flow dynamics; however, the patient’s anatomy will dictate which view provides the best interrogation of
transvalvular blood flow. For this reason it is advised that both views be sought out and the highest veloci-
ties obtained are used in calculations of AS. In a small minority of individuals, the ME LAX view (at 120
degrees) allows the best alignment to the transaortic flow.
A note of caution is necessary in a discussion of Doppler imaging and the angle of incidence. Some
echocardiographic systems provide a means to correct the angle of interrogation visually by multiplying
the Doppler shift velocity by the cosine of the incident angle of the beam to the aortic flow as manually
input by the echocardiographer. It is generally accepted that this is not a reliable method since the interac-
tion of beam and blood flow occurs in three dimensions and 2D imaging is unable to provide the true angle of
incidence to the jet accurately. With turbulent jets, as in AS, judging the alignment with flow is particularly
difficult. Such jets may be very eccentrically directed to the 2D plane visualized, so that apparent “correc-
tion” by looking at a color flow map of the jet can be very imprecise. Obtaining the highest velocity smooth
envelope is a better way to confirm accuracy. Feathered velocities at the tip of the velocity envelope are
artifactual and should not be included in the analysis. Orientation by sound of the Doppler signal to the
purest tone also may help in defining the optimal orientation of the interrogating beam in parallel to flow.
Ideally the beam should align to within 0 to 15 degrees of the actual jet.
Doppler Determination of the Aortic Valve Gradient: The Modified Bernoulli Equation
The modified Bernoulli equation is used to calculate transaortic valve pressure gradients (Table 12.2). The
modified Bernoulli equation states that the maximal pressure gradient equals four times the square of the
peak jet velocity and allows calculation of the peak instantaneous gradient across any orifice. Thus, if the
peak blood flow velocity across the AV is 4 m/s, the calculated peak gradient = 4 × 42 = 64 mm Hg. The mean
gradient is calculated by averaging the instantaneous gradients over time. This function is accomplished by
tracing the aortic flow velocity profile and using the analysis program of the ultrasound machine (Fig. 12.1).
The mean velocity cannot be used to estimate the mean gradient in the Bernoulli equation. Averaged
instantaneous gradients must be averaged (by the trace function). A less accurate alternative mean gradient
can be calculated from the peak velocity as 2.4(Vmax)2. The mean gradient, in particular, correlates well with
invasively determined gradients and is most often used in evaluating the severity of AS. It is imperative that
a true peak velocity be obtained for this estimate to be valid. A well-defined velocity curve with a smooth
envelope is generally a valid one.
The peak gradient can be influenced by the flow volume on the ventricular side of the valve plane.
Remember that the simplified Bernoulli equation ignores the impact of the LVOT blood flow velocity.
However, the Bernoulli equation must factor in the LVOT blood flow velocity when it exceeds 1.5 m/s, as
commonly occurs in associated aortic insufficiency and other high output states, to avoid overestimation of
the pressure gradient (Table 12.2). For example, if the outflow tract velocity is 1.7 m/s and the peak trans-
valvular velocity is 4 m/s, the actual gradient is 4 × (42 − 1.72) = 4 × (16 − 2.89) = 52.4 mm Hg, instead of the
64 mm Hg predicted by the simplified Bernoulli equation.
TABLE 12.2 Equations for Aortic Transvalvular Gradients
Peak gradient (simplified Bernoulli equation)

Peak gradient (mm Hg) = 4(aortic peak velocity)2
Mean gradient
Mean gradien (estimate) = 2.4(Vmax)2
Peak gradient with significant aortic regurgitation (modified Bernoulli equation)
Gradient = 4 ([peak aortic velocity)2 – [LVOT velocity]2)
LVOT, left ventricular outflow tract.

FIGURE 12.1 Deep transgastric view with parallel continuous wave Doppler beam alignment in a patient with severe
aortic stenosis. Aortic stenosis tracing is labeled 2 (outer envelope), with a maximal aortic valve velocity of 4.95 m/s and a
Bernoulli equation–derived peak aortic valve gradient of 97.9 mm Hg. Aortic valve time–velocity integral (TVI) is 141.1 cm.
Tracing 1 is of the left ventricular outflow tract (LVOT) velocity. LVOT maximal velocity is 1.19 m/s and LVOT TVI is 33.1 cm.
Discrepancies often occur between catheterization and echocardiographic pressure gradients in AS.
The peak echocardiographic gradient measures the peak instantaneous gradient between the LV and aorta.
This is generally higher than the peak-to-peak gradient (between the peak LV pressure and the generally
later peak aortic pressure) routinely entered on cardiac catheterization reports (Fig. 12.2). In addition, the
phenomenon of pressure recovery (PR), the recovery of pressure energy from the kinetic energy of accel-
eration through the narrowed orifice that occurs distal to the stenotic valve, can cause an elevation in the
200
Peak-to-peak
gradient Mean
Maximum
gradient
Pressure (mm Hg)
gradient
100
Ao
LV
0
Time (s)
FIGURE 12.2 Example of left ventricular (LV) and aortic (Ao) pressures measured with fluid-filled catheters in a patient
with severe aortic stenosis. The maximal instantaneous gradient is greater than the peak-to-peak gradient. The shaded
area indicates the mean gradient. (From Otto CM. Textbook of Clinical Echocardiography. 2nd ed. Philadelphia, PA: WB
Saunders; 2000:238, with permission.)

FIGURE 12.3 Demonstrates the concept of parallel Doppler beam alignment and the concept of “what goes in has to
come out.” Hence LVOTVTI × LVOTCSA = ASVTI × Aorta Valve Area (AVA).
estimated transvalvular gradient by Doppler as compared to measurements by catheterization. In general

this only becomes a factor in patients with small aortas (sinotubular junction ≤3 cm). (See below.)
Hemodynamically significant AS is generally associated with a mean gradient of 40 mm Hg or more
or a maximal velocity of 4 m/s or more (Table 12.1). The exception is in patients with a low ejection frac-
tion who may not be able to generate a high gradient. In these patients, peak gradients as low as 20 to
30 mm Hg may be associated with critical stenosis, and the continuity equation and planimetry as well as
a dobutamine challenge should be considered to further evaluate the significance of AS. Systemic hyper-
tension during the assessment also impacts both on the apparent gradient and the left ventricular ejection
fraction (LVEF) and must also be considered in evaluating the validity of the assessment of the gradient.
(See below.)
Doppler Estimation of the Aortic Valve Area: The Continuity Equation (Fig. 12.3)
The continuity equation states that the volume of blood that enters the stenotic aortic orifice is equal to
the volume of blood that exits it. If we can calculate the volume of flow entering a stenotic AV through the
LVOT and measure the velocity at which it exits the stenotic valve, then the equation can be rearranged to
solve for the area of the stenotic valve (Table 12.3). The valve area derived from the equation is the effective
area, as opposed to the anatomic area derived from planimetry of the valve. The effective area has been
TABLE 12.3 Calculation of Aortic Valve Area with the Continuity Equation
Continuity equation (“What goes in must come out.”)

LVOT stroke volume = AV stroke volume
Stroke volume = CSA × TVI
Therefore,
TVILVOT × AreaLVOT = TVIAV × AreaAV
TVILVOT × AreaLVOT
AreaAV =
TVIAV
Aortic valve area
LVOT velocity (m/s, maximal)
LVOT diameter (cm, inner to inner, midsystole)
LVOT area (cm2) = πr 2
AV area (cm2, continuity equation)
LVOT, left ventricular outflow tract; AV, aortic valve; CSA, cross-sectional area; TVI, time–velocity integral.

FIGURE 12.4 A: Midesophageal aortic valve short-axis view of a normal aortic valve with a planimetric area of 3.06 cm2.
B: Two-dimensional M-mode (motion mode) midesophageal aortic valve long-axis view demonstrating cusp separation
of 18 mm in the same patient.
clinically validated even though it is slightly smaller than the anatomic area as the primary predictor of
clinical outcome (5). The area of the normal AV is between 3 and 4 cm2 (Fig. 12.4, Videos 12.3, 12.4). Guide- Video 12.3
lines viewing the disease as a continuum based on hemodynamic and natural history data, define severe AS Video 12.4
as a valve area <1 cm2, and a mean gradient >40 mm Hg or peak jet velocity >4 m/s (3) (Table 12.1).
One first calculates the cross-sectional area of the LVOT. In the ME AV LAX view, the LVOT annular
diameter, an initial estimate, is obtained by measuring the inner dimension (endocardium to endocardium)
of the LVOT at the insertion point of the AV leaflets in midsystole with the electronic calipers (Fig. 12.5B).
However, measurement of the outflow tract ideally should be where the optimal outflow tract velocity
profile is obtained in the apical view (see below). This is generally either at, or within a centimeter of, the
aortic leaflet insertions into the valve annulus. The diameter of the LVOT is generally 2 ± 0.2 cm and var-
ies somewhat in proportion to body size. Inaccuracies in measurement of the outflow tract can account
for much of the error in this technique because the radius is squared in the continuity equation. The most
common discrepancies occur during the imaging of elderly women, who often have a smaller outflow tract
(and body surface area) than average, and large men, who often have a larger outflow tract (and body sur-
face area). If we assume that the LVOT is a circle, one calculates its area as πr 2 (or π[D/2]2). Observations
in small numbers of patients assessing the size of the LVOT by CT angiography and TTE 3D echo (6–8),
show that it is often not circular but ovoid and that its true size is best determined by planimetry using

FIGURE 12.5 A: Midesophageal aortic valve short-axis view demonstrating aortic stenosis and a tricuspid aortic valve
with heavy calcification. Aortic valve area by planimetry is 0.65 cm2. B: Midesophageal aortic valve long-axis view in mid-
systole with measurement of the left ventricular outflow tract (LVOT) diameter (1.94 cm). The diameter is measured from
the inner surfaces (endocardium to endocardium) of the LVOT at the insertion points of the aortic cusps. The continuity
equation–derived aortic valve area is 0.70 cm2. Continuous wave Doppler values are from Figure 12.1.
these techniques. Using the assumption it is round by 2D echo can result in up to a 15% underestimation
of LVOT area. The more accurate measurement is important when sizing percutaneous transvalvular aortic
prostheses as undersizing often causes paraprosthetic aortic regurgitation. However, the circular assump-
tion has held up well for clinical assessment of severity and the need for more accurate measurement will
require additional corroboration.
Secondly, the LVOT time–velocity integral (TVI) is then determined by either of the two methods. PWD
can be used, with the sample volume just proximal to the AV cusps within the LVOT (Fig. 12.6). The sample
volume is gradually moved toward the AV until a smooth LVOT velocity profile is obtained at the level of
the outflow tract where the annular dimension was obtained. If this is slightly below the aortic leaflet inser-
tion point, the LVOT dimension should be remeasured at the same place. The internal calculation package
available on all echocardiographic machines traces the LVOT velocity, allowing calculation of the LVOT
TVI. PWD is essential for this flow measurement because it must be made at the precise level at which
the outflow tract was measured due to the acceleration of blood flow from LV into the stenotic AV orifice.
A second alternative method, which is less well validated, uses CWD interrogation through the AV. If the
alignment is correct, a more intense lower velocity inner envelope representing the lower velocity LVOT
flow is imaged within the higher velocity aortic jet envelope and can be traced as previously described to

FIGURE 12.6 Deep transgastric view of the aortic valve with pulsed wave Doppler assessment of the left ventricular
outflow tract (LVOT) flow velocity. The LVOT time–velocity integral is assessed to be 39.1 cm. Note correlation with inner
envelope technique valve area of 33.1 cm (same patient as in Fig. 12.1).
calculate the LVOT TVI (Fig. 12.1). However, this envelope peak can be erroneously high because the sub-
aortic jet accelerates into the stenotic orifice to form a proximal isovelocity surface area as it narrows to fit
into the orifice (see MR Chapter 8). This can raise the apparent peak velocity to a level higher that it would
be at the annular level and result in an overestimation of the valve area. The “double envelope” configura-
tion defines proper alignment with the jet and facilitates PWD confirmation of the velocity at the annular
level. As such, it may help to identify an optimal window for interrogation of the actual LVOT velocity with
PWD.
Finally, the AV TVI is traced from the larger envelope of the CWD profile (Fig. 12.1) obtained in the
deep TG and/or TG LAX views, depending on which is optimal. These measurements require that the
Doppler probe be as close to parallel as possible to the direction of flow. The resulting values for the LVOT
diameter, LVOT TVI, and AV TVI are entered into the continuity equation to solve for the AV area. Some
clinicians use the peak velocity instead of the TVI in these analyses, although the TVI should correlate bet-
ter from a theoretic standpoint.
Planimetry of the Aortic Orifice

Early echocardiographers looked at the characteristics of aortic leaflet motion in an attempt to determine
the severity of aortic obstruction. Separation of the aortic leaflets by less than 8 mm in a 2D long-axis
view suggested critical disease, whereas separation by more than 12 mm suggested noncritical disease (9)
(Fig. 12.4). In addition, fluttering of an aortic leaflet on M-mode echocardiography was felt to be better
than 2D separation as a discriminator of noncritical disease (10). These findings have been superseded
by later techniques.
Two-dimensional echocardiography in the ME AV SAX view, at an approximate angle of 45 to 60 degrees,
images the short-axis plane of the AV and allows planimetry of the AV orifice. Accurate planimetry requires
that the imaging plane and machine settings be optimized to identify the minimal total orifice as follows:
1. Obtain a short-axis view of the AV with all three leaflets in view.
2. Use color flow Doppler imaging (with minimal color gain) to aid in adjusting the probe depth and angle
of the imaging plane so as to interrogate the narrowest orifice and to localize the edges of the orifice.
3. Optimize the 2D image by adjusting the gain settings to the minimum showing an entire orifice. Excessive
gain leads to an underestimation of valve area because of a “blooming artifact” from the bright echoes
of the thickened valve leaflets. Acoustic shadowing caused by bright echoes from valve calcification can
also make determination of the orifice problematic. Slight changes in angulation, gain, and in the depth
of the probe may be necessary for optimization.

FIGURE 12.7 Using dedicated software, orthogonal views can be visualized and aligned to allow planimetry of the
valve orifice at its smallest dimension regardless of its orientation relative to the aortic long axis.
4. Use the electronic tracing caliper of the ultrasound machine to trace the orifice and so obtain its area
(Figs. 12.4 and 12.5A).
Although successful measurement by TTE, planimetry has been reported, TEE, with its superior reso-
lution, has been more effective in making this measurement accurately (11–13). Although changes in CO
can cause discrepancy of Doppler and invasive valve area estimates (14), it should not cause changes in
a planimetered area, so that the technique should be as good in patients with a low or normal CO, and
it has been suggested to be more accurate than the Gorlin equation in patients with either low or high
output (15).
All planimetric techniques are limited by an inability to determine whether the actual minimal orifice
is being imaged or whether the plane chosen for measurement is either below or at an angle to the true
minimal orifice. Although errors are minimized using the above techniques, when adequate images can be
obtained, 3D imaging allows determination of angulation of the true orifice to the long axis of the aorta
and permits a more accurate alignment of the plane of the orifice to be measured. The optimal 3D view is
the short axis of the valve in cross section using real time, full volume, and the zoom mode of acquisition
from the ME AV SAX and LAX views (16). Using dedicated software, orthogonal views can be visualized
and aligned to allow planimetry of the valve orifice at its smallest dimension regardless of its orientation
relative to the aortic long axis (Fig. 12.7).
The accuracy of planimetry has been assessed by comparing it with the “gold standard” reference tech-
nique used in the catheterization laboratory to calculate AV area, the Gorlin equation:
cardiac output
AVA =
44.3(SEP)(HR) mean gradient
where 44.3 is an empiric correction factor. The systolic ejection period (SEP) is factored in because we are
assessing flow through the valve only in systole. Initial studies using 3D TTE compared to the continuity
equation and 3D TEE compared to the Gorlin equation suggest 3D to be more accurate and reproducible
than 2D TEE planimetry (17–19). TEE is not as accurate in the presence of significant valvular calcifica-
tion (which is generally present), and not all observers have reported uniformly good correlations of TEE
planimetric valve areas with Gorlin formula valve areas (20,21). Although 3D may ultimately prove to be
more definitive, the results of 2D imaging and Doppler assessment remain the current basis for the standard
assessment of the severity of AS.

TECHNICAL CONSIDERATIONS
AS is a technically challenging valvular lesion to assess by Doppler TTE, and the limitations imposed by the
angle of incidence of the Doppler beam in TEE are even more of a challenge. Often, the orientation of the
jet is such that the transducer cannot be positioned such that the beam is aligned parallel to the jet. Accep-
tance of an inadequate jet as representative of the true jet is a significant source of error in underestimating
the severity of stenosis. Unless a clearly defined velocity envelope can be seen, no quantitative estimate of
severity should be made.
The jet of mitral insufficiency can easily be mistaken for that of AS. Both jets have several features in
common: They are negative, high velocity jets when interrogated from the TG and lower esophageal win-
dows, tend to peak in midsystole, and may lie in the same path of interrogation because the Doppler beam
often traverses both the anterior left atrium and the adjacent posterior aortic root. In the latter situation,
anteriorly oriented mitral regurgitant (MR) jets and stenotic aortic jets can be interrogated. It is impor-
tant to document visually that an MR jet is not traversed using color Doppler imaging. In cases in which
this is difficult, it is useful to look at the time of onset of an MR jet during PWD recording to determine
the relationship of the onset of flow velocity to the electrocardiographic QRS complex for reference. MR
jets start early (during isovolumic systole) because the LV pressure exceeds the LA pressure (normal, 0 to
12 mm Hg) almost as soon as LV contraction begins. AS jets start later in systole because flow begins when
the LV pressure exceeds the central aortic diastolic pressure (60 to 90 mm Hg). This is generally in the mid
or latter portion of the QRS complex. This determination is facilitated by recording the jets at a faster sweep
speed (100 mm/s). It may be helpful to look at the AV morphology to assess whether significant obstruction
is suggested by the mobility of the valve on 2D imaging. It should be borne in mind, however, that in a low
output state, AV motion may be decreased by reduced CO rather than by significant stenosis.
SPECIAL CONSIDERATIONS
Pressure Recovery
Convergence of flow through the stenotic AV to the vena contracta (the convergence point of flow imme-
diately distal to the stenotic orifice) converts potential (pressure) energy into kinetic energy with a result-
ing reduction in pressure at the vena contracta. Divergence of flow distally allows reconversion of some
kinetic energy to potential (pressure) energy with recovery of a proportion of the pressure lost within a few
centimeters (Fig. 12.8). Since Doppler-based methods detect the peak velocity at the vena contracta, the
transvalvular gradient estimated by Doppler will be greater than that calculated from simultaneous inva-
sive pressure measurements between the LVOT and the aortic root. Therefore, Doppler pressure gradient
estimates are higher and estimated valve areas smaller than catheter measurements (5) (Fig. 12.2).
PR is predominantly a factor in patients with small ascending aortas (≤3 cm in diameter) and there-
fore of greatest clinical relevance in small individuals and children. The relationship between the AV area
obtained by the continuity equation (AVAce) and the cross-sectional area of the ascending aorta (Aa) mea-
sured at the sinotubular junction (Aa = πr2, where r = half the diameter of the aorta at the sinotubular
junction) is given by the following equations (22–24):
Pressure Recovery (mm Hg) = 4V2 × (2AVA/Aa)[1 – AVA/Aa]
PR Corrected AVA = AVAce × Aa/(Aa – AVAce)
Consideration should be given to applying this correction in cases where the clinical and valvular mor-
phologic findings do not appear to be consistent with the echo-derived assessment, particularly in the
presence of a small ascending aorta.
Systemic Hypertension and Arterial Compliance

Systemic blood pressure and arterial compliance are significant factors in the load against which the left
ventricle must work, despite the interposition of a stenosed valve, with an increase in systemic pressure or
reduced arterial compliance causing a lowering of the gradient and of ejection fraction. Since significant

FIGURE 12.8 Concept of pressure recovery: The convergence of flow through the stenotic aortic valve to the vena
contracta converts potential (pressure) energy into kinetic energy with a resulting reduction in pressure at the vena con-
tracta. Divergence of flow distally allows reconversion of some kinetic energy to potential (pressure) energy with recovery
of a proportion of the pressure lost within a few centimeters. PLV = pressure in the left ventricular; PGmax = maximum pres-
sure gradient; LV = left ventricular; VC = vena contracta; Ao = aortic root; PVC = pressure at the vena contracta; PGnet = net
change in pressure gradient; PAo = pressure in the aorta.
elevations in systolic blood pressure will cause an apparent decrement in estimated gradients, systolic
blood pressure should always be recorded and factored into the analysis of the patient data, particularly in
serial comparisons (25,26).
Assessment in the Presence of Low Gradient, Low Stroke Volume Critical AS

As previously noted, the gradient across a stenosis varies with the flow across the stenosis. The gradient will
increase during exercise or in a hyperadrenergic state (e.g., in the operating room) because it is directly pro-
portional to the CO, but the valve area remains constant. This relationship is reflected in the Gorlin formula
used to calculate valve areas, in which the CO is in the numerator and the gradient is in the denominator.
In patients with a normal CO, significant and possibly critical stenosis usually results in a peak pressure
gradient of >64 mm Hg and often significantly higher.
In patients with a low CO, a peak gradient in potentially critical stenosis may be in the range of 20 to 30 mm Hg.
Gradients this low with a normal CO are generally minor and not hemodynamically important. Therefore,
the CO is an important determinant of the significance of a given valve gradient. Accordingly, an echocar-
diographic assessment of LV function should routinely be performed before “small” gradients are reported as
insignificant. With reduced ejection fraction and a low CO, gradients can be quite low despite critical disease.
Recently a new cohort of patients has been described with normal ejection fractions and both low
stroke volumes (<35 cc/M2) and transvalvular gradients but critically stenosed valve areas. Clinical
correlates include an increased incidence of female patients, often with a moderate-to-severe degree of
concentric left ventricular hypertrophy (LVH) and small LV cavities. Analysis of global LV strain, a subtle
indicator of global LV function in these patients, shows it generally to be reduced, suggesting that despite
a normal LVEF these ventricles are compromised. The course of these patients if unoperated, appears to
progress in a manner similar to those with moderate-to-severe valve disease. It has been recently proposed
that subclassification of patients to include the incorporation of outflow parameters (< or >35 cc/M2) and

ejection fraction may better characterize the population at risk. The subject will likely be further addressed
in upcoming revisions of clinical management guidelines (27–31).
Because of the limitations of pressure gradients in assessing AS in patients with suspected intrinsic
heart disease, valve area estimates by the continuity equation and the dimensionless index (see following)
are relied upon. In addition, assessment of whether these patients have a low ejection fraction due to intrin-
sic heart disease or critical AS can be determined using dobutamine stress echocardiography.
Dimensionless Index
In patients with a decreased LVEF, in addition to calculation of estimated AV area, the echocardiographer
can use the LVOTTVI/AV TVI ratio or LVOTPV/AVPV ratio to assess the degree of AS. This approach is a modi-
fication of the continuity equation (Table 12.3) but eliminates the aortic root area (AreaLVOT), which is a
common source of (squared) measurement error, to provide a dimensionless index (32). The aortic root area
is essentially a constant and therefore can be eliminated from the equation to provide this alternative index
of severity. A ratio of ≤0.25 denotes critical disease. This approach is also helpful in determining whether
an erroneous measurement of the aortic annular dimension may have resulted in an estimated AV area that
seems disproportionately high or low to the measured gradient across the valve. It is also a useful index for
following patients with prosthetic AVs where measurement of an aortic annular dimension is often difficult.
Dobutamine Stress Testing

The fact that patients with poor LV function may be unable to mount a significant gradient has led to the
use of dobutamine stress testing to determine whether a low gradient is caused by intrinsic myocardial
disease or valvular disease. A low dose of dobutamine (usually starting at 2.5 to 5 μg/kg/min increasing by
2.5 to 5 μg/kg/min increments every 3–5 minutes) is infused intravenously to increase the CO while the
relevant Doppler parameters are monitored. An end point of 10–20 beats per minute, an increase in resting
heart rate to 100 beats per minute or an increase in resting cardiac output by 20% or more is required. An
increase in CO and in valve gradient with a constant valve area suggests severe valvular disease. An increase
in valve area with increase in CO suggests primary myocardial disease as an issue and would contraindicate
valve replacement as sole definitive therapy. In general, but not invariably, the surgical outcome of these
patients may be poorer than that of patients with high gradients and normal baseline function. However,
AS is unique in being one of the few cardiovascular conditions where patients with a low ejection fraction
preoperatively may normalize after valve replacement (5).
Assessment of Aortic Stenosis Gradient in Aortic Regurgitation

As a result of the leak in aortic insufficiency, the volume of blood that must be ejected from the ventricle dur-
ing systole increases. The reason is that the forward stroke volume now equals the volume of blood return-
ing from the lungs plus the volume leaking back from the aorta. The latter can exceed 50% of the forward
stroke volume. This increased volume must be ejected through the LVOT, which has only a limited ability
to dilate to accommodate it. Therefore, velocity in the LVOT increases because the area is relatively stenotic
for the volume of blood traversing it. The increased velocity in the outflow tract is further exaggerated in
the aorta by the acceleration resulting from the narrowing caused by the valvular stenosis. The full modified
Bernoulli equation must be used to calculate the true valve gradient accurately when the LVOT flow velocity
is 1.5 m/s or more, whether from aortic regurgitation or from another hyperdynamic state (Table 12.3). The
outflow tract velocity should be sampled using PWD at the level at which the LVOT diameter was measured.
Pre- and Postoperative Subaortic Obstruction

The anterior MV leaflet and the intraventricular septum are relatively close to each other. In a small percent-
age of patients in whom the septum is hypertrophic as an adaptive response to AS, the septum bulges into
the outflow tract and may appear to underlie most of the right coronary cusp in the ME LAX view (mirrored
in the parasternal long-axis TTE view preoperatively). The so-called sigmoid septum, seen in some older
patients with or without hypertrophy, has a similar appearance. This situation is frequently encountered
in elderly hypertensive women who have marked LVH and, frequently, small left ventricular cavities with

significant mitral annular calcification (33). Occasionally, systolic anterior motion (SAM) of the MV with
true subaortic stenosis physiology is present. Replacement of the AV, with the resultant decrease in afterload
on the ventricle, may then cause SAM to develop or worsen, resulting in new or worsening subaortic stenosis.
Valvular AS can also coexist with true idiopathic hypertrophic subaortic stenosis and SAM of the MV
(34). In this situation, the accelerated velocity due to the subaortic stenosis can extend into the LVOT and
makes it impossible to calculate the transvalvular gradient. In this situation the best approach to estimating
the severity of the valvular stenosis is by planimetry of the short-axis view of the aortic orifice. AVR may
bring the anterior mitral leaflet closer to the septum, and SAM may develop or worsen, causing a secondary
subaortic stenosis physiologically identical to that of idiopathic hypertrophic subaortic stenosis. The classic
finding is the so-called dagger-shaped (or late peaking) jet seen in dynamic subaortic obstruction, caused
by an increase in the gradient late in systole as the MV moves closer to the septum when the ventricle
becomes smaller (Fig. 12.9). A similar phenomenon can occur with redundant, elongated mitral leaflets
FIGURE 12.9 A: Midesophageal long-axis view demonstrating profound asymmetric septal hypertrophy involving the
left ventricular outflow tract (LVOT). Note the acute narrowing of the LVOT at the proximal border of the area of septal
hypertrophy. B: High pulse repetition frequency Doppler demonstrating the classic “dagger” flow velocity pattern of
dynamic outflow obstruction.

after a “floppy” MV is repaired (8,35). Occasionally, postoperative intracavitary gradients or midcavity

obliteration occurs with the decrease in afterload after valve replacement in ventricles that are markedly
hypertrophic in response to the stenotic valve.
The result of all of these phenomena is that weaning from bypass may be impossible unless the subval-
vular obstruction is recognized as a cause of postoperative hypotension. In this situation, interrogation
of the LVOT in the long-axis view demonstrates SAM of the MV. Color flow Doppler shows the mosaic
appearance of high velocity aliasing flow caused by the resultant gradient across the LVOT (or within the
cavity at an area of intracavitary narrowing) and often concomitant mitral regurgitation. Interrogation
by CWD demonstrates a high velocity proportional to the gradient caused by the obstruction that can be
quantified with the modified Bernoulli equation. The treatment for the resultant hypotension is counterin-
tuitive; the patient requires volume loading to increase the LV volume and the negative inotropic effect of
beta-blocker therapy to decrease contractility and prolong the diastolic filling period by slowing the heart.
On rare occasions, the obstruction may be intractable, and septal myomectomy or MV replacement with a
low profile prosthetic valve is required.
SUMMARY
Assessment of the stenotic AV remains a challenge. Echocardiography provided valuable insights into the
rate of progression by permitting serial noninvasive measurements for the first time. As is generally the
case in echocardiography, the application of a variety of techniques allows a more reliable estimate of
the severity of disease, particularly if the results support each other. In clinical practice, however, the inte-
gration of patient data is essential, and a good correlation of the clinical and echocardiographic findings
remains essential. Accordingly, echocardiographers must be thoroughly familiar with the application of all
these techniques for an optimal assessment of AS in the operating room.
REFERENCES
1. Roger VL, Tajik AJ. Progression of aortic stenosis in adults: New insights provided by Doppler echocardiography. J Heart Valve
Dis. 1993;2:114–118.
2. Rosenhek R, Binder T, Porenta G, et al. Predictors of outcome in severe, asymptomatic aortic stenosis. N Engl J Med.
2000;343:611–617.
3. American College of Cardiology/American Heart Association Task Force on Practice Guidelines, Society of Cardiovascular
Anesthesiologists, Society for Cardiovascular Angiography and Interventions, et al. ACC/AHA 2006 guidelines for the manage-
ment of patients with valvular heart disease: A report of the American College of Cardiology/American Heart Association Task
Force on Practice Guidelines (writing committee to revise the 1998 Guidelines for the Management of Patients With Valvular
Heart Disease): Developed in collaboration with the Society of Cardiovascular Anesthesiologists: Endorsed by the Society for
Cardiovascular Angiography and Interventions and the Society of Thoracic Surgeons. Circulation. 2006;114:e84–e231.
4. Vahanian A, Otto CM. Risk stratification of patients with aortic stenosis. Eur Heart J. 2010;31:416–423.
clinical practice. J Am Soc Echocardiogr. 2009;22:1–23.
6. Pibarot P, Dumesnil JG. Paradoxical low-flow, low-gradient aortic stenosis adding new pieces to the puzzle. J Am Coll Cardiol.
2011;58:413–415.
7. Cooper J, Pinheiro L, Fan P, et al. A practical approach to cardiovascular Doppler ultrasound. In: V N, ed. Doppler
Echocardiography. Baltimore, MD: Williams & Wilkins; 1993:59–68.
8. Mihaileanu S, Marino JP, Chauvaud S, et al. Left ventricular outflow obstruction after mitral valve repair (Carpentier’s tech-
nique). Proposed mechanisms of disease. Circulation. 1988;78:I78–I84.
9. Godley RW, Green D, Dillon JC, et al. Reliability of two-dimensional echocardiography in assessing the severity of valvular
aortic stenosis. Chest. 1981;79:657–662.
10. Chin ML, Bernstein RF, Child JS, et al. Aortic valve systolic flutter as a screening test for severe aortic stenosis. Am J Cardiol.
1983;51:981–985.
11. Hoffmann R, Flachskampf FA, Hanrath P. Planimetry of orifice area in aortic stenosis using multiplane transesophageal
echocardiography. J Am Coll Cardiol. 1993;22:529–534.
12. Okura H, Yoshida K, Hozumi T, et al. Planimetry and transthoracic two-dimensional echocardiography in noninvasive assess-
ment of aortic valve area in patients with valvular aortic stenosis. J Am Coll Cardiol. 1997;30:753–759.
13. Stoddard MF, Arce J, Liddell NE, et al. Two-dimensional transesophageal echocardiographic determination of aortic valve area
in adults with aortic stenosis. Am Heart J. 1991;122:1415–1422.
14. Burwash IG, Dickinson A, Teskey RJ, et al. Aortic valve area discrepancy by Gorlin equation and Doppler echocardiography
continuity equation: Relationship to flow in patients with valvular aortic stenosis. Can J Cardiol. 2000;16:985–992.

15. Tardif JC, Miller DS, Pandian NG, et al. Effects of variations in flow on aortic valve area in aortic stenosis based on in vivo
planimetry of aortic valve area by multiplane transesophageal echocardiography. Am J Cardiol. 1995;76:193–198.
echocardiography. J Am Soc Echocardiogr. 2012;25:3–46.
17. Blot-Souletie N, Hebrard A, Acar P, et al. Comparison of accuracy of aortic valve area assessment in aortic stenosis by real time
three-dimensional echocardiography in biplane mode versus two-dimensional transthoracic and transesophageal echocar-
diography. Echocardiography. 2007;24:1065–1072.
18. Goland S, Trento A, Iida K, et al. Assessment of aortic stenosis by three-dimensional echocardiography: An accurate and novel
approach. Heart. 2007;93:801–807.
19. Adda J, Mielot C, Giorgi R, et al. Low-flow, low-gradient severe aortic stenosis despite normal ejection fraction is associ-
ated with severe left ventricular dysfunction as assessed by speckle-tracking echocardiography: A multicenter study. Circ
Cardiovasc Imaging. 2012;5:27–35.
20. Bernard Y, Meneveau N, Vuillemenot A, et al. Planimetry of aortic valve area using multiplane transoesophageal echocardiog-
raphy is not a reliable method for assessing severity of aortic stenosis. Heart. 1997;78:68–73.
21. Awtry EH, Davidoff R. Low-flow low-gradient aortic stenosis: In search of optimal risk stratification. Circ Cardiovasc Imaging.
2012;5:6–8.
22. Baumgartner H, Schima H, Tulzer G, et al. Effect of stenosis geometry on the Doppler-catheter gradient relation in vitro: A
manifestation of pressure recovery. J Am Coll Cardiol. 1993;21:1018–1025.
23. Garcia D, Dumesnil JG, Durand LG, et al. Discrepancies between catheter and Doppler estimates of valve effective orifice
area can be predicted from the pressure recovery phenomenon: Practical implications with regard to quantification of aortic
stenosis severity. J Am Coll Cardiol. 2003;41:435–442.
24. Bahlmann E, Cramariuc D, Gerdts E, et al. Impact of pressure recovery on echocardiographic assessment of asymptomatic
aortic stenosis: A SEAS substudy. JACC Cardiovasc Imaging. 2010;3:555–562.
25. Kadem L, Dumesnil JG, Rieu R, et al. Impact of systemic hypertension on the assessment of aortic stenosis. Heart. 2005;91:354–
361.
26. Pibarot P, Dumesnil JG. New concepts in valvular hemodynamics: Implications for diagnosis and treatment of aortic stenosis.
Can J Cardiol. 2007;23 suppl B:40B–47B.
27. Flachskampf FA, Kavianipour M. Varying hemodynamics and differences in prognosis in patients with asymptomatic severe
aortic stenosis and preserved ejection fraction: A call to review cutoffs and concepts. J Am Coll Cardiol. 2012;59:244–245.
28. Jander N, Minners J, Holme I, et al. Outcome of patients with low-gradient “severe” aortic stenosis and preserved ejection
fraction. Circulation. 2011;123:887–895.
29. Lancellotti P, Magne J, Donal E, et al. Clinical outcome in asymptomatic severe aortic stenosis: Insights from the new proposed
aortic stenosis grading classification. J Am Coll Cardiol. 2012;59:235–243.
30. Pibarot P, Dumesnil JG. Improving assessment of aortic stenosis. J Am Coll Cardiol. 2012;60:169–180.
31. Pibarot P, Dumesnil JG. Low-flow, low-gradient aortic stenosis with normal and depressed left ventricular ejection fraction.
J Am Coll Cardiol. 2012;60(19):1845–1853.
32. Oh JK, Taliercio CP, Holmes DR Jr, et al. Prediction of the severity of aortic stenosis by Doppler aortic valve area determination:
Prospective Doppler-catheterization correlation in 100 patients. J Am Coll Cardiol. 1988;11:1227–1234.
33. Topol EJ, Traill TA, Fortuin NJ. Hypertensive hypertrophic cardiomyopathy of the elderly. N Engl J Med. 1985;312:277–283.
34. Chung KJ, Manning JA, Gramiak R. Echocardiography in coexisting hypertrophic subaortic stenosis and fixed left ventricular
outflow obstruction. Circulation. 1974;49:673–677.
35. Kronzon I, Cohen ML, Winer HE, et al. Left ventricular outflow obstruction: A complication of mitral valvuloplasty. J Am Coll
Cardiol. 1984;4:825–828.

QUESTIONS
1. Use of the Gorlin equation in the 4. A patient is determined to have the
catheterization suite has all of the following Doppler parameters: Left
following limitations EXCEPT: ventricular outflow tract (LVOT) velocity,
a. In patients with aortic insufficiency, the 1.7 m/s; aortic valve velocity, 4.6 m/s. The
aortic valve area may be falsely elevated pressure gradient across the aortic valve is:
b. The cardiac output (CO) of multiple beats a. 84.64 mm Hg
must be averaged for patients in atrial b. 73 mm Hg
fibrillation c. 33.64 mm Hg
c. The peak-to-peak gradient is required d. 11.56 mm Hg
d. The systolic ejection period must be calcu-
5. In regard to pressure gradients in the
lated
left ventricular (LV) and aortic valve, the
e. The gradient across a stenotic aortic valve
following is/are true:
varies directly with cardiac output
a. The Doppler-derived mean transvalvular
2. The following statements regarding the gradient approximates the catheterization-
usefulness of planimetry in the evaluation derived mean transvalvular gradient
of AS are true EXCEPT: b. The peak-to-peak catheter gradient is usu-
a. The midesophageal (ME) aortic valve short- ally the highest gradient recorded
axis view is preferred c. The Doppler-derived maximal instanta-
b. The results of planimetry correlate neous gradient is comparable with the
extremely well with catheterization-derived peak-to-peak catheterization gradient
determinations of the aortic valve area d. All of the above
c. An adequate planimetry-derived determi-
6. A patient has an LV ejection fraction of
nation of the aortic valve area depends on
10%. Which measurement is preferred in
an adequate CO
determining the severity of the AS?
d. Significant valvular calcification decreases
a. Peak aortic valve flow velocity
the accuracy of planimetry-derived deter-
b. Aortic valve area response to dobutamine-
minations of area
mediated increase in cardiac output
e. Three-dimensional planimetry facilitates
c. Aortic valve mean gradient
obtaining the true minimal cross-sectional
d. Planimetered aortic valve area
valve area by orienting this in a third dimen-
e. LVOT time–velocity integral (TVI)/aortic
sion
valve TVI ratio
3. All of the following statements regarding
7. Preoperative evaluation of a patient
continuous wave Doppler evaluation of the
undergoing valve replacement for critical
aortic valve are true EXCEPT:
aortic stenosis shows that the basal
a. The preferred view is the deep transgastric
interventricular septum has hypertrophied
(TG) long-axis view because of the parallel
into the left ventricular outflow tract
alignment of the Doppler beam with flow
(“sigmoid septum”). When coming
b. The deep TG long-axis view offers a corre-
off bypass after valve replacement the
lation of more than 0.9 with transthoracic
patient is hypotensive. The appropriate
echocardiography (TTE)-derived aortic
intervention is:
valve flow velocities
a. Administer pressors with positive inotropy
c. If a mitral prosthetic valve is present, the
to maintain adequate peripheral perfusion
TG long-axis view at 120 degrees can be
pressure
used to obtain aortic valve flow velocities
b. Administer pressors and volume load because
d. Accurate flow velocities can be obtained
the hypertrophied left ventricle requires a high
with the ME views by electronically steering
filling pressure due to its lack of compliance
(angle correcting) the resulting signal to the
c. Reassess the status of the left ventricle to
jet direction as visualized on the 2D color
determine if subaortic obstructive physiol-
Doppler image
ogy has developed postoperatively (systolic
anterior motion of the mitral valve or “SAM”)
d. Volume load, withdraw pressors and con-
sider adding beta blockers

8. Which of the following parameters does not 13. All of the following have been shown to
impact on the measured aortic valve area? be associated with decrease in myocardial
a. Arterial blood pressure perfusion reserve EXCEPT:
b. Diameter of the sinotubular junction a. Aortic valve pressure gradients
c. Left ventricular systolic function b. LV mass index
d. Mitral regurgitation c. Male sex
d. LV filling pressure
9. Which of the following may be associated
e. Myocardial fibrosis
with a low transvalvular gradient in the
presence of critical aortic stenosis? 14. Of the choices given below, which one
a. Dilated cardiomyopathy correlates most with a decrease in
b. Nonobstructive hypertrophic cardiomyop- myocardial perfusion reserve?
athy a. Aortic valve pressure gradients
c. Normal ejection fraction in a small non- b. LV mass index
compliant LV c. Male sex
d. All of the above d. LV filling pressure
e. None of the above e. Myocardial fibrosis
10. In the presence of aortic stenosis with 15. Treatment for SAM can include which of
subaortic obstruction due to hypertrophic the following?
cardiomyopathy the best method for a. MV replacement
assessing aortic valve area is: b. Volume expansion
a. Continuity equation using the peak veloc- c. Reduction of intraoperative inotropes
ity in the LV outflow tract above the area of d. Beta blockade
obstruction e. All of the above
b. Planimetry of the aortic valve orifice
16. A patient is determined to have the
c. Dimensionless index
following Doppler parameter: Aortic valve
d. Continuity equation using the peak veloc-
velocity, 5 m/s. The mean pressure gradient
ity in LV just below the area of subaortic
across the aortic valve is:
obstruction
a. 30
11. When the continuity equation is used, b. 50
which of the following statements regarding c. 60
measurement of the LVOT is true? d. 100
a. The diameter is measured 1 cm proximal to
17. 3D TEE of the aortic valve is not limited by:
the aortic valve
a. High temporal resolution
b. Inner to inner edge, parallel and adjacent
b. Thin AV leaflets
to the aortic valve at its leaflet insertions, or
c. Anterior location
at the site of velocity measurement.
d. Low frame rates
c. The diameter is measured at the leaflet tips
d. The chance of introducing error into this 18. A 40-year-old man develops syncope while
measurement is small playing golf. Despite poor TTE 2D imaging,
the patient’s aortic valve mean gradient is
12. A patient is found to have aortic stenosis.
40 mm Hg. What is the most common cause
What maneuvers will increase the gradient
of his aortic stenosis?
across the aortic valve?
a. Bicuspid aortic valve
a. Exercise
b. Calcific aortic stenosis
b. Aortic insufficiency
c. Rheumatic heart disease
c. Acute myocardial infarction
d. Marfan’s syndrome
d. Both a and b
e. All the above

19. A patient with a heart rate of 80 bpm, 20. A patient with a heart rate of 80 bpm,
CO of 2 L/min, AV peak gradient of CO of 2 L/min, AV peak gradient of
30 mm Hg, and 20% LVEF, undergoes 30 mm Hg, and 20% LVEF, undergoes
dobutamine stress testing. His results are dobutamine stress testing. His results are
in the following table. Which example is in the following table. Which example
consistent with severe aortic stenosis? is consistent with primary myocardial
disease?
Cardiac AV peak Aortic
Heart output gradient valve area Cardiac AV peak Aortic
Choice rate (L/min) (mm Hg) (cm3) Heart output gradient valve area
a. 80 2 30 1 Choice rate (L/min) (mm Hg) (cm3)
b. 100 2 30 1 a. 80 2 30 1
c. 100 3.5 50 1 b. 100 2 30 1
d. 100 3.5 50 1.4 c. 100 3.5 50 1
e. 100 2 30 1.4 d. 100 3.5 50 1.4
e. 100 2 30 1.4

13 Prosthetic Valves
Albert T. Cheung and Scott C. Streckenbach
INTRODUCTION
The first successful artificial heart valves were implanted in 1960. Starr implanted a Starr–Edwards caged-
ball valve in a patient with rheumatic mitral stenosis and Harken implanted the Harken caged-ball pros-
thesis in the subcoronary aortic position in a patient with rheumatic aortic stenosis and regurgitation.
Over the next 45 years, numerous manufacturers have produced prosthetic valves of various designs for
clinical use. In the past 10 years, increased attention to the risk of prosthetic-patient mismatch has been an
important factor driving the development of prosthetic valves with larger effective orifice sizes and thus
more favorable hemodynamic properties. The production of prosthetic valves has also become a competi-
tive business with each manufacturer creating unique products and individual cardiac surgeons developing
specific preferences in their choice of valves. As a consequence, the design, construction, and marketing
of prosthetic valves is an ongoing process and incremental refinements are continually being made in an
effort to improve the biocompatibility, durability, hemodynamic performance, and ease of implantation
that are evidenced by the frequent appearance of new models with new trade names. One of the challenges
of assessing prosthetic valve function is to recognize and appreciate the distinct echocardiographic fea-
tures and hemodynamic performance of each of the many varieties of prosthetic valve types, models, and
sizes that have been commercially available and may be encountered in the existing contemporary patient
population.
ROLE OF TRANSESOPHAGEAL ECHOCARDIOGRAPHY IN THE

EVALUATION OF PROSTHETIC CARDIAC VALVES
Multiplane transesophageal echocardiography (TEE) is considered the diagnostic technique of choice for
identifying the type of prosthesis, assessing its function, and diagnosing prosthetic dysfunction (1–6). The
ability of TEE to combine two-dimensional (2D) and three-dimensional (3D) with color Doppler and spec-
tral Doppler imaging enables TEE to generate diagnostic information based on both the structure and the
hemodynamic function of the prosthetic valve. However, the evaluation of prosthetic heart valves using
ultrasound imaging poses special problems because mechanical valves and components of bioprosthetic
valves have poor acoustic properties, making it difficult to image the valve and the surrounding soft tissues
in detail. In addition, the small size of the valves and their mechanical components make detailed examina-
tion of the motion of the stent and occluder mechanisms challenging.
Despite incremental improvements in instrumentation, the imaging resolution that can be achieved
using transthoracic echocardiography (TTE) does not match that achieved by TEE. The improved imaging
resolution provided by TEE with the ultrasound transducer close to the cardiac valve structures permits a
detailed assessment of both prosthetic valve function and determining the etiology of prosthetic valve dys-
function. High resolution 2D and 3D imaging can distinguish between normal and abnormal motion of the
valve leaflets and occluder mechanisms. Abnormal motion of the valve stent or dehiscence of the prosthetic
valve annulus can also be detected. In addition, vegetations, calcifications, pannus, and thrombus forma-
tion on the prosthetic valve can be detected using 2D and 3D imaging.
Color Doppler imaging can distinguish normal closure and leakage regurgitant jets (washing jets) from
pathologic transvalvular or paravalvular regurgitant jets. Quantification of blood flow velocity using spec-
tral Doppler techniques often permits the estimation of transvalvular pressure gradients and the effective
orifice area of the prosthetic valves (1,7–10).
258

13. Prosthetic Valves 259
TABLE 13.1 Prosthetic Heart Valves and Clinical Indications for TEE
TEE evaluation prior to valve replacement

1. Verify disease of native valve
2. Assess the extent of annular calcification
3. Estimate the annular diameter of the native valve. In aortic valve disease, a small annulus may dictate the type of
valve to be implanted
4. Evaluate the feasibility of valve repair. Considering the limitations of prosthetic valves, it is almost always preferable
to repair a valve rather than replace it
TEE evaluation immediately after valve replacement
1. Verify that the prosthetic valve apparatus is stable and well seated within the native valve annulus
2. Verify that all leaflets or occluders move normally
3. Verify the presence and location of characteristic transvalvular washing regurgitant jets
4. Verify the absence of paravalvular or pathologic transvalvular regurgitation
5. Verify that there is no left ventricular outflow tract obstruction caused by prosthetic valve struts or retained
subvalvular apparatus
6. Verify satisfactory hemodynamic function of the prosthetic valve by measuring the transvalvular pressure
gradient, Doppler velocity index, and effective orifice area
TEE evaluation to assess for collateral damage to other cardiac structures as a consequence of valve replacement
1. Mitral regurgitation from a misplaced suture through the anterior mitral valve leaflet after aortic valve
replacement
2. Aortic regurgitation from a misplaced suture through an aortic valve cusp after mitral valve replacement
3. Coronary obstruction after aortic valve replacement manifested by right or left ventricular dysfunction
4. Left circumflex coronary artery injury or obstruction after mitral valve replacement manifested by left ventricular
segmental wall motion abnormality
5. Ventricular or atrial septal defect after mitral or aortic valve replacement
6. Left ventricular outflow tract obstruction after mitral valve replacement
TEE diagnosis of prosthetic valve dysfunction
1. Identify prosthetic valve type
2. Detect and quantify the severity of transvalvular or paravalvular regurgitation
3. Detect annular dehiscence
4. Detect vegetations associated with endocarditis
5. Detect thrombosis or pannus formation on the valve
6. Detect and quantify valve stenosis
7. Detect structural valvular degeneration or calcification
Clinical indications for TEE include the evaluation of the native valve prior to valve replacement, the
evaluation of prosthetic valve function immediately after implantation, the diagnosis of prosthetic valve
dysfunction, the assessment of prosthetic patient mismatching, and the diagnosis of early complications
associated with valve replacement (Table 13.1).
TECHNICAL CONSIDERATIONS IN PERFORMING

TEE EXAMINATIONS OF PROSTHETIC VALVES
Many of the ultrasound imaging techniques used to evaluate native valve function can be applied to the
evaluation of prosthetic heart valves, but certain special considerations are necessary. Ultrasound does
not penetrate through the metallic and polymeric components of mechanical and biologic valves. These
material components produce highly specular echoes and impair the imaging of distal structures because
of acoustic shadowing. For these reasons, decreasing the transmit gain helps to decrease imaging artifacts
and to resolve structural details in the vicinity of nonbiologic materials. To overcome some of the prob-
lems created by acoustic shadowing, it is necessary to image the prosthetic valve from different transducer
positions that provide views of both the upstream and the downstream sides of the prosthetic valve. For
example, the midesophageal aortic valve long-axis imaging plane will not reliably display the motion of the
mechanical aortic prosthesis because of shadowing from the valve sewing ring (Fig. 13.1). By advancing the
TEE probe to the transgastric position, prosthetic aortic leaflet motion can be observed from the apical or

FIGURE 13.1 Bileaflet mechanical prosthesis in the aortic position. Transesophageal echocardiographic midesopha-
geal aortic valve long-axis view at a multiplane angle of 135 degrees in a patient with a bileaflet mechanical prosthesis
in the aortic position. Color Doppler flow imaging in diastole shows the normal appearance of the two leakage regurgi-
tant jets that originate at the leaflet hinge points (arrows). Note that ultrasound shadowing caused by the annular stent
makes it difficult to assess the motion of the leaflets from this imaging angle. The transgastric long-axis or the deep
transgastric long-axis views through the aortic valve are necessary to evaluate the motion of the individual leaflets.
mid-left ventricular transgastric long-axis view through the aortic valve without interference from the sew-
ing ring (Fig. 13.2). Similarly, imaging the ventricular side of mitral prosthetic valves using the transgastric
mid-ventricular or deep transgastric long-axis imaging planes provides detail that cannot be observed with
the midesophageal views alone.
Doppler echocardiography can be used to estimate the transvalvular pressure gradient across bileaflet,
tilting disc, and biologic valves that have a centrally directed, linear transvalvular flow. In contrast, for
caged-ball or caged-disc valves where the occluder alters the direction of blood flow through the valve, the
Bernoulli equation will not accurately estimate the transvalvular pressure gradient.
ECHOCARDIOGRAPHIC CHARACTERISTICS OF THE INDIVIDUAL

PROSTHETIC CARDIAC VALVE TYPES
Each type of prosthetic valve has distinct echocardiographic features and hemodynamic characteristics.
The type, shape, and motion of the structural components of the valve allow it to be identified by the TEE
examination. Knowing the published and manufacturers’ specifications for the normal range of motion of
the valve components, the average transvalvular pressure gradient, and average effective orifice area is nec-
essary to verify normal functioning of the prosthesis and to diagnose prosthetic dysfunction (1,8–10). In
general, prosthetic valves are classified as mechanical or biologic and by the manufacturer, model number,
and outside diameter of the sewing ring (Table 13.2 and Appendix D).

A B
FIGURE 13.2 Bileaflet mechanical prosthesis in the aortic position. Transesophageal echocardiographic deep transgas-
tric apical long-axis view at a multiplane angle of 0 degrees permits imaging of prosthetic valve leaflets (arrows) and their
motion. In diastole (panel A), both leaflets are in the fully closed position at an angle of 30 degrees in relation to the plane
of the valve annulus. In systole (panel B), both leaflets are in the fully open position at an angle of 90 degrees in relation
to the plane of the valve annulus. LV, left ventricle; Ao, aorta.
Mechanical Heart Valves

Mechanical heart valves are more durable than biologic valves, but are thrombogenic and require sys-
temic anticoagulation. For these reasons, mechanical valves are traditionally considered for younger
patients who are more likely to experience structural failure after implantation of a biologic prosthetic as
a consequence of their longer life expectancy. Mechanical prosthetics may also be preferred in patients
who require anticoagulation therapy for other reasons or in whom the risk of re-operation is unaccept-
able. The silastic, metal, and pyrolytic carbon components of mechanical valves are poor conductors of
TABLE 13.2 Prosthetic Valve Types
Bioprosthetic Description
Allograft Indistinguishable from the native valve, used only in the aortic position (CryoLife aortic allograft)
Porcine Porcine aortic valve on polypropylene or elgiloy mount with three support struts (e.g., Hancock,
Carpentier–Edwards, Medtronic Mosaic, St. Jude Bioimplant, St. Jude Medical Epic, Wessex)
Pericardial Trileaflet valve fashioned from bovine or porcine pericardium mounted on a Dacron-covered
support frame with three struts (e.g., Bioflo pericardial, Carpentier–Edwards Pericardial, Labcor-
Santiago pericardial, Sorin Mitroflow, Ionescu–Shiley, Sorin Pericarbon, St. Jude Medical Trifecta)
Stentless Reinforced porcine aortic root (Biocor stentless, CryoLife-O’Brien stentless, Edwards Prima
stentless, Medtronic Freestyle, Toronto Stentless Porcine valve, Medtronic ATS 3f )
Transcatheter Trileaflet pericardial valve supported within a wireform stent for implantation through a catheter
(Edwards SAPIEN, Medtronic CoreValve)
Mechanical Description
Ball-in-cage Circular sewing ring with U-shaped arches containing a silastic ball (e.g., Braunwald-Cutter,
Harken, Starr–Edwards)
Caged-disc Circular sewing ring with short cage containing a lightweight silastic centrally occluding disc (e.g.,
Beall, Kay–Shiley, Kay–Suzuki, Starr–Edwards Model 6520)
Tilting disc Eccentrically hinged single tilting disc in circular ring opening to form two orifices (e.g., Bjork–
Shiley, Lillehei–Kaster, Medtronic Hall, Omnicarbon, Omniscience, Sorin Allcarbon monoleaflet,
Wada-Cutter)
Bileaflet Two semicircular hinged leaflets in a circular ring opening almost perpendicularly to form three
orifices (e.g., ATS, Carbomedics, Duromedics, Edwards MIRA, Jyros bileaflet, ON-X, St. Jude
Medical, Sorin Allcarbon, Sorin Bicarbon)

Leaflet
Annular stent
Sewing ring
FIGURE 13.3 Photograph of a Carbomedics R-series mechanical bileaflet prosthetic aortic valve. The valve consists of
two semicircular pyrolytic carbon leaflets supported within a pyrolytic carbon annular stent surrounded by the sewing
ring. The inset shows a close-up of the hinge points of the leaflets. The valve is designed to permit a small amount of
leakage backflow at the hinge points.
ultrasound and cause acoustic shadowing, reverberations, and strong specular signals. The echocardio-
graphic appearance and characteristics of mechanical prosthetic valves can be categorized based on the
occluder mechanism.
Bileaflet Valves
The bileaflet mechanical valve prostheses are the most commonly implanted mechanical valves because of
their outstanding record of durability and large valve orifice area in relation to sewing ring diameter. They
can be implanted in the aortic, mitral, or tricuspid positions. The valves are constructed of two semicircu-
lar leaflets suspended from four hinge points in a circular annulus surrounded by a sewing ring (Fig. 13.3).
When the leaflets open, three separate orifices are formed within the valve annulus. Minor variations in
design include the shape of the leaflets, the width of the sewing ring, and the materials used to construct
the valve components.
A systematic TEE examination of the prosthetic valve includes verification of normal leaflet motion,
proper seating of the prosthesis within the native valve annulus, and normal blood flow pattern through the
valve. In addition, the TEE examination should verify the presence of normal washing jets and the absence
of significant paravalvular regurgitation and the absence of abnormal transvalvular regurgitation. Finally,
TEE can be used to estimate the transvalvular pressure gradient and calculate the effective orifice area of
the valve.
1. Confirm leaflet motion: 2D and 3D imaging confirms the opening and closure of the two mechanical
Video 13.1 leaflets (Video 13.1). In the short-axis imaging plane, the two leaflets in the open position produce
two linear shadows within a circular annulus (Fig. 13.4). For valves implanted in the mitral position,
leaflet motion is best examined using the midesophageal long-axis views (Fig. 13.5). Multiplane rotation
through the valve to generate a cross-sectional imaging plane that is perpendicular to the two leaflets
permits the motion of both leaflets to be observed simultaneously (Fig. 13.5). The two leaflets tilt open
symmetrically to an angle of 85 to 90 degrees and close at an angle of 30 degrees in relation to the plane
of the annulus for a travel arc of approximately 60 degrees. Leaflet motion of a valve implanted in the
aortic position is more difficult to evaluate (Figs. 13.1 and 13.4). Acoustic shadowing from the sewing
ring and leaflets typically obscure leaflet motion in the midesophageal aortic valve long-axis view.
Individual leaflet motion is better visualized in the transgastric long axis and deep transgastric long-axis
views that provide unobstructed views of the aortic valve in the far field through the left ventricle and
Video 13.2 left ventricular outflow tract (LVOT) (Figs. 13.2 and 13.6, Video 13.2).

FIGURE 13.4 Bileaflet mechanical prosthesis in the aortic position. Transesophageal echocardiographic midesopha-
geal short-axis image just above the plane of the valve annulus in systole provides cross-sectional imaging of the two
parallel leaflets (arrows) of the mechanical valve in the open position. Note the acoustic shadowing caused by the
mechanical leaflets in the far field making it difficult to resolve detail in the distal portion of the valve annulus. LA, left
atrium; RA, right atrium.
A B C D E
FIGURE 13.5 Multiplane TEE midesophageal images of a normally functioning bileaflet mechanical valve in
the mitral position. Panels A and D show the appearance of the prosthetic valve at mid-systole with both leaflets in the
closed position at a multiplane angle perpendicular to the pivot axis (two-leaflet view). The arrow in panel A shows the
location of the pivot guard that contains the hinge points. Panels B and C show the appearance of the prosthetic valve
in diastole with both leaflets in fully opened position at a multiplane angle perpendicular to the pivot axis (two-leaflet
view). The arrow in panel C shows the position of the central orifice. Doppler color flow imaging at mid-systole (panels
D and E) shows the typical appearance of normal regurgitant jets that originate from the hinge points or between the
leaflets and the valve stent. Rotating the multiplane angle 90 degrees forward from the two-leaflet view produces
the single-leaflet view that is parallel to the pivot axis (panel E). In the single-leaflet view, Doppler color flow imaging
shows the origin of the centrally directed regurgitant jets from the hinge points (panel E) (Courtesy of Drs. Cheung
and Streckenbach).

FIGURE 13.6 Doppler color flow full-volume 3D TEE transgastric aortic valve long-axis view at a multiplane angle of
155 degrees of a normally functioning mechanical bileaflet valve in the aortic position viewed from the left ventricular
side in systole with the occluders open (top panels) and in diastole with the occluders closed (bottom panels). Color
suppression (left panels) demonstrates the position of the occluders in the open (top left panel) and closed positions
(bottom left panel). Doppler color flow imaging (right panels) demonstrates the normal pattern of transvalvular flow
through the three orifices of the prosthetic valve during systole (top right panel) and normal pattern of regurgitant jets
at the hinge points of the occluders during diastole (bottom right panel). Small transvalvular regurgitant jets can often
be detected between the occluder and the annular stent in a normally functioning mechanical bileaflet prosthetic valve
(not shown) (Courtesy of Drs. Cheung and Streckenbach).
2. Confirm proper valve seating: Incomplete fixation of the prosthetic sewing ring to the native annulus
or dehiscence of the sewing ring will cause paravalvular regurgitation. Paravalvular regurgitation is
defined as regurgitation originating outside of the prosthetic valve annulus or sewing ring (Fig. 13.7,
Video 13.3 Video 13.3). The most common cause for incomplete fixation immediately after prosthetic implantation
is a severely calcified native valve annulus or an avulsed annular suture. Prosthetic endocarditis is
the most common cause for late valve dehiscence and can produce a “rocking” motion of the entire
valve apparatus on 2D imaging. Proper seating of the prosthetic valve, paravalvular regurgitation, and
dehiscence are best identified from the multiplane long-axis images of the valve.
3. Confirm normal blood flow patterns and the absence of pathologic transvalvular and paravalvular
regurgitation: Color flow Doppler imaging will demonstrate central antegrade flow through the valve
annulus when the leaflets open and small characteristic regurgitant jets during leaflet closure. A small
amount of regurgitation is normal for bileaflet prosthetic valves and is caused by closure backflow and
leakage backflow. Closure backflow is the reversal of flow required for closure of the leaflets. Leakage
backflow occurs after closure of mechanical valves, originates from the four hinge points of the leaflets
and at other locations between the edges of the occluder and the prosthetic valve stent. The leakage

A B
C D
FIGURE 13.7 Transesophageal midesophageal long-axis view in a patient with a caged-ball prosthesis in the mitral
position complicated by prosthetic valve endocarditis and dehiscence. Two-dimensional imaging (panel A) demon-
strated a rocking motion of the prosthetic valve and separation of the sewing ring from the native annulus in the region
of the posterior mitral valve annulus (arrow, panel A) that was characteristic of dehiscence. Vegetations on the prosthetic
valve that were diagnostic for endocarditis were detected also by 2D imaging (arrows, panel B). Doppler color flow imag-
ing in diastole showed antegrade flow around the open occluder into the left ventricle (arrow, panel C). Doppler color
flow imaging in systole demonstrated paravalvular regurgitation in the region of dehiscence (arrow, panel D) (Courtesy of
Drs. Cheung and Streckenbach). LA, left atrium; Ao, aorta.
backflow jets originating from the hinge points produces four centrally directed regurgitant jets that
are best visualized in the long-axis image through the prosthetic valve at a multiplane angle aligned
Video 13.2
parallel to the leaflets (Figs. 13.1, 13.5, 13.6, Videos 13.2, 13.4, and 13.5). These washing jets originate
Video 13.4
laterally near the inner border of the prosthetic annulus and are directed medially into the left atrium.
The bileaflet valves are designed to permit a small amount of regurgitation at the hinge points to prevent Video 13.5
the formation of thrombus within the hinge mechanism. Sometimes, small leakage regurgitant jets
originating along the edge of the leaflet where it meets the annulus during closure can also be imaged by
color Doppler imaging (Fig. 13.5). Normal physiologic regurgitant jets are small and short in duration
and can be distinguished from pathologic transvalvular regurgitation based on their size, location,
direction, and duration.
Pathologic regurgitation with a jet originating within the sewing ring is called transvalvular
regurgitation. Pathologic transvalvular regurgitation immediately after valve implantation indicates
malfunctioning of the valve leaflets. Intraoperative causes of leaflet malfunction causing transvalvular
regurgitation include retained tissue preventing valve closure, a misplaced suture interfering with
leaflet motion, or debris within the hinges causing trapping of the leaflet in a fixed position (Fig. 13.8).
Significant regurgitant jets originating outside of the sewing ring are always pathologic and called
paravalvular regurgitation.
4. Calculate valve gradient and effective orifice area: The hemodynamic performance of the prosthetic
valve can be assessed using Doppler echocardiography (Fig. 13.9). The interpretation of Doppler-derived
prosthetic valve hemodynamic parameters is complicated because even normally functioning prosthetic
valves are inherently obstructive to blood flow, and blood flow velocity profiles across prosthetic valves
are not uniform depending upon prosthetic valve type, model, and annular diameter. Since the blood
flow velocity through the central rectangular orifice is greater than the blood flow velocity through the
two semicircular orifices of the bileaflet valves, some studies suggest that Doppler-derived gradients
based on the Bernoulli equation may overestimate the true transvalvular gradient (11). Yet the same and
other studies suggest also that differences observed between Doppler- and catheter-derived gradients

A B
FIGURE 13.8 Intraoperative TEE midesophageal commissural view at a multiplane angle of 64 degrees displaying a
mechanical bileaflet prosthetic in the mitral position. TEE imaging of the bileaflet view in diastole immediately after
implantation demonstrated that the anterior leaflet was trapped in a closed position (arrow, panel A). TEE examination
after surgical revision to free trapped leaflet showed that both leaflets were fully open in diastole (panel B) and moved
normally throughout the cardiac cycle.
A B C
FIGURE 13.9 The functional performance of prosthetic valves implanted in the aortic position can be assessed by TEE
in mid-systole by using 2D imaging to measure the diameter of the left ventricular outflow tract in the midesophageal
aortic valve long-axis view (panel A), pulsed wave Doppler to measure the blood flow velocity in the left ventricular
outflow tract in the transgastric aortic valve long-axis view (panel B), and continuous wave Doppler to measure the
transvalvular blood flow velocity in the transgastric aortic valve long-axis view (panel C). In this example of a 29-mm bio-
prosthetic valve implanted in the aortic position, the transvalvular peak gradient was 21 mm Hg and mean gradient was
10 mm Hg using the simplified Bernoulli equation. Using the nonsimplified Bernoulli equation, the transvalvular peak
gradient was 12 mm Hg and mean gradient was 6 mm Hg. The Doppler velocity index (DVI) was 0.66, and the effective
orifice area was 2.4 cm2 (Courtesy of Drs. Cheung and Streckenbach).

TABLE 13.3 Determining the Effective Orifice Area (EOA) Using the Continuity Method
EOA = LVOTarea (VTILVOT/VTItransvalvular)
Where:
EOA = effective orifice area of prosthetic valve
LVOTarea = cross-sectional area of left ventricular outflow tract (LVOT)
= π (diameter of LVOT/2)2
VTItransvalvular = velocity–time integral of blood flow across valve
VTILVOT = velocity–time integral of blood flow across LVOT
across prosthetic valves can be explained by localized gradients and pressure recovery downstream
from the valve orifice (11,12). Based on this interpretation, differences between Doppler- and catheter-
derived pressure gradients may not represent an overestimation of catheter-derived gradients, but
represent instead inherent differences in measurement technique, line of interrogation, and precise
location of pressure gradients relative to the prosthetic valve orifices. Furthermore, the equation used to
estimate mitral valve area based on pressure half-time (MVA = 220/PT1/2) may not apply to prosthetic
valves that differ in structure and flow characteristics to the native valve. For clinical purposes of
quantifying prosthetic valve function, several approaches can be applied for interpretation of Doppler-
derived measurements. One approach is to report only actual values of Doppler transvalvular peak and
mean flow velocities across the prosthetic valve and compare the values to established normal values
for the specific type, model, and size of the prosthetic valve based on clinical reports, specifications
published by the manufacturers that can be obtained from their respective websites or the package insert
accompanying the prosthetic valve (9), or in the appendix of the American Society of Echocardiography
guidelines for the evaluation of prosthetic valves (Appendix D) (1,10). Similarly, Doppler-derived
effective orifice areas calculated using the continuity equation for a prosthetic valve can be compared
to those observed for that specific prosthetic valve type, model, and size (Table 13.3 and Appendix
D) (1,10). Another variable adding to the complication of interpreting Doppler-derived hemodynamic
information in patients with prosthetic valves is that Doppler-derived pressure gradients are dependent
on blood flow and even blood viscosity. Decreased blood viscosity from hemodilution or increased
cardiac output from inotropic support immediately after prosthetic valve implantation may lead to
overestimation of prosthetic valve gradients using the simplified Bernoulli equation. One approach to
address this problem of assessing aortic valve prosthetics is to index transvalvular Doppler blood flow
velocity through the prosthetic valve to the blood flow velocity through the LVOT using the Doppler
velocity index (DVI = VLVOT/VAoV) (Table 13.4) (1,13,14). For example, using the DVI or the “double
envelope” technique for assessing the function of a prosthetic valve in the aortic position, a peak blood
flow velocity in the LVOT (VLVOT) to peak transvalvular blood flow velocity (VAoV) ratio less than 0.25
(VLVOT/VAoV < 0.25) suggests significant prosthetic valve stenosis (Table 13.5) (1,13). Another approach
is to estimate prosthetic valve gradients using the nonsimplified Bernoulli equation that accounts for the
velocity of blood flow on the upstream side of the valve ([P1 − P2] = 4[V22 − V12]). Similarly, for assessing
the function of a prosthetic valve in the mitral position, a transvalvular velocity–time integral (VTIMV)
to LVOT velocity–time integral (VTILVOT) ratio greater than 2.5 (VTIMV/VTILVOT > 2.5) suggests
significant prosthetic valve stenosis (Tables 13.4 and 13.6) (14).
TABLE 13.4 Determining the Doppler Velocity Index (DVI)
Aortic valve DVI = VmaxLVOT/VmaxAoV

Mitral valve DVI = VTIMV/VTILVOT
Where:
DVI = Doppler Velocity Index
VmaxLVOT = Maximum blood flow velocity in the left ventricular outflow tract
VmaxAoV = Maximum transvalvular blood flow through the prosthetic aortic valve
VTIMV = Velocity–time integral for flow across the prosthetic mitral valve
VTILVOT = Velocity–time integral for flow through the left ventricular outflow tract

TABLE 13.5 Doppler Parameters for Diagnosis of Prosthetic Aortic Stenosisa
Parameter Normal Possible stenosis Suggests significant stenosis

Peak velocity (m/s)b <3 3–4 >4
Mean gradient (mm Hg)b <20 20–35 >35
DVI ≥0.30 0.29–0.25 <0.25
EOA (cm2) >1.2 1.2–0.8 <0.8
Transvalvular velocity profile Triangular, early peaking Intermediate Rounded, symmetric contour
a
In conditions of normal stroke volume (50–70 mL) through the aortic valve.
b
These parameters are more affected by flow, including concomitant aortic regurgitation.
Adapted from: Zoghbi WA, Chambers JB, Dumesnil JG, et al. Recommendations for evaluation of prosthetic valves with
echocardiography and Doppler ultrasound. J Am Soc Echocardiogr. 2009;22:975–1014.
Caged Ball
Caged-ball valves were the first prosthetic valves implanted in humans. They consist of a silastic or metal
ball occluder housed in a wire cage with three or four struts. The ball occluder casts a large acoustic shadow
and its motion within the cage is best imaged in the long-axis plane of the valve (Fig. 13.10). In the short-
axis imaging plane, the ball occluder can be imaged within the wire struts. Doppler color flow imaging
in the short-axis plane of the valve demonstrates blood flow between the wire struts through the outside
perimeter of the ball occluder (Fig. 13.10).
Tilting Disc
Tilting disc valves have been utilized in the aortic, mitral, and tricuspid positions. They consist of a single-
disc occluder supported by struts. The single-disc occluder pivots open 60 to 80 degrees to form two ori-
fices of different size and shape. They have a low profile and offer the advantage of providing a large orifice
size in relation to its stent size. Although tilting disc valves are no longer in production for implantation
in the United States, there are still many patients with these mechanical valves in the population. The
two primary models of tilting disc valves can be distinguished by the presence of a central aperture in the
Medtronic Hall and the absence of a central aperture in the Bjork Shiley valve when examined by color
Doppler imaging (Figs. 13.11 and 13.12).
Echocardiographic examination includes the following:
1. Confirm proper tilting action of the occluder in the long-axis imaging plane.
2. In the short-axis imaging plane, one edge of the disc occluder should move in and out of the imaging
plane as the valve tilts open.
TABLE 13.6 Doppler Parameters for Diagnosis of Prosthetic Mitral Stenosis
Possible Suggests significant

Normal Stenosisa stenosisa
Peak velocity (m/s)b,c <1.9 1.9–2.5 ≥2.5
Mean gradient (mm Hg)b,c ≤5 6–10 >10
VTIMV/VTILVOTb,c <2.2 2.2–2.5 >2.5
EOA (cm2) ≥2 1–2 <1
PHT (ms) <130 130–200 >200
a
Abnormal values should prompt a closer evaluation of valve function and consideration of other conditions such as high
cardiac output, tachycardia, or prosthesis–patient mismatch.
b
Slightly higher cutoff values than shown may be seen in some bioprosthetic valves.
c
These parameters are also abnormal in the presence of significant prosthetic mitral regurgitation.
PHT, pressure half-time; VTILVOT, velocity–time integral in left ventricular outflow tract; VTIMV, velocity–time integral through
prosthetic mitral valve.

A B
FIGURE 13.10 Starr–Edwards caged-ball mechanical valve. Panel A is a transesophageal echocardiographic mid-
esophageal four-chamber view of a caged-ball valve prosthesis in the mitral position at end-diastole. Ultrasound shad-
owing caused by the silastic ball occluder (arrow) contained within the wire form cage makes it difficult to image the
distal side of the valve. Panel B is a TEE midesophageal aortic valve short-axis view at a multiplane angle of 50 degrees
during systole in a patient with a caged-ball valve in the aortic position. Note the three metal struts of the cage. Color
Doppler flow imaging demonstrates blood flow through the valve at the perimeter of the silastic ball occluder. Again, the
silastic ball occluder causes ultrasound shadowing.
A B C
FIGURE 13.11 Transesophageal midesophageal images with color Doppler imaging in mid-systole demonstrating
the normal pattern of leakage regurgitant jets in patients with a bileaflet mechanical (panel A), Bjork–Shiley tilting disc
(panel B), and Medtronic Hall tilting disc (panel C) prosthetic valves in the mitral position. The bileaflet mechanical valve
is distinguished by medially directed regurgitant jets originating from the hinge points of the occluders at a multiplane
cross-sectional image parallel to the axis of rotation of the occluders (panel A). The Bjork–Shiley valve is distinguished by
a leakage regurgitant jet through a central orifice of the tilting disc occluder (panel C). The Medtronic Hall valve has no
central orifice, but small leakage regurgitant jets originate between the tilting disc and the annular stent that are directed
laterally. (panel B) (Courtesy of Drs. Cheung and Streckenbach).

A B C
FIGURE 13.12 Transillumination of a bileaflet (St. Jude Medical, panel A), tilting disc (Medtronic Hall, panel B), and caged-
ball (Starr–Edwards, panel C) mechanical prosthetic valves that demonstrate the typical sites of origin for normal washing
and leakage regurgitant jets that appear on Doppler color flow imaging (Courtesy of Drs. Cheung and Streckenbach).
3. Doppler color flow imaging showing a centrally directed leakage regurgitant jet originating from the
hinge point of the disc occluder or small leakage regurgitant jets originating at the site of contact
between the disc and the annular stent are normal findings for the Bjork–Shiley valve (Figs. 13.11 and
13.12). Two regurgitant jets originating from the inner edges of the annular stent that are directed
laterally are a normal characteristic of the Bjork-Shiley valve (Fig. 13.11).
4. Strut fracture is a serious complication that can cause occluder malfunction and even disc embolization
and is manifest by severe transvalvular regurgitation. Thrombus or pannus ingrowth on the valve can
limit occluder opening or impair the occluder from closing completely, causing stenosis or transvalvular
regurgitation (Fig. 13.13).
FIGURE 13.13 Pannus formation on a Bjork–Shiley tilting disc mechanical prosthesis in the mitral position. Trans-
esophageal echocardiographic midesophageal four-chamber view during systole in a patient with a tilting disc mechani-
cal prosthesis in the mitral position. The single-disc occluder (single arrow) failed to close completely during systole and
open completely during diastole (not shown). Pannus formation on the valve (double arrows) limited the motion of
the disc occluder causing both prosthetic mitral stenosis and transvalvular mitral regurgitation. LA, left atrium; LV, left
ventricle.

Leaflets
Stent
Sewing ring
FIGURE 13.14 Photograph of a Carpentier–Edwards model 6625 porcine bioprosthetic mitral valve. The valve is con-
structed from a porcine aortic xenograft mounted on a wire form stent surrounded by a sewing ring.
Biologic Valves or Tissue Valves

Biologic valves do not require systemic anticoagulation, but have an effective life span of only 12 to
15 years. The biologic components of bioprosthetic valves are susceptible to structural valvular dete-
rioration such as leaflet calcification, tear, or perforation. Unstented bioprosthetic aortic valves are also
susceptible to regurgitation from annular or aortic root dilatation. Bioprosthetic valves are typically pre-
ferred for elderly patients with a life expectancy less than 15 years or for patients who cannot tolerate
anticoagulation therapy or in whom anticoagulation therapy is not feasible. The biologic components of
bioprosthetic valves have favorable acoustic properties and permit imaging by ultrasound. In general, the
same principles used to examine native cardiac valves can be applied to the TEE examination of biologic
valve prostheses.
Stented Porcine Heterografts

Stented porcine heterografts are constructed from a glutaraldehyde-preserved porcine aortic xenograft
mounted on a cloth-covered wire or polymer frame with an attached sewing ring (Fig. 13.14). They can be
implanted in the aortic, mitral, or tricuspid positions. In short axis, the three leaflets supported by struts
open to form a central orifice in the shape of a bulging triangle. In long axis, the valve leaflets separate sym-
metrically when open and coapt at the center of the valve when closed. The stent struts that support the
leaflets extend from the base of the annulus and point toward the downstream side of the valve. Doppler
color flow imaging can sometimes detect a small closure or leakage regurgitant jet originating from the
central coaptation point.
Stented Pericardial Valves

Stented pericardial valves are constructed from bovine or porcine pericardium fashioned into three leaf-
lets supported by a wire frame with three struts attached to a sewing ring (Video 13.6). The pericar- Video 13.6
dial leaflets can be mounted either on the internal side of the struts (Carpentier–Edwards Perimount)
(Fig. 13.15) or on the external side of the struts (Sorin Mitroflow or St. Jude Medical Trifecta) (Figs. 13.16
and 13.17). In addition, the strut apparatus can be mounted above the annular sewing ring for supra-annular
implantation. These modifications were designed to maximize the effective orifice area for the prosthetic
valve relative to its outside annular dimension. The pericardial bioprosthetic valves have a lower profile
compared to the stented porcine bioprosthetic valves, but the echocardiographic appearance of these
valves is similar, though not exactly the same as that of stented porcine aortic heterografts. Mild central
transvalvular regurgitation can be normal immediately after implantation for some models of pericardial

Leaflet
Stent
Annulus
Sewing
ring
A B
FIGURE 13.15 Photograph of a Carpentier–Edwards model 6900 bovine pericardial bioprosthetic mitral valve (panel
A). The valve leaflets are constructed from bovine pericardium mounted on a wire form stent surrounded by a sewing
ring. In contrast, the Carpentier–Edwards Perimount Magna valve (panel B) is a bovine pericardial bioprosthetic valve for
implantation in the aortic position with a supra-annula design where the valve apparatus is mounted above the sewing
ring in an effort to maximize the effective orifice area relative to the outside diameter of the sewing ring (Courtesy of
Drs. Cheung and Streckenbach).
bioprosthetic valves (Fig. 13.18). In addition, small transvalvular regurgitant leakage jets can sometimes
be identified originating from the fabric-covered regions of the stent struts or from the region between
the stent and the sewing ring (Fig. 13.18). These transvalvular regurgitant leakage jets through the fabric
of bioprosthetic valves typically disappear over time as the fabric becomes sealed with cellular elements
or endothelium.
Stentless Valves
The first generation stentless bioprosthetic valves were fabric-reinforced glutaraldehyde-preserved porcine
aortic heterografts constructed without the wireform frame, stents, and sewing ring. They were designed
for use in the aortic position or for replacement of the aortic root. Elimination of the stent and sewing ring
FIGURE 13.16 Photograph of a St. Jude Medical Trifecta porcine pericardial bioprosthetic aortic valve. The valve leaf-
lets are constructed from porcine pericardium externally mounted on a titanium stent in an effort to maximize the effec-
tive orifice size relative to the outside diameter of the sewing ring (Courtesy of Drs. Cheung and Streckenbach).

A,B C
FIGURE 13.17 Transesophageal midesophageal aortic valve short-axis (panels A, B, and C) views of stented biopros-
thetic valves in the aortic position with corresponding photographs of the actual prosthetic valves (lower panel). The
struts protruding into the aortic root of the porcine (Hancock II) bioprosthetic valve (arrow, panel A) can be distinguished
in the short-axis cross-sectional view (panel A), but acoustic shadowing from the prosthetic valve stent obscures the bio-
prosthetic leaflets. Both the struts (arrow, panel B) and individual leaflets (arrowhead, panel B) of a Carpentier–Edwards
bovine pericardial bioprosthetic valve in systole can be imaged in the short-axis cross-sectional view (panel B). Detailed
examination can distinguish that the pericardial leaflets on the Sorin Mitroflow prosthetic valve (arrow, panel C) are
mounted on the external surface of the struts. Edema or thickening of the wall of the aortic root is sometimes present
after aortic valve replacement (asterisks, panels A and B). (Courtesy of Drs. Cheung and Streckenbach).
A B
FIGURE 13.18 Mild transvalvular regurgitation can normally be detected sometimes immediately after implantation
of bovine pericardial bioprosthetic valves. Midesophageal four-chamber view with color Doppler flow imaging demon-
strated mild central regurgitation (arrow) through the leaflet commissures in a bovine pericardial bioprosthetic valve
implanted in the mitral position (panel A). Transgastric mid-left ventricular long-axis view through the aortic valve with
color Doppler flow imaging detected mild regurgitation through the fabric-covered stent struts (arrows) in a bovine
pericardial bioprosthetic valves implanted in the aortic position (panel B). These transvalvular regurgitant jets typically
decrease in severity over time. LA, left atrium; LV, left ventricle; Ao, aorta.

A B
FIGURE 13.19 Intraoperative transesophageal midesophageal aortic valve long-axis view immediately after implan-
tation of a stentless porcine bioprosthetic aortic root (Medtronic Freestyle) in the aortic position (panel A). Periaortic
thickening (arrow, panel A) is common immediately after implantation and can be attributed to tissue edema. Only the
cloth-reinforced annular sewing ring produces an acoustic shadow on 2D (asterisk, panel A) and Doppler color flow imag-
ing (asterisk, panel B) (Courtesy of Drs. Cheung and Streckenbach).
increases the effective orifice area that can be achieved after valve replacement making them particularly
useful in patients with a native aortic valve annulus less than 20 mm in diameter. Elimination of the stent
also permits greater freedom of movement of the valve leaflets and annulus and, in theory, may decrease
the risk of structural valvular degeneration. However, the competency of the stentless aortic valve is con-
tingent on the geometry of the aortic root. Mismatching of the annular size, malalignment of the leaflets
in the annular plane, or dilatation of the aortic root will alter leaflet coaptation and cause regurgitation.
For this reason, it is important for the intraoperative echocardiographic examination to accurately size the
native annulus and verify that the ascending aorta is not dilated and that the diameter of the sinotubular
junction matches or is within 10% the diameter of the stentless valve (15). The echocardiographic appear-
ance of the stentless valve is virtually indistinguishable from the native aortic valve except for the presence
of an acoustic shadow caused by the Dacron reinforcement at the base of the valve annulus (Fig. 13.19).
Implantation of the stentless valve within the native aortic root increases the thickness of the vessel wall
at the region of overlap and makes paravalvular regurgitation possible (Fig. 13.19). Trace or mild central
aortic regurgitation is detectable up to 25% of the time immediately after implantation of the stentless
bioprosthetic valve.
The Medtronic ATS 3f is a new generation pericardial stentless valve constructed from three equine
pericardial leaflets shaped in the form of a tube attached directly to a polyester annular sewing ring. After
implantation within the aortic valve annulus, the three commissural tabs on the distal side of the valve
attached directly to the native aortic wall and the prosthetic sewing ring can be distinguished by TEE. The
absence of regurgitation by color Doppler examination after implantation is useful to ensure that the valve
and the commissural suspension points are properly positioned within the aortic root.
Allograft Valves
Cryopreserved human aortic root allografts are commercially available for implantation. They are sized
according to the aortic valve annulus diameter in a range from 20 to 26 mm. Absence of a stent requires
that the annular size of the allograft matches the size of the native valve annulus to ensure valve compe-
tence. Implantation of an undersized or oversized allograft may result in aortic regurgitation. The echo-
cardiographic appearance of the aortic allograft is indistinguishable from the native aortic valve and aortic
root. Replacement of the aortic root and reimplantation of the coronary arteries with a human aortic root
allograft, stentless porcine aortic root, or mechanical valved conduit is performed for aortic valve endo-
carditis with aortic root abscess, bicuspid aortic valve with dilated aortic root, type A aortic dissection, or
aneurysms involving the aortic root and ascending aorta.

CLINICAL CAVEATS FOR THE ECHOCARDIOGRAPHIC

DIAGNOSIS OF PROSTHETIC VALVE DYSFUNCTION
Prosthetic valve dysfunction can result in regurgitation, stenosis, or hemolysis. TEE is recognized as the
diagnostic examination of choice for the diagnosis and evaluation of suspected prosthetic valve dysfunction.
1. Prosthetic valve regurgitation. When the Doppler examination reveals regurgitation in a prosthetic
valve, it is important to distinguish physiologic regurgitation from pathologic regurgitation.
a. A small amount of regurgitation is normally observed in all mechanical prosthetic valves except for
caged-ball valves and in approximately 10% of bioprosthetic valves. Closure backflow is the rever-
sal of flow required for closure of the valve. In contrast, leakage backflow occurs after closure of
mechanical valves and originates from the hinges and the regions of coaptation between the occlud- Video 13.2
ers and the valve ring (Figs. 13.1, 13.5, 13.6, 13.12, 13.18, Videos 13.2, 13.4, and 13.5). Physiologic
Video 13.4
regurgitation jets are small and short in duration. The leakage backflow patterns for each valve type
Video 13.5
are unique and distinct from pathologic regurgitation (Fig. 13.11). Mild transvalvular regurgita-
tion can often be detected by TEE Doppler flow imaging in bioprosthetic valves immediately after
implantation (Fig. 13.18). Regurgitant jets that originate at the sites of leaflet coaptation are directed
centrally. Regurgitant jets from leakage at the fabric-covered regions of the valve stent originate at
the valve struts and are directed toward the center of the valve. Mild physiologic transvalvular regur-
gitation in bioprosthetic valves detected by TEE immediately after implantation typically decreases
or even disappears by the end of the operation.
b. Pathologic transvalvular regurgitation in bioprosthetic valves is commonly associated with
chronic degenerative changes that may include leaflet calcification, perforation, tears, or prolapse
(Figs. 13.20 and 13.21), or from leaflet destruction caused by endocarditis. In mechanical prosthetic
valves, pathologic transvalvular regurgitation can be caused by pannus, thrombus, vegetations, or
foreign material on valve components that prevent complete closure of the occluder (Fig. 13.22).
Two-dimensional and three-dimensional imaging of leaflet or occluder motion in mechanical valves
is useful for detecting transvalvular regurgitation caused by impingement of the occluder by pannus,
thrombus, or vegetations (Video 13.7). Grading systems based on Doppler measurements of regurgi- Video 13.7
tant fraction, regurgitant jet area, jet length, and vena contracta or jet width also apply for assessing the
clinical severity of prosthetic valve regurgitation. However, the pattern and location of regurgita-
tion associated with prosthetic valve dysfunction differ from those associated with native valvular
heart disease and sometimes require an alternative or integrative approach to grade the severity of
regurgitation. For example, in the case of paravalvular regurgitation, the annular extent of the defect
A B C
FIGURE 13.20 Transesophageal midesophageal aortic valve long-axis view of a porcine bioprosthetic valve in the
aortic position demonstrating structural valvular degeneration with prolapse and perforated valve cusps (arrow, panel
A). Doppler color flow imaging in diastole demonstrated severe transvalvular regurgitation through the defects (arrow,
panel B) that were also apparent on the explanted prosthetic valve (panel C) (Courtesy of Drs. Cheung and Streckenbach).
LV, left ventricle; Ao, aorta; LA, left atrium.

A B C D
FIGURE 13.21 Transesophageal midesophageal four-chamber view of a stented bovine pericardial bioprosthetic valve
implanted in the mitral position. Two-dimensional imaging demonstrated restricted leaflet motion in diastole (arrow,
panel B) and incomplete coaptation in systole (panel A). Doppler color flow imaging demonstrated severe central mitral
regurgitation (panel C). Pannus formation at the base of the prosthetic valve leaflets (arrows, panel D) and thickening of
the leaflet edges (asterisk, panel D) causing leaflet restriction and transvalvular regurgitation was seen in the explanted
specimen (Courtesy of Drs. Cheung and Streckenbach). LV, left ventricle; LA, left atrium.
can be used to quantify the severity of regurgitation along with regurgitant jet width, size, length,
eccentricity, density, and proximal flow convergence (Tables 13.7 and 13.8).
c. Paravalvular regurgitation is always pathologic and is caused by prosthetic endocarditis, incom-
plete fixation of the prosthetic sewing ring to the native annulus, or dehiscence of the sewing ring.
Incomplete fixation is typically caused by native annular calcification that increases the difficulty of
prosthetic implantation or an avulsed annular suture. Paravalvular regurgitant jets imaged using color
Doppler flow imaging originate at a point outside of the sewing ring, characteristically produce eccen-
tric jets that track along the walls of the receiving chamber, and are usually accompanied by zones
of proximal flow convergence adjacent to the site of the defect in the upstream cardiac chamber
Video 13.3 (Fig. 13.7, Video 13.3). Evidence to support the best course of action in response to the TEE detection
of paravalvular regurgitation immediately after prosthetic valve implantation is limited. Some clinical
A B
FIGURE 13.22 Severe transvalvular regurgitation caused by a leaflet trapped in the open position due to pannus
ingrowth. Transgastric mid-left ventricular long-axis view through the aortic valve in a patient with a bileaflet mechanical
prosthetic valve in the aortic position. Two-dimensional imaging (panel A) demonstrated one of the valve leaflets was
immobile and trapped in the open position (arrow). Color Doppler flow imaging (panel B) demonstrated severe trans-
valvular regurgitation through the region of the prosthetic valve with the leaflet trapped in the open position (arrow).
LA, left atrium; LV, left ventricle; Ao, aorta.

TABLE 13.7 Echocardiographic Parameters for Grading the Severity of Prosthetic Aortic Regurgitation
Parameter Mild Moderate Severe

■ 2D and 3D parameters
Valve stent Normal Abnormala Abnormala
Leaflets or occluders Normal Abnormalb Abnormalb
Jet width (% LVOT diameter)c Narrow (≤25) Intermediate (26–64) Large (>65)
Jet density (CW Doppler) Incomplete/faint Dense Dense
Jet deceleration rate (PHT, ms)d Slow (>500) Variable (200–500) Steep (<200)
LVOT flow:pulmonary flow ratio Slightly increased Intermediate Greatly increased
Diastolic flow reversal (Desc. Ao) Absent or brief Intermediate Prominent
Regurgitant volume (mL/beat) <30 30–59 >60
Regurgitant fraction (%) <30 30–50 >50
a
Examples of abnormal motion include dehiscence or rocking.
b
Examples of abnormal motion include immobile occluder, limited occluder range of travel, or prolapsed bioprosthetic leaflet.
c
At a Nyquist limit set at 50–60 cm/s. Parameter is less accurate for eccentric jets.
d
Influenced by left ventricular compliance.
CW, continuous wave; Desc. Ao, descending thoracic aorta; LVOT, left ventricular outflow tract; PHT, pressure half-time.
TABLE 13.8 Echocardiographic Parameters for Grading the Severity of Prosthetic Mitral Regurgitation
Parameter Mild Moderate Severe

■ 2D and 3D parameters
Valve stent Normal Abnormala Abnormala
Leaflets or occluders Normal Abnormalb Abnormalb
Color flow jetc Small central jet Variable Large central jet
<4 cm2 4–8 cm2 >8 cm2
Eccentric wall impinging jet
Flow convergenced None or minimal Intermediate Large
Pulmonary venous flowe Systolic dominance Systolic blunting Systolic flow reversal
Vena contracta width (cm)f <0.3 0.3–0.59 ≥0.6
Regurgitant volume (mL/beat)f <30 30–59 ≥60
Regurgitant fraction (%)f <30 30–49 ≥50
EROA (cm2)f <0.20 0.20–0.49 ≥0.50
a
Examples of abnormal motion include dehiscence or rocking.
b
Examples of abnormal motion include immobile occluder, limited occluder range of travel, or prolapsed bioprosthetic leaflet.
c
At a Nyquist limit set at 50–60 cm/s.
d
Minimal and large flow convergence defined as a flow convergence radius <0.4 cm and ≥0.9 cm for central jets, respectively, at
a Nyquist limit of 40 cm/s; thresholds for eccentric jets may be greater.
e
Other reasons for systolic blunting include atrial fibrillation and increased left atrial pressure.
f
Quantitative Doppler parameters for grading prosthetic mitral regurgitation are less well validated compared to use in native
mitral regurgitation.
EROA, effective regurgitant orifice area.

A B
FIGURE 13.23 Dehiscence, bovine pericardial bioprosthesis in the aortic position. Transesophageal echocardiographic
midesophageal aortic valve long-axis image at a multiplane angle of 113 degrees showing dehiscence of a pericardial
bioprosthesis in the aortic position. In systole (panel A), the anterior region of the prosthetic stent (arrow) is displaced
toward the left ventricular side of the native aortic valve annulus. In diastole (panel B) the anterior region of the pros-
thetic stent is completely detached from the aortic valve annulus (arrow). Dehiscence with partial annular detachment
produced a “rocking” motion of the prosthetic valve and paravalvular regurgitation in the region of separation (arrow).
LA, left atrium; LVOT, left ventricular outflow tract; Ao, aorta.
series suggested that intraoperative TEE was useful for detecting paravalvular regurgitation and
prompted revision of the valve replacement (16). In a very small series, two out of six patients with
mild paravalvular regurgitation and two out of two patients with moderate paravalvular regurgitation
detected by TEE immediately after mitral valve replacement had subsequent clinical deterioration
(17). Another study examining 27 patients after aortic or mitral valve replacement found that small
paravalvular regurgitant jets detected by TEE using Doppler color flow imaging were common after
valve replacement, decreased in size and number after protamine administration, and were not asso-
ciated with early postoperative morbidity (18). Finally, in a large series of 608 consecutive patients
undergoing aortic or mitral valve replacement, trivial or mild paravalvular regurgitation defined as
a regurgitant jet area less than 3 cm2 by Doppler color flow imaging was detected by intraoperative
TEE in 18.3% of patients (19). At early follow-up, paravalvular regurgitation had resolved in 50% of
the patients. At late follow-up, only 4 out of the original 113 patients with mild paravalvular regur-
gitation had worsening of regurgitation. Precise characterization of the location, annular extent, and
multimodal assessment of the severity of paravalvular regurgitant jets detected by TEE after valve
implantation is important for guiding intraoperative decisions whether surgical revision is necessary.
Paravalvular regurgitation as a consequence of dehiscence is a late complication after valve replace-
ment and is commonly associated with endocarditis. Dehiscence of part of the sewing ring may desta-
bilize the prosthetic valve producing a “rocking” motion of the entire prosthesis and a visible separa-
tion of the native and prosthetic valve annulus detected by 2D imaging (Figs. 13.7 and 13.23).
2. Prosthetic valve stenosis. Compared to the native valve, all prosthetic valves are mildly stenotic depending
upon the valve type, size, and the hemodynamic condition of the patient. The mean pressure gradient
across prosthetic valves calculated using the simplified Bernoulli equation depends on the prosthetic
valve type, its position, its size, the blood flow velocity proximal to the prosthetic valve, and the cardiac
output. For this reason, the package insert or published normal values that lists the hemodynamic
specifications for the particular valve type and model according to annular size is often used as a
reference when examining the hemodynamic performance of a specific prosthetic valve (Appendix D)
(1,8–10). The peak transvalvular gradient for valves in the mitral position ranges from 3 to 4 mm Hg
and the peak transvalvular gradient for valves in the aortic position ranges from 10 to 30 mm Hg.

TABLE 13.9 Doppler Parameters for Diagnosis of Prosthetic Tricuspid Stenosis
Parameter Consider valve stenosisa

Peak velocityb >1.7 m/s
Mean gradientb ≥6 mm Hg
Pressure half-time ≥230 ms
a
Because of respiratory variation use the average of at least 5 cardiac cycles.
b
Prosthetic valvular regurgitation may also increase these parameters.
Threshold values of echocardiographic parameters that suggest significant prosthetic valve stenosis are
also available in published guidelines (Tables 13.5, 13.6, and 13.9) (1).
3. The continuity method can also be used to estimate the effective orifice area (EOA) of prosthetic valves
in the mitral or aortic positions (Table 13.3). The continuity method uses Doppler to measure the velocity–
time integral (VTI) across the prosthetic valve in relation to the cross-sectional area of the LVOT and
the VTI through the LVOT. A normal value of the EOA estimated by the continuity equation is ≥2 cm2
for prosthetic valves in the mitral position and >1.2 cm2 for prosthetic valves in the aortic position
(Tables 13.5 and 13.6). Stenosis of bioprosthetic valves is caused by chronic degenerative changes
resulting in leaflet calcification, thickening, and rigidity, restricting their ability to open completely.
Degenerative changes and restricted leaflet mobility can be detected by the 2D and 3D examination.
In mechanical valves, stenosis can be caused by thrombus, pannus, vegetation, suture, or even retained
subvalvular structures that trap the occluder mechanism in the closed position or impinge its ability to
open completely (Figs. 13.8 and 13.13).
4. Prosthesis–patient mismatch. Prosthetic heart valves are inherently stenotic relative to native cardiac
valves. Although still somewhat controversial, several clinical studies have provided evidence that
implantation of a prosthetic valve that is sized too small for an individual patient has the potential
to cause significant obstruction to flow (20–23). The hemodynamic consequences of flow obstruction
caused by a normally functioning prosthetic valve increased the likelihood of mortality and cardiac
complications after aortic valve replacement (21–23). Implantation of a stenotic prosthetic valve in
the aortic position for aortic stenosis has also been shown to be associated with decreased ventricular
mass regression after operation (24). This condition is called prosthesis–patient mismatch and may be
particularly important in patients with decreased left ventricular ejection fraction. Prosthesis–patient
mismatching has been best described after aortic valve replacement because the diameter of the native
aortic valve annulus limits the size of the prosthetic valve that can be implanted. However, several studies
have also suggested that prosthesis–patient mismatching may occur also after mitral valve replacement
and was manifested by pulmonary hypertension (25). Intraoperative TEE provides an opportunity to
measure the diameter of the native aortic valve annulus to determine the size of prosthetic valve that can
be implanted, thus helpful for predicting the risk of prosthetic–patient mismatch based on the indexed
effective orifice area (EOAi = EOA/BSA, where EOAi is the indexed effective orifice area, EOA is the
effective orifice area of the prosthetic valve, and BSA is the body surface area of the patient in m2) (see
Table 13.3). Prosthesis–patient mismatch is considered severe after aortic valve replacement if the EOAi
is ≤0.65 cm2/m2, moderate if the EOAi is between 0.65 and 0.85 cm2/m2, and not significant if the EOAi is
≥0.85 cm2/m2 (21). Prosthesis–patient mismatch is considered significant after mitral valve replacement
if the EOAi is ≤1.2 cm2/m2 (21). If intraoperative TEE measurements detect a small aortic valve annulus
prior to aortic valve replacement, operative options to decrease the risk of patient prosthetic mismatch
include implanting the prosthetic valve in the supra-annular position, choosing a prosthetic valve model
with the greatest EOA for the given annular diameter, performing an aortic root enlargement procedure
to permit implantation of a larger prosthetic valve, or replacing the aortic root.
5. Thrombosis and pannus. Acute thrombosis, usually as a result of inadequate anticoagulation, can cause
stenosis or regurgitation by obstructing blood flow through the valve or by interfering with occluder opening
and closure. Stenosis or regurgitation can also be caused by ingrowth of pannus, a subacute condition. 2D
and 3D imaging may demonstrate abnormal masses attached to the prosthetic valve sometimes interfering

FIGURE 13.24 Endocarditis and aortic root abscess, mechanical bileaflet valve, aortic position. Transesophageal echo-
cardiographic midesophageal aortic valve long-axis image at a multiplane angle of 139 degrees demonstrating pros-
thetic endocarditis in a patient with a mechanical bileaflet valve in the aortic position. A vegetation attached to the
prosthetic valve was imaged in the left ventricular outflow tract during diastole (single arrow). Thickening of the posterior
wall of the aortic root (double arrows) suggested aortic root abscess.
with or limiting the range of motion of the occluder device (Fig. 13.13). Pannus, with its fibrous composition,
is echodense and firmly fixed to the valve apparatus. Thrombus tends to be more mobile, larger in size,
and sometimes associated with spontaneous echocontrast in the cardiac chambers indicating regions of
low flow (26). Color Doppler imaging may demonstrate transvalvular regurgitation or an eccentric inflow
pattern across the affected leaflet (Fig. 13.22). Sometimes, pannus ingrowth is diagnosed only indirectly by
demonstrating significant prosthetic valve stenosis or abnormal patterns of regurgitation.
6. Hemolysis. Hemolysis is unusual with modern valve prostheses, but hemolysis can occur when blood
is subjected to high peak shear stresses. These hydrodynamic conditions can occur when blood
accelerates rapidly or decelerates rapidly upon collision or impingement with prosthetic material (27).
Regurgitant jets associated with hemolysis often exhibit patterns of flow fragmentation, collision, or
rapid acceleration by color Doppler flow imaging. Free regurgitant jets or jets that decelerate gradually
are less likely to produce hemolysis.
7. Endocarditis. Prosthetic endocarditis occurs in approximately 3% to 6% of patients after valve replacement
and has a mortality that ranges between 20% and 80% (3). TEE is currently the best diagnostic technique
for detecting vegetations, dehiscence, or annular abscess for the diagnosis of prosthetic endocarditis
(Figs. 13.7 and 13.24) (28). Because of acoustic shadowing artifacts, it is important to use both
midesophageal and transgastric imaging planes to examine both sides of the prosthetic valve for the
presence of vegetations.
8. LVOT obstruction. LVOT obstruction causing subvalvular aortic stenosis is uncommon, but is a recognized
complication of mitral valve replacement (29–31). After mitral valve replacement performed using the
valve sparing or chordal sparing techniques, residual mitral valve leaflet or chordal apparatus remaining in
the LVOT can cause LVOT obstruction. LVOT obstruction can also be caused by a bioprosthetic valve in
the mitral position with a strut protruding into the LVOT causing obstruction to left ventricular outflow.
The transgastric long-axis view provides a means to image the LVOT after mitral valve replacement and
Video 13.8 to estimate the LVOT pressure gradient using continuous wave Doppler (Video 13.8).
CONCLUSION
The evaluation of prosthetic heart valves, the diagnosis of prosthetic valve dysfunction, and the detection of
complications associated with valve replacement are important clinical applications of TEE. A systematic

TABLE 13.10 General Principles for Applying TEE in Valve Replacement Procedures
1. Know the make and models of prosthetic valves used in your hospital and their characteristic 2D, 3D, and
Doppler echocardiographic features
2. Perform and record a baseline (prebypass) complete standardized TEE examination
3. Watch and listen to the surgeons as they implant the prosthetic valve
4. Start TEE assessment of the prosthetic valve before separation from bypass
5. Use TEE to assist with de-airing the cardiac chambers
6. Become an expert at examining the cardiac valves from the transgastric views
7. Use 2D, 3D, zoom, and slow-motion replay to examine a prosthetic valve
8. Use Doppler echocardiography to quantify the hemodynamic performance of the prosthetic valve
9. Get a second opinion to confirm a difficult diagnosis
10. Have available reference of the hemodynamic specifications for commonly used prosthetic valve models and
sizes
approach to the TEE examination in patients undergoing valve replacement operations and in patients
with prosthetic cardiac valves is necessary to verify the proper functioning of the prosthetic valves and
to diagnose prosthetic valve dysfunction or complications associated with valve replacement procedures
(Table 13.10).
REFERENCES
1. Zoghbi WA, Chambers JB, Dumesnil JG, et al. Recommendations for evaluation of prosthetic valves with echocardiography
and Doppler ultrasound. J Am Soc Echocardiogr. 2009;22:975–1014.
2. Seward JB, Labovitz AJ, Lewis JF, et al. ACC position statement. Transesophageal echocardiography. J Am Coll Cardiol.
1992;20:506.
3. Vongpatanasin W, Hillis DL, Lange RA. Medical progress: Prosthetic heart valves. N Engl J Med. 1996;335:407–416.
4. Daniel WG, Mugge A, Grote J, et al. Comparison of transthoracic and transesophageal echocardiography for detection of
abnormalities of prosthetic and bioprosthetic valves in the mitral and aortic positions. Am J Cardiol. 1993;71:210–215.
5. Khandheria BK, Seward JB, Oh JK, et al. Value and limitations of transesophageal echocardiography in assessment of mitral
valve prostheses. Circulation. 1991;83:1956–1968.
6. Karalis DG, Chandrasekaran K, Ross JJ, et al. Single-plane transesophageal echocardiography for assessing function of
mechanical or bioprosthetic valves in the aortic position. Am J Cardiol. 1992;69:1310–1315.
7. Chambers J, Fraser A, Lawford P, et al. Echocardiographic assessment of artificial heart valves: British Society of
Echocardiography position paper. Br Heart J. 1994;71(4 suppl):6–14.
8. Panidis IP, Ross J, Mintz GS. Normal and abnormal prosthetic valve function as assessed by Doppler echocardiography. J Am
Coll Cardiol. 1986;8:317–326.
9. Reisner SA, Meltzer RS. Normal values of prosthetic valve Doppler echocardiographic parameters: A review. J Am Soc
Echocardiogr. 1988;1:201–210.
10. Rosenhek R, Binder T, Maurer G, et al. Normal values for Doppler echocardiographic assessment of heart valve prostheses.
J Am Soc Echocardiogr. 2003;16:1116–1127.
11. Baumgartner H, Khan S, DeRobertis M, et al. Discrepancies between Doppler and catheter gradients in aortic prosthetic valves
in vitro. A manifestation of localized gradients and pressure recovery. Circulation. 1990;82:1467–1475.
12. Bech-Hanssen O, Gjertsson P, Houltz E, et al. Net pressure gradients in aortic prosthetic valves can be estimated by Doppler.
13. Maslow AD, Haering JM, Heindel S, et al. An evaluation of prosthetic aortic valves using transesophageal echocardiography:
The double-envelope technique. Anesth Analg. 2000;91:509–516.
14. Malouf JF, Ballo M, Connolly HM, et al. Doppler echocardiography of 119 normal-functioning St Jude Medical mitral valve
prostheses: A comprehensive assessment including time-velocity integral ratio and prosthesis performance index. J Am Soc
Echocardiogr. 2005;18:252–256.
15. Guarracino F, Zussa C, Polesel E, et al. Influence of transesophageal echocardiography on intraoperative decision making for
Toronto stentless prosthetic valve implantation. J Heart Valve Dis. 2001;10:31–34.
16. Shapira Y, Vaturi M, Weisenberg DE, et al. Impact of intraoperative transesophageal echocardiography in patients undergoing
valve replacement. Ann Thorac Surg. 2004;78:579–583.
17. Movsowitz HD, Shah SI, Ioli A, et al. Long-term follow-up of mitral paraprosthetic regurgitation by transesophageal echocar-
diography. J Am Soc Echocardiogr. 1994;7:488–492.
18. Morehead AJ, Firstenberg MS, Shiota T, et al. Intraoperative echocardiographic detection of regurgitant jets after valve
replacement. Ann Thorac Surg. 2000;69:135–139.
19. O’Rourke DJ, Palac RT, Malenka DJ, et al. Outcome of mild periprosthetic regurgitation detected by intraoperative trans-
esophageal echocardiography. J Am Coll Cardiol. 2001;38:163–166.

20. Koch CG, Khandwala F, Estafanous FG, et al. Impact of prosthesis-patient size on functional recovery after aortic valve
replacement. Circulation. 2005;111:3221–3229.
21. Blais C, Dumesnil JG, Baillot R, et al. Impact of valve prosthesis-patient mismatch on short-term mortality after aortic valve
replacement. Circulation. 2003;108:983–988.
22. Tasca G, Mhagna Z, Perotti S, et al. Impact of prosthesis-patient mismatch on cardiac events and midterm mortality after
aortic valve replacement in patients with pure aortic stenosis. Circulation. 2006;113:570–576.
23. Mohty-Echahidi D, Malouf JF, Girard SE, et al. Impact of prosthesis-patient mismatch on long-term survival in patients with
small St. Jude Medical mechanical prostheses in the aortic position. Circulation. 2006;113:420–426.
24. Tasca G, Brunelli F, Cirillo M, et al. Impact of valve prosthesis-patient mismatch on left ventricular mass regression following
aortic valve replacement. Ann Thorac Surg. 2005;79:505–510.
25. Li M, Dumesnil JG, Mathieu P, et al. Impact of valve prosthesis-patient mismatch on pulmonary arterial pressure after mitral
valve replacement. J Am Coll Cardiol. 2005;45:1034–1040.
26. Barbetseas J, Nagueh SF, Pitsavos C, et al. Differentiating thrombus from pannus formation in obstructed mechanical pros-
thetic valves: An evaluation of clinical, transthoracic, and transesophageal echocardiographic parameters. J Am Coll Cardiol.
1998;32:1410–1417.
27. Garcia MJ, Vandervoort P, Stewart WJ, et al. Mechanisms of hemolysis with mitral prosthetic regurgitation. Study using trans-
esophageal echocardiography and fluid dynamic simulation. J Am Coll Cardiol. 1996;27:399–406.
28. Piper C, Korfer R, Horstkotte D. Prosthetic valve endocarditis. Heart. 2001;85:590–593.
29. Jett GK, Jett MD, Banhart GR, et al. Left ventricular outflow tract obstruction with mitral valve replacement in small ventricu-
lar cavities. Ann Thorac Surg. 1986;41:70–74.
30. Come PC, Riley MF, Weintraub RM, et al. Dynamic left ventricular outflow tract obstruction when the anterior leaflet is
retained at prosthetic mitral valve replacement. Ann Thorac Surg. 1987;43:561–563.
31. Gallet B, Berrebi A, Grinda JM, et al. Severe intermittent intraprosthetic regurgitation after mitral valve replacement with
subvalvular preservation. J Am Soc Echocardiogr. 2001;14:314–316.

QUESTIONS
1. A 62-year-old male underwent aortic valve 4. A 70-year-old female underwent TEE
replacement for aortic stenosis with a examination to assess the function of a
bioprosthetic valve prosthesis. Continuous mechanical bileaflet mechanical prosthetic
wave Doppler echocardiography valve implanted in the mitral position for
measured a peak velocity of 231 cm/s and mitral stenosis 15 years ago. Continuous wave
a mean velocity of 141 cm/s across the Doppler echocardiography measured a peak
prosthetic valve. Pulsed wave Doppler velocity across the prosthetic valve of 1.5 m/s,
echocardiography measured a peak velocity a mean gradient across the valve of 4 mm Hg,
of 154 cm/s and a mean velocity of and a pressure half-time of 110 milliseconds.
86 cm/s in the left ventricular outflow tract. These findings are consistent with:
The most accurate peak pressure gradient a. A normally functioning prosthetic valve in
across the bioprosthetic aortic valve is: the mitral position
a. 30 mm Hg b. Possible stenosis of the prosthetic valve
b. 21 mm Hg c. Significant stenosis of the prosthetic valve
c. 12 mm Hg d. Significant stenosis of the prosthetic valve if
d. 10 mm Hg the cardiac output is normal
e. 4 mm Hg e. Echocardiography cannot be used to diag-
nosis prosthetic mitral stenosis
2. An 82-year-old female who was 5′2″ and
148 lbs with a body surface area (BSA) of 5. A 56-year-old male with a height of 5′10″,
1.68 m2 underwent aortic valve replacement weight of 180 lbs, and body surface area
with a 19-mm bioprosthetic valve. of 2 m2, and a left ventricular ejection
Echocardiographic measurements after fraction of 60% is scheduled for aortic
prosthetic valve implantation yielded a left valve replacement for calcific aortic
ventricular outflow tract (LVOT) diameter of stenosis. Intraoperative TEE demonstrated
1.8 cm, a velocity–time integral of 30 cm in a native aortic valve annulus of 19.5 mm
the left ventricular outflow tract (VTILVOT), in diameter. To avoid severe patient–
and a velocity–time integral (VTIAoV) of prosthetic mismatching, the following
60 cm across the prosthetic aortic valve. needs to be performed:
These findings are consistent with: a. Aortic root enlargement
a. No prosthetic–patient mismatching b. Avoid using a mechanical prosthetic valve
b. Mild prosthetic–patient mismatching c. Aortic root replacement
c. Moderate prosthetic–patient mismatching d. Myomectomy
d. Severe prosthetic–patient mismatching e. Select a prosthetic valve with an estimated
e. Cannot determine the severity of prosthetic– orifice area greater than 1.3 cm2
patient mismatching based on the information
6. A 50-year-old male with bicuspid aortic
3. A 74-year-old male underwent aortic valve, aortic regurgitation, and a dilated
valve replacement for aortic stenosis. ascending aorta underwent a composite
Intraoperative TEE examination after aortic root replacement, ascending aorta, and
implantation of the prosthetic aortic valve partial aortic arch graft with a mechanical
revealed paravalvular regurgitation. The valved conduit. A leak at the proximal aortic
best echocardiographic method to grade valve annular suture line would:
the severity of prosthetic regurgitation is a. Have no clinical consequences
performed by: b. Cause paravalvular regurgitation that can
a. Measuring the width of the regurgitant jet be detected by TEE
with Doppler color flow imaging c. Cause nonpathologic transvalvular regurgi-
b. Estimating the density of the regurgitant jet tation
using continuous wave Doppler d. Cause cardiac tamponade
c. Detecting the presence of proximal flow e. Lead to an aortic pseudoaneurysm
acceleration at the site of regurgitation
d. Calculating the regurgitant volume
e. Combining qualitative and quantitative echo-
cardiographic parameters of regurgitation

7. The best TEE view to assess the individual d. TEE upper esophageal aortic arch short-
motion of the occluders of a mechanical axis view
bileaflet prosthetic valve implanted in the e. There is no TEE imaging plane that can be
aortic position is the: used to measure the velocity of blood flow
a. TEE midesophageal aortic valve short-axis across a prosthetic valve in the pulmonic
view position
b. TEE midesophageal aortic valve long-axis
11. The TEE midesophageal aortic valve short-
view
axis view (see image below) indicates
c. TEE midesophageal right ventricular
that the patient has the following type of
inflow–outflow view
prosthetic valve in the aortic position:
d. TEE transgastric long-axis view
e. TEE cannot be used to assess the individual
motion of occluders of a mechanical pros-
thetic valve implanted in the aortic position
8. The best TEE view to assess the individual
motion of the occluders of a mechanical
bileaflet prosthetic valve implanted in the
mitral position is the:
a. TEE midesophageal four-chamber view
b. TEE midesophageal aortic valve short-axis
view
c. TEE transgastric long-axis view
d. TEE transgastric two-chamber view
e. TEE deep transgastric long-axis view a. Mechanical bileaflet prosthesis
9. An 85-year-old female who had a caged-disc b. Tilting disc mechanical prosthesis
prosthetic valve implanted in the mitral c. Caged-ball mechanical prosthesis
position for mitral stenosis presents with d. Stentless porcine bioprosthesis
congestive heart failure. TEE was ordered e. Pericardial bioprosthesis
to assess the function of the prosthetic 12. The continuous wave Doppler spectral
valve. The following can be most accurately display of blood flow velocity through the
determined from the TEE examination: mitral valve indicates that the patient had
a. Prosthetic–patient mismatching what type of prosthetic valve implanted in
b. The severity of prosthetic valve stenosis the mitral position (see image below)?
c. The severity of paravalvular regurgitation
d. The left ventricular end-diastolic pressure
e. The estimated orifice area of the prosthetic
valve
10. A 48-year-old female who underwent
Tetralogy of Fallot repair as a child had
a pulmonic valve replacement with a
bioprosthetic valve for severe pulmonic
regurgitation. TEE examination can be
used to estimate the pulmonary artery
pressure in the presence of mild physiologic
transvalvular regurgitation through
the bioprosthetic valve in the pulmonic
position using the following imaging plane: a. Bileaflet mechanical prosthetic valve
a. TEE midesophageal aortic valve short-axis b. Porcine bioprosthetic valve
view c. Bovine pericardial prosthetic valve
b. TEE midesophageal right ventricular d. Prosthetic mitral annular ring
inflow–outflow view e. Did not have a prosthetic valve implanted in
c. TEE transgastric right ventricular inflow view the mitral position

13. The following prosthetic valve is no longer 18. Accurate application of the Doppler
available for clinical use: velocity index to quantify the severity of the
a. Caged-ball valve prosthetic valve stenosis in a patient with
b. Porcine bioprosthetic valve a bioprosthetic valve in the aortic position
c. Bovine pericardial bioprosthetic valve requires:
d. Human aortic allograft a. Measurement of blood flow velocity in the
e. Mechanical bileaflet prosthetic valve left ventricular outflow tract
b. Calculation of the cardiac output
14. TEE examination is requested to evaluate
c. Knowledge of the prosthetic valve size
a patient with a bioprosthetic valve in the
d. Estimation of the cross-sectional area of the
mitral position who presents with fever.
left ventricular outflow tract
The following echocardiographic findings
e. Normal sinus rhythm
are consistent with prosthetic valve
endocarditis: 19. A 52-year-old male who had a mitral valve
a. Paravalvular regurgitation replacement 5 years ago for rheumatic
b. Vegetation on the prosthetic valve leaflet mitral stenosis presents with fever and
c. Transvalvular regurgitation leukocytosis. Blood cultures had no
d. Rocking motion of the valve stent bacterial growth. The most sensitive and
e. All of the above specific test to evaluate this patient for
prosthetic endocarditis is:
15. Which of the following sites of regurgitant
a. Transthoracic echocardiography
flow across a prosthetic valve detected by
b. Transesophageal echocardiography
color Doppler flow imaging immediately
c. Fluoroscopy
after valve implantation are most likely
d. Cine computed tomography
considered pathologic?
e. Cardiac catheterization
a. At the hinge points in mechanical bileaflet
prosthetic valves 20. TEE midesophageal four-chamber view
b. At the central commissure of bovine peri- with Doppler color flow imaging in systole
cardial bioprosthetic valves from a 56-year-old patient with a normally
c. At the site of a suture through the sewing functioning prosthetic valve in the mitral
ring position (see image below). The TEE
d. Between the native annulus and the sewing examination indicates that the prosthetic
ring valve is a:
e. All regurgitation after valve implantation is
considered pathologic
16. Echocardiographic findings that indicate
structural valvular degeneration of a
bioprosthetic valve are:
a. Leaflet prolapse
b. Leaflet calcification
c. Leaflet perforation
d. Restricted leaflet opening
e. All of the above
17. Pannus ingrowth impairing the function
of a bileaflet mechanical prosthetic valve
implanted in the aortic position would most a. Starr–Edwards caged-ball prosthesis
likely produce the following pathologic b. Bjork–Shiley tilting disk prosthesis
echocardiographic finding: c. Medtronic Hall tilting disk prosthesis
a. Mass on the prosthetic valve d. St. Jude Medical bileaflet prosthesis
b. Disappearance of the normal transvalvular e. Sorin Mitroflow prosthesis
regurgitant jets at the hinge points
c. A Doppler velocity index less than 0.25
d. Abnormal motion of the valve stent
e. Paravalvular regurgitation

14 Right Ventricle, Right Atrium, Tricuspid
and Pulmonic Valves
Rebecca A. Schroeder, Barbora Parizkova, and Jonathan B. Mark
INTRODUCTION
Right ventricular (RV) dysfunction is a common concern in the perioperative period. Inadequate myocar-
dial protection, increases in pulmonary vascular resistance, air embolism to the RV coronary supply, and
acute valvular dysfunction can compromise RV performance. This chapter surveys the echocardiographic
approaches for evaluating the right side of the heart, the tricuspid valve (TV) and pulmonic valve (PV).
RIGHT VENTRICLE
Anatomy
Echocardiographic evaluation of the RV is complicated by the nongeometric, asymmetric, crescent shape
of this chamber. The RV consists of a free wall and a septum that is shared with the left ventricle (LV). The
RV free wall is divided into basal, mid, and apical segments corresponding to the adjacent LV segments as
seen in the midesophageal (ME) four-chamber view. The RV is also described in terms of its inflow and
outflow tracts. An encircling muscular band includes parietal and septal portions, separates these two
regions, and reflects their embryologic origins. Its most apical portion with the distinctive moderator band
is often well visualized with transesophageal echocardiography (TEE). Present in most normal individuals,
the moderator band is a muscular trabeculation extending from the lower interventricular septum to the
anterior RV free wall and serves as an anchoring structure for the tricuspid papillary muscles (Fig. 14.1).
Crista
supraventricularis
Parietal
band
Septal band
Moderator
band
FIGURE 14.1 Schematic drawing of anatomic structures in the right ventricle.

286

14. Right Ventricle, Right Atrium, Tricuspid and Pulmonic Valves 287
FIGURE 14.2 Transgastric midpapillary short-axis view. This image demonstrates the tricuspid valve in short axis during
diastole (i.e., with the leaflets in the open position). RV, right ventricle.
Transesophageal Echocardiographic Views

1. ME four-chamber view. This long-axis view of the RV allows assessment of all three segments of the RV.
In this view, the RV appears triangular in comparison with the elliptic LV, and its length is only two-
third the length of the LV (see Chapter 2 and Appendices).
2. ME RV inflow–outflow view. Often termed the wraparound view, the right atrium (RA), RV, and
pulmonary artery (PA) appear to “wraparound” the aortic valve and left atrium, describing a 270-degree
arc from left to right of the video display (see Chapter 2 and Appendices).
3. Transgastric (TG) midpapillary short-axis view. In addition to the monitoring of LV function, this view
serves to assess the function of the RV free wall and interventricular septum (Fig. 14.2, Video 14.1). Video 14.1
4. TG RV inflow view. Analogous to the two-chamber view of the LV, this view is acquired by advancing the
multiplane angle 90 degrees from the TG short-axis view of the RV (see above) or until the RA and RV
are seen in long axis, with the RV inflow and TV centered in the image. Alternatively, one develops the
TG two-chamber view of the left atrium and ventricle and then rotates the probe clockwise (rightward)
until the two right-sided chambers are displayed. Both techniques should result in the similar images of
the RV inflow tract and the long axis of the RA and the RV (Fig. 14.3, Video 14.2). Video 14.2
FIGURE 14.3 Transgastric right ventricular (RV) inflow view. RA, right atrium; RV, right ventricle.

FIGURE 14.4 Right ventricular (RV) dilation. Note the change in shape of the dilated right ventricle from triangular to
round. There is also a pulmonary artery catheter visible in the right atrium and ventricle. RA, right atrium; RV, right ven-
tricle; LA, left atrium; LV, left ventricle.
Additional TEE views may allow more complete assessment of RV function, particularly regional assess-
ment of RV wall motion (1).
Assessment of Global Right Ventricular Function

Hypertrophy
The normal thickness of the RV free wall measures less than 5 mm at end-diastole (2). RV hypertrophy
is present when the RV free wall thickness exceeds 5 mm, indicating elevated PA pressure or pulmonic
stenosis (PS) (3). In patients with chronic cor pulmonale, the RV wall thickness may exceed 10 mm while
intracavitary trabecular patterns become more prominent, particularly at the apex.
Dilation
RV dilation may be seen with RV volume or chronic RV pressure overload. Normally, the RV end-diastolic
cross-sectional area is approximately 60% of the area of the LV. As the RV dilates, its shape changes from
triangular to round. In addition, the cardiac apex, which should be made up solely of the LV, may be equally
shared between the ventricles or even dominated by the RV, indicating significant RV dilation. With mild RV
dilation, the RV area is >70% of the LV area on two-dimensional (2D) imaging. With moderate RV dilation,
the RV area may equal the LV area, and with severe RV enlargement, the RV area exceeds that of the LV (3,4)
Video 14.3 (Fig. 14.4, Video 14.3).
Systolic Function
Quantitative assessment of RV systolic function is limited by the unique geometry of RV, while variations in
shape occur readily with changes in RV volume. RV ejection is accomplished by inward motion of the RV free
wall, with lesser contributions from the right ventricular outflow tract (RVOT). Longitudinal shortening of the
RV with systolic descent of the tricuspid annulus also contributes significantly to RV ejection (3,4). Signs of RV
dysfunction include severe hypokinesis or akinesis of the RV free wall, RV enlargement, change in shape of the
RV from crescent to round, and flattening or bulging of the interventricular septum toward the left side.
Tricuspid Annular Plane Systolic Excursion

Long-axis systolic excursion of the lateral aspect of the tricuspid annulus may be used as an indicator
of RV systolic function. Normal tricuspid annular plane systolic excursion (TAPSE) is 20 to 25 mm with

ECG T
P
a
c v
CVP
y
x
S
D
HVQ
V
A A
FIGURE 14.5 A: Schematic diagram of the correlation of hepatic vein flow (HVQ) with central venous pressure (CVP) and
electrocardiogram (ECG). B: Pulsed wave Doppler image of normal hepatic venous flow with forward flow in systole (S)
and diastole (D) and two small retrograde waves (A and V).
<15 mm being considered significantly depressed. The angle of excursion is toward the cardiac apex, and is
slightly greater than normal mitral annular plane excursion (2). The tricuspid annulus tilts toward the apex,
whereas the mitral annulus moves more symmetrically toward the apex, somewhat like a piston, emphasiz-
ing the importance of measuring motion at the lateral annulus (4). Depressed TAPSE measurements sug-
gest depressed RV systolic function from a variety of causes.
Hepatic Venous Flow Patterns

Examination of flow velocity patterns during phases of the cardiac cycle with pulsed wave Doppler can
contribute useful information about RV function. Normal hepatic venous flow patterns have four phasic
components. Initial forward flow during systole is associated with atrial relaxation and apical movement of
the TV during RV systole and corresponds to the x-descent in atrial pressure measurements. Subsequent
diastolic flow, associated with early ventricular filling, corresponds to the y-descent. Two small retrograde
waves are often detectable, corresponding to atrial contraction at end-diastole (A) and at end-systole (V),
prior to the y-descent (Fig. 14.5A and B). When RV systolic function is impaired, the systolic inflow wave
of hepatic venous flow is attenuated and may even be reversed.

Assessment of Regional Right Ventricular Function

RV perfusion is supplied primarily by the right coronary artery, although a small portion of the anterior free
wall may be supplied by a conus branch of the left anterior descending artery (4,5). Since the thin-walled
RV is a volume-dependent chamber, its ejection fraction (EF) is extremely sensitive to changes in afterload.
In contrast, the thick-walled LV is a pressure-dependent chamber, and its EF is largely preserved over large
changes in afterload demand. Furthermore, the irregularity and asymmetry of the RV make changes in
inotropic function difficult to detect or quantify. More dramatic changes in function such as akinesis or
dyskinesis are more readily identified and are sensitive indicators of RV infarction (3,6). Less common find-
ings associated with RV infarction include RV dilation, papillary muscle dysfunction, tricuspid regurgita-
tion (TR), and paradoxic motion of the interventricular septum (IVS) (3,6).
Interventricular Septum
Examination of interventricular septal motion can help distinguish RV volume overload from RV pressure
overload (2).
Right Ventricular Volume Overload

RV volume overload is characterized by a prominent, rounded ventricular cavity that often extends to the car-
diac apex, sometimes eclipsing the LV in size in the four-chamber views. Ventricular enlargement usually devel-
ops as an adaptation to the increased total blood flow resulting from atrial or ventricular septal defects, TR, or
pulmonic regurgitation (PR). Although features of RV volume and pressure overload may overlap, RV volume
overload more consistently produces dilation of the RV. Examination of the IVS may yield additional clues to the
etiology of RV dysfunction. Normally, the IVS functions as part of the LV and maintains a convex shape toward
the LV throughout the cardiac cycle. As the RV dilates or becomes hypertrophic, its total mass increases, the
septum flattens, and paradoxic septal motion develops. It is important to note that in contrast to chronic pres-
sure overload, chronic volume overload eventually results in septal distortion that is greatest at end-diastole with
paradoxical motion toward the RV (i.e., away from the center of the LV) during systole (2).
Right Ventricular Pressure Overload

RV pressure overload accompanies pulmonary hypertension or PS and is characterized by hypertrophy of
the RV free wall and eventually hypertrophy of the interventricular septum and free wall. In contrast to RV
volume overload, RV pressure overload produces maximal septal distortion at end-systole and early diastole (2).
RIGHT ATRIUM
Anatomy
The RA is a thin-walled, irregularly shaped structure with the superior vena cava entering near the anterior
portion of the superior wall and the inferior vena cava entering near the right posterior portion of the infe-
rior wall. The tricuspid annulus forms the inferior portion of the RA, and the coronary sinus opens into the
RA just above this structure. The Eustachian valve and Chiari network are associated with the orifice of the
inferior vena cava. Failure of regression of the right or inferior valve of the sinus venosus during gestation
may result in a persistent Eustachian valve. The Chiari network is a fenestrated, strand-like structure within
the RA cavity. Although it most often arises from the orifice of the IVC, it may originate from the RA free
wall, the coronary sinus, or interatrial septum.

TEE evaluation of the RA may be performed from the standard ME four-chamber view or the ME RV
inflow–outflow view. The ME bicaval view is also very useful (see Chapter 2 and Appendices), particularly
for the evaluation of RA free wall and interatrial septum. The upper limit of normal for RA size is 18 cm2,
or 5.3 cm × 4.4 cm (5).

Aortic valve
Pulmonary valve
Anterior cusp Tricuspid valve
Right cusp Medial (septal) cusp
Left cusp Anterior cusp
Posterior cusp
Mitral valve
FIGURE 14.6 Schematic drawing of tricuspid valve anatomy.
TRICUSPID VALVE
Anatomy
The TV consists of valve leaflets, chordae tendineae, papillary muscles, an annular ring, and the RV myo-
cardium. The TV is trileaflet, with anterior, septal, and posterior leaflets of unequal size (Fig. 14.6). The
anterior papillary muscle is the largest and originates from the moderator band while the chordae tendin-
eae connect the papillary muscles to the tricuspid leaflets. The TV annulus is larger and located in a slightly
more apical position than the mitral valve annulus.

TEE evaluation of the TV focuses on the same standard views as for the RV.
1. ME four-chamber view. From the standard ME four-chamber view, slight rightward (clockwise)
rotation of the probe moves the TV to the center of the scan plane; advancing and withdrawing
the transducer allows imaging of the entire TV. This view demonstrates the anterior and septal
leaflets.
2. ME RV inflow–outflow view. This view provides a nearly orthogonal view of the TV, with the orifice more
nearly parallel to the ultrasound beam. As such, quantitative measurements of TV flow velocities are
optimized.
3. ME modified bicaval view. From the standard ME bicaval view at approximately 120 degrees, the
omniplane angle is increased slightly until the TV appears in the far left of the display. This view provides
the best alignment of the ultrasound beam and the direction of the regurgitant TR jet, minimizing error
in continuous or pulsed wave Doppler measurements.
4. TG views. The TG views used to evaluate the RV also provide useful windows for imaging the TV.
Rightward (clockwise) rotation of the TEE transducer from the TG midshort-axis view of the LV provides
a good view of the TV in short axis, allowing identification of its septal, anterior, and posterior leaflets. The
TG RV inflow view provides the best image of the chordae tendineae and RV papillary muscles supporting
the TV.

Tricuspid Regurgitation
TR is the most common right-sided valvular lesion in adults. It is most often caused by tricuspid annular
dilation secondary to RV enlargement or chronic pulmonary hypertension.
Echocardiographic features of TR include RA, RV, and tricuspid annular dilation causing incomplete TV
closure or even TV leaflet prolapse.
Doppler Echocardiography
Color Flow Doppler
Regurgitation severity is most easily assessed with color flow Doppler, with severe dysfunction defined
as an abnormal color flow signal filling >50% of the RA, or appearing as a laminar color signal. When the
regurgitant jet is directed toward the atrial septum, it must be distinguished from normal caval inflow or
Video 14.4A flow through an atrial septal defect (Fig. 14.7A,B, Video 14.4A,B).
Video 14.4B
Pulsed Wave Doppler
Severe TR may also be documented by measurement of reversed or retrograde systolic hepatic vein or caval
flow (Fig. 14.8).
Estimation of Pulmonary Artery Systolic Pressure

A visible TR jet may be interrogated with continuous wave Doppler to measure its peak velocity. The sim-
plified Bernoulli equation (ΔΡ = 4v2; v = peak TR jet velocity) may then be used to estimate the transvalvular
pressure gradient, which when added to the RA pressure yields an estimate of RV peak systolic pressure. In
the absence of obstruction to RV outflow, this calculated RV systolic pressure provides a good estimate of
the PA systolic pressure. It is critical, however, to align the ultrasound beam with the direction of regurgi-
tant jet to avoid an underestimation error (Fig. 14.7C).
Tricuspid Stenosis
Tricuspid stenosis (TS) is diagnosed by visualization of structural abnormalities of the leaflets and quanti-
fied by continuous wave Doppler examination of transtricuspid flow.
Features consistent with TS include increased echo density of the thickened leaflets, diastolic leaflet dom-
ing, and decreased size of the TV orifice.
Being the largest of the cardiac valves, transtricuspid flow velocities are often very low, typically <0.7 m/s.
Although normal prosthetic valves in the tricuspid position may demonstrate peak velocities nearly twice
normal, peak flow velocity >1.5 m/s suggests significant TS. As with any suspected valve dysfunction, effec-
tive orifice area should be calculated to confirm peak flow estimates of severity (5).
Etiology of Tricuspid Valve Disease

Annular Dilation
Annular dilation results in decreased leaflet coaptation and progressive TR. The severity of the regurgita-
tion is directly related to the degree of annular dilation and may be treated with ring annuloplasty.

FIGURE 14.7 A: Midesophageal four-chamber view showing a color flow Doppler image of severe tricuspid regurgita-
tion. B: Midesophageal, RV inflow–outflow view showing a color flow Doppler image of severe tricuspid regurgitation
with the jet wrapping around a prominent Eustachian valve. C: Continuous wave Doppler image of tricuspid regurgita-
tion. A sample calculation of the pulmonary artery systolic pressure follows: ΔΡ = 4(3.7)2; systolic pulmonary artery pres-
sure = 54 + right atrial pressure; systolic pulmonary artery pressure is approximately 59 to 64 mm Hg (13).

FIGURE 14.8 Pulsed wave Doppler image of hepatic venous flow with retrograde systolic flow, indicating severe
tricuspid regurgitation.
Rheumatic Disease
Rheumatic disease is the most common cause of acquired TS, resulting in fibrosis and scarring of the valve
leaflets, doming, and eventually frank commissural fusion. Rheumatic tricuspid disease often includes
regurgitation, and the mitral valve is almost uniformly involved.
Endocarditis
TV vegetations usually are oscillating, echo-dense masses attached to the leaflets or the annulus. Typically,
they involve the atrial surface of affected leaflets and are often larger and bulkier than those found on the
left side. Leaflet destruction may eventually result in flail segments and severe TR.
Carcinoid Syndrome
Carcinoid tumors typically occur in the distal small bowel and secrete serotonin, bradykinins, histamine,
and prostaglandins. Damage from these substances is usually limited to right-sided valvular structures as
they are inactivated by monamine oxidase abundantly present in normal lung tissue. Typical features of
carcinoid heart disease include TV and/or PV leaflet thickening and fibrosis with moderate to severe TR, mild
TS, and PS (6). TR is caused primarily by restricted leaflet mobility preventing adequate coaptation of the
leaflet tips. In contrast to rheumatic heart disease, carcinoid syndrome does not result in tricuspid leaflet
doming or commissural fusion.
Ebstein’s Anomaly
Ebstein’s anomaly is a congenital condition in which a malformed TV arises from a location abnormally
displaced toward the RV apex. Typically, the anterior leaflet is redundant, often fenestrated and “sail-like,”
while the septal and posterior leaflets are either rudimentary or completely absent. Ebstein’s anomaly
should be suspected when the long-axis separation between the mitral and tricuspid annular planes
exceeds 8 mm/m2. This marked apical displacement of the TV causes a portion of the morphologic RV to
become atrialized (7). Associated features include an atrial septal defect, impaired RV function, conduction
abnormalities, and TR.

FIGURE 14.9 Midesophageal aortic valve short-axis view of the pulmonic valve and main pulmonary artery. Note the
presence of a vegetation attached to the pulmonic valve, but visible in the proximal main pulmonary artery. Main PA,
main pulmonary artery.
PULMONIC VALVE
Anatomy
The PV is a trileaflet valve with anterior, right, and left posterior semilunar cusps. The leaflets are thinner
than the aortic valve leaflets and are directly connected to the musculature of the RV.

Because of its anterior position, high-resolution images of the PV are difficult to obtain with TEE. Trans-
thoracic imaging with its greater flexibility in transducer positioning and angulation may in some cases be
superior.
1. ME RV inflow–outflow view. The most consistent TEE scan plan for imaging the PV is the ME RV
inflow–outflow view. The PV appears adjacent to the commissure separating the right and left coronary
cusps of the aortic valve. Since the PV is oriented at approximately 90 degrees to the aortic valve, it is
usually viewed in long axis when the aortic valve is seen in short axis.
2. ME aortic valve short-axis view. With gradual withdrawal of the probe from the ME AV short-axis
position, the PV will come into view, again in long axis adjacent to the AV, but also with a significant
portion of the main PA and even its bifurcation into right and left branches in the extreme near field
(commonly known as the Y-view) (Fig. 14.9, Video 14.5). Video 14.5
3. Upper esophageal PV long-axis/aortic arch short-axis view. This view may be reached by rotating the
transducer angle to 90 degrees from either a long-axis view of the aortic arch, or from the Y-view
described above. The close alignment of blood flow with the ultrasound signal vector makes this an
excellent position from which to detect PR or quantify PS with continuous wave Doppler.
4. TG PV view. From the TG LV midpapillary short-axis view, the probe is turned to the right and the transducer
is rotated to 110 to 140 degrees, the RVOT and PV in long axis will appear in the far field (Fig. 14.10, Video
14.6). This view is useful for obtaining Doppler measurements of cardiac output from the RVOT (8). Video 14.6
Pulmonic Regurgitation
Congenital PR results from abnormal cusp structure, while acquired PR often complicates pulmonary
hypertension, annular dilation, or other structural distortion. PR severity is usually quantified by its appear-
ance on color flow Doppler mapping. PA catheters have a minimal effect on the severity of PR or TR (9).

FIGURE 14.10 Transgastric long-axis view of the RV outflow tract and pulmonic valve. RV, right ventricle; RVOT, right
ventricular outflow tract; PV, pulmonic valve.
Pulmonic Stenosis
PS is most commonly congenital but may also result from rheumatic or carcinoid heart disease, or infective
endocarditis. Severity of stenosis is quantified with 2D examination of leaflet motion or color flow Doppler
appearance of transvalvular flow.
Features of PS include abnormal initial systolic leaflet motion and subsequent doming of stenotic leaflets
into the PA. Other common findings are RV hypertrophy and RA enlargement.
Doppler features of PS include increased flow velocities through the stenotic valve and poststenotic turbulence.
Ross Procedure
In 1967, Donald Ross described the replacement of a diseased aortic valve using the patient's native PV (i.e.,
pulmonary autograft). In this procedure, TEE is important in establishing candidate suitability by assessing
for PR and providing dimensions of pulmonic and aortic valves. In addition, new intraoperative LV septal
wall motion abnormalities may indicate ligation of a septal coronary artery branch during dissection and
excision of the PV. Postoperatively, the patients are followed for development of aortic insufficiency, an
early sign of autograft failure (10).
REALTIME THREEDIMENSIONAL
TRANSESOPHAGEAL ECHOCARDIOGRAPHY
Real-time three-dimensional transesophageal echocardiography (RT-3D TEE) zoom and full-volume
modalities are proving useful for imaging the right-sided cardiac structures, including views of the TV leaf-
Video 14.7 lets and subvalvular supporting structures (Fig. 14.11, Video 14.7). RT-3D can help in estimating the sever-
ity of TR using CF Doppler, by obtaining the area of vena contracta of the tricuspid regurgitant jet and crop-
ping the RT-3D CF Doppler data set with imaging planes exactly parallel to the TV orifice. This is especially
useful in advanced stages of TR, as the valve's natural saddle configuration becomes more round and flat in
shape (11). In the stenotic valve, the orifice may be more easily visualized and planimetered using RT-3D.

FIGURE 14.11 Transgastric short-axis 3D image of the tricuspid valve showing the valve leaflets at end-diastole in the
open position. Anterior leaflet (A), Posterior leaflet (P), Septal leaflet(S)
Conventional 2D imaging techniques support RV volumetric assessments but provide only surrogates
of EF. However, with RT-3D capability, rapid acquisition of a 3D RV data set is becoming more feasible and
has been shown to be reproducible over a wide range of RV dimensions (12). Furthermore, it appears to
be less prone to underestimation of both end-systolic and end-diastolic volume measurements, yielding
more accurate measurements of chamber volumes and EF than 2D techniques (5). At present, though RV
quantification software exists, it has not yet been integrated into clinical practice. Significant limitations to
3D TEE are the variable quality of available acoustic windows, especially for the PV, and the time required
for data collection and analysis (5). As of now, there is no evidence that 3D assessment improves surgical
outcomes.
REFERENCES
1. Kasper J, Bolliger D, Skarvan K, et al. Additional cross-sectional transesophageal echocardiography views improve periopera-
tive right heart assessment. Anesthesiology. 2012;117(4):726–734.
2. Haddad F, Couture P, Tousignant C, et al. The right ventricle in cardiac surgery, a perioperative perspective: I. Anatomy, physi-
ology, and assessment. Anesth Analg. 2009;108(2):407–421.
3. Horton KD, Meece RW, Hill JC. Assessment of the right ventricle by echocardiography: A primer for cardiac sonographers.
J Am Soc Echocardiogr. 2009;22(7):776–792; quiz 861–862.
4. Vitarelli A, Terzano C. Do we have two hearts? New insights in right ventricular function supported by myocardial imaging
echocardiography. Heart Fail Rev. 2010;15(1):39–61.
5. Rudski LG, Lai WW, Afilalo J, et al. Guidelines for the echocardiographic assessment of the right heart in adults: A report from
the American Society of Echocardiography endorsed by the European Association of Echocardiography, a registered branch
of the European Society of Cardiology, and the Canadian Society of Echocardiography. J Am Soc Echocardiogr. 2010;23(7):
685–713; quiz 786–788.
6. Bruce CJ, Connolly HM. Right-sided valve disease deserves a little more respect. Circulation. 2009;119(20):2726–2734.
7. Attenhofer Jost CH, Connolly HM, Dearani JA, et al. Ebstein's anomaly. Circulation. 2007;115(2):277–285.
8. Maslow A, Comunale ME, Haering JM, et al. Pulsed wave Doppler measurement of cardiac output from the right ventricular
outflow tract. Anesth Analg. 1996;83(3):466–471.
9. Goldman ME, Guarino T, Fuster V, et al. The necessity for tricuspid valve repair can be determined intraoperatively by two-
dimensional echocardiography. J Thorac Cardiovasc Surg. 1987;94(4):542–550.
10. Marino BS, Pasquali SK, Wernovsky G, et al. Accuracy of intraoperative transesophageal echocardiography in the prediction
of future neo-aortic valve function after the Ross procedure in children and young adults. Congenit Heart Dis. 2008;3(1):39–46.
11. David TE. Functional tricuspid regurgitation: A perplexing problem. J Am Soc Echocardiogr. 2009;22(8):904–906.
12. Karhausen J, Dudaryk R, Phillips-Bute B, et al. Three-dimensional transesophageal echocardiography for perioperative right
ventricular assessment. Ann Thorac Surg. 2012;94(2):468–474.
13. Zoghbi WA, Enriquez-Sarano M, Foster E, et al. Recommendations for evaluation of the severity of native valvular regurgita-
tion with two-dimensional and Doppler echocardiography. J Am Soc Echocardiogr. 2003;16(7):777–802.

QUESTIONS
1. The red color flow Doppler signal shown in pulmonary artery systolic pressure in this
the image results from: patient is approximately:
a. Normal tricuspid inflow

b. Severe pulmonic regurgitation
c. Severe tricuspid regurgitation a. 20 mm Hg
d. Severe tricuspid stenosis b. 32 mm Hg
c. 44 mm Hg
2. In the image shown above, which of the
d. Indeterminate
following additional findings supports the
diagnosis? 5. This hepatic vein PW Doppler trace shows:
a. Aliasing spectral Doppler signal
b. Inverted spectral Doppler signal
c. Laminar spectral Doppler signal
d. Variance spectral Doppler signal
3. Which of the following TEE scan planes
provides the best alignment of the ultrasound
beam for assessment of tricuspid stenosis?
a. ME four-chamber view
b. ME two-chamber view
c. Modified ME bicaval view
d. TG RV inflow view
4. The TR CW spectral Doppler trace shown
in the figure was obtained when right atrial
pressure was 12 mm Hg and there was no
pulmonary stenosis. The estimated
a. Dominant A-wave
b. Giant V-wave
c. Normal systolic inflow
d. Reversed systolic flow
6. Which of the following structures is located
in the RA?
a. Chiari network
b. Crista supraventricularis
c. Moderator band
d. Parietal band

7. In which of the following is apical a. Atrial septal defect

displacement of the tricuspid valve a b. Patent foramen ovale
characteristic finding? c. Tricuspid valve stenosis
a. Carcinoid syndrome d. Ventricular septal defect
b. Ebstein's anomaly
10. Which of the following structures is shown
c. Rheumatic heart disease
in this image?
d. Ross procedure
8. This image was recorded from a
patient with valvular heart disease that
predominately involved a single valve.
Which of the following is the most likely
diagnosis?
a. Descending aorta
b. Left atrium
c. Pulmonary artery
d. Right atrium
11. The predominant wave shown in the PW
Doppler image is an:
a. Aortic stenosis
b. Mitral stenosis
c. Pulmonic stenosis
d. Tricuspid stenosis
9. In the image shown, which of the following
is the most likely explanation for the
appearance of the right ventricle?
a. A wave
b. D wave
c. S wave
d. V wave
12. The most likely diagnosis in the previously
shown image is:
a. Mitral stenosis
b. Pulmonary hypertension
c. Tricuspid regurgitation
d. Normal tracing

13. In the image shown, the best description of 16. In the image shown, which of the following
the echocardiographic findings is: is present?
a. Left atrial dilation a. Pulmonary hypertension

b. Right atrial dilation b. Pulmonic regurgitation
c. Right ventricular dilation c. Tricuspid regurgitation
d. All of the above d. Tricuspid stenosis
14. In the previously shown image, which of the 17. The two 3D color Doppler images shown
following is also seen? were recorded during different phases
a. Chiari network of the cardiac cycle from a patient with
b. Crista terminalis valvular heart disease. Which of the
c. Eustachian valve following is the most likely diagnosis?
d. Right heart catheter
15. Using the image shown, which of the
following may be assessed using spectral
Doppler measurements?
a. Aortic stenosis
b. Cardiac output
c. Left ventricular outflow tract obstruction
a. Pulmonic regurgitation
b. Pulmonic stenosis
c. Tricuspid regurgitation

18. Which of the following TEE scan planes is 20. Which of the following chronic conditions
most useful to assess severity of pulmonic would most likely be present in a patient
stenosis? with a 22-mm tricuspid annular plane
a. Midesophageal aortic valve short-axis view systolic excursion?
b. Midesophageal aortic valve long-axis view a. Mitral stenosis
c. Upper esophageal aortic arch long-axis b. Patent foramen ovale
view c. Pulmonary hypertension
d. Upper esophageal aortic arch short-axis view d. Tricuspid regurgitation
19. The moderator band has anatomic
importance because:
a. It defines the infundibular right ventricular
outflow tract
b. It divides the right atrium into inflow and
outflow portions
c. It supports papillary muscle attachments to
the tricuspid valve
d. It supports the crista terminalis

IV CLINICAL CHALLENGES
15 Transesophageal Echocardiography
for Coronary Revascularization
Donna L. Greenhalgh and Justiaan L.C. Swanevelder
INTRODUCTION
TEE provides an astutely trained clinician with essential information which can significantly influence clin-
ical management and improve patient outcome in both cardiac and noncardiac procedures (1,2). In 2011,
the American Society of Anesthesiologists/Society of Cardiovascular Anesthesiologists (SCA) Task Force
published updated practice guidelines and classified hemodynamic instability as a Category I indication
for the use of TEE and the use in coronary revascularization for patients with poor ventricular function
as category IIa (3). The use of TEE in routine coronary artery surgery is also now considered IIa (3,4). The
European Association of Echocardiography (EAE) and the SCA recommend that TEE should be used for
both elective and emergency cardiac surgery unless contraindicated (3,4).
TEE provides an enormous amount of information during cardiac surgery that may directly change
surgical case management in up to 13% of cases prebypass and in 6% postbypass (5–8) as well as anesthetic
management in approximately 50% of coronary artery bypass graft (CABG) patients (Table 15.1) (5). The
new information provided and subsequent interventions have been shown to be cost-effective (9). Skinner
and Klein have also shown that preoperative studies may not accurately reflect patient pathology due to
inadequacies of transthoracic echo, an inaccurate or incomplete report, and/or disease progression (7,10).
TEE provides a rational basis for decision-making during weaning from bypass by being able to continuously
assess cardiac function, cardiac output, volume replacement, inotropic and vasoactive therapies as well as guide
placement of intra-aortic balloon pumps (IABPs). TEE allows immediate assessment of the adequacy of revas-
cularization by examination of regional wall motion abnormalities (RWMAs) both during on-pump and off-
pump coronary artery procedures. Furthermore, TEE has proved reliable and comparable with the pulmonary
artery catheter (PAC) and standard thermodilution techniques for monitoring and quantifying cardiac output.
The increasing age and comorbidity of patients undergoing coronary revascularization procedures
make TEE an invaluable part of our monitoring armamentarium. For example, it allows us to optimally
fluid resuscitate the patient and note the corresponding value of central venous pressure (CVP) or pulmo-
nary artery pressure which can then be used in the intensive care unit. This is particularly important in
hypertensive patients and those with ventricular systolic or diastolic dysfunction, in which venous pressure
does not accurately reflect intracardiac volume (11,12).
SAFETY AND COMPLICATIONS

The risk of major complications, notably perforation of the esophagus, is small at 0.01% to 0.02% as assessed
by a number of large studies. Minor complications such as sore throat and odynophagia are common but
can be minimized by using a laryngoscope for placement (13–15). Antibiotic prophylaxis is not indicated
for the majority of cases, though in high-risk cases, for example, ventilated patients with prosthetic valves
on intensive care where oropharyngeal transfer of bacteria can occur, prophylaxis may be advisable. In
every case, there is a balance of risks to be assessed with absolute and relative contraindications. In many
enthusiasts’ eyes, the only absolute contraindications to a TEE will be an esophagectomy, recent esophageal
surgery, or significant esophageal pathology.
302

15. Transesophageal Echocardiography for Coronary Revascularization 303
TABLE 15.1 Role of TEE in Patients Undergoing CABG
To supplement cardiac workup

t Confirm diagnosis and evaluate cardiac function for patients undergoing emergent surgery
t Provide an updated examination of cardiac and valvular functions
t Evaluate potential target sites of coronary revascularization by administration of contrast agents (evaluate coronary
perfusion) or dobutamine (stress test to evaluate viability)
To diagnose impact of previously unrecognized pathology on surgical procedure
t Valvular pathology:
t Aortic insufficiency—distension of the ventricle during cardiopulmonary bypass
t Mitral regurgitation (MR)—dynamic MR, ischemic MR
t Aortic stenosis—previously undetected, underestimated, or disease progression
t Patent foramen ovale/atrial septal defect
t Emboli, thrombus, or mass
t Persistent left superior vena cava
t Regional wall motion abnormalities—pre- or postbypass
t Aortic dissection—iatrogenic or previously undetected
t Atherosclerotic disease
To assist the surgeon in the conduct of circulatory management
Positioning/placement of:
t Aortic cross-clamp
t Coronary sinus cardioplegia catheter
t Intra-aortic balloon pump
t Femoral venous cannula
Port access (endoaortic catheter, venous cannula, coronary sinus catheter)
t Ventricular assist device
To facilitate the conduct of circulatory management or surgical procedure
t Redo sternotomy
t Conduct of bypass: Assess left ventricle chamber size for distension
t Plan management strategies for separation from cardiopulmonary bypass for patients with poor cardiac
function
t Separation from cardiopulmonary bypass (titration of volume and pharmacologic or mechanical support)
To diagnose cause of acute cardiovascular compromise
t New myocardial ischemia
t New valvular lesions
t Ventricular failure
t Ventricular filling
PREBYPASS EXAMINATION
The prebypass intraoperative examination should target the pathology at hand, be performed in a sys-
tematic manner, and be organized into a comprehensive study. In contrast, the postcardiopulmonary
bypass (CPB) examination is usually targeted toward assessing the results of the intervention and trou-
bleshooting of possible complications. Preoperatively digital echo loops should be recorded to review
and compare with examination findings during the postbypass period. A TEE examination should
always include a written report for the patient’s records and a discussion of the findings with the cardiac
surgeon.
Assessment of Ventricular Function

Traditionally, LV filling and cardiac output have been quantified by using a PAC. Intraoperative TEE often
supplements or replaces these measures in current practice. Real-time echo images allow accurate qualita-
tive evaluation of cardiac output, quantification of ventricular and valvular functions, intraoperative hemo-
dynamic assessment, and most importantly contractility. Hypovolemia or severe LV dysfunction is easy to
detect but various degrees of RWMAs can often be subtle as well as subjective and operator dependent.

304 IV. Clinical Challenges
TABLE 15.2 Assessment of Cardiac Function by TEE
Preload
LV end-diastolic area
LV end-diastolic pressure (estimated from AI jet)
LA pressure (estimated from pulmonary vein flow)
Contractility
Fractional area change (calculated)
Ejection fraction (visual estimate)
Segmental wall motion
Fractional shortening
Tissue Doppler
Quantitative hemodynamics
Stroke volume/cardiac output
Systemic vascular resistance
RV systolic pressure
Diastolic function
Mitral inflow velocities
Pulmonary vein blood flow velocities
LV, left ventricle; AI, aortic insufficiency; LA, left atrium; RV, right ventricle.
The standard views used to evaluate global LV function or regional ischemia (16) are discussed in
Chapter 4. Table 15.2 summarizes the other TEE tools available to access cardiac function.
New Advances in Intraoperative Assessment of Global and

Regional Cardiac Function
The automated border detection technique of acoustic quantification (AQ) introduced in the mid-90s to
obtain area changes has been a step toward real-time, quantitative assessment of ventricular filling and
Video 15.1 ejection (Video 15.1). Tissue Doppler imaging (TDI) and real-time three-dimensional (RT3D) echocar-
diography echo may bring us closer to accurately measuring and quantifying myocardial function (17).
However, because of angle dependency, fast-changing hemodynamic conditions, and lack of accurate vali-
dation studies, intraoperative TDI has never found its way into routine intraoperative TEE practice and has
been replaced by other techniques to display myocardial deformation.
RT3D is useful to search for myocardial ischemia in high-risk surgical patients, in addition to assessing
LV volumes and ejection fraction (EF) (18). Multiple slices from the apex to the base can now be displayed
simultaneously (19,20). A computer-generated endocardial cast can graphically display the timing of con-
traction of each of the 17 segments to detect delays that may represent myocardial ischemia (Figs. 15.1 and
15.2). Evaluation of RWMAs with RT3D is still qualitative and therefore subject to observer bias. Initial
studies of RT3D using dobutamine stress echo suggest that these multisliced displays are highly specific
for the detection of angiographically confirmed ischemic myocardial regions (20). There are other new
quantitative methods of detecting myocardial ischemic deformation. For example, strain measured by
speckle tracking uses two-dimensional (2D) images and analyzes the movement of stable acoustic markers
(speckles) between frames (19–21).
Monitoring of Ischemia
Visualizing the Aortic Root, Coronary Arteries, and Coronary Blood Flow
TEE imaging of the coronaries is discussed in detail in Chapter 4. As the aortic root runs oblique to the sag-
ittal plane, the origin of the LCA is interrogated in a more superior (cephalad) plane than the RCA in TEE
SAX views. TEE visualizes approximately 70% to 88% of the left and 25% to 50% of the right coronary artery
ostia (22). Although difficult to quantify, flow can often be visualized with TEE in more distal branches of the
larger coronary arteries, that is, the circumflex coronary artery in the atrioventricular groove (23) (Fig. 15.3,
Video 15.2 Video 15.2). It is important to recognize, both for ischemia detection and revascularization procedures, the
patient variability in the coronary blood supply to the various myocardial segments (Figure 4.2).

FIGURE 15.1 The “bull’s eye” depicts the standard deviation of the time taken of the individual segments in cross sec-
tion to contract maximally. This may aid resynchronization therapy.
It is important to score any myocardial segments with RWMAs prior to bypass and evaluate post-CABG
for improvement (Table 15.3). Unfortunately, not all RWMAs benefit from coronary revascularization.
Most akinetic and dyskinetic regions are the result of myocardial infarction and thus represent nonviable
myocardium. In general, hypokinetic segments are viable and may represent active ischemia.
Shortcomings of TEE
RWMAs can be difficult to quantify because the ventricle twists when contracting, causing different myo-
cardial segments to move in and out of the imaging plane during one cardiac cycle. The endocardial and
epicardial borders cannot always be completely identified, limiting accurate quantification of wall thick-
ening. Bear in mind that interpreting regional wall motion is an operator-dependent skill, therefore very
subjective. RWMAs may also occur in the absence of coronary artery disease, for example, when paced.
NEW RWMA AFTER CARDIOPULMONARY BYPASS

What Does it Signify?
In two classic studies by Roizen and Smith, the occurrence of postoperative myocardial infarction was
increased in patients who exhibited new RWMAs during CABG or aortic vascular surgery (24,25). The
incidence of postoperative infarction was more strongly associated with new RWMAs than with new elec-
trocardiographic changes. Although TEE may be sensitive in diagnosing ischemia, a new RWMA does not
always predict myocardial infarction. In the study of Leung et al. (26), a myocardial infarction was subse-
quently diagnosed in only one of eight patients in whom a new, persistent RWMA had developed. This
apparent discrepancy is consistent with the concept of “myocardial stunning,” in which an acute episode

FIGURE 15.2 Complete 3D regional wall motion map. The regional segments’ movements are displayed in milliseconds.
of myocardial ischemia can result in wall motion abnormalities that later resolve without any permanent
injury. Alternatively, new RWMAs may be related to loading conditions of the ventricle, electrolyte abnor-
malities, blood viscosity, level of inotropic support, hypothermia, off-pump CABG stabilizing devices, car-
diac pacing, and bundle branch conduction abnormalities. Any apparent dyskinesis due to conduction
abnormalities can be differentiated from ischemia by looking for myocardial thickening.
FIGURE 15.3 A 2D demonstration of the circumflex coronary artery visualized in the atrioventricular groove.

TABLE 15.3 Segmental Scores in Increasing Order of Severity
Normal—1
Hypokinesis—2
Akinesis (negligible thickening)—3
Dyskinesis (paradoxical systolic motion)—4
Aneurysmal (diastolic deformation)—5
What Should We Do?

The appearance of new RWMAs after bypass is common, but the interpretation is complicated by fac-
tors such as infusion of inotropic drugs, inadequate recovery from cardioplegia, conduction abnormalities,
and transient ischemia resulting from the distal coronary embolization of air or debris. Although some
investigators have suggested that the detection of new RWMAs warrants further surgical intervention, no
prospective study is available to support such an aggressive approach. The additional morbidity/mortality
associated with the resumption of bypass to place another graft would likely outweigh the potential benefit
in most cases. A more progressive approach is presented in Table 15.4.
The surgeon can assess graft patency and flow by visual inspection to confirm the absence of graft kink-
ing or torsion, by stripping the vein graft to confirm refill, by palpation, and by the use of a Doppler flow
probe. Decreased flow in an arterial conduit can result from poor distal runoff, a compromised anastomo-
sis, or vasospasm that can be effectively treated with nitroglycerin or a calcium channel antagonist such as
nicardipine or nifedipine.
Ventricular septal hypokinesis and dyskinesia is common immediately after separation from CPB and
usually recovers within 10 to 15 minutes (Video 15.3). The abnormal conduction progression inherent Video 15.3
with RV pacing results in contractile dyssynchrony, which may be interpreted as a septal RWMA. Atrial
pacing commonly restores the normal ventricular conduction pathway and contractile synchrony of the
ventricular septum. If septal dyskinesia persists then the surgeon should be advised to check the LAD
and RCA grafts if present. RWMAs in other areas of the left ventricle need the patency of the graft to
be checked sooner. If a RWMA persists or, more commonly, global dysfunction is seen with TEE, then
circulatory support should be started either with inotropes or by inserting a circulatory assist device.
The level of assist depends on the dysfunction seen. TEE aids placement of the devices and monitoring
of recovery.
Differentiation between poor perfusion and stunned myocardium is more difficult. Possible strategies
include epicardial scanning and the administration of a contrast agent to determine coronary flow patterns.
If the area demonstrates flow of the contrast agent, the RWMA may resolve with time. The absence of
contrast agent suggests a technical problem at the anastomosis or distal obstruction in the native coronary.
Such information can help guide any possible surgical intervention. The technique of contrast perfusion
can also be performed before bypass. If a specific area is likely to be infarcted, as demonstrated by the
absence of contrast flow and significant wall thinning, surgical interventions are not likely to be of value.
Both these techniques are uncommonly applied in routine operative practice, and their impact remains to
be determined.
TABLE 15.4 Strategy for Management of a New RWMA Abnormality after Separation from Cardiopulmonary Bypass
Increase the coronary perfusion pressure

Restore normal conduction pathways (sinus rhythm, A-pace)
Normalize electrolytes and arterial blood gases
Inspect coronary grafts
Visual inspection and stripping
Doppler flow examination
Echo contrast examination
Return to cardiopulmonary bypass

TABLE 15.5 Echocardiographic Findings in Hypotension and Cardiac Dysfunction
LVEDA LVESA FAC CO

Decreased LV preload ↓ ↓ 0 ↓↓
Decreased LV afterload 0 ↓↓ ↑↑ ↑
Increased LV afterload ↑ ↑ ↓ ↓
LV dysfunction ↑ ↑↑ ↓↓ ↓
RV dysfunction ↓ ↓ ↓/0 ↓
Acute mitral regurgitation LV distension ↑↑ 0/↑ ↓ ↓
LVEDA, left ventricular end-diastolic diameter; LVESA, left ventricular end-systolic diameter; FAC, fractional area change; CO,
cardiac output; LV, left ventricle; RV, right ventricle; ↑, increased; ↓, decreased; 0, unchanged.
ACUTE CARDIAC DYSFUNCTION: ASSESSMENT AND MANAGEMENT

Cardiac dysfunction may develop at any time during the perioperative period. TEE examination of the
heart and great vessels can provide a quick assessment of the primary factors related to hypotension: Pre-
load, afterload, myocardial contractility, valvular function, and integrity of the aorta. TEE can significantly
affect the surgical and anesthetic management, especially in high-risk patients or in patients with acute
hemodynamic collapse. The reader is reminded that post-CPB cardiac function must be interpreted in the
context of the prebypass examination findings and the occurrence of any significant bypass events.
The TEE examination quickly provides data that guides pharmacologic therapy and volume resuscita-
tion. In several studies, TEE significantly modified both surgical and hemodynamic decision-making dur-
ing the perioperative period (26,27). The echocardiographic findings associated with common causes of
hypotension and cardiac dysfunction are presented in Table 15.5 and discussed below:
Hypovolemia
Hypovolemia, a common cause of perioperative hypotension, is often related to the obstruction of venous
inflow as a consequence of prebypass cannula placement, volume re-equilibration after separation from
bypass, and bleeding. The assessment of LV chamber size by TEE has been shown to be a sensitive measure
of LV preload. In the study of Cheung et al. (28) the quantitative analysis of changes in the TG short-axis
area could reliably detect even a 2.5% decrease in intravascular volume.
After separation from CPB, the left ventricle is often noncompliant, especially when the LV is hypertro-
phied. This makes assessment of filling difficult when relying on a pressure reading from a CVP or PAC as
higher pressures will be necessary to achieve optimal preload. TEE allows direct visualization of diastolic
chamber size (which can be correlated with a pressure reading) and assessment of fluid therapy.
Dynamic Mitral Regurgitation

The development of mitral regurgitation (MR) may be associated with hypotension, increased pulmonary
pressures, RV failure, and decreased CO. Excessive volume resuscitation or increased afterload can result
in LV distension with incomplete coaptation of the mitral leaflets and a central jet of regurgitation. Alter-
natively, ischemia or LV dysfunction can lead to papillary muscle dysfunction or LV distension. Significant
MR may require mitral valve surgery or hemodynamic management, such as adjusting the systemic vascu-
lar resistance, administering inotropic agents, or decreasing the LV preload.
Right Ventricular Dysfunction

RV dysfunction is another common cause of perioperative hypotension. RV dysfunction is associated with
RV dilation, tricuspid regurgitation, abnormal septal wall motion, and decreased LV chamber size. Man-
agement includes checking for ischemia (though more difficult to assess for the RV), optimizing the pul-
monary vascular resistance (PVR), systemic arterial pressure, and contractility. The RV can be affected by
pathology of the LV and vice versa. Following myocardial infarction, this ventricular interdependence can

affect the shape (e.g., septal shift), size, and function (pressure–volume relationship) of the other ventricle,
and is a predictor of outcome. The use of only retrograde cardioplegia can be associated with inadequate
RV protection as the balloon on the cannula can obstruct the right cardiac vein preventing cardioplegia
reaching the territory supplied by it.
RV systolic dysfunction following CABG is commonly diagnosed by 2D echo images using ME
four-chamber, ME RV inflow/outflow, and the TG SAX views. After open-heart surgery any residual
intraventricular air is more likely to enter the right coronary because of its anterior position causing
temporary RV ischemia and dysfunction. With the open chest, impairment of the free wall and RV dis-
tension can be visualized directly. Dysfunction and recovery can also be monitored by TEE while treat-
ment is instituted using rest, administration of inotropic agents that also decrease PVR (e.g., milrinone,
dobutamine), and titration of pulmonary vasodilators (nitric oxide, prostaglandin E1, or nitroglycerin)
Video 15.4
(Videos 15.4, 15.5).
Video 15.5
Low Ejection Fraction

Patients who have reduced left ventricular ejection fraction (LVEF) as evaluated prebypass (<40% EF)
may need supplemental inotropic or chronotropic support as they are often on β-blockers and the
ventricles can appear sluggish on TEE initially upon separation from bypass. This may be short lived
and is monitored by TEE and therapy may be discontinued relatively quickly. LVEF <30% prebypass
invariably needs inotropic support and TEE is useful in assessing filling and changes in contractility in
these patients. An increasingly sluggish LV post-CPB is an indication for insertion of an IABP. If this,
in combination with inotropes, does not help then a left ventricular assist device (LVAD) is the next
consideration.
Unexpected Diagnosis of Coexisting Problems

Unexpected findings are not uncommon in patients who have undergone a standard workup (7,10) and can
be secondary to disease progression or previously undetected findings. Diagnosis of previously undetected
pathologies can dramatically alter the surgical plan, for example, insertion of a mitral ring for severe MR,
as well as impact the postoperative management and outcome.
Intracardiac Shunts; Patent Foramen Ovale or Atrial Septal Defect

Up to 25% of adult cardiac surgical populations have an intracardiac shunt which can affect the surgical
plan and long-term neurologic prognosis due to paradoxical air embolism. If a patent foramen ovale (PFO)
is found incidentally during CABG surgery, the decision regarding closure depends on individual surgical
preference (29). When an open-chamber procedure is performed in conjunction with CABG surgery or in
a patient with a stroke history, an incidental PFO should be closed.
A PFO can be most reliably detected when the interatrial septum is examined with both color flow
Doppler and after air contrast injection in the ME four-chamber and bicaval views. The passage of contrast
bubbles in the left atrium within five cardiac cycles confirms the diagnosis of a PFO.
Intraoperative detection of a previously unsuspected PFO has relevance to ICU management and
emphasizes the need for an echocardiographic report in the medical record and communication with the
ICU staff. For example, if atelectasis develops post-CABG surgery resulting in an increase in RV afterload,
the increase in right heart pressures can cause the shunt direction to change or exacerbate an existing right-
to-left intracardiac shunt, with subsequent worsening hypoxia.
Pleural Effusions
Iatrogenic pleural effusions often develop when the pleura is opened during internal mammary artery har-
vesting and may be already present in patients with impaired ventricular function. This may have a marked
effect on post-CPB ventilation and oxygenation as well as affecting the hemodynamic status of a patient
with borderline cardiac function. Ultrasound can easily detect both left- and right-sided pleural effusions.
Left pleural effusions can be seen in the ME descending aortic SAX view. Right-sided effusions are seen by
turning the probe from the ME four-chamber view to the right (Videos 15.6, 15.7). Video 15.6
Video 15.7

Previously Unknown Aortic Valve Pathology

Moderate aortic stenosis may be discovered during intraoperative TEE for CABG surgery. Quantification
of AV disease and the decision when to perform a combined CABG and aortic valve replacement (AVR)
procedure can be difficult, especially when LV function is compromised and the loading conditions may
be altered. Evidence shows that a subsequent AVR after a previous CABG has a higher mortality than a
single combined procedure (30). The degree of calcification is important because even in the asymptom-
atic patient progression of the disease process may be rapid. Progression is quite variable, with a decrease
in effective valve area ranging from approximately 0.1 to 0.3 cm2/y. In a primary CABG procedure, it is
therefore recommended that AVR should be considered in a patient with even moderate AS.
A patient with coronary artery disease may need insertion of an IABP during ischemic or unstable peri-
ods after CPB. If aortic regurgitation is diagnosed intraoperatively, the use of an IABP is contraindicated
due to its effect on the LV end-diastolic volume and wall tension.
Coexisting Mitral Valve Regurgitation—Combined CABG and MVR

Patients presenting for CABG often have coexisting functional or ischemic MR (e.g., Carpentier Class I
and III) of a mild or moderate degree. The team needs to decide whether or not to surgically address the
MV pathology during the coronary operation. The altered loading conditions under anesthesia should be
taken into consideration when quantifying the regurgitation. The reduction in ventricular chamber size,
systemic vascular resistance, and blood pressure that typically occurs in anesthetized patients can signifi-
cantly reduce the degree of mitral incompetence compared to the awake state. In order to gain more reli-
able information we advise to simulate awake loading conditions by increasing both preload and afterload
with a vasopressor.
In patients with functional ischemic mild (graded as 1 to 2) mitral regurgitation, the MV is often left
untouched. The need for surgical intervention in patients with moderate (>2+) ischemic MR under anes-
Video 15.8 thesia remains a point of debate (Fig. 15.4, Video 15.8). The risk of leaving the MV untouched with the
possibility that CABG surgery will successfully decrease the severity of MR by improving LV function and
geometry are weighed against the risk of MV surgery with extending aortic cross-clamp times. In patients
with ≥3+ ischemic MR, repair or replacement is recommended to improve functional status (31). The final
decision whether to proceed with mitral surgery in the setting of ischemic heart disease depends on the
surgeon. Importantly, moderate MR secondary to a structural leaflet abnormality (e.g., Carpentier Class II)
should be corrected as the disease is progressive and revascularization alone will not improve valve function.
FIGURE 15.4 ME four-chamber view of a patient with a central jet of moderate mitral regurgitation based on a vena
contracta of 0.546 cm.

Use of 3D Echo in Coronary Artery Revascularization

RT3D TEE technology is an exciting advance in evaluating ventricular function and although its appli-
cation during CABG is not routine at present, 3D TEE is emerging as an adjunct to 2D in revascular-
ization procedures to assess cardiac chamber volumes, ischemia, and cardiac output. Compared to 2D
imaging, RT3D has lower spatial resolution and also lower temporal resolution but it is more accurate for
volumetric measurements. Some have advocated its use for EF and volume assessment in all cases as it
removes some of the geometrical assumptions made in 2D, improves accuracy, and removes subjectivity
(20,19). Pre- and postvalues of stroke volume are used as an objective measurement to assess improvement
post-CABG surgery.
Three-dimensional measurement of LVEF and volumes are made from the ME four- and two-chamber
views. The echocardiographer must ensure that the whole of the LV is in view for full-volume acquisition
to minimize foreshortening. Ideally ventilation should be stopped while acquiring the image to minimize
stitch artifacts for the 5 to 7 beats 3D acquisition. The full-volume image is acceptable when the landmarks
of the mitral annulus, septal and lateral points, and apex are easily seen.
There is a high correlation of 3D volume reconstruction by echo with magnetic resonance imaging (MRI)
but in general 3D echo slightly underestimates the LV volume due to under tracing of the endocardium.
Three dimensional is superior to 2D as surface rendering is not dependent on geometrical assumptions
which is important if an aneurysm is present. Changes in EF following revascularization can be quantita-
tively measured this way (Fig. 15.2).
Segmental wall function can be visualized in both the 3D volume reconstruction and a trace of each of
the 17 segments with a different color depicting the time taken to reach minimal volume (i.e., maximum
contraction) against time. This should be simultaneous as any delay reveals LV dyssynchrony. The standard
deviation of regional ejection times is referred to as the systolic dyssynchrony index (SDI). The report page
depicts a bull’s-eye map displaying the 17 segments of contraction as parametric images with color shading
for timing differences (Fig. 15.1). All these maps make it easy to assess which segments have delayed con-
traction and by inference, ischemia and are again imaged postrevascularization to assess for improvement
in contractility objectively. LVSDI may be used to predict the response to resynchronization therapy and
where to best position the LV lead in the future. The RV is susceptible to ischemia in coronary revascular-
ization. Three-dimensional imaging is a useful adjunct to 2D in assessing function, size, and volume as its
crescent shape makes measurement of these parameters difficult in 2D (Video 15.9). Video 15.9
TEE for Specific Surgical Situations

Redo Sternotomy
TEE can be useful in detecting adherence of the right ventricle to the sternum. This is best viewed in the ME
RV inflow–outflow plane where restriction of the free wall of the RV can be seen (Video 15.10). Femoral Video 15.10
cannulation may be a preferred option in these circumstances.
Off-pump CABG
TEE intraoperative evaluation has aided off-pump coronary artery bypass (OPCAB) graft or minimally
invasive direct (MIDCAB) surgery techniques (32). Patient tolerance to the procedure can be monitored in
real time with TEE as patients undergoing OPCAB are susceptible to cardiovascular instability especially
when the myocardial stabilizer is applied. Application of the stabilizer and displacement of the heart can also
cause transient occlusion of the coronary arteries and ischemia which can be detected by TEE. Intraoperative
detection of moderate-to-severe MR may indicate that the OPCAB approach is not warranted.
RWMA during OPCABG: Transgastric images are often lost when the heart is displaced to access the
right and circumflex coronary arteries. However, evaluating the ME four-chamber, two-chamber, and LAX
views, during OPCAB surgery, allows for >14 segments to be evaluated for new RWMAs (33). Placement
of a sterile glove filled with saline instead of lap pads posterior to the heart has been shown to improve
image acquisition of the TG views (34). If a new RWMA is detected then repositioning of the stabilizer
or insertion of an intercoronary perfusion shunt may be beneficial. Persistent abnormalities may predict
postoperative problems and graft patency (Video 15.11). Video 15.11

MR during OPCABG: This can be a new development when the heart is displaced and the annulus dis-
torted. It is easily detected by CFD in the ME views. Pre-existing MR may preclude OPCAB surgery as it
Video 15.12 increases the risk of progressing to severe persistent MR and pulmonary edema (Video 15.12).
IABP insertion during OPCABG: An IABP is used occasionally to support the heart during OPCAB
surgery, especially if the LV is poor or the patient has unstable angina. TEE guidance is useful for insertion
as the OPCAB approach is commonly selected in patients with severe atheromatous disease of the aorta.
Preload assessment during OPCABG: Diastolic filling can be impaired by the use of a myocardial sta-
bilization suction system and compression of the right atrium can occur when the heart is elevated. The
Trendelenburg position helps maintain ventricular filling and TEE can distinguish between hypovolemia
and impaired cardiac function.
Conversion to CPB during OPCABG: This decision can be elective or as an emergency response.
TEE can anticipate deterioration of ventricular function, persistent RWMAs requiring graft revision, or
development of severe MR, before sudden hemodynamic collapse occurs. New information, for example,
valvular abnormalities or atrial septal defects, indicating a need for CPB may also be found in these
patients.
Graft patency during OPCABG: The patency of the grafts is assessed with TEE by looking for normal
function and resolution of RWMAs prior to chest closure. The intraoperative use of myocardial contrast
echocardiography may differentiate causes of LV dysfunction immediately after separation from CPB fol-
lowing revascularization by looking at regional flow patterns. Hence, TEE can modify OPCAB cases and
may improve morbidity and mortality in these patients (35).
Role of TEE in Vascular Cannulations

Aortic cannula: As part of a complete examination during coronary revascularization, the ascending and
descending aorta should be examined for atheromatous plaques or calcification. This will influence surgi-
cal decision-making when instrumentation of the aorta is considered, for example, aortic cannula, aortic
cross-clamp, or intra-aortic balloon counterpulsation. Detection of severe atheromatous disease of the
ascending aorta is a risk factor for poor outcome and modification of surgical technique may be warranted.
Changing the aortic cannulation and cross-clamp sites, avoiding an aortic side-clamp by performing all
proximal and distal coronary anastomoses during one single ischemic cross-clamp period, and using endo-
aortic balloon occlusion are all options to reduce embolic consequences. Furthermore, OPCAB surgery or
CABG under hypothermic circulatory arrest can also be considered.
The ME ascending aorta LAX and SAX, the ME AV LAX, UE aortic arch SAX and LAX views examine
the ascending aorta and arch, and the ME descending aorta SAX and LAX views examine the descending
aorta. Due to the anatomical location of the trachea and the left main stem bronchus, which lies between
the esophagus and the aortic arch, TEE only visualizes 50% to 80% of the ascending aorta. Atheroma is
measured perpendicularly from the outer vessel wall to the intimal surface and graded 1 to 4 depending
Video 15.13 on the thickness. Grade 5 is a mobile plaque (Fig. 15.5, Videos 15.13, 15.14). Severe atheroma (grade 4 to
Video 15.14 5) found in the descending aorta has been correlated with the presence of a similar grade atheroma in the
ascending aorta. Detection of severe or mobile plaques in the aortic arch may change the surgical plan
converting an on-pump coronary revascularization to OPCAB procedure to avoid the “sand blasting”
effect of the aortic inflow cannula disrupting plaque and sending it into the systemic circulation as emboli
(35–37). Postcannulation and decannulation assessments are made to check for iatrogenic aortic dissec-
tion originating from the aortic cannulation and antegrade cardioplegia sites as well as the proximal vein
graft sites. When there is inadequate visualization of the aorta with TEE, epiaortic scanning should be
considered.
1. Cardioplegia
Cardioplegia is given either by antegrade and/or retrograde routes. Prior to placement of the antegrade
cardioplegia cannula, TEE and epiaortic imaging are used to check for the presence of aortic atheroma in
the ascending aorta, arch, and descending aorta. Aortic dissection is a rare complication of antegrade car-
dioplegia cannulation but may be detected by TEE in the ME ascending aorta LAX view.
TEE is useful to guide and confirm placement of the retrograde cannula in the coronary sinus. The ME
four-chamber with slight retroflexion and advancement of the probe provide the most reliable view of the
Video 15.15 coronary sinus (Fig. 15.6, Video 15.15). Alternatively, the coronary sinus can be visualized in a modified

FIGURE 15.5 Grade 4 plaques in the arch of the aorta. This changed the operation from on-pump to off-pump CABG to
avoid the “sandblasting” effect. The patient woke up neurologically intact.
bicaval view with the imaging plane at approximately 130 degrees. The presence of a valve at the entrance
to the coronary sinus (Thebesian valve) may impede insertion. It is essential that a persistent left-sided
superior vena cava (SVC) be excluded when retrograde cardioplegia is being used as it will render the
cardioplegia ineffective. This persistent left-sided SVC is best seen in the ME four-chamber view with the
probe slightly withdrawn and is seen next to the left upper pulmonary vein (LUPV) although an enlarged
coronary sinus showing positive contrast echo from a left-sided IV is more reliable (Fig. 15.7).
2. IABP
IABPs remain essential tools to stabilize patients with left main coronary artery disease and unstable
symptoms prior to surgery as well as intraoperatively in patients with deteriorating ventricular function.
TEE is useful to ensure correct placement and avoid associated complications. First, confirm proper intra-
luminal position of the guidewire. Second, guide correct IABP position from the ME descending aorta SAX
view with the tip positioned just distal (2 to 3 cm) to the left subclavian artery (Videos 15.16, 15.17). Video 15.16
Video 15.17
FIGURE 15.6 Insertion of a retrograde cannula for cardioplegia showing the coronary sinus catheter within the coro-
nary sinus in the ME four-chamber view with slight probe retroflexion.

FIGURE 15.7 Patient with a persistent left SVC seen in this view anterior to the LUPV.
3. Femoral vascular cannulation

Arterial and venous femoral lines are inserted for a variety of clinical indications including aortic sur-
gery and coronary artery bypass surgery. Severe atheromatous disease or dilation of the ascending aorta
can preclude cannulation at this site. Redo surgery is increasing and femoral cannulation allows decom-
pression of the heart prior to sternotomy decreasing injury to the RV when adherent to the posterior
surface of the sternum. It also limits anatomical dissection around the heart that conventional cannulation
requires.
The femoral vessels are exposed and guidewires are passed up the aorta and inferior vena cava (IVC).
Dissection is ruled out by the presence of the wire within the lumen of the aorta and is visualized in the ME
descending aorta SAX and LAX views. The wire has bright echogenicity. The femoral venous wire is passed
up into the right atrium and is best seen in the ME bicaval view. SVC cannulation can also be performed
under echo guidance with the wire passing down from the right internal jugular vein (RIJV) into the right
atrium. This is best seen in the ME bicaval view and the tip of the cannula is adjusted to allow isolation of
Video 15.18 the cava if necessary (Video 15.18).
4. Port access surgery

The ascending aorta is sized by measuring it in the ME AV LAX view 2 to 3 cm above the aortic valve
and the valve competence is assessed by CFD. Femoral and SVC cannulation are performed and verified
by echo as described above. The aortic endoclamp is positioned under echo guidance in the ascending
aorta just distal to the sinotubular junction. Cardioplegia is administered through the port and monitored
by the use of CFD. Aortic regurgitation can develop if the aortic balloon migrates toward the aortic valve
and prolapses through it. The balloon can be repositioned under TEE guidance. Decompression of the LV
is difficult in port access surgery and it is important to monitor the LV for distension while on bypass. It
is advisable to do this in the ME LAX view as making large changes in the echo window is fraught with
hazard as orientating the images on bypass is difficult. De-airing is also aided by the use of echo as normal
de-airing methods are not available. The apex of the LV and left atrial appendage (LAA) are closely checked
for air. Air appears as multiple, small, bright echogenic reflections or as a wobbling collection at the apex
Video 15.19 (Fig. 15.8, Video 15.19).
Endoscopic Vein Harvesting (EVH)

Recent advances in harvesting the long saphenous vein endoscopically, while reducing morbidity from
the leg incision and increasing early mobility, have produced its own problems. The insufflation of carbon
dioxide (CO2) at 10 to 15 mm Hg pressure to facilitate harvesting has resulted in reports of CO2 embolism.
The ME bicaval and TG views of the hepatic veins and the IVC are used to detect the presence of bubbles in

FIGURE 15.8 ME four-chamber view with bright echogenic shadows “fireflies” and a large wobbling bright echogenic
shadow at the apex of the LV. The bright echogenic shadows are intracavity air.
the right atrium (38). Rapid diagnosis by TEE allows prompt treatment. The incidence has been reported to
be between 0.5% for severe and 3.5% for moderate emboli (38). Using the lowest pressures for insufflation
and monitoring with TEE allows for early CO2 embolism detection.
Ventricular Assist Devices

The use of ventricular assist devices (VADs) is becoming increasingly common both as rescue therapy,
a bridge to transplant, or destination therapy. The use of TEE to assist in implantation and management
is now a category 1 indication (3). LVADs are the most frequently implanted but right ventricular assist
device (RVAD) and biventricular assist devices (BIVADs) are also used occasionally. Echocardiography is
an essential tool for pre-, peri-, and postoperative assessments (39,40). Three-dimensional TEE is increas-
ingly useful to guide spatial positioning of cannulas and to assess problems (41). Prior to implantation it
is necessary to assess baseline ventricular function and to exclude various pathologies. A comprehensive
examination should be performed with special attention to the following:
1. Intracardiac thrombus, ventricular and atrial

There will be sluggish flow in both chambers by virtue of the fact that an assist device is needed.
Ventricular aneurysms are also common and may harbor thrombus. Along with scarred ventricular regions,
these sites should be avoided for insertion of the inflow cannula. Thrombus can obstruct the inflow cannula
when placed at the ventricular apex, the most common site, but alternative sites can be in the left atrium or
pulmonary veins (Figs. 15.9 and 15.10, Videos 15.20, 15.21). Video 15.20
Video 15.21
2. Intracardiac shunts (PFO, ASD)
PFOs are common in up to 27% of the population. All can increase hypoxia and complications such as
stroke if undiagnosed. Timing of assessment of PFOs is important as in the failing LV with high left atrial
pressure the PFO may not be apparent until the LVAD is in place and decompression of the chambers has
occurred. Accordingly, it is essential to check after placement of the cannula to determine if a PFO has
opened. If a significant shunt is present this may be closed formally or percutaneously.
3. Valvular abnormalities
Aortic regurgitation decreases forward flow from the LVAD and increases recirculation as aortic blood
returns to the ventricle. Because of reduced gradients in failing ventricles regurgitation should be reas-
sessed on CPB as it can be underestimated on the initial examination. If it is significant then the valve may
need to be replaced if the VAD is for bridging or sutured shut if it is for destination therapy. Allowing the

FIGURE 15.9 2D TEE four-chamber view demonstrating thrombus in the LV apex in a patient scheduled for LVAD
placement.
aortic valve to open intermittently (this is achieved by decreasing the LVAD contribution under echo guid-
ance) helps in reducing stasis and the potential for thrombosis. In a similar manner, pulmonary insuffi-
ciency should be assessed prior to placement of RVADs.
MR is a feature of end-stage heart failure and should be improved by LVAD insertion. Mitral stenosis
impairs filling of the LVAD placed in the left ventricle. Atrial or pulmonary venous placement will avoid this
limitation or a valvotomy preinsertion can be performed.
4. Right ventricular function
Although the RV may improve following LVAD insertion, as afterload is reduced, RV failure is common
and can occur in up to 40% of patients (42). Increasing preload may precipitate RV failure, and the intraven-
tricular shift of the septum to the left following implantation can also reduce RV contractility.
Predictors of good RV function are normal function or mild hypokinesis of the free wall, absence of
severe tricuspid regurgitation, fractional shortening >20% of the right ventricular outflow tract (RVOT),
and tricuspid annular plane systolic excursion (TAPSE) of 10 to 15 mm (42). Severe tricuspid regurgitation
can reduce filling of the left ventricle and the LVAD.
FIGURE 15.10 3D TEE four-chamber view demonstrating thrombus in the LV apex in a patient scheduled for LVAD
placement.

FIGURE 15.11 ME four-chamber view of inflow cannula at the LV apex.
5. Aortic atheroma
The presence of mobile atheroma in the arch and ascending aorta is associated with an increased risk of
stroke following LVAD placement. Although part of the ascending aorta is not well seen, atheroma in the
proximal ascending, arch, and descending aorta is associated with cerebral dysfunction.
6. Positioning of ventricular assist device cannulas
a. Inflow cannula
As previously mentioned, the inflow cannula can be in various positions. The most common is through
the left ventricular apex and either the right ventricle(RV) or the right atrium for RVADs, more common
for RVADs. (Fig. 15.11, Videos 15.22, 15.23). Two-dimensional echo of LV inflow cannula should be aligned Video 15.22
with the mitral inflow and not obstructed by any walls (Fig. 15.12). Two-dimensional echo using at least Video 15.23
two orthogonal views, for example, ME four-chamber and ME two-chamber, is very useful to assess proper
placement. Three-dimensional real-time TEE is extremely useful in checking the orientation of the cannula.
CFD should demonstrate unidirectional laminar flow with the pattern specific to the particular device.
Pulsatile LVADs such as HeartMate I, Thoratec, and Novacor will have a pulsatile pattern of flow where
normal velocities should be <2.3 m/s (which is compatible with a 16-mm cannula) and flow rates of 65 mL/s.
FIGURE 15.12 ME four-chamber view showing LVAD inflow via color Doppler.

FIGURE 15.13 2D ME four-chamber view of “suckdown” where the intraventricular septum bows toward the LV inflow
cannula potentially causing obstruction.
The impeller driven axial flow devices (e.g., HeartMate II and Javik) are implanted directly through
the LV apex and have no inflow cannula per se, will show continuous inflow throughout the cardiac cycle
as well as a pulsatile pattern that synchronizes with the ECG (39,40,43). These axial flow devices have
peak filling velocities of 1 to 2 m/s depending on preload and residual cardiac output from the heart. An
increase in pulsed wave Doppler (PWD) velocities in the LV cavity, incomplete emptying of the LV, high-
velocity flow through the AV, or frequent opening of the AV (which should not occur as only minimal
flow should pass through the AV with a properly functioning LVAD) suggests that the inflow cannula is
malfunctioning.
A “suckdown effect” results when hypovolemia and/or rapid decompression from excessive LVAD
speed causes intermittent obstruction of the inflow cannula. This situation can occur during weaning of
CPB to LVAD support. There is a prominent bowing of the intraventricular septum toward the LV which
Video 15.24 then occludes the inflow cannula (Figs. 15.13 and 15.14, Videos 15.24, 15.25). When faced with a suckdown
Video 15.25 effect in a hemodynamically unstable patient it is important not to increase LVAD speed in an attempt to
improve flow and blood pressure but rather to decrease LVAD speed and increase preload. Later progressive
FIGURE 15.14 3D image of the intraventricular septum encroaching on the LVAD LV inflow cannula.

FIGURE 15.15 2D ME LAX showing color flow out of the outflow aortic cannula of LVAD.
increases in LVAD support can be initiated. If the LV cavity image consistently looks small on TEE, it may
be due to poor cannula position or an intercavity clot.
Causes of cannula obstruction in RVADs can be associated with the tricuspid anterior leaflet, subvalvu-
lar apparatus, or an aneurismal intra-atrial septum.
b. Outflow cannula
The most common site for attaching the LVAD outflow cannula is the ascending aorta. The attachment
should be perpendicular to the ascending aorta and is assessed by CFD looking for laminar flow in the ME
AV LAX view (Fig. 15.15, Video 15.26). Video 15.26
For RVADs, the pulmonary artery is the most common attachment site for the outflow cannula either
using direct anastomosis or from the RV via the pulmonary valve. Assessment is made using the ME
ascending aortic SAX and the ME RV inflow/outflow views (Figs. 15.16 and 15.17, Videos 15.27, 15.28). Video 15.27
Normal peak velocities of 1.7 to 2.5 m/s have been suggested (40) but lower velocities 1 to 2 m/s for axial Video 15.28
flow pumps as detected by PWD at 1 cm proximal to the aortic anastomosis (39,40) are acceptable.
Obstruction of the outflow cannula or incompetence of the valve may be indicated by increased flow
velocity measured proximally in the graft compared to distally. Causes of outflow obstruction can be
thrombus, vegetations or extrinsic compression by mediastinal hematoma, or kinking of the graft during
FIGURE 15.16 2D ME RV inflow–outflow view of the RVOT showing the outflow cannula for the RVAD going into the PA.

FIGURE 15.17 3D LAX image of RVAD outflow cannula into PA.
sternal closure. Other indications that obstruction has occurred are septal deviation to the right, LV dila-
tion, and increased MR. Table 15.6 summarizes post-VAD implantation checks and complications.
7. VAD follow-up and device dysfunction
Regular follow-up is needed as device failure and malfunction can be as high as 35% (40,44). For pulsa-
tile LVADs, inflow regurgitation secondary to mechanical failure of the inflow valve is the most common
cause of LVAD dysfunction. Inflow cannula regurgitation results in turbulent flow at the inflow cannula
during LVAD ejection. It is detected on Doppler examination as a biphasic inflow pattern as opposed to
the unidirectional laminar flow seen in the normally functioning VAD. PWD demonstrates flow reversal
in the inflow cannula during LVAD ejection as well as decreased peak velocities (<1.8 m/s) in the outflow
cannula. Other indications of a malfunctioning inflow cannula with a pulsatile LVAD are a full or dilated
LV and frequent opening of the AV.
Axial flow VAD designs (Jarvik 2000 and HeartMate II) eliminated the use of valves. Diastolic regurgita-
tion through the outflow graft from the aorta into the LV secondary to pump failure is associated with an
abnormal retrograde apical flow pattern on Doppler examination. Thromboembolic problems can occur
and result in inflow obstruction. Detection inside the devices is not possible with TEE but thrombi in the
LAA, LV apex and intraventricular septum, and around the cannula may indicate intradevice thrombi. For
pulsatile pumps, a peak inflow velocity >2.3 m/s or interruptions of the usual laminar inflow pattern are
consistent with inflow cannula obstruction. With continuous-flow devices, inflow obstruction is suggested
by turbulent flow and Doppler-derived peak inflow velocities of >2 m/s.
TABLE 15.6 Summary Post-VAD Implantation Checks and Complications
t De-airing, both intracardiac and device

t Re-evaluation for PFO
t Presence of MR, this should be reduced, if not then it possibly indicates poor positioning of the inflow cannula.
Frequent arrhythmias are also a sign of poor cannula positioning
t Decompression of the LV
t Septal position should be neutral. Right shift indicates inadequate emptying. Left shift can result from excessive
decompression due to excessive pump speeds
t Doppler interrogation of the cannulas
t Aortic valve opening. This can be intermittent with axial flow devices but in pulsatile devices it should be closed at
all times
t Right ventricular failure
t Rule out cardiac tamponade

Aortic dissection can occur as there is increased stress on the aortic intima by the blood being reinfused
at high velocities against the aortic wall. Endocarditis may develop resulting in vegetations on native valves
and conduits causing obstruction and even rupture in extreme cases.
8. Weaning from VADs
The criteria for weaning from VADs are not fully defined at the time of writing but involve a combina-
tion of echo and clinical features. Recovery of the LV can occur and is assessed visually and objectively:
LVEF >45%, left ventricular end diastolic diameter <45 mm, and fractional area change >40%. RVAD sup-
port following LVAD insertion is usually only needed for 2 to 4 weeks and can be discontinued when
recovery of the RV occurs; however, when to remove it is more difficult to assess than for the LV. The PVR
must be optimized and support from the RVAD gradually weaned by reducing the rate and vacuum while
monitoring the RV function visually. The ME four-chamber and ME RV inflow/outflow views are used for
assessment as well as observing the venous pressures and LV function.
Echo in Extra Corporeal Membrane Oxygenation

1. Cannulation placement
Extra corporeal membrane oxygenation (ECMO) is increasingly being chosen to treat refractory respi-
ratory failure. Veno-venous (V-V) ECMO is used for respiratory failure with preserved cardiac function
and both the inflow and outflow cannulas are placed in the venous system. Veno-arterial (V-A) ECMO is
used when there is inadequate cardiac function associated with respiratory failure and as support for the
RV following LVAD placement until it recovers. V-V is preferred as there are fewer complications associ-
ated with large-bore venous cannulas than with large bore cannulas in arteries for V-A.
TEE is invaluable in assessing patient selection, cannula insertion, correct placement, detection of com-
plications, monitoring improvement, and weaning from V-A ECMO by assessing recovery of cardiac func-
tion (45). A preinsertion TEE should be performed to check any structural abnormalities like a PFO (45),
ASD, large Eustachian valve, Chiari network, or TV pathology which may impede the placement of the
inflow cannula. Closure or management of any right-to-left shunt may result in ECMO being unnecessary.
A comprehensive TEE will determine if V-V will be sufficient or if V-A ECMO is indicated.
For V-V ECMO, dual lumen cannulas are now available and are inserted into the SVC via the RIJV.
Blood from the SVC and IVC enters one lumen positioned just above the IVC entry into the RA and pro-
vides inflow to the oxygenator. Outflow blood is returned via a separate lumen, positioned so that flow from
the side hole is directed through the tricuspid valve into the RV. TEE is essential for the correct placement
and positioning. CFD from the ME views is used to adjust the position of the outflow hole toward the TV
(Fig. 15.18). If it is incorrectly positioned, the outflow of oxygenated blood instead of passing into the RV
FIGURE 15.18 ECMO cannula showing CFD with outflow positioned in-line with the tricuspid valve.

is taken back to the oxygenator by the inflow port and recirculation occurs. A marked difference between
the color of the blood in the dual lumens assists in assessing correct position so recirculation is minimized.
Separate cannulas may be inserted with the inflow tip positioned as the IVC enters the RA and the out-
flow cannula above the TV. Large patients (over 100 kg) often need a second oxygenator. The second inflow
cannula is usually placed in the femoral vein. TEE is used to visualize the guidewire in the RA as it passes
via the RIJV into the SVC passing through the heart down the IVC or in the IVC passed from the femoral
vein. The SVC approach is the most common route for placement of the cannula.
In V-A ECMO, TEE is used to assess the ascending aorta for aortic dissection before proceeding. The
ME AV LAX, UE aortic arch, and ME descending aorta SAX and LAX views are used during cannulation
to check for the location of the guidewire and to rule out the presence of aortic atheroma. TEE evaluation
of ventricular decompression is made in the ME and TG views. Once ECMO is established, TEE is used to
monitor the effect on the heart.
With V-A ECMO, preload is decreased but afterload is increased due to the pressurized arterial return.
In severe LV dysfunction, this can lead to further LV failure, severe MR, and the AV not opening at all.
Spontaneous echo contrast from stasis can lead to thrombosis and this should be looked for in the LV,
aorta, and pulmonary veins. Anticoagulation needs to be increased and flow reduced until the spontaneous
echo contrast improves. If it does not then a LVAD may be more appropriate than ECMO.
In V-V ECMO there are fewer hemodynamic changes. The increase in oxygen content of the blood can
decrease the RV afterload as the PVR falls improving RV and LV function.
2. ECMO complications
Thrombosis is a concern and the presence of venous casts when the cannulas are removed should be
evaluated in the ME bicaval and ME four-chamber views. TEE can show complications such as tamponade
and cannula displacement, for example, migration across the atrial septum or through the TV. TEE is used to
assess ventricular filling and function, and aids repositioning of cannulas if required. Normal clinical param-
eters for detecting tamponade may be hidden as the heart is in a partial bypass state with V-A ECMO so
collapse of the ventricles is normal and if flow is maintained then tamponade may be only detected by TEE.
Another recognized problem is difficulty in removing the SVC cannula after being in situ for a pro-
longed period. Tethering usually occurs at the level of insertion. TEE is useful in checking that the cannula
is not tethered in the ventricle.
3. ECMO weaning
TEE is not very useful for weaning from V-V ECMO due to the fact that weaning is primarily determined
by improvement in pulmonary compliance and oxygenation. However, TEE is useful to assess the recovery of
LV function and weaning from V-A ECMO. There are no specific parameters utilized and weaning is similar
to that performed when weaning from a VAD. Indications of a successful wean include an LVEF >35%, LVOT
TVI >10 cm, and absence of cardiac tamponade or LV dilation. Flow is gradually decreased under TEE guid-
ance but not to a value of less than 1 to 2 L/min to minimize the risk of thrombosis.
SUMMARY
TEE can significantly influence clinical management and improve patient outcome in coronary revascu-
larization (2). Recent recommendations from both sides of the Atlantic recommend its routine use in all
patients undergoing coronary revascularization. As surgical approaches to revascularization develop along
with associated technologies, TEE has proven to be an increasingly valuable tool for patient care.
REFERENCES
1. Swanevelder J, Chin D, Kneeshaw J, et al. Accreditation in transoesophageal echocardiography: Statement from the
Association of Cardiothoracic Anaesthetists and the British Society of Echocardiography Joint TOE Accreditation Committee.
Br J Anaesth. 2003;91:469–472.
2. Kolev N, Brase R, Swanevelder J, et al. The influence of transoesophageal echocardiography on intra-operative decision mak-
ing. A European multicentre study. European Perioperative TOE Research Group. Anaesthesia. 1998;53:767–773.
3. American Society of Anesthesiologists and Society of Cardiovascular Anesthesiologists Task Force on Transesophageal
Echocardiography. Practice guidelines for perioperative transesophageal echocardiography. An updated report by the

American Society of Anesthesiologists and the Society of Cardiovascular Anesthesiologists Task Force on Transesophageal
4. Flachskampf FA, Badano L, European Association of Echocardiography, et al. Recommendations for transoesophageal echo-
cardiography: Update 2010. Eur J Echocardiogr. 2010;11:557–576.
5. Eltzschig HK, Rosenberger P, Löffler M, et al. Impact of intraoperative transesophageal echocardiography on surgical decisions
in 12,566 patients undergoing cardiac surgery. Ann Thorac Surg. 2008;85:845–852.
6. Qaddoura FE, Abel MD, Mecklenburg KL, et al. Role of intraoperative transesophageal echocardiography in patients having
coronary artery bypass graft surgery. Ann Thorac Surg. 2004;78:1586–1590.
7. Klein AA, Snell A, Nashef SAM, et al. The impact of intra-operative transoesophageal echocardiography on cardiac surgical
practice. Anaesthesia. 2009;64:947–952.
8. Desjardins G, Cahalan M. The impact of routine trans-oesophageal echocardiography (TOE) in cardiac surgery. Best Pract Res
Clin Anaesthesiol. 2009;23:263–271.
9. Fanshawe M, Ellis C, Habib S, et al. A retrospective analysis of the costs and benefits related to alterations in cardiac surgery
from routine intraoperative transesophageal echocardiography. Anesth Analg. 2002;95:824–827, table of contents.
10. Skinner HJ, Mahmoud A, Uddin A, et al. An investigation into the causes of unexpected intra-operative transoesophageal
echocardiography findings. Anaesthesia. 2012;67:355–360.
11. Schwann NM, Hillel Z, Hoeft A, et al. Lack of effectiveness of the pulmonary artery catheter in cardiac surgery. Anesth Analg.
2011;113:994–1002.
12. Guarracino F. [The role of transesophageal echocardiography in intraoperative hemodynamic monitoring]. Minerva Anestesiol.
2001;67:320–324.
13. Piercy M, McNicol L, Dinh DT, et al. Major complications related to the use of transesophageal echocardiography in cardiac
surgery. J Cardiothorac Vasc Anesth. 2009;23:62–65.
14. Hilberath JN, Oakes DA, Shernan SK, et al. Safety of transesophageal echocardiography. J Am Soc Echocardiogr. 2010;23:1115–
1127; quiz 1220–1221.
15. Na S, Kim CS, Kim JY, et al. Rigid laryngoscope-assisted insertion of transesophageal echocardiography probe reduces oropha-
ryngeal mucosal injury in anesthetized patients. Anesthesiology. 2009;110:38–40.
17. Piérard LA, Lancellotti P. Risk stratification after myocardial infarction: Toward novel quantitative assessment of left ventricu-
lar mechanics? J Am Coll Cardiol. 2010;56:1823–1825.
18. Ng A, Swanevelder J. Perioperative monitoring of left ventricular function: What is the role of recent developments in echo-
cardiography? Br J Anaesth. 2010;104:669–672.
19. Vegas A, Meineri M. Core review: Three-dimensional transesophageal echocardiography is a major advance for intraoperative
clinical management of patients undergoing cardiac surgery: A core review. Anesth Analg. 2010;110:1548–1573.
echocardiography. J Am Soc Echocardiogr. 2012;25:3–46.
21. Saito K, Okura H, Watanabe N, et al. Comprehensive evaluation of left ventricular strain using speckle tracking echocar-
diography in normal adults: Comparison of three-dimensional and two-dimensional approaches. J Am Soc Echocardiogr.
2009;22:1025–1030.
22. Ballal RS, Nanda NC, Gatewood R, et al. Usefulness of transesophageal echocardiography in assessment of aortic dissection.
Circulation. 1991;84:1903–1914.
24. Roizen MF, Beaupre PN, Alpert RA, et al. Monitoring with two-dimensional transesophageal echocardiography. Comparison
of myocardial function in patients undergoing supraceliac, suprarenal-infraceliac, or infrarenal aortic occlusion. J Vasc Surg.
1984;1:300–305.
25. Smith JS, Cahalan MK, Benefiel DJ, et al. Intraoperative detection of myocardial ischemia in high-risk patients:
Electrocardiography versus two-dimensional transesophageal echocardiography. Circulation. 1985;72:1015–1021.
26. Leung JM, O’Kelly B, Browner WS, et al. Prognostic importance of postbypass regional wall-motion abnormalities in patients
undergoing coronary artery bypass graft surgery. SPI Research Group. Anesthesiology. 1989;71:16–25.
27. Bergquist BD, Leung JM, Bellows WH. Transesophageal echocardiography in myocardial revascularization: I. Accuracy of
intraoperative real-time interpretation. Anesth Analg. 1996;82:1132–1138.
28. Cheung AT, Savino JS, Weiss SJ, et al. Echocardiographic and hemodynamic indexes of left ventricular preload in patients with
normal and abnormal ventricular function. Anesthesiology. 1994;81:376–387.
29. Sukernik MR, Goswami S, Frumento RJ, et al. National survey regarding the management of an intraoperatively diagnosed
patent foramen ovale during coronary artery bypass graft surgery. J Cardiothorac Vasc Anesth. 2005;19:150–154.
30. Bonow RO, Carabello BA, American College of Cardiology/American Heart Association Task Force, et al. 2008 Focused
update incorporated into the ACC/AHA 2006 guidelines for the management of patients with valvular heart disease: A report
of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee
to Revise the 1998 Guidelines for the Management of Patients With Valvular Heart Disease): Endorsed by the Society of
Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic
Surgeons. Circulation. 2008;118:e523–e661.
31. Shuhaiber J, Anderson RJ. Meta-analysis of clinical outcomes following surgical mitral valve repair or replacement. Eur J
Cardiothorac Surg. 2007;31:267–275.

32. Kapoor PM, Chowdhury U, Mandal B, et al. Trans-esophageal echocardiography in off-pump coronary artery bypass grafting.
Ann Card Anaesth. 2009;12:167.
pump coronary artery bypass surgery. Anesth Analg. 2004;99:965–973, table of contents.
34. Kim SH, Yeo JS, Yoon TG, et al. Placing a saline bag underneath the displaced heart enhances transgastric transesophageal
echocardiographic imaging during off-pump coronary artery bypass surgery. Anesth Analg. 2009;109:1038–1040.
35. Gurbuz AT, Hecht ML, Arslan AH. Intraoperative transesophageal echocardiography modifies strategy in off-pump coronary
artery bypass grafting. Ann Thorac Surg. 2007;83:1035–1040.
36. Gold JP, Torres KE, Maldarelli W, et al. Improving outcomes in coronary surgery: The impact of echo-directed aortic cannula-
tion and perioperative hemodynamic management in 500 patients. Ann Thorac Surg. 2004;78:1579–1585.
37. Evered LA, Silbert BS, Scott DA. Postoperative cognitive dysfunction and aortic atheroma. Ann Thorac Surg. 2010;89:1091–
1097.
38. Lin TY, Chiu KM, Wang MJ, et al. Carbon dioxide embolism during endoscopic saphenous vein harvesting in coronary artery
bypass surgery. J Thorac Cardiovasc Surg. 2003;126:2011–2015.
39. Chumnanvej S, Wood MJ, MacGillivray TE, et al. Perioperative echocardiographic examination for ventricular assist device
implantation. Anesth Analg. 2007;105:583–601.
40. Sheinberg R, Brady MB, Mitter N. Intraoperative transesophageal echocardiography and ventricular assist device insertion.
Semin Cardiothorac Vasc Anesth. 2011;15:14–24.
41. Castillo JG, Anyanwu AC, Adams DH, et al. Real-time 3-dimensional echocardiographic assessment of current continuous-
flow rotary left ventricular assist devices. J Cardiothorac Vasc Anesth. 2009;23:702–710.
42. Hsu PL, Parker J, Egger C, et al. Mechanical circulatory support for right heart failure: Current technology and future outlook.
Artif Organs. 2012;36(4):332–347.
43. Nicoara A, Mackensen GB, Podgoreanu MV, et al. Malpositioned left ventricular assist device cannula: Diagnosis and manage-
ment with transesophageal echocardiography guidance. Anesth Analg. 2007;105:1574–1576.
44. Kirkpatrick JN, Wiegers SE, Lang RM. Left ventricular assist devices and other devices for end-stage heart failure: Utility of
echocardiography. Curr Cardiol Rep. 2010;12:257–264.
45. Platts DG, Sedgwick JF, Burstow DJ, et al. The role of echocardiography in the management of patients supported by extracor-
poreal membrane oxygenation. J Am Soc Echocardiogr. 2012;25:131–141.

QUESTIONS
1. Regarding insertion of a TEE probe: 6. In using TEE to assess cannulation:
a. Bacteremia is common with TEE insertion a. The presence of a Eustachian valve is a con-
b. Arrhythmias are uncommon following TEE traindication to retrograde cardioplegia
insertion b. The right main bronchus results in poor
c. A hiatus hernia is an absolute contraindica- views of the ascending aorta
tion c. Dissection of the ascending aorta from the
d. Odynophagia is uncommon following TEE retrograde cardioplegia cannula is usually
insertion seen in the ME LAX 135-degree view
e. Recurrent laryngeal palsy is a complication d. The bicaval view is the best view for assess-
of TEE insertion ing atrial septal transverse by the long
venous wire
2. In 3D TEE:
a. Stitching artifacts are seen frequently in live 7. Which is true?
3D a. Rapid hemodynamic deterioration during
b. 3D is less reliant on endocardial border EVH should be assessed by the bicaval view
tracking than 2D b. The subclavian vein can be seen by rotat-
c. Spatial resolution is lower but temporal ing left after obtaining the SAX view of the
resolution is higher than 2D ascending aorta at 90 degrees
d. 3D is more resistant to artifacts produced c. In port access surgery aortic stenosis is a
by atrial fibrillation contraindication
d. Plaques in the descending aorta are usually
3. In 3D echo:
1 to 2 grades worse than in the ascending
a. The paramagnetic image on the report page
aorta
reflects the time taken to relax
b. The LV dyssynchrony index is the standard 8. In a VAD placement which of the following
deviation of regional contraction times is not a contraindication requiring
c. The LV dyssynchrony index may be use- intervention:
ful for placing the right ventricular lead in a. Intraventricular thrombus
resynchronization therapy b. Ventricular septal defect
d. Segmental analysis is useful in assessing c. Aortic regurgitation
diastolic dysfunction d. Mitral regurgitation
4. Concerning right ventricular function: 9. In assessment of LVADs:
a. Right ventricular failure occurs in <1% of a. Intraventricular shift to the left can decrease
patients post-CABG right ventricular function
b. Left ventricular dysfunction occurs because b. Intraventricular shift to the left can aid fill-
of ventricular interdependence ing of the LVAD
c. The right cardiac vein is well protected with c. Fractional shortening of the basal segments
retrograde cardioplegia >20% is a predictor of right ventricular fail-
d. E/A waves of the tricuspid valve are a good ure
marker of ventricular systolic dysfunction d. Assessment for a PFO should only be made
early in the insertion process
5. In off-pump coronary revascularization:
a. The transgastric view is the best to detect 10. In a patient with a LVAD:
wall motion abnormalities a. The afterload is reduced to the left ventricle
b. Infusion of normal saline can assist in TEE b. Turbulence in the inflow cannula detected
views by PW can be an indication of malfunction
c. Mitral valve regurgitation can develop with c. The aortic valve may open intermittently
application of the octopus with pulsatile devices
d. Mitral valve regurgitation is a contraindica- d. An increase in proximal flow velocity com-
tion to off-pump coronary surgery pared to distal can indicate valvular incom-
petence

11. Which of the following is true? 16. In case of the unexpected intraoperative
a. In LVADs increasing the preload can pre- discovery of moderate functional mitral
cipitate RV failure regurgitation during a CABG procedure:
b. Echo is useful in weaning from V-V ECMO a. A more reliable quantification of regurgita-
c. Inflow to the ECMO cannula should be tion severity should be made by increasing
positioned just above the tricuspid valve contractility with a positive inotropic agent
d. LVOT VTI <10 cm support weaning from b. A more reliable quantification of regurgita-
V-A ECMO tion severity should be made by increasing
preload and afterload with a vasopressor
12. With TEE, coronary artery blood flow:
c. The MV should be left untouched when
a. Can be accurately quantified with pulsed
severity is less than grade 3
wave Doppler
d. Revascularization of the ischemic papillary
b. Can usually be visualized in the atrioven-
muscle usually decreases the MR severity
tricular groove
c. Can be seen in 80% of the right and 50% of 17. During intraoperative visualization of
the left coronary ostia RWMAs:
d. Cannot be demonstrated in the distribution a. An akinetic region is the result of myocar-
areas of all three arteries while using one dial infarction and reflects nonviable myo-
view cardium
b. A hypokinetic region is the result of myo-
13. Dyskinesis with myocardial thickening may
cardial infarction and reflects nonviable
occur when there is:
myocardium
a. Ventricular epicardial pacing
c. Ventricular rotation and twist during sys-
b. Electrolyte disturbances
tole complicates quantification
c. Epinephrine infusion during separation
d. Most WMAs benefit from coronary revas-
from bypass
cularization
d. Decreased volume loading
18. During a CABG procedure acute right
14. The intraoperative discovery of a small
ventricular dysfunction:
secundum ASD or patent foramen ovale:
a. Should be minimized by providing retro-
a. Is very rare
grade cardioplegia via the coronary sinus
b. Can most reliably be quantified with pulsed
b. Is caused by a poor coronary anatomizes to
wave Doppler
the right coronary artery
c. Can most reliably be assessed with color
c. May be caused by air embolism down the
flow Doppler and agitated saline contrast
right coronary artery
injection in the transgastric short-axis view
d. Should be accurately quantified with myo-
d. May affect the postoperative management
cardial deformation techniques
and outcome of any cardiac patient
19. During OPCAB surgery, is most useful to
15. In case of the unexpected intraoperative
access RWMAs during grafting of which
discovery of moderate aortic stenosis
coronary artery?
during a CABG procedure:
a. Right coronary artery
a. The patient should be woken up and con-
b. Circumflex coronary artery
sented for a combined surgical procedure
c. Left anterior descending coronary artery
before progressing
d. All the above
b. A subsequent AVR after the CABG has a
higher mortality than a single combined 20. Acute septal hypokinesis immediately after
procedure separation from CPB:
c. The progression of stenosis is 0.3 cm2/y and a. Requires immediate revision of the internal
should not change the surgical approach mammary artery graft anastomosis
d. An intra-aortic balloon pump should be b. Will require inotropic support to improve
inserted to assist coronary perfusion after ejection fraction
bypass c. May be due to right ventricular pacing
d. Is relatively common and may resolve spon-
taneously after 15 minutes

16 Echocardiography for Percutaneous Aortic Valve
and Mitral Clip Implantation
Chirojit Mukherjee
INTRODUCTION
The most frequent valvular disease in adults is calcification of the aortic valve. The average age of patients
presenting for surgery has increased to 70 years or older and many are asymptomatic until late in the dis-
ease process. Medically treated patients with symptomatic aortic stenosis (AS) show poor survival after
occurrence of symptoms (25% at first year and 50% in second year), and the incidence of sudden death
approaches 50%. Iung et al. (1) have shown that surgery is denied in 30% of octogenarians predominantly
due to a low LV ejection fraction and associated comorbidities (2). Transcatheter aortic valve implantation
(TAVI) is an innovative and evolving alternative for elderly, high-risk patients suffering with severe, symp-
tomatic AS (3,4).
The first human TAVI was performed in 2002 using a balloon-expandable pericardial stent via the
antegrade approach (5). This led to a series of trials establishing TAVI as a feasible and effective option
for multimorbid patients with symptomatic aortic valve stenosis who were denied surgical aortic valve
replacement (4,6–8).
CURRENT DEVICES: VALVES AND DELIVERY SYSTEMS

The greatest experience with TAVI has been with the SAPIEN valve (Edwards Lifesciences, Inc., Irvine, CA)
and the CoreValve (Medtronic, Inc., Minneapolis, MN). Both of these percutaneous valve delivery systems
offer the advantage of avoiding usage of cardiopulmonary bypass (CPB). Ongoing trials continue to explore
new options for transcatheter valve systems aimed at improving the mechanism of implantation, the valve
and stent material, valve hemodynamics, lowering the incidence of paravalvular leakage, and providing
improved mechanisms to retrieve the valve after deployment.
The SAPIEN valve is a balloon-expandable system on a stainless steel stent, into which a trileaflet bovine
pericardial valve is mounted (Fig. 16.1). The stents are skirted with a polyethylene terephthalate material
designed to decrease paravalvular leaks. The cobalt–chromium alloy allows for better apposition into the
annulus and walls of the aorta. The SAPIEN valve is available in three sizes (23, 26, and 29 mm) in Europe
and two sizes (23 and 26 mm) in the United States. Currently, the NovaFlex delivery system utilizes an
18-French (Fr) sheath for valve deployment.
The CoreValve is inserted by a retrograde approach using either transfemoral, subclavian, or direct aor-
tic access (Fig. 16.2). The valve consists of a porcine pericardial tissue mounted on a nitinol stent. It consists
of three parts (low, middle, and high) and three sizes 26, 29, and 31 mm. The lowest portion corresponds
to the annular region and applies the highest radial force to prevent device migration. The middle portion
lies within the sinus of Valsalva and is designed to reduce the incidence of paravalvular leaks. The higher
portion increases the quality of fixation into the ascending aorta. With progressive design improvements,
the delivery system has been reduced in size from the initial 25-Fr to an 18-Fr sheath which may decrease
vascular complications. The valve is partially retrievable, repositionable, and excludes the need for rapid
pacing during implantation.
Recently, the JenaValve (JenaValve Technology, Munich, Germany) and Acurate valve (Symetis, Inc.,
Lausanne, Switzerland) obtained CE approval for transapical implantation (9).
327

A B
FIGURE 16.1 The Edwards SAPIEN (Edwards Lifesciences, Inc., Irving, CA) is a low-profile valve available in three sizes:
23, 26, and 29 mm catering to annulus sizes between 18 and 27 mm. These valves are pretreated with Carpentier-Edwards
ThermaFix process and are presumed to prevent calcification and improve durability. A: Edwards SAPIEN valve. B: The
Edwards SAPIEN-XT valve. (Courtesy of Edwards Lifesciences, Inc., Irving, CA.)
FIGURE 16.2 The CoreValve (Medtronic, Inc., Minneapolis, MN) has three parts (lower, middle, and higher) and three sizes
26, 29, and 31 mm. The valve is partially retrievable with facility to recapture. (Courtesy of Medtronic, Inc., Minneapolis,
MN.)

16. Echocardiography for Percutaneous Aortic Valve and Mitral Clip Implantation 329
PROCEDURAL PERFORMANCE
Transapical Aortic Valve Implantation

This approach is through the left ventricular apex via a left anterior thoracotomy incision. After inser-
tion of rescue access, (guidewires and sheath for emergency initiation of CPB), an aortic root pigtail
catheter is placed in the ascending aorta to angiographically determine aortic root disease, cusp and
root anatomy, and ascending aortic dimensions. The apex of the heart is prepared with purse string/mat-
tress sutures, and bipolar epicardial pacing wires are placed for rapid ventricular pacing (RVP) required
during valve implantation. Apical access is established and guidewires are placed and subsequently
exchanged with an apical sheath and balloon valvuloplasty catheter. Balloon aortic valvuloplasty is per-
formed using RVP (usually 180 to 200 beats/min), the apical sheath is withdrawn, and the valve delivery
system is introduced through the apical access. After correct valve position is confirmed by fluoroscopy
and TEE, a second episode of RVP facilitates valve implantation. Optimal positioning and valve deploy-
ment are then achieved using either fluoroscopy, multidetector computerized tomography (MDCT), or
TEE (10).
Transfemoral Aortic Valve Implantation

The transfemoral approach is considered in patients when the anatomy of the iliac vessels is favorable
for the insertion of the delivery system. Femoral access is achieved using the contralateral approach and
multiple progressive dilations may be required to accommodate the large deployment sheath which is then
fixed in place with a stay suture. A pigtail catheter is placed in the abdominal aorta for continuous arte-
rial monitoring and angiographic facilitation of the anatomy of iliofemoral vessels. Pacing leads may be
inserted via the internal jugular or femoral veins. After guidewire insertion, a 14-Fr sheath is introduced.
A J-tip guidewire is positioned cross the native aortic valve and is then replaced with an Amplatz Super Stiff
(260 cm) guidewire. Balloon valvuloplasty is then performed using RVP. The delivery system (RetroFlex
for CoreValve) along with the crimped valve is directed toward the annulus of the native valve using fluo-
roscopic guidance. After satisfactory positioning using central and coaxial orientation, valve deployment
is performed. When the Edwards Sapien prosthesis is used a second episode of RVP is required. Correct
positioning is achieved by full root angiographic evaluation. After satisfactory implantation of the valve, the
delivery system along with the guidewire is withdrawn, femoral access is repaired, and a pressure bandage
is applied (11,12).
Transaortic Approach
In this retrograde access, the valve is employed through a ministernotomy incision or a right minithora-
cotomy in the second or third intercostal space (13,14). Both self-expanding and balloon-expandable valves
have been deployed using this method. This approach offers the surgeon easier manipulation and better
control of the valve delivery system. Postoperative pain control is better due to a smaller incision compared
to transapical access.
ECHOCARDIOGRAPHIC CONSIDERATIONS DURING TAVI

TEE is an essential tool to guide deployment of transcatheter aortic valves (15,16). Given the risk of acute
kidney injury with iodinated contrast administration required during angiography, intraoperative TEE may
emerge as the primary modality used for TAVI (17–19).
The advanced echocardiographer involved with the TEE guidance for the TAVI procedure must be
familiar with the nuances of TAVI deployment. Patients undergoing TAVI tend to be elderly, with multiple
comorbidities, and thus, vigilance must be maintained by the anesthesiologists when performing both the
clinical care and TEE guidance for the TAVI procedure.

TEE is used for both transfemoral and transapical deployment, but with transfemoral procedures
increasingly being performed under local anesthesia combined with conscious sedation (20), the role of
TEE in this setting may decrease, though transnasal or intracardiac TEE may allow prolonged monitor-
ing even without general anesthesia (21). During transapical aortic valve implantation, the surgeon has
very limited direct visualization of the heart, so imaging plays a pivotal role during the entire procedure.
TEE, intraoperative angiography, and intraoperative rotational MDCT scanning are the imaging armamen-
tarium at the surgeon's disposal in the hybrid operating room. However, the utility of intraoperative TEE is
complementary to the other imaging modalities used in the operating room.
A PRACTICAL APPROACH TO TAVI TEE DEPLOYMENT GUIDANCE

As the procedure involves an elderly high-risk population, a comprehensive initial examination is per-
formed. Following the initial comprehensive examination, focus shifts to the aortic valve and then aortic
root, corresponding to the sequence of the procedure.
Step 1: Annulus Measurement

This is a critical first step before commencing with TAVI, as faulty measurements can lead to serious compli-
cations. When measuring the annulus the echocardiographer has to bear in mind the concept of “oversizing,”
by which, for example, a 25-mm valve will be selected for a 23-mm aortic annulus. This approach is justi-
fied as that these valves are sutureless and hence need an anchoring sheath or landing zone to prevent
the valve from being dislodged. The heavily calcified and stenosed native valve provides the ideal environ-
ment and facilitates implantation. Unfortunately, bulky and eccentric calcification poses an increased risk
for a paravalular leakage. While standard multiplane TEE can be used to measure the annulus, real-time,
three-dimensional (3D) TEE in a biplane mode provides simultaneous long- and short-axis views of the
valve and annulus which may improve the accuracy of these measurements. The observer starts from the
ME AV LAX view, placing the cursor in the middle to transect the aortic valve. With 3D, the biplane view
is used to generate the corresponding short-axis view ME AV SAX in the orthogonal plane (Fig. 16.3,
Video 16.1 Video 16.1). The ME AV SAX view should demonstrate all three commissures along with the base of any
calcified leaflet, which further ensures a true short-axis plane. The annulus of the aortic valve and aortic
FIGURE 16.3 Annulus can be reliably measured using biplane technique. The measurements are done at the aortic
valve insertion sites (hinge points) within the left ventricular outflow tract from trailing edge to leading edge.

root is then measured in the long and short axis in systole. With standard two-dimensional (2D) TEE,
the annulus is generally measured from the ME LAX view, with the short-axis plane viewed by rotating
the plane to ∼40 to 50 degrees. To avoid underestimates of annual size, it is important to identify the true
annulus, rather than the common overlying calcification. Measurements (trailing edge to leading edge)
are made in systole at the AV leaflet insertion sites (hinge points) within the left ventricular outflow tract.
Alternatively, the annulus can be measured with postprocessing using commercial software from a full 3D
volume data set obtained in the ME AV LAX view, but owing to time constraints in the operating room,
this currently is more for research purposes. In the future, improvements in automated 3D echo processing
should allow rapid extraction of annular anatomy.
Step 2: Guidewire Placement

We suggest that the ME AV LAX view be used to position the guidewire. For transapical TAVI, this view
is adjusted to focus on the LV apex, the mitral valve (MV) and its subvalvular apparatus, the aortic valve
and annulus, the sinus and sinotubular junction, and the proximal part of the ascending aorta. The probe
is manipulated using the lateral and retroflex controls to fully image the apex by identifying the longest
long-axis dimension of the LV.
Complications that can occur during transapical TAVI include the following:
1. Nonapical punctures can be avoided by echo-guided digital palpation of the apex before proceeding
with the puncture.
2. Guidewire entrapped in the secondary chords of the MV (Video 16.2). Video 16.2
3. Guidewire is not able to align with the aortic valve and reaches the left atrium (Video 16.3) or has a Video 16.3
difficult alignment owing to a hypertrophied LV (Video 16.4). By utilizing ME AV LAX view (Fig 16.4), Video 16.4
one can ascertain the degree of septal hypertrophy (Video 16.5) and be prepared to take precautionary Video 16.5
measures to avoid “physiologic” systolic anterior motion (SAM) (22). Despite the fact that placement of
the guidewire is more straightforward using the transfemoral approach, TEE may still be helpful during
this approach.
Step 3: Stage of Balloon Valvuloplasty

After the guidewire is positioned and exchanged with a Super Stiff guidewire, the balloon is loaded and
positioned for valvuloplasty. Biplane TEE imaging is ideal for this purpose as the balloon needs to be
FIGURE 16.4 Placement of guidewire: Surrounding structures include the anterior mitral leaflet, subvalvular appa-
ratus, secondary chords of mitral valve and septal hypertrophy need to be monitored during insertion of guidewire. ME
AV LAX view in live 3D-TEE mode may be beneficial for quick and accurate assessment.

FIGURE 16.5 A and B: Presence of calcified plaques in front of ostium of right coronary artery. Echocardiographer
should be alert of a new regional wall motion abnormality post balloon aortic valvuloplasty or after the implantation
of the new valve. Arrow showing the presence of calcium before right coronary ostium in both 2D (Fig. 16.5A) and 3D
images (Fig. 16.5B).
Video 16.6 positioned midvalve for universal and complete dilation of the calcified valve (Video 16.6). The presence
Video 16.7a of eccentric calcification as opposed to regular calcification (Video 16.7a,b) may predispose for postim-
Video 16.7b plantation paravalvular leak. The presence of calcified plaques in the region of right coronary ostium can
Video 16.8 be seen well in 2D and real-time 3D TEE (Fig. 16.5A,B). Rupture or sliding of the balloon during valvulo-
Video 16.9 plasty (Video 16.8) necessitates another episode of valvuloplasty with a bigger balloon (Video 16.9) before
Video 16.10 valve implantation. Balloon valvuloplasty may cause aortic regurgitation (Video 16.10) which may require
a change in inotrope management. The phase following valvuloplasty should be brief to prevent acute
ventricular failure and the valve should be deployed immediately after the ballooning phase. If general
anesthesia is used for the transfemoral approach, TEE can be helpful in placement of the pigtail catheter
Video 16.11 used to guide valve placement (Video 16.11).
Step 4: Stage of Valve Implantation

After the insertion of the applicator device along with the valve, the valve position is determined by TEE
and angiography. The exchange of guidewires and insertion of the applicator device may cause a sudden
Video 16.12 air entry into the heart and should be evaluated (Video 16.12). When implanting a CoreValve, TEE should
confirm that the nitinol stent is well within the borders of the calcified native annulus. The CoreValve
frame has a longer length and can vary from 52 to 55 mm depending on the valve size. However, an aortic
dimension above 43 mm is a contraindication for CoreValve implantation due to the risk of the device
being dislodged or migrating after implantation. The SAPIEN valve should be positioned at midannulus,

FIGURE 16.6 Real-time 3D allows depth perception which cannot be appreciated in 2D. The crimped SAPIEN valve
before deployment is imaged in this figure. The arrow on the left of the picture shows the distal end of the valve whereas
the arrow on the right demonstrates the tip of the delivery system.
(Video 16.13), and for the XT valve, slightly more than half should be below the annulus (Figs. 16.1 and Video 16.13
16.6). Echocardiographers involved in implantation guidance need to familiarize themselves with the
structure of the implantable valves and their delivery systems to ensure that these landmarks are identi-
fied during the procedure.
During implantation, the status of the MV also needs to be considered. The applicator device can
obstruct, distort, or perforate the anterior mitral leaflet causing severe regurgitation (Videos 16.14, 16.15) Video 16.14
leading to rapid deterioration in hemodynamics. TEE guidance is valuable during the RVP phase of implan- Video 16.15
tation (Fig. 16.7, Video 16.16). Video 16.16
FIGURE 16.7 Well-positioned SAPIEN valve demonstrating good coaptation in midesophageal aortic valve LAX view.

FIGURE 16.8 Biplane view showing good implantation of the prosthetic mitral valve without a paravalvular leak.
Biplane imaging allows rapid and simultaneous assessment of the aortic valve in both the short- and long-axis views.
Step 5: Postimplantation Aortic Valve Assessment

After TAVI, immediate evaluation of the replaced AV is required. The following approach is recom-
mended:
A. Confirm proper AV position and function:
1. The ME AV LAX and ME AV SAX views (ideally in combination using biplane views) are observed
Video 16.17a to assess how well the valve is implanted (Fig. 16.8, Video 16.17a) and to rule out the presence of
Video 16.17b para/transvalvular leak (Video 16.17b,c). If valvular regurgitation is present, the guidewire may be
Video 16.17c withdrawn for a second assessment. Typically, the leaflet's seating improves over the first minutes
following implantation and the valvular regurgitation will lessen.
Video 16.22 2. The TG LAX (Video 16.22) and deep TG views are used to measure the postimplantation gradient
and to determine the severity of any regurgitation (Fig. 16.9). Owing to the nature of the valves,
the postoperative gradients are relatively low when compared to conventional surgical aortic valve
replacement (Fig. 16.10). When a significant leak is identified, a second episode of valvuloplasty
FIGURE 16.9 The presence of a trans or paravalvular leak can be readily recognized from TG LAX or deep TG views.

FIGURE 16.10 The gradients post valve implantation are generally low owing to the stentless nature of the trans-
catheter valves.
or a valve-in-valve (Fig. 16.11, Video 16.18) option may be considered. Similarly, valve-in-valve Video 16.18
approaches have been described to manage degenerated xenografts (23). Any malpositioned, reverse
Video 16.19
positioned (Videos 16.19, 16.20), or unsuccessfully implanted valve (Video 16.21) is readily diag-
Video 16.20
nosed with TEE (Figs. 16.12, 16.13).
Video 16.21
B. Rule out aortic dissection.
The aortic root should be assessed for dissection (Video 16.23) and the presence or absence of pre- Video 16.23
existing atheromatous plaques (Fig. 16.14, Video 16.24). Video 16.24
C. Evaluate for a new RWMA.
The TG SAX views provide rapid detection of RWMA which should caution the echocardiographer of a
possible occlusion of one or both coronary ostium. The recent expert consensus document from EAE/ASE
FIGURE 16.11 A valve in valve implantation performed in an attempt to decrease the intensity of a paravalvular leak.
The presence of a second valve is difficult to identify with echocardiography.

FIGURE 16.12 The presence of a parvalvular leak due to a malpositioned valve. The heavily calcified annulus inhibited
complete balloon valvuloplasty and proper valve positioning thereby causing a leak.
(24) suggests that real-time 3D TEE and/or MDCT be used to visualize the annular-left coronary ostium
distance. The measurement of annular-left coronary distance can be measured using the coronal plane
in multiplanar reconstruction (MPR) mode. Unfortunately, standard 2D imaging prohibits this technical
procurement and real-time 3D TEE is obligatory for MPR mode acquisition. Two-dimensional TEE can be
utilized for visualization of the annular-right coronary distance using the ME LAX view of the left ventricu-
lar outflow tract and proximal aortic root.
ROLE OF 3D ECHOCARDIOGRAPHY
The present usage of real-time 3D echocardiography is confined to determination of annulus measurements
using the biplane method and to detect the extent and severity of paraprosthetic leakage postdeployment
FIGURE 16.13 The valve being dislodged after implantation. Retrospective analysis showed inadequate and asymmet-
ric calcification of the native annulus where calcification acts as “landing zone” or anchoring sheath for valve deployment.
The danger of device migration in patients with a bicuspid aortic valve is due to similar mechanisms.

FIGURE 16.14 The presence of atheroma in descending aorta may change the surgical approach from transfemoral
to transapical access.
(15,25). Accuracy of annulus measurement may be further enhanced using MPR techniques using com-
mercially available software (QLAB-software, Philips, Netherlands). “Zoom” mode may be used during any
part of the examination in 2D or real-time 3D to concentrate on any specific pathology.
LIMITATIONS
The TEE probe may need to be withdrawn during fluoroscopy and needs frequent adjustments. TEE can-
not definitively diagnose an obstruction to the coronaries occurring during TAVI, although appearance of
a new RWMA should alert the multidisciplinary team to this possibility.
TAVI CONCLUSION
TAVI is an image-guided procedure necessitating a multidisciplinary team approach. For better patient
outcome it is essential for all personnel involved in the hybrid operating room to have an understanding
of TAVI procedures and to be acquainted with the sequence of surgical steps. Intraoperative communica-
tion is imperative for procedural success. The armamentarium of imaging modalities presently available
includes TEE, fluoroscopy, and MDCT. TEE is valuable not only during insertion and deployment but also
as means to assess complications associated with the surgical procedure.
ECHOCARDIOGRAPHY FOR MITRAL CLIP INTERVENTION

Percutaneous MV repair has evolved as a new technology for the treatment of MV regurgitation in a certain
subset of patients with both functional and degenerative mitral regurgitation (26). The mitral clip interven-
tion improves New York Heart Association Functional Class, quality-of-life score and left ventricular size
(27). However, surgical repair more effectively reduces the grade of mitral regurgitation as compared to the
mitral clip procedures. One-year follow-up results demonstrate a reduced LV end-diastolic volume in both
the groups.
This minimally invasive off-pump repair can be performed in patients with MR-associated prolapse and
those with ischemic MR by opposing and clipping the edges of the leaflets, resulting in an edge-to-edge repair.

A B
FIGURE 16.15 Mitral clip delivery system. A: Mitral Clip. B: Delivery system. (Courtesy of Abbott Vascular, USA.)
The Mitral Clip catheter-based system (Abbott Vascular) includes the following:
a. A steerable guide catheter on a mounted stabilizer
b. A clip delivery system
c. The Mitral Clip device (implant) attached to the distal end of the catheter.
The Mitral Clip device has a gripper and an arm 4 mm wide, with a cobalt or chromium implant. This
can be maneuvered by the clip delivery system (Fig. 16.15).
INCLUSION CRITERIA
Patients with moderate to severe MR, compromised LV function, a centrally originating jet, and adequate coap-
tation length of the leaflets to enable leaflet “capture” by the device are eligible for a mitral clip intervention.
EXCLUSION CRITERIA
An MV with restrictive pathology, excessive prolapse with a coaptation defect >10 mm (also known as flail
gap), flail width of 15 mm, and/or a dilated ventricle >55 mm internal systolic diameter are currently ineli-
gible for the mitral clip intervention.
PROCEDURE: STEPBYSTEP
The mitral clip deployment involves the following steps:
A. Transseptal puncture:
A 24-Fr catheter system is advanced from the femoral vein into the left atrium. The puncture posi-
tion can be well seen by the use of biplane TEE imaging which permits simultaneous visualization of
Video 16.25 the ME AV SAX and ME bicaval views (Fig. 16.16, Video 16.25). The superior and inferior positions
of the device are evaluated in the ME bicaval view whereas the anterior and posterior positions of the
device are evaluated in relation to the anterior positioned aorta in the ME AV SAX view. The 90-degree
biplane imaging assists the echocardiographer in identifying the puncture location in relation to fossa
ovalis and the aorta.

FIGURE 16.16 Biplane positioning demonstrating 90-degree ME AV SAX and ME bicaval views used for intra-atrial
septal puncture site evaluation.
At the point of indentation or tenting of the atrial septum, the ME four-chamber view is used to
make measurements within the left atrium before proceeding with transseptal puncture (Fig. 16.17).
A left atrium (LA) diameter <4 cm impairs manipulation of the delivery system between the transseptal
catheter and the MV annulus. Second, a >4.5 cm distance from the site of the transseptal puncture to
the MV annulus results in the delivery system having inadequate length to access the mitral leaflets.
Superior puncture in the intra-atrial septum is preferred in cases of prominent or bileaflet prolapse to
provide greater movement of the delivery system. Prophylactic placement of the guidewire into the left
upper pulmonary vein prevents iatrogenic injury to the left atrial wall and surrounding structures.
B. Device orientation and catheter positioning:
After septal puncture, the catheter tip is seen in LA (Fig. 16.18A, Video 16.26) and clip is advanced Video 16.26
toward the A2, P2 region of the MV. Real-time 3D TEE, using the “en face” view, permits superior
FIGURE 16.17 Measurements in the ME four-chamber view utilized to evaluate for difficulty with device manipulation.

A B
FIGURE 16.18 A: Biplane view for device guidance. B: En face view for mitral clip guidance with the device seen in the
center of the mitral valve.
Video 16.27 orientation and guidance of the delivery system (Fig. 16.18B, Video 16.27). Assessment of individual
prolapsed segments can be well visualized with TEE during positioning of catheter and prior to deploy-
ment of the clip. Comprehensive orientation with conventional 2D TEE is possible, but difficult. Real-
time 3D TEE is an excellent supportive imaging adjunct.
C. Clip implantation:
Implantation of the clip is performed when the mitral clip is positioned at the midportion of the MV leaf-
Video 16.28 let and perpendicularly aligned to the MV leaflet coaptation point (Fig. 16.19, Video 16.28). “Capture” of
FIGURE 16.19 Application of the mitral valve clip demonstrating placement within the center of the mitral valve and
in alignment with mitral valve leaflet coaptation.

FIGURE 16.20 Biplane imaging before clipping deployment demonstrating the mitral anterior and posterior leaflets.
the leaflets is visualized with 2D TEE using the ME LAX view as this facilitates simultaneous visualiza-
tion of the A2 and P2 segments (Fig. 16.20, Video 16.29). Alternatively, 3D TEE guidance can be particu- Video 16.29
larly helpful using the biplane view for imaging the anterior and posterior segments (Fig. 16.21, Video Video 16.30
16.30). The biplane view permits simultaneous imaging of the entire posterior mitral leaflet (P1–P3) and
A2 segment of the anterior leaflet.
D. Postintervention assessment:
All standard views for MV assessment using 2D TEE should be utilized for detailed evaluation. To
rule out a stenotic gradient postclip implantation spectral Doppler examination is performed. A gradient
of >5 mm Hg, signifying mitral stenosis, should avert the use of a second clip. Assessment for residual
mitral regurgitation is then performed using 2D TEE or real-time 3D TEE color Doppler. The dual ori-
fice presentation of the mitral leaflet following clip implantation is well appreciated by the “en face” view
(Fig. 16.22, Video 16.31). Three-dimensional TEE color Doppler aids 2D-TEE color Doppler in locating Video 16.31
the site of any residual regurgitation (Video 16.32). If significant regurgitation remains, a second clip may Video 16.32
be deployed. Three-dimensional planimetry can provide estimate of the MV orifice area following edge-
to-edge repair (Fig. 16.23).
FIGURE 16.21 Biplane imaging showing anterior and posterior leaflets.

FIGURE 16.22 “Edge-to-Edge” repair as demonstrated in the mitral valve “en face” view.
FIGURE 16.23 Planimetry using commercial software to determine mitral valve area.

FIGURE 16.24 Transgastric basal short-axis view showing leaflet coaptation.
Intraoperative complications include failure to capture a leaflet. Successful leaflet coaptation can be
evaluated in the TG SAX and LAX views (Fig. 16.24). Pericardial tamponade can result from injury to Video 16.17a
surrounding structures. A postprocedure left-to-right shunt may sometimes be seen as a complication of Video 16.17b
the transseptal puncture. Depending on the shunt intensity, closure with a percutaneous occluder device Video 16.17c
may be considered (Videos 16.17a–c, 16.18, 16.19). Rare complications like perforation of pulmonary Video 16.18
veins and delayed thrombus formation after invagination of the left atrial appendage is also possible. Video 16.19
Mitral clip conclusion: Percutaneous mitral clip procedures have shown promising results. Real-time
3D TEE, conventional 2D TEE, and fluoroscopy are routinely used imaging modalities for clip deploy-
ment. With further development and miniaturization of these devices, these procedures will likely gain
popularity and will be routinely used in advanced centers. Comprehensive echocardiographic knowl-
edge is imperative for procedural execution and successful patient outcome.
REFERENCES
1. Iung B, Cachier A, Baron G, et al. Decision-making in elderly patients with severe aortic stenosis: Why are so many denied
surgery? Eur Heart J. 2005;26:2714–2720.
2. Gardin JM, Kaplan KJ, Meyers SN, et al. Aortic stenosis: Can severity be reliably estimated noninvasively? Chest. 1980;77:130–
131.
3. Walther T, Simon P, Dewey T, et al. Transapical minimally invasive aortic valve implantation: Multicenter experience.
Circulation. 2007;116:I240–I245.
4. Tamburino C, Capodanno D, Ramondo A, et al. Incidence and predictors of early and late mortality after transcatheter aortic
valve implantation in 663 patients with severe aortic stenosis. Circulation. 2011;123:299–308.
5. Cribier A, Eltchaninoff H, Tron C, et al. Early experience with percutaneous transcatheter implantation of heart valve prosthe-
sis for the treatment of end-stage inoperable patients with calcific aortic stenosis. J Am Coll Cardiol. 2004;43:698–703.
6. Avanzas P, Munoz-Garcia AJ, Segura J, et al. Percutaneous implantation of the CoreValve self-expanding aortic valve prosthesis
in patients with severe aortic stenosis: Early experience in Spain. Rev Esp Cardiol. 2010;63:141–148.
7. Godino C, Maisano F, Montorfano M, et al. Outcomes after transcatheter aortic valve implantation with both Edwards-
SAPIEN and CoreValve devices in a single center: The Milan experience. JACC Cardiovasc Interv. 2010;3:1110–1121.
8. Leon MB, Smith CR, Mack M, et al. Transcatheter aortic-valve implantation for aortic stenosis in patients who cannot undergo
surgery. N Engl J Med. 2010;363:1597–1607.
9. Chiam PT, Ruiz CE. Percutaneous transcatheter aortic valve implantation: Evolution of the technology. Am Heart J.
2009;157:229–242.
10. Walther T, Mollmann H, Van LA, et al. Transcatheter aortic valve implantation transapical: Step by step. Semin Thorac
Cardiovasc Surg. 2011;23:55–61.
11. Piazza N, Grube E, Gerckens U, et al. Procedural and 30-day outcomes following transcatheter aortic valve implantation using
the third generation (18 Fr) corevalve revalving system: Results from the multicentre, expanded evaluation registry 1-year
following CE mark approval. EuroIntervention. 2008;4:242–249.
12. Buellesfeld L, Gerckens U, Schuler G, et al. 2-year follow-up of patients undergoing transcatheter aortic valve implantation
using a self-expanding valve prosthesis. J Am Coll Cardiol. 2011;57:1650–1657.
13. Etienne PY, Papadatos S, El KE, et al. Transaortic transcatheter aortic valve implantation with the Edwards SAPIEN valve:
Feasibility, technical considerations, and clinical advantages. Ann Thorac Surg. 2011;92:746–748.

14. Bapat V, Khawaja MZ, Attia R, et al. Transaortic transcatheter aortic valve implantation using Edwards Sapien valve: A novel
approach. Catheter Cardiovasc Interv. 2012;79(5):733–740.
15. Goncalves A, Marcos-Alberca P, Zamorano JL. Echocardiography: Guidance during valve implantation. EuroIntervention.
2010;6 suppl G:G14–G19.
16. Marcos-Alberca P, Zamorano JL, Sanchez T, et al. Intraoperative monitoring with transesophageal real-time three-dimensional
echocardiography during transapical prosthetic aortic valve implantation. Rev Esp Cardiol. 2010;63:352–356.
17. Strauch JT, Scherner MP, Haldenwang PL, et al. Minimally invasive transapical aortic valve implantation and the risk of acute
kidney injury. Ann Thorac Surg. 2010;89:465–470.
18. Van LA, Kempfert J, Rastan AJ, et al. Risk of acute kidney injury after minimally invasive transapical aortic valve implantation
in 270 patients. Eur J Cardiothorac Surg. 2011;39:835–842.
19. Bagur R, Rodes-Cabau J, Doyle D, et al. Usefulness of TEE as the primary imaging technique to guide transcatheter transapical
aortic valve implantation. JACC Cardiovasc Imaging. 2011;4:115–124.
20. Fassl J, Seeberger MD, Augoustides JG. Transcatheter aortic valve implantation: Is general anesthesia superior to conscious
sedation? J Cardiothorac Vasc Anesth. 2011;25:576–577.
21. Bartel T, Bonaros N, Muller L, et al. Intracardiac echocardiography: A new guiding tool for transcatheter aortic valve replace-
ment. J Am Soc Echocardiogr. 2011;24:966–975.
22. Suh WM, Witzke CF, Palacios IF. Suicide left ventricle following transcatheter aortic valve implantation. Catheter Cardiovasc
Interv. 2010;76:616–620.
23. Kempfert J, Van LA, Linke A, et al. Transapical off-pump valve-in-valve implantation in patients with degenerated aortic
xenografts. Ann Thorac Surg. 2010;89:1934–1941.
24. Zamorano JL, Badano LP, Bruce C, et al. EAE/ASE recommendations for the use of echocardiography in new transcatheter
interventions for valvular heart disease. Eur J Echocardiogr. 2011;12:557–584.
25. Goncalves A, Almeria C, Marcos-Alberca P, et al. Three-dimensional echocardiography in paravalvular aortic regurgitation
assessment after transcatheter aortic valve implantation. J Am Soc Echocardiogr. 2012;25:47–55.
26. Rogers JH, Franzen O. Percutaneous edge-to-edge MitraClip therapy in the management of mitral regurgitation. Eur Heart J.
2011;32:2350–2357.
27. Feldman T, Foster E, Glower DD, et al. Percutaneous repair or surgery for mitral regurgitation. N Engl J Med. 2011;364:1395–
1406.

QUESTIONS
1. The current delivery system for transcather 8. The SAPIEN valve (Edwards Lifesciences,
valve is: Inc., Irvine, CA) can be used for valve
a. Ascendra delivery system with a 33-Fr sheath implantation via the:
b. Ascendra delivery system with a 34-Fr sheath a. Antegrade approach only
c. NovaFlex delivery system with an 18-Fr sheath b. Retrograde approach only
d. NovaFlex delivery system with a 17-Fr sheath c. Both antegrade and retrograde approach
2. Cohort B in the PARTNER Trial for aortic
valve replacement demonstrated: 9. Cohort A from the PARTNER aortic valve
a. Inoperable patients requiring medical replacement trial suggests that:
therapy have better outcome a. Surgical AVR is better than TAVI
b. Surgical AVR has better outcome b. TAVI is an acceptable alternative to high-
c. Transapical AVR has beneficial effects risk patients who are operable
compared to surgical AVR c. TAVI is not feasible for patients who can be
d. The benefits of transfemoral AVR outweighs surgically operated
the risk when compared to conservative treat- d. TAVI has proven to be much better than
ment surgical AVR
3. The present role of real-time 3D echo for 10. The present indications for TAVI in 2013
TAVI is: include:
a. To detect the extent and severity of any para- a. Any aged high-risk patient
valvular leaks b. Selected high-risk patients above 80 years
b. For proper valve placement of age
c. For proper guidewire placement c. Selected high-risk patients above 40 years
d. To assist balloon valvuloplasty of age
d. Young patients with high-risk for cardiac
4. The best view for valve assessment
surgery
postdeployment is:
a. ME AV LAX view 11. Intraoperative occlusion of the coronary
b. TG AV LAX view ostium during valve implantation is best
c. Biplane mode showing ME AV SAX and ME detected by:
LAX views a. 2D echocardiography
d. Deep TG view b. Fluoroscopic imaging
c. Real-time 3D echocardiography
5. The SAPIEN valve (Edwards Lifesciences,
d. Intraoperative rotational multislice com-
Inc., Irvine, CA) has 3 sizes:
puter tomography
a. 23, 25, and 27 mm
b. 21, 23, and 25 mm 12. Annulus measurements before valve
c. 23, 25, and 27 mm implantation have the best correlation
d. 23, 26, and 29 mm between:
a. 3D echocardiography and 2D echocardiog-
6. The CoreValve (Medtronic, Inc.,
raphy
Minneapolis, MN) has 3 sizes:
b. 3D echocardiography and fluoroscopy
a. 26, 29, and 31 mm
c. 3D echocardiography and computer tomog-
b. 26, 28, and 30 mm
raphy
c. 25, 27, and 29 mm
d. 2D echocardiography and fluoroscopy
d. 23, 26, and 29 mm
13. If aortic regurgitation persists after valve
7. The CoreValve (Medtronic, Inc., Minneapolis,
implantation then the following may be tried
MN) can be used for valve implantation via
to reduce the degree of aortic regurgitation:
the:
a. Deployment of a second valve
a. Both the antegrade and retrograde approach
b. Surgical AVR
b. Retrograde approach only
c. Balloon valvuloplasty followed by a valve in
c. Antegrade approach only
valve procedure
d. Once deployed no maneuver can decrease
the level of regurgitation

14. Compared to surgical AVR the TAVI tends 18. Modern iterations of the valve and delivery
to have: system aim toward:
a. Higher postoperative gradients a. Miniaturization of delivery system
b. Lower postoperative gradients b. Valve which can be repositioned and
c. Similar gradients retrievable
d. Similar gradients to mechanical valves c. To decrease paravalvular leak
d. All of the above
15. Asymmetric calcification of the native valve
may lead to: 19. The TEE findings of regional wall motion
a. Device migration abnormality post-TAVI may be secondary
b. Paravalvular leak to:
c. Transvalvular leak a. Aortic dissection
d. All of the above b. Valve migration
c. Coronary occlusion
16. Present indications for TAVI exclude:
d. Patient prosthetic mismatch
a. Octogenarians
b. Patients above the age of 60 years and above 20. During implantation of a CoreValve with
with symptomatic AS the nitinol stent in ME AV LAX view the
c. Old patients with high-risk comorbidities valve should be positioned:
with symptomatic AS a. Above the annulus extending into the ven-
d. Old patients with AS whom surgery has tricle
been denied b. Below and within the calcified annulus
c. More than halfway between the annulus
17. Complications during TAVI may include:
and left ventricular outflow tract
a. Aortic dissection and coronary artery occlu-
sion
b. Rupture of aortic annulus and pericardial
tamponade
c. Rupture of apex of left ventricle
d. All of the above

17 Transesophageal Echocardiography
of the Thoracic Aorta
Roman M. Sniecinski
A LTHOUGH SIMPLE IN STRUCTURE , THE thoracic aorta is a crucial component of the routine periopera-
tive transesophageal echocardiography (TEE) examination. Pathologies such as atheroma, aneurysms, and
dissections can be readily diagnosed and inspected in the operating room. Likewise, TEE can help guide
the insertion of cannulas, stents, and intra-aortic balloon pumps during the actual surgical procedure. It is
therefore imperative that the intraoperative echocardiographer have a firm grasp on both the anatomy and
potential abnormalities of this vital blood vessel.
ANATOMY AND TEE IMAGING

The basic structure of the aorta is similar to that of an upside-down letter “J,” albeit with a slight twist (see
Fig. 17.1). The aortic valve annulus, leaflets, and sinuses of Valsalva comprise the beginning of the thoracic
FIGURE 17.1 Basic anatomy of the aorta and TEE views. The thoracic aorta resembles a slightly twisted “J” and is com- 347
monly divided into six zones (shown as 1 to 6 in figure).

aorta, collectively known as the aortic root. The ascending aorta, which is the start of the tubular portion,
begins at the sinotubular junction (STJ), travels cephalad, and extends to the origin of the innominate
(a.k.a. brachiocephalic) artery. The aortic arch begins at this point and travels horizontally to the origin on
the left subclavian artery. The descending aorta begins just distal to the left subclavian artery, at a region
known as the aortic isthmus, and travels caudad going through the diaphragm.
It is important to keep this overall shape of the aorta in mind during its examination. The vertical nature
of the descending portion explains why a short-axis (SAX) view of this section is typically obtained at an
omniplane angle of around 0 degrees, while the SAX view of the arch, which is horizontal in nature, is at
90 degrees. The reverse is true for the long-axis (LAX) views, with the descending and arch portions of
the aorta obtained at 90 degrees and 0 degrees, respectively (1). It is also important to keep in mind that
the relationship between the esophagus and the aorta switches as they travel from the abdomen into the
thoracic cavity (see Fig. 17.2). At the level of the diaphragm, the aorta is posterior to the esophagus, while
at the level of the arch, the aorta is anterior to it. Because of this changing orientation, it is very difficult for
the echocardiographer to designate anterior/posterior and left/right while examining the descending aorta.
P
E
R L
15 cm
P 2
R 2 L
Ao E
3
3 20 cm
E
E 1
R L
4 E
1 4 25 cm
A
5
E
R 6 L 5 30 cm
A
R L
E 6
35 cm
A
FIGURE 17.2 Relationship between the esophagus and aorta at different levels of the thoracic esophagus. (From
Estafanous FG, Barash PG, Reves JG, eds. Cardiac anesthesia principles and clinical practice, 2nd ed. Philadelphia: Lippincott
Williams & Wilkins, 2001:785, with permission).

17. Transesophageal Echocardiography of the Thoracic Aorta 349
For purposes of surgery and echocardiography, the thoracic aorta can be divided into six zones (2). The
first three zones are within the ascending aorta, with zone 1 closest to the aortic root, zone 2 the typical site
for proximal anastomosis of coronary grafts, and zone 3 where aortic cross-clamping for cardiopulmonary
bypass (CPB) occurs. The aortic arch is divided into two halves, creating zones 4 and 5. The aortic cannula
is often placed within the distal region of zone 3 to proximal region of zone 4. The descending aorta com-
prises zone 6. Because of the interposition of the trachea and left mainstem bronchus, TEE cannot reliably
image zones 3 and 4, which is the rationale for performing epiaortic scanning (3) (Fig.17.1).
Because of the sheer length of the structure, the thoracic aorta can be viewed in many of the standard
imaging planes. However, a systematic approach to its examination is recommended to ensure all possible
sections are visualized. One common method is to begin its examination after obtaining the transgastric
views of the left ventricle and turning the probe to the left until the descending aorta is seen in SAX at 0
degrees. From here, the depth is typically set to 6 to 8 cm and the probe is withdrawn, following the aorta
until the circular view of the descending in SAX becomes the tubular view of the arch in LAX (Video 17.1). Video 17.1
The omniplane angle can then be adjusted to about 90 degrees to obtain the SAX of the arch and the probe
advanced, following the descending aorta down to the diaphragm in LAX (Video 17.2). The process can be Video 17.2
repeated using color flow Doppler to help visualize dissections or coarctations of the descending aorta.
The ascending aorta can be visualized by first obtaining a midesophageal LAX of the aortic valve at a
typical omniplane angle of 110 to 140 degrees, and slowly withdrawing the probe to obtain imaging of the
ascending aorta. By using the right pulmonary artery as an imaging window it is usually possible to see up
to zone 2. The omniplane angle can then be decreased by 90 degrees to obtain a SAX of the ascending
aorta and the probe advanced to follow the aortic root down to the aortic valve in SAX (Video 17.3). The Video 17.3
views used to scan the thoracic aorta are provided in Figure 17.1, and while their order of acquisition is not
important, all are required for a complete examination.
ACUTE AORTIC SYNDROMES

Acute aortic syndromes are a collection of life-threatening conditions including aortic dissection, intramu-
ral hematoma (IMH), and penetrating aortic ulcers. Acute dissection of the ascending aorta, perhaps the
best studied of these entities, has a widely quoted mortality rate of 1% to 2% per hour upon presentation (4).
Timely diagnosis is obviously critical so that appropriate surgical intervention can be instituted.
Acute Aortic Dissection

An aortic dissection begins with a tear in the intimal layer of the aorta. The tear allows blood to enter and
separate the intima from the media or adventitia, creating a “flap” of tissue separating the true aortic lumen
from the false lumen (Fig. 17.3, Video 17.4). It is the visualization of this flap that makes the diagnosis. Video 17.4
While in the past, aortography was considered the “gold standard” for diagnosis of aortic dissection, it is
very rarely used as a first-line test today due to its invasiveness and lower sensitivity than other modalities.
A recent survey of the International Registry of Acute Aortic Dissection (IRAD) database showed that
contrast-enhanced computed tomography (CT) was the first diagnostic test in 68% of cases since the year
2000, with TEE used for initial diagnosis in almost all of the remainder (28%). Even if surgical intervention
is initiated based upon CT findings, intraoperative TEE still plays an essential role in confirming the diag-
nosis and helping to guide surgical repair. Important aspects for the intraoperative echocardiographer to
address during the examination are summarized in Table 17.1(5).
Thoracic aortic dissections are commonly classified by either the Stanford (Type A or B) or DeBakey
(Type I, II, or III) system (Fig. 17.4). Acute dissections of the ascending aorta (i.e., Stanford A, or DeBakey
Types I and II) are considered surgical emergencies since medical management has a 14-day mortality
of about 50% (6). Dissections of the descending aorta (i.e., Stanford B, or DeBakey Type III) are less lethal
and not generally taken to the operating room emergently unless there are ischemic complications such
as renal or visceral malperfusion.
As stated earlier, the hallmark finding of an acute aortic dissection on TEE is the visualization of the
intimal flap. The proximal extent of the flap is important to determine, since this typically governs the need
for acute surgical treatment. In an ascending aorta dissection, most patients do not undergo angiography

FIGURE 17.3 Aortic dissection flap. Once a tear in the intimal layer of the aorta occurs, blood enters and separates the
intima from the medial or adventitial layers. This creates two lumens, the native or “true” lumen (denoted by purple arrow),
and the space due to the separation known as the “false” lumen (denoted by green arrow).
due to the acuity of the situation, so it is also useful to determine if the proximal extension involves any
Video 17.5 coronary arteries. The dissection flap is usually very irregularly shaped and highly mobile (Video 17.5).
Visualizing the flap in two separate imaging planes (Fig. 17.5) is important in order to distinguish artifacts
from true dissection flaps. One such confounder is the presence of a pulmonary artery catheter, which can
create reverberation artifacts mimicking a flap (Fig. 17.6). When in doubt, this can be remedied by pulling
the catheter back and seeing if the flap remains. Other sources of linear artifacts include calcifications on
the aortic valve or root and atherosclerosis of the ascending aorta (7). They can typically be distinguished
from a true dissection by their lack of rapid, oscillatory movement, their tendency to cross known anatomic
boundaries, and their indistinct structural borders.
Once the dissection flap is visualized, it is useful to determine where the break in the intima (a.k.a. the
“tear” or “entry point”) has occurred, since one of the primary aims of surgical treatment is to excise this
region. Color flow Doppler is often used to visualize a turbulent jet flowing from the true lumen into the
Video 17.6 false lumen (Fig. 17.7, Video 17.6). The true lumen can usually be differentiated from the false lumen due
Video 17.7 to its expansion during systole (Video 17.7). In addition, the false lumen is often larger, and frequently has
spontaneous echo contrast or thrombus within it, particularly in the descending aorta (8).
TABLE 17.1 Role of Intraoperative TEE in Acute Ascending Aortic Dissection
(1) Confirm the diagnosis t Visualize the intimal flap in two separate imaging planes
t Determine the proximal extent of the flap
(2) Identify the entry points t Color flow Doppler to see flow from true to false lumen
t There may be multiple tears
(3) Determine coronary involvement t Look for flap extending into aortic root and coronary ostia
t Look for regional wall motion abnormalities
t Assess ventricular function
(4) Assess aortic valve t Grade severity of any aortic regurgitation
t Determine if aortic valve may be repairable
(5) Look for effusions t Pericardial and pleural effusions are common
(6) Rule out additional cardiac t Preoperative workup is often minimal due to the urgency of the
pathology surgery—a complete examination is essential

I II III
A A B
III-A
III-B
FIGURE 17.4 The Stanford (A and B) and DeBakey (I, II, III) classification systems for thoracic aorta dissections. (From
Crawford ES, Crawford JL. Diseases of the aorta. Baltimore: Williams & Wilkins, 1984:174, with permission.)
FIGURE 17.5 Ascending aorta dissection flap in short and long axis. A dissection flap is irregularly shaped and typically
mobile. It should be visualized in two separate views to minimize the chance of mistaking an artifact for a flap.

FIGURE 17.6 Pulmonary artery catheter mimicking aortic dissection flap. The false appearance of a dissection flap in
the ascending aorta is often due to the presence of a pulmonary artery catheter in the right ventricle (delineated by blue
arrows) causing a reverberation artifact (delineated by yellow arrows).
Intramural Hematoma
While the initiating event for the classical aortic dissection is a break in the intimal layer, the underlying
cause of an IMH is thought to be a rupture of vasa vasorum in the medial layer (9). This blood accumulation
causes a thickening of the medial layer which may progress to intimal fracture, and subsequent flap forma-
tion like a classic aortic dissection, or frank aortic rupture. The mortality from IMH is dependent on the
location (i.e., ascending or descending aorta) and is similar to that of classic aortic dissection (10). As such,
the Stanford classification system is applied, with Type A considered a surgical emergency.
Unlike the classic aortic dissection, there is no intimal flap. On TEE imaging, IMH appears as a thick-
ening of the medial layer of the aorta (Fig. 17.8). This typically measures 7 ± 2 mm in Type A cases, and
15 ± 6 mm in Type B (11). Other features may include echolucency within the medial layer, and medial dis-
placement of calcium in the intimal layer. It is important to note that atherosclerotic plaques appear above
the intimal layer, while IMHs occur below the intimal layer.
FIGURE 17.7 Identification of the entry point. The break in the intimal layer is known as the entry point or tear. Use of
color flow Doppler, as seen in this color compare image, can help visualize blood flow entering the false lumen at the
site of the tear.

FIGURE 17.8 Intramural hematoma of the ascending aorta. Thickening of the media beneath the intimal layer is dem- Video 17.8
onstrated in this Type A intramural hematoma. Video 17.8.
Penetrating Atherosclerotic Ulcer

Of the acute aortic syndromes, penetrating atherosclerotic ulcer (PAU) is the least common, accounting
for somewhere between 2% and 7% of cases (12). While most atherosclerotic disease protrudes above the
intimal layer into the vessel lumen, PAU consists of plaque that has eroded through the internal elastic
lamina into the aortic media. No dissection flap is created, but the localized erosion of the medial wall can
lead to aneurysm formation or even aortic rupture. Like IMHs, PAUs of the ascending aorta are often con-
sidered for emergent surgical intervention due to the risk of rupture (13). However, most PAUs occur in the
descending aorta, where there is controversy among advocates of stent placement, frequent monitoring,
or open repair (14,15).
No dissection flap or false lumen is visualized on TEE in cases of PAU. Instead, there is a crater-like
ulcer with jagged edges and possible echolucent areas within the plaque (Fig. 17.9). The erosion into the
medial layer can make it difficult to clearly see the exact borders of the aortic lumen. There are typi-
cally extensive surrounding areas of atherosclerotic disease, and adjacent effusions or fluid collections are
common.
FIGURE 17.9 A penetrating atherosclerotic ulcer in the descending aorta. Note the crater-like appearance and echo-
lucent areas of the atherosclerotic plaque. Disruption of the medial layers has made it difficult to determine where the
adventitia layer is.

FIGURE 17.10 Typical ascending aorta measurements obtained in the OR.
THORACIC AORTIC ANEURYSMS

Dilation of the thoracic aorta can occur due to a variety of clinical conditions including altered flow dynamics,
underlying connective tissue disorders, and atherosclerosis. While the size of a “normal” aorta will depend upon
both the age and the overall body surface area (16), the expected values for typical measurements performed
in the operating room are provided in Figure 17.10/Table 17.2 (17–19). Measurements more than 50% greater
than these values are considered aneurysmal. Aneurysms can be broadly divided into either saccular, meaning
a focal out-pouching, or fusiform, meaning cylindrical and affecting the entire circumference of the aorta.
Aneurysms of the ascending aorta, sometimes referred to (properly or not) as Type A aneurysms, are
typically fusiform. The dilation can be proximal to the STJ, in which case it is called a “root” aneurysm, or
it can start distal to the STJ, in which case it is known as a “tubular,” or “supracoronary” aneurysm (20). The
distinction is important because root type aneurysms require coronary artery reimplantation and possible
aortic valve repair/replacement, while tube types frequently do not. Dilation involving both the root and
ascending aorta are referred to as “diffuse,” and typically result in effacement of the STJ (Fig. 17.11). The risk
of aortic rupture significantly increases with ascending diameters of ≥6 cm and so, as a margin of safety,
surgical treatment is recommended for asymptomatic patients with any aortic measurements ≥5.5 cm,
or diameters of 4.2 to 5 in patients with known connective tissue disorders (21). Recent guidelines also
suggest that patients undergoing cardiac surgery with either root or ascending aorta dilation >4.5 cm be
considered for concomitant aortic repair (22).
TABLE 17.2 Normal Aortic Parameters based upon BSA of ∼2 m2
Diameter measurement Mean ± SD

Subaortic (annulus) 21 ± 3 mm
Maximum sinus 32 ± 4 mm
STJ 27 ± 4 mm
Ascending aorta 33 ± 4 mm
Descending aorta 24 ± 4 mm
STJ, sinotubular junction.
Adapted from: Wolak A, Gransar H, Thomson LE, et al. Aortic size assessment by noncontrast cardiac computed tomography:
Normal limits by age, gender, and body surface area. JACC Cardiovasc Imaging. 2008;1:200–209; Tamas E, Nylander E.
Echocardiographic description of the anatomic relations within the normal aortic root. J Heart Valve Dis. 2007;16:240–246;
and Hager A, Kaemmerer H, Rapp-Bernhardt U, et al. Diameters of the thoracic aorta throughout life as measured with helical
computed tomography. J Thorac Cardiovasc Surg. 2002;123:1060–1066.

FIGURE 17.11 Types of ascending aortic aneurysms. Root type aneurysms (top) are commonly found in patients with
connective tissue disorders (e.g., Marfan’s Syndrome). The sinotubular junction is visible in both root and tube types, but
is effaced and indistinguishable on TEE in cases of diffuse ascending aneurysms.
Thoracoabdominal aneurysms, that is, those involving the descending aorta with or without ascending
involvement, are typically classified according to the Crawford scheme (Fig. 17.12). Although TEE is less
useful for characterizing aneurysms below the diaphragm, associated findings such as dissection flaps,
thrombus within the false lumen, and atherosclerotic plaques can frequently be visualized. Since the risk
of rupture is significantly increased with diameters ≥7 cm (21), open repair or stent placement is recom-
mended at sizes of ≥6 cm, or >5.5 cm if chronic dissection or connective tissue disorders are present (22).
EVALUATION OF AORTIC GRAFTS

Following repair of dissections and aneurysms, efforts should be made to identify both the proximal and
distal ends of the graft. Most synthetic grafts are made from either polytetrafluoroethylene (PTFE) or poly-
ester fiber (Dacron) (23). On TEE, these materials can usually be distinguished from native tissue by their
serrated appearance (Fig. 17.13). Thoracoabdominal aneurysms are often done as staged repairs, with the
ascending portion replaced first. In this situation, an “elephant trunk” is frequently placed for easy proxi-
mal connection or as a landing zone for stent deployment during the second stage of repair. The elephant
trunk can be visualized floating in the descending aorta (Fig. 17.14, Video 17.9) and color flow Doppler Video 17.9
should be utilized to verify flow within it.
Thoracic endovascular aortic repair (TEVAR) has significantly evolved since its introduction in the
early 1990s. Although there are a variety of manufacturers and models, the basic structure of an endo-
graft is either a PTFE or polyester tube with either an endo- or exoskeleton of metal wires (24). The metal

I II III IV
FIGURE 17.12 Crawford classification of thoracoabdominal aneurysms.
FIGURE 17.13 Distal end of graft in the aortic arch long-axis view. Note the serrated appearance of the synthetic graft
material compared to the native aortic tissue.
FIGURE 17.14 Elephant trunk for staged aortic repairs. A view of the elephant trunk in the descending aorta, both
short (SAX) and long (LAX) axes.

FIGURE 17.15 Small endoleak. Descending aorta long-axis (LAX) view with color flow Doppler compare demonstrat-
ing a small leak with flow into the false lumen of a Type B aortic dissection.
structure creates significant reverberation artifact, making TEE imaging of the actual endograft difficult.
Nevertheless, TEE is useful for confirming guidewire placement into the true lumen, aiding fluoroscopy
in stent positioning, and detecting leaks postdeployment (Fig. 17.15) (25). In the case of Type B dissections,
successful deployment will cover the entry site, reducing flow into the false lumen and eventually causing
it to thrombose (Video 17.10). Video 17.10
AORTIC ATHEROMA
Atherosclerotic plaques in the aorta have been shown to be a marker for coronary artery disease (26). It is
therefore not surprising that patients presenting for cardiac surgery often have visible plaques on intraop-
erative TEE examinations. From a surgical perspective, it is useful to know the location of these plaques
in order to avoid manipulation of those areas and reduce the chance of embolic events. However, TEE can
only visualize about 60% of the ascending aorta (3), and misses the segment most frequently utilized for
cannulation and cross-clamping. Nevertheless, plaques in the descending aorta are well visualized and TEE
has been advocated as a screening tool to decide what patients should undergo epiaortic scanning (27).
Plaques in the descending aorta may also impact the decision to place an intra-aortic balloon pump,
so it is important to note their presence. Although multiple classification schemes exist to determine the
FIGURE 17.16 Measurement of aortic plaque. The maximal plaque height/intimal thickness is used to determine the
grade of the lesion (Table 17.3).

TABLE 17.3 Five-Point TEE Grading System for Atheroma of the Aorta
Grade TEE findings

I Normal intimal thickness
II Intimal thickening without protrusion into lumen
III Plaque protrudes <5 mm into aortic lumen
IV Plaque protrudes ≥5 mm into aortic lumen
V Any plaque with a mobile component
Based on the classification scheme by Katz et al. (Katz ES, Tunick PA, Rusinek H, et al. Protruding aortic atheromas predict stroke
in elderly patients undergoing cardiopulmonary bypass: experience with intraoperative transesophageal echocardiography.
J Am Coll Cardiol. 1992;20:70–77.)
severity of atherosclerotic plaques, the five-point scale developed in 1992 by Katz et al. (28) is widely used
for intraoperative TEE. The normal intimal layer of the aorta is less than 2 mm thick, and atherosclerosis
first leads to an increase in this thickness. With disease progression, the atheroma becomes more complex
Video 17.11 in shape and protrudes into the lumen of the aorta (Fig. 17.16, Video 17.11). The Katz grading system is
provided in Table 17.3.
Because of TEE’s blind spots on the ascending aorta, epiaortic scanning is often employed to determine
the location of atherosclerotic plaques in these areas. Changes in surgical management occur in 4% to 29%
of cases, and may reduce stroke rates (29–31). Guidelines for an intraoperative epiaortic examination have
been published, which recommend using a high-frequency probe (≥7 MHz) in a sterile sheath that can
be used in the surgical field (32). Linear array transducers, that is, “vascular probes,” provide the advantage
of being able to be placed directly on the aorta, but may not be wide enough to include all walls in a single
image. A phased-array transducer, such as a pediatric transthoracic probe, can typically visualize all walls
at once, but must be held about 1 cm above the aortic wall to prevent near-field clutter. In either case, SAX
views of the proximal, mid, and distal segments of the ascending aorta should be obtained (Fig. 17.17). It
is also helpful to obtain a LAX view of the ascending and proximal arch if possible.
FIGURE 17.17 Epiaortic imaging of the aorta. Aortic plaques in the blind spots of TEE can effectively be imaged using
epiaortic ultrasound. The proximal ascending aorta begins just above the sinotubular junction. The superior vena cava
(SVC) is seen on the right. The probe is then moved distally up the ascending aorta until the right pulmonary artery (PA)
is seen posterior to the aorta. This marks the midportion of the ascending. As the epiaortic probe is moved even more
distally, the right PA disappears from view.

CONCLUSION
The thoracic aorta is the site for both acute (dissections, IMHs) and progressive (aneurysms, atheroscle-
rosis) diseases. Although not all segments can be evaluated using TEE, a systematic evaluation can help
confirm diagnoses and guide surgical therapy.
REFERENCES
1. Blanchard DG, Kimura BJ, Dittrich HC, et al. Transesophageal echocardiography of the aorta. JAMA. 1994;272:546–551.
2. Royse C, Royse A, Blake D, et al. Assessment of thoracic aortic atheroma by echocardiography: A new classification and esti-
mation of risk of dislodging atheroma during three surgical techniques. Ann Thorac Cardiovasc Surg. 1998;4:72–77.
3. Konstadt SN, Reich DL, Quintana C, et al. The ascending aorta: How much does transesophageal echocardiography see?
Anesth Analg. 1994;78:240–244.
4. Tsai TT, Nienaber CA, Eagle KA. Acute aortic syndromes. Circulation. 2005;112:3802–3813.
5. Meredith EL, Masani ND. Echocardiography in the emergency assessment of acute aortic syndromes. Eur J Echocardiogr.
2009;10:i31–i39.
6. Hagan PG, Nienaber CA, Isselbacher EM, et al. The International Registry of Acute Aortic Dissection (IRAD): New insights
into an old disease. JAMA. 2000;283:897–903.
7. Appelbe AF, Walker PG, Yeoh JK, et al. Clinical significance and origin of artifacts in transesophageal echocardiography of the
thoracic aorta. J Am Coll Cardiol. 1993;21:754–760.
8. Ballal RS, Nanda NC, Gatewood R, et al. Usefulness of transesophageal echocardiography in assessment of aortic dissection.
Circulation. 1991;84:1903–1914.
9. Song JK, Kim HS, Kang DH, et al. Different clinical features of aortic intramural hematoma versus dissection involving the
ascending aorta. J Am Coll Cardiol. 2001;37:1604–1610.
10. Evangelista A, Mukherjee D, Mehta RH, et al. Acute intramural hematoma of the aorta: A mystery in evolution. Circulation.
2005;111:1063–1070.
11. Harris KM, Braverman AC, Gutierrez FR, et al. Transesophageal echocardiographic and clinical features of aortic intramural
hematoma. J Thorac Cardiovasc Surg. 1997;114:619–626.
12. Nathan DP, Boonn W, Lai E, et al. Presentation, complications, and natural history of penetrating atherosclerotic ulcer disease.
J Vasc Surg. 2012;55:10–15.
13. Troxler M, Mavor AI, Homer-Vanniasinkam S. Penetrating atherosclerotic ulcers of the aorta. Br J Surg. 2001;88:1169–1177.
14. Tittle SL, Lynch RJ, Cole PE, et al. Midterm follow-up of penetrating ulcer and intramural hematoma of the aorta. J Thorac
Cardiovasc Surg. 2002;123:1051–1059.
15. Coady MA, Rizzo JA, Elefteriades JA. Pathologic variants of thoracic aortic dissections. Penetrating atherosclerotic ulcers and
intramural hematomas. Cardiol Clin. 1999;17:637–657.
Echocardiogr. 2005;18:1440–1463.
17. Wolak A, Gransar H, Thomson LE, et al. Aortic size assessment by noncontrast cardiac computed tomography: Normal limits
by age, gender, and body surface area. JACC Cardiovasc Imaging. 2008;1:200–209.
18. Tamas E, Nylander E. Echocardiographic description of the anatomic relations within the normal aortic root. J Heart Valve
Dis. 2007;16:240–246.
19. Hager A, Kaemmerer H, Rapp-Bernhardt U, et al. Diameters of the thoracic aorta throughout life as measured with helical
computed tomography. J Thorac Cardiovasc Surg. 2002;123:1060–1066.
20. Elefteriades JA. Thoracic aortic aneurysm: Reading the enemy’s playbook. Curr Probl Cardiol. 2008;33:203–277.
21. Coady MA, Rizzo JA, Hammond GL, et al. What is the appropriate size criterion for resection of thoracic aortic aneurysms?
J Thorac Cardiovasc Surg. 1997;113:476–491; discussion 489–491.
22. Hiratzka LF, Bakris GL, Beckman JA, et al. 2010 ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/SIR/STS/SVM Guidelines for the
diagnosis and management of patients with thoracic aortic disease: Executive summary: A report of the American College of
Cardiology Foundation/American Heart Association Task Force on Practice Guidelines, American Association for Thoracic
Surgery, American College of Radiology, American Stroke Association, Society of Cardiovascular Anesthesiologists, Society
for Cardiovascular Angiography and Interventions, Society of Interventional Radiology, Society of Thoracic Surgeons, and
Society for Vascular Medicine. Anesth Analg. 2010;111:279–315.
23. Leon L, Greisler HP. Vascular grafts. Expert Rev Cardiovasc Ther. 2003;1:581–594.
24. Kiguchi M, Chaer RA. Endovascular repair of thoracic aortic pathology. Expert Rev Med Devices. 2011;8:515–525.
25. Swaminathan M, Lineberger CK, McCann RL, et al. The importance of intraoperative transesophageal echocardiography in
endovascular repair of thoracic aortic aneurysms. Anesth Analg. 2003;97:1566–1572.
26. Fazio GP, Redberg RF, Winslow T, et al. Transesophageal echocardiographically detected atherosclerotic aortic plaque is a
marker for coronary artery disease. J Am Coll Cardiol. 1993;21:144–150.
27. Konstadt SN, Reich DL, Kahn R, et al. Transesophageal echocardiography can be used to screen for ascending aortic athero-
sclerosis. Anesth Analg. 1995;81:225–228.
28. Katz ES, Tunick PA, Rusinek H, et al. Protruding aortic atheromas predict stroke in elderly patients undergoing cardiopulmo-
nary bypass: Experience with intraoperative transesophageal echocardiography. J Am Coll Cardiol. 1992;20:70–77.

29. Rosenberger P, Shernan SK, Loffler M, et al. The influence of epiaortic ultrasonography on intraoperative surgical management
in 6051 cardiac surgical patients. Ann Thorac Surg. 2008;85:548–553.
30. Djaiani G, Ali M, Borger MA, et al. Epiaortic scanning modifies planned intraoperative surgical management but not cerebral
embolic load during coronary artery bypass surgery. Anesth Analg. 2008;106:1611–1618.
31. Hangler HB, Nagele G, Danzmayr M, et al. Modification of surgical technique for ascending aortic atherosclerosis: Impact on
stroke reduction in coronary artery bypass grafting. J Thorac Cardiovasc Surg. 2003;126:391–400.
32. Glas KE, Swaminathan M, Reeves ST, et al. Guidelines for the performance of a comprehensive intraoperative epiaortic ultra-
sonographic examination: Recommendations of the American Society of Echocardiography and the Society of Cardiovascular
Anesthesiologists; endorsed by the Society of Thoracic Surgeons. J Am Soc Echocardiogr. 2007;20:1227–1235.

QUESTIONS
1. TEE can reliably image which of the 7. In the image shown, what is the yellow
following zones of the aorta? arrow pointing to?
a. Zone 2
b. Zone 3
c. Zone 4
d. All of the above
2. What is the hallmark finding of an acute
aortic dissection on TEE?
a. Severe aortic regurgitation
b. A large pericardial effusion
c. An intimal flap
d. Regional wall motion abnormalities of the
left ventricle
3. The aortic arch is typically seen in long axis
at an omniplane angle of ______ and short
axis at an omniplane angle of ______ when
using TEE.
a. 120 degrees, 30 degrees
b. 0 degrees, 90 degrees a. The distal end of an elephant trunk graft
c. 90 degrees, 0 degrees b. A dissection flap
d. The aortic arch is not visible using TEE c. An aortic cannula
d. A pulmonary artery catheter
4. Which of the following aortic pathologies
are generally NOT taken to the operating 8. Which of the following is a characteristic of
room emergently? a Type A intramural hematoma?
a. Asymptomatic DeBakey Type III aortic a. The underlying etiology is a tear in the inti-
dissection mal layer of the aorta
b. Stanford Type B dissection with evidence of b. There is thickening of the medial layer of at
ischemic bowel least 15 mm
c. DeBakey Type I aortic dissection c. There is protrusion above the intimal layer
d. All of the above require immediate surgical into the lumen of the aorta
intervention d. Left untreated, it may progress to aortic
rupture
5. All of the following are typical of the false
lumen of an aortic dissection EXCEPT: 9. In the image shown, this patient with aortic
a. Color flow Doppler demonstrates flow into stenosis can be said to have______
it at the tear site
b. It expands during systole
c. It is often the larger of the two lumens
d. It may contain spontaneous echo contrast
6. Acute aortic syndromes encompass all of
the following entities EXCEPT:
a. Acute aortic dissection
b. Penetrating atherosclerotic ulcer
c. Ascending aortic aneurysm
d. Intramural hematoma
a. A root type aneurysm

b. A supracoronary (tubular) type aneurysm
c. A Type A aneurysm
d. A normal ascending aorta

10. All of the following are characteristic of an 14. What type of thoracoabdominal aneurysm
acute aortic dissection flap EXCEPT: involves the greatest length of the
a. Irregularly shaped descending aorta?
b. Highly mobile a. Crawford Type I
c. Indistinct borders b. Crawford Type II
d. Contained within the lumen of the aorta c. Crawford Type III
d. Crawford Type IV
11. In a patient undergoing elective aortic
valve replacement, poststenotic dilation 15. What is the pathology shown in the image
of what size should warrant consideration below?
of surgical treatment?
a. 4 cm
b. 4.5 cm
c. 5 cm
d. 5.5 cm
12. In the image shown, the letter “X” is seen
within what lumen?
a. The true lumen of a dissection at the level of

the descending aorta
a. Acute aortic dissection
b. The false lumen of a dissection at the level
b. Reverberation artifact
of the descending aorta
c. Intramural hematoma
c. The true lumen of a dissection at the level of
d. Severe atherosclerotic disease
the aortic arch
d. The false lumen of a dissection at the level
of the aortic arch
13. What is the major disadvantage of using
a phased-array transducer for epiaortic
scanning?
a. All walls of the aorta cannot typically be
imaged at once.
b. The frequency is usually too low for detailed
imaging.
c. The probe requires a “stand-off ” to prevent
near-field clutter.
d. They must be autoclaved to maintain sterility.

16. What is the pathology shown in the image 19. What is the next appropriate step in
below? management of the patient seen in the
image below?
a. Grade 3 atherosclerosis of the ascending

aorta
b. Acute aortic dissection
c. Grade 3 atherosclerosis of the descending
aorta
d. Penetrating atherosclerotic ulcer
17. Assuming no chronic dissection or
connective tissue disorders are present,
at what diameter is it recommended to
surgically address the descending aorta in
an asymptomatic patient? a. Obtain angiography, including cardiac cath-
a. ≥4.5 cm eterization
b. ≥5 cm b. Attempt placement of a percutaneous aor-
c. ≥5.5 cm tic valve
d. ≥6 cm c. Obtain an MRI to rule out artifact
d. Proceed directly to the operating room
18. The size of a “normal” aorta depends upon:
a. Weight 20. According to the Katz grading system, an
b. Height atherosclerotic plaque with any type of
c. Age mobile component to it would be graded:
d. All of the above a. Grade M
b. Grade V
c. Type A
d. Type IV

18 Critical Care Echocardiography
Heidi K. Atwell and Michael H. Wall
INTRODUCTION
Critical care ultrasound (CCUS) comprises ultrasound evaluation of the heart, lungs, pleural space,
abdomen, vascular access, and evaluation of venous thrombosis. CCUS has been used by emergency
medicine and critical care physicians for at least 15 years (1,2). Recently, several societies have published
position papers, training guidelines, competency statements, and educational curricula on CCUS (3–7).
It is important to recognize that CCUS is not meant to replace traditional diagnostic ultrasound (US).
CCUS is designed to be used as a series of simplified, focused examinations that can quickly rule in or
rule out a diagnosis, or support the need for additional testing, imaging, or procedures. The advantages
to CCUS are that it is noninvasive, performed and interpreted by the physician caring for the patient
at the bedside, can be easily repeated, and is rapidly available 24 hours a day. This chapter will review
the use of focused transthoracic echocardiography (TTE) and transesophageal echocardiography (TEE)
in critically ill patients, and during advanced cardiac life support (ACLS). The chapter will also briefly
review the use of focused echocardiography in the diagnosis of common complications seen in the inten-
sive care unit (ICU).
FOCUSED, GOALDIRECTED ECHOCARDIOGRAPHY

Multiple protocols for echocardiography in critically ill patients have been described and all have common
concepts including:
1. They are all rapidly applied, focused examinations.
2. They can all be learned with relatively brief training.
3. They all use some combination of four to six limited views (subcostal, apical, parasternal, and pleural).
4. They are all performed real time, by the treating physicians at the patient’s bedside.
5. The examination can and should be repeated over time to evaluate the effects of therapeutic
interventions.
6. The examinations are not meant to replace traditional diagnostic examinations.
FOCUSED GOALDIRECTED TRANSTHORACIC ECHOCARDIOGRAPHY

This section will describe the standard views for a focused, goal-directed echo (GDE) and transthoracic
echocardiography (TTE). Views can be grouped according to probe position, namely parasternal, apical,
and subcostal views. This can be further divided into axis (long and short) and chambers views (two and
four) (Fig. 18.1).
Parasternal Long Axis

The parasternal window is found immediately adjacent to the sternum, in the third or fourth intercostal
space. Images obtained in this window are greatly improved by left lateral decubitus positioning, which
brings the heart closer to the chest wall. The parasternal long axis (Fig. 18.2) provides images of the aortic
Video 18.1 and mitral valves, the left atrium and ventricle, and a small portion of the right ventricular outflow tract.
The septum and posterior walls of the left ventricle are seen in this view (Video 18.1).
364

18. Critical Care Echocardiography 365
Suprasternal
Right
parasternal Parasternal
Right
apical Apical
Subcostal
FIGURE 18.1 This diagram demonstrates the various transducer locations used in echocardiography. (From Henry WL,
DeMaria A, Gramaik R, et al. Report of the American Society of Echocardiography Committee on Nomenclature and
Standards in Two-dimensional Echocardiography. Circulation. 1980;62:212–217, with permission.)
Parasternal Short Axis

By rotating the probe 90 degrees, the parasternal short axis is seen. Views at the midventricular level at the
level of the papillary muscles allow for evaluation of left and right ventricular chamber size and wall motion
abnormalities (Fig. 18.3, Video 18.2). Video 18.2
FIGURE 18.2 Transthoracic two-dimensional echocardiogram recorded in a parasternal long-axis view revealing the
right ventricle, left ventricle, left atrium, and proximal aorta as well as septal and posterior wall thickness (double-headed
arrows).

FIGURE 18.3 A parasternal short-axis view at the level of the mitral valve is shown.
Apical Four-chamber
This window is found at the ventricular apex, or point of maximal impulse (PMI), near the anterior axillary
line. Images are greatly improved with lateral decubitus positioning, making this view more difficult to
accomplish in ICU patients. The apical four-chamber view (Fig. 18.4) provides a global picture of all four
Video 18.3 chambers. Chamber size and ventricular interdependence can be evaluated (Video 18.3).
Apical Two-chamber
Accomplished by rotating the transducer 90 degrees, the apical two-chamber allows visualization of the left
ventricular anterior and inferior walls (Fig. 18.5).
Subcostal Four-chamber
The subcostal window is found just inferior to the xiphoid process. This image is difficult to obtain in
patients with midline abdominal incisions or mediastinal chest tubes. All chambers of the heart can
Video 18.4 be visualized with this view (Fig. 18.6, Video 18.4). The inferior vena cava (IVC) can also be examined
by rightward angulation of the probe allowing the ultrasound beam to transmit through the liver
Video 18.5 (Fig. 18.7, Video 18.5).
FIGURE 18.4 The apical four-chamber view is shown. LA, left atrium; LV, left ventricle; RA, right atrium; RV, right
ventricle.

FIGURE 18.5 Apical two-chamber view. In the apical two-chamber view, small portions of the posterior mitral leaflet
are seen laterally and medially with the anterior leaflet filling most of the annulus area. Part of a papillary muscle has
been shown for orientation, but the papillary muscles are located symmetrically posterior to the image plane. The tomo-
graphic plane has been rotated with the apex of the sector at the top.
FIGURE 18.6 A subcostal four-chamber view is demonstrated. LA, left atrium; LV, left ventricle; RA, right atrium; RV,
right ventricle.
FIGURE 18.7 The inferior vena cava near the hepatic vein. Note the liver provides the acoustic window.

A B
FIGURE 18.8 Ultrasonograph scan lines. A: Anterior scan line. The ultrasound probe is held firmly perpendicular to
chest wall. The ultrasonographer moves the ultrasound probe cephalad and caudad in one longitudinal line and then
moves either lateral or medial and repeats a longitudinal scan. Transducer marker points cephalad. B: Midaxillary scan
line. C: Posterior scan line. (The patient provided written consent for the use of this photograph.) (From Koenig SJ,
Narasimhan M, Mayo PH. Thoracic ultrasonography for the pulmonary specialist. Chest. 2011;140:1332–1341.)
Pleural Ultrasound
Although not included in conventional TTE protocols, evaluation of the pleural spaces should be included
when assessing causes of hypotension and hypoxia. Many lung pathologies are definitively diagnosed with
radiographic studies, but ultrasound provides real time evaluation, especially in circumstances where x-ray
or CT scan is not available. In unstable patients, “the usefulness of thoracic ultrasonography rests with
its immediate application” (8). Evaluation of the pleural and lung parenchyma can be done by placing the
transducer between the ribs, and serially scanning the lungs in multiple longitudinal planes. If findings are
abnormal, comparison with normal lung tissue is imperative. Images are actually of the interface between
chest wall and lung, as the air-filled lung provides poor images. A normal examination consists of the
movement of the pleura caused by normal ventilation, called the sliding, or gliding sign (9,10). Absence of
this sign is indicative of a pneumothorax (Figs. 18.8 and 18.9).
FIGURE 18.9 Normal pleural line. Longitudinal anterior chest ultrasonograph displaying typical anatomic landmarks
in normal lung (8).

TABLE 18.1 Causes of Cardiac Arrest with TEE Findings
Diagnosis TEE finding

Hypovolemia Empty, hyperdynamic LV and RV
Pulmonary embolism Dilated RV
Tamponade Pericardial effusion, compression/collapse of low-pressure chambers
Pneumothorax Absence of gliding sign
Cardiac standstill No organized ventricular contraction
ECHOCARDIOGRAPHY AND ADVANCE CARDIAC LIFE SUPPORT

Use of TTE during cardiopulmonary resuscitation (CPR) has become increasingly widespread, as famil-
iarity and skills increase. It is most useful in pulseless electrical activity (PEA) and very low flow states,
which carry a high mortality rate, but may be associated with identifiable and potentially treatable
causes. The use of TTE during ACLS can identify several of these potentially correctable causes (11)
(Table 18.1).
TTE is also beneficial in differentiating low flow states versus true PEA, as well as the return of sponta-
neous circulation. Many authors have found that clinicians are inconsistent in their ability to detect a pulse
during CPR (12–15). Other monitors, such as pulse oximetry or noninvasive blood pressure measurement,
are often unreliable in severe hypotension. TTE provides direct visualization of cardiac wall motion, allow-
ing assessment of organized cardiac contraction and return of circulation. The focused echocardiographic
evaluation in resuscitation (FEER) examination (16) and cardiac arrest ultrasound examination (CAUSE)
(17) are two protocols specifically created for cardiac arrest and resuscitation.
The diagnostic abilities of echocardiography are proven, but the ability to appropriately utilize the
technology is still questionable. Concerns regarding interruption of chest compressions and training of
responders utilizing echo has been addressed in several studies, with promising results (16). The 10-second
pulse check has been utilized in several of the aforementioned studies as a period to perform a scan without
interruption of CPR, with evidence of rapid image acquisition and interpretation (16–18). The utility of
echocardiography in cardiac arrest will continue to evolve.
FOCUSED GOALDIRECTED TEE

There are many critically ill patients where performing a goal-directed TTE is not possible due to dressings,
drains, chest tubes, patient characteristics, or positioning difficulties. Provided there are no contraindica-
tions to placement of the TEE probe, it is reasonable to perform a focused goal-directed TEE examination
using standard views that are similar to those described for goal-directed TTE, in these patients. Immedi-
ate clinical decision-making can be greatly aided by goal-directed TEE, followed by a comprehensive TEE
examination once hemodynamic stability is restored.
GOALDIRECTED TEE VIEWS

Similar to goal-directed TTE, goal-directed TEE would use the following views:
t ME four- and five-chamber views
t ME bicaval
t ME RV inflow–outflow
t TG midpap SAX
t TG midpap LAX
t ME evaluation of pleural spaces

ME FOUR AND FIVECHAMBER VIEWS

This ME four- and five-chamber views (Figure Chapter 2) provide a quick overview of atrial size and func-
tion, right ventricle and left ventricle size and function, tricuspid and mitral valve function, and the presence
or absence of pericardial fluid. The five-chamber view adds additional information about the aortic valve.
ME RV INFLOWOUTFLOW VIEW
In the ME RV inflow–outflow, the RVOT and the pulmonic valves are seen (Figure Chapter 2) allowing for
evaluation of RV size and function and pulmonic valve function.
ME BICAVAL VIEW
The bicaval view shows the intra-atrial septum, right atrium (RA), SVC, and IVC allowing for size determi-
nation of these structures plus placement of intracardiac lines (Figure Chapter 2).
TG MIDPAP SAX VIEW

The TG midpap SAX view (Figure Chapter 2) provides information on right and left ventricle size and func-
tion, and regional wall motion in the major distribution of the left, right, and circumflex coronary arteries.
TG LAX
The TG LAX view allows evaluation of LV size, function, and wall motion, as well as assessment of the
mitral valve, and left atrium (Figure Chapter 2).
BILATERAL PLEURAL SPACE VIEWS

In the midesophageal position, rotation of the probe to the patient’s right can evaluate the right pleural
space; rotation to the patient’s left can evaluate the left pleural space and descending thoracic aorta.
The use of these views should allow the rapid assessment of hypotension, global right and left dys-
function, myocardial ischemia, volume status, severe valvular disease, pleural and pericardial effusion, and
pericardial tamponade.
Recently, a small miniaturized TEE probe (Fig. 18.10) has been approved by the FDA and can be left in
place for 72 hours (ImaCor, Inc. Garden City, New Jersey). This technology may prove to be a useful device
to aid in the ongoing assessment and treatment of hemodynamically unstable patients.
ECHO FINDINGS IN COMMON INTENSIVE CARE UNIT ICU

COMPLICATIONS
Intensive care patients are frequently characterized by rapidly changing hemodynamic parameters. The
cause for such fluctuations is often difficult to determine, requiring multiple studies and time. Use of echo-
cardiography and CCUS can aid in the differential diagnosis of the causes of hypotension and hypoxia.
HYPOTENSION
Hypotension is a common symptom in ICU patients. The causes of hypotension are numerous, and include
hypovolemia, sepsis, ventricular failure, tamponade, aortic dissection or aneurysm, and pneumothorax,
just to name a few. With the use of echo, several causes can be diagnosed and treated within minutes of
onset of hypotension.

FIGURE 18.10 Miniaturized transesophageal echocardiography (TEE) probe has been approved by the FDA and can
be left in place for 72 hours.
HYPOVOLEMIA
Hypovolemia is frequently seen in ICU patients. Echocardiographic evaluation of a hypovolemic patient
would show an empty, often hyperdynamic left ventricle (LV). In the short-axis view, the LV chamber size is
very small. Giving a therapeutic fluid bolus while directly observing LV diameter with ultrasound will dem-
onstrate an increasing end-diastolic area in the hypovolemic patient, while other hemodynamic parameters
(blood pressure, central venous pressure, heart rate), may remain unchanged (19,20). Inferior and superior
vena cava collapsibility is frequently used as an indicator of volume status (21,22). The IVC can be easily
viewed with ultrasound (Fig. 18.7, Video 18.5), and its diameter and changes with ventilation can provide Video 18.5
an idea of a patient’s volume status. Spontaneously ventilating patients increase their venous return dur-
ing inspiration, causing narrowing of the IVC as blood flows quickly into the RA (23). Positive pressure
ventilation (PPV) decreases venous return (24), causing the IVC to become more dilated. In hypovolemic
patients the IVC will collapse by >50% with a sniff test, whereas a patient with high right atrial pressures
will not demonstrate any change in diameter (25). The easily imaged IVC makes this an ideal indicator of
volume status.
LEFT VENTRICULAR FAILURE

Left ventricular failure often presents with gross hypokinesis (or akinesis) of the chamber in question. In
LV failure, the visual presentation of the chamber may vary (eccentric or concentric hypertrophy, etc.), but
overt hypokinesis is always present. Visual estimation often provides an accurate assessment of ejection
fraction, and is less time-consuming than more quantitative methods (26).
RIGHT VENTRICULAR FAILURE

Right ventricular failure can be easily missed, and can quickly become fatal. The RV will acutely dilate as
it fails, as seen with massive pulmonary embolism (PE). In right ventricular failure, the left ventricle often
appears under-filled, as the RV is unable to maintain forward flow. RV dilatation can have various etiolo-
gies, including PE, right-sided MI, and lung pathologies (chronic obstructive pulmonary disease, obstructive

FIGURE 18.11 Parasternal short-axis view demonstrated a dilated right ventricular (RV) failure consistent with RV failure.
sleep apnea, and pulmonary hypertension). Knowledge of the patient’s underlying pathology can help aid in
the determination of acute versus chronic RV dilatation. Treatment differs from the treatment of LV failure;
Video 18.6 therefore, it is imperative to distinguish between the two (Fig. 18.11, Video 18.6).
CARDIAC TAMPONADE
Cardiac tamponade is a life-threatening condition that must be diagnosed quickly. It is frequently seen
following cardiac surgery, but can occur following trauma, or in patients with malignant or infectious
processes. Clinical symptoms of elevated central venous pressure, distended neck veins, muffled heart
sounds, tachycardia, and hypotension are often of little use in the postoperative cardiac patient. Echo-
cardiography provides evaluation of chamber compromise and may frequently show the effusion (Video
Video 18.7 18.7). Cardiac chamber collapse is the hallmark of a hemodynamically significant effusion. Compression
is initially seen in the chambers with the lowest pressure (27,28). Right atrial compression, RV collapse
in early diastole, and dilated IVC without respiratory variation are all indicatives of tamponade (29,30).
Absence of these echo findings does not necessarily preclude tamponade, especially in cardiac surgery
patients, as they frequently have posterior focal hematoma obstructing venous return to the left side of
the heart.
AORTIC DISSECTION
Aortic dissection, if suspected, must be immediately diagnosed. Although uncommon to present in the
ICU, dissection remains a possibility in postoperative open heart patients, as well as patients who had a
recent cardiac catheterization. Transthoracic echo does not provide adequate imaging for a thoracic dis-
section (31). Conversely, the sensitivity and specificity of TEE approaches that of CT or MRI (32). TTE
remains vital in assessment of aortic regurgitation and pericardial effusion, both sequelae of acute dissec-
Video 18.8
tion (Videos 18.8 and 18.9).
Video 18.9
CAUSES OF ACUTE HYPOXIA

Acute hypoxia is a common symptom in the ICU. A multitude of causes exist, including cardiac, extrinsic,
and intrinsic pulmonary diseases. Pneumothorax, although most frequently diagnosed on chest x-ray or

FIGURE 18.12 Ultrasound showing a complex pleural effusion (Pleff ) with alveolar consolidation (Alv Cons) and air
bronchograms (AB). CW, chest wall; HD, hemi-diaphragm.
CT, can be visualized with transthoracic echo. The “gliding or sliding sign” is caused by the movement of
the parietal and visceral pleural over each other during respiration. When imaging the pleura, absence of
the gliding sign is indicative of pneumothorax, and presence is confirmation that there is no pneumothorax
(8). This is a rapid way to assess for iatrogenic pneumothorax following procedures. Hydropneumothorax
will also have a visible air–fluid interface (33).
Comparison of pathologic findings to those of the patient’s normal lung helps elucidate the diagno-
sis (34). Consolidated lung tissue has a density similar to that of the liver and spleen; occasionally, air
bronchograms can be seen within the lung parenchyma (35). Pleural effusion is visible on both TTE
and TEE. Appearing hypoechoic, the effusion fluid can be localized with ultrasound prior to drainage
(Fig. 18.12).
ACUTE PULMONARY EMBOLISM

Acute PE is an important cause of morbidity and mortality, but is often underdiagnosed. Although echo-
cardiography is not the preferred imaging study to diagnose PE, it does provide useful information when
the patient is too unstable for transport to the CT or MRI scanner, as occasionally a thrombus can be
visualized in the right ventricle or pulmonary artery. PE causes acute RV dysfunction as the pulmonary
artery pressure abruptly increases. As this happens, there is a distinct pattern of wall motion abnormali-
ties, called the McConnell sign (akinesis of the RV midfree wall, with normal wall motion of the apex).
These findings are both sensitive and specific for PE (36,37). Furthermore, resultant RV dysfunction is
a good predictor of increased mortality (38,39). Echocardiography, finally, is a useful tool for assess-
ing cardiac function following therapeutic interventions, such as thrombectomy or inotropic support
(Video 18.10). Video 18.10
CONCLUSION
The use of focused or goal-directed echocardiography in the ICU to evaluate, diagnose and manage shock,
hypotension, hypoxia, and CPR in ICU patients is now a common accepted practice. The ability to rapidly
obtain diagnostic information and then repeat the examination as often as needed by the treating intensiv-
ist is ideal in the management of the ICU patient. Echocardiography really has become an extension of the
physical examination—similar to the use of a stethoscope.

REFERENCES
1. Heller M, Melanson SW. Applications for ultrasonography in the emergency department. Emerg Med Clin North Am.
1997;15:735–744.
2. Benjamin E, Griffin K, Leibowitz AB, et al. Goal-directed transesophageal echocardiography performed by intensivists to assess
left ventricular function: Comparison with pulmonary artery catheterization. J Cardiothorac Vasc Anesth. 1998;12:10–15.
3. Price S, Via G, Sloth E, et al. Echocardiography practice, training and accreditation in the intensive care: Document for the
World Interactive Network Focused on Critical Ultrasound (WINFOCUS). Cardiovasc Ultrasound. 2008;6:49.
4. Mayo PH, Beaulieu Y, Doelken P, et al. American College of Chest Physicians/La Société de Réanimation de Langue Française:
Statement on competence in critical care ultrasonography. Chest. 2009;135:1050–1060.
5. Kaplan A, May PH. Echocardiography performed by the pulmonary/critical care medicine physician. Chest. 2009;135:529–
535.
6. Bennett S. Training guidelines for ultrasound: Worldwide trends. Best Pract Res Clin Anaesthesiol. 2009;23:363–373.
7. Vignon P, Mucke F, Bellec F, et al. Basic critical care echocardiography: Validation of a curriculum dedicated to noncardiologist
residents. Crit Care Med. 2011;39:636–642.
8. Koenig SJ, Narasimhan M, Mayo PH. Thoracic ultrasonography for the pulmonary specialist. Chest. 2011;140:1332–1341.
9. Lichtenstein DA, Menu Y. A bedside ultrasound sign ruling out pneumothorax in the critically ill. Lung sliding. Chest.
1995;108:1345–1348.
10. Dulchavsky SA, Hamilton DR, Diebel LN, et al. Thoracic ultrasound diagnosis of pneumothorax. J Trauma. 1999;47:970.
11. Deakin CD, Nolan JP, Soar J, et al. European resuscitation council guidelines for resuscitation 2010 section 4. Adult advanced
life support. Resuscitation. 2010;81:1305–1352.
12. Dick WF, Eberle B, Wisser G, et al. The carotid pulse check revisited: What if there is no pulse? Crit Care Med. 2000;
28:N183–N185.
13. Lapostolle F, Le Toumelin P, Agostinucci JM, et al. Basic cardiac life support providers checking the carotid pulse: Performance,
degree of conviction, and influencing factors. Acad Emerg Med. 2004;11:878–880.
14. Ochoa FJ, Ramalle-Gomara E, Carpintero JM, et al. Competence of health professionals to check the carotid pulse.
Resuscitation. 1998;37:173–175.
15. Eberle B, Dick WF, Schneider T, et al. Checking the carotid pulse check: Diagnostic accuracy of first responders in patients
with and without a pulse. Resuscitation. 1996;33:107–116.
16. Breitkreutz R, Walcher F, Seeger FH. Focused echocardiographic evaluation in resuscitation management: Concept of an
advanced life support-conformed algorithm. Crit Care Med. 2007;35:S150–S161.
17. Hernandez C, Shuler K, Hannan H, et al. C.A.U.S.E.: Cardiac arrest ultra-sound exam—a better approach to managing patients
in primary non-arrhythmogenic cardiac arrest. Resuscitation. 2008;76:198–206.
18. Price S, Uddin S, Quinn T. Echocardiography in cardiac arrest. Curr Opin Crit Care. 2010;16:211–215.
19. Salem R, Vallee F, Rusca M, et al. Hemodynamic monitoring by echocardiography in the ICU: The role of the new echo tech-
niques. Curr Opin Crit Care. 2008;14:561–568.
20. Tousignant CP, Walsh F, Mazer CD. The use of transesophageal echocardiography for preload assessment in critically ill
patients. Anesth Analg. 2000;90:351.
21. Barbier C, Loubieres Y, Schmit C, et al. Respiratory changes in inferior vena cava diameter are helpful in predicting fluid
responsiveness in ventilated septic patients. Intensive Care Med. 2004;30:1740–1746.
22. Vieillard-Baron A, Slama M, Cholley B, et al. Echocardiography in the intensive care unit: From evolution to revolution?
Intensive Care Med. 2008;34:243–249.
23. Morgan BC, Abel FL, Mullins GL, et al. Flow patterns in cavae, pulmonary artery, pulmonary vein, and aorta in intact dogs.
Am J Physiol. 1966;210:903–909.
24. Morgan BC, Martin W, Hornbein TF, et al. Hemodynamic effects of intermittent positive pressure respiration. Anesthesiology.
1966;27:584–590.
25. Rudski LG, Lai WW, Afilalo J, et al. Guidelines for the echocardiographic assessment of the right heart in adults: A report
from the American Society of Echocardiography endorsed by the European Association of Echocardiography, a registered
branch of the European Society of Cardiology, and the Canadian Society of Echocardiography. J Am Soc Echocardiogr.
2010;23:685–713.
26. Mueller X, Stauffer JC, Jaussi A, et al. Subjective visual echocardiographic estimate of left ventricular ejection fraction as
an alternative to conventional echocardiographic methods: Comparison with contrast angiography. Clin Cardiol. 1991;14:
898–902.
27. Gillam LD, Guyer DE, Gibson TC, et al. Hydrodynamic compression of the right atrium: A new echocardiographic sign of
cardiac tamponade. Circulation. 1983;68:294–301.
28. Asher C, Klein AL. Diastolic heart failure: Restrictive cardiomyopathy, constrictive pericarditis, and cardiac tamponade:
Clinical and echocardiographic evaluation. Cardiol Rev. 2002;10:218–229.
29. Tsang TSM, Oh JK, Seward JB. Diagnosis and management of cardiac tamponade in the era of echocardiography. Clin Cardiol.
1999;22:446–452.
30. Armstrong WF, Schilt BF, Helper DJ, et al. Diastolic collapse of the right ventricle with cardiac tamponade: An echocardio-
graphic study. Circulation. 1982;65:1491–1496.
31. Cigarroa JE, Isselbacher EM, DeSanctis RW, et al. Diagnostic imaging in the evaluation of suspected aortic dissection. Old
standards and new directions. N Engl J Med. 1993;328:35–43.
32. Nienaber CA, von Kodolitsch Y, Nicolas V, et al. The diagnosis of thoracic aortic dissection by noninvasive imaging proce-
dures. N Engl J Med. 1993;328:1–9.

33. Targhetta R, Bourgeois JM, Chavagneux R, et al. Ultrasonographic approach to diagnosing hydropneumothorax. Chest.
1992;101:931–934.
34. Tsai TH, Yang P. Ultrasound in the diagnosis and management of pleural disease. Curr Opin Pulm Med. 2003;9:282–290.
35. Lichtenstein DA, Lascols N, Mezière G, et al. Ultrasound diagnosis of alveolar consolidation in the critically ill. Intensive Care
Med. 2004;30:276–281.
36. Goldhaber SZ. Echocardiography in the management of pulmonary embolism. Ann Intern Med. 2002;136:691–700.
37. McConnell MV, Solomon SD, Rayan ME, et al. Regional right ventricular dysfunction detected by echocardiography in acute
pulmonary embolism. Am J Cardiol. 1996;78:469–473.
38. Ribeiro A, Lindmaker P, Juhlin-Dannfelt A, et al. Echocardiography Doppler in pulmonary embolism: Right ventricular dys-
function as a predictor of mortality rate. Am Heart J. 1997;134:479–487.
39. Grifoni S, Olivotto I, Cecchini P, et al. Short-term clinical outcome of patients with acute pulmonary embolism, normal blood
pressure, and echocardiographic right ventricular dysfunction. Circulation. 2000;101:2817–2822.

QUESTIONS
1. A 75-year-old woman arrives in the shows moderate tricuspid regurgitation,
ICU from the emergency room with the no effusions, and RV area > LV area in the
diagnosis of urosepsis. She is intubated and four-chamber view. Which of the following
mechanically ventilated. BP is 90/55, HR interventions is the most appropriate next
is 110. Bedside echo shows normal valves, step?
no effusions, and a left ventricular internal a. One liter normal saline bolus
dimension (LVID) at end-diastole of 3.5 cm b. Dobutamine infusion
and LVID at end-systole of 0.5 cm. Which c. Norepinephrine infusion
of the following interventions is the most d. Heparin infusion
appropriate next step?
5. A 75-year-old woman arrives in the
a. One liter normal saline bolus
ICU from the emergency room with the
b. Dobutamine infusion
diagnosis of urosepsis. She is spontaneously
c. Norepinephrine infusion
breathing. BP is 90/55, HR is 110. Bedside
d. Heparin infusion
echo shows normal valves, no effusions,
2. A 75-year-old woman arrives in the and a left ventricular internal dimension
ICU from the emergency room with the (LVID) at end-diastole of 6 cm and LVID
diagnosis of urosepsis. She is intubated and at end-systole of 4 cm. In addition, her
mechanically ventilated. BP is 90/55, HR IVC diameter is 1 cm at end expiration
is 110. Bedside echo shows normal valves, and 0.3 cm at end inspiration. Which of
no effusions, and a left ventricular internal the following interventions is the most
dimension (LVID) at end-diastole of 6 cm appropriate next step?
and LVID at end-systole of 4 cm. Which a. One liter normal saline bolus
of the following interventions is the most b. Dobutamine infusion
appropriate next step? c. Norepinephrine infusion
a. One liter normal saline bolus d. Heparin infusion
b. Dobutamine infusion
6. A 60-year-old man with normal LV function
c. Norepinephrine infusion
is in the ICU for 4 hours following CABG.
d. Heparin infusion
His chest tube output per hour for the last
3. A 75-year-old woman arrives in the 4 hours has been 400, then 300, then 300,
ICU from the emergency room with the then 10. He is now requiring increasing
diagnosis of urosepsis. She is intubated and norepinephrine to maintain his blood
mechanically ventilated. BP is 90/55, HR pressure. He remains intubated, but is
is 110. Bedside echo shows normal valves, breathing spontaneously. Bedside TTE
no effusions, and a left ventricular internal shows the following:
dimension (LVID) at end-diastole of 8 cm t No effusions
and LVID at end-systole of 7 cm. Which t Left ventricular internal dimension (LVID)
of the following interventions is the most at end-diastole is 6 cm
appropriate next step? t LVID end-systole is 4 cm
a. One liter normal saline bolus t IVC diameter at end expiration is 2 cm
b. Dobutamine infusion t IVC diameter and end inspiration is 1 cm
c. Norepinephrine infusion Which of the following is the most appropriate
d. Heparin infusion next step?
4. A 75-year-old woman arrives in the a. One liter normal saline bolus
ICU from the emergency room with the b. Dobutamine infusion
diagnosis of urosepsis. She is intubated c. Increase norepinephrine infusion
and mechanically ventilated. BP is 105/55, d. Re-exploration
HR is 90, and ScvO2 is 75%. Bedside echo

7. A 60-year-old man with normal LV function 11. What is the best time to obtain a
is in the ICU for 4 hours following CABG. transthoracic echo image during
His chest tube output per hour for the last ACLS for ventricular fibrillation?
4 hours has been 400, then 300, then 300, a. Before CPR starts
then 10. He is now requiring increasing b. As soon as the echo machine arrives
norepinephrine to maintain his blood c. Immediately following defibrillation
pressure. He remains intubated, but is d. After 2 minutes of CPR
breathing spontaneously. Bedside TTE
12. Focused TTE during ACLS shows the
shows the following:
following:
t No effusions
t Left ventricular internal dimension (LVID) t Limited wall motion
at end-diastole is 6 cm
t No pulse
t LVID end-systole is 4 cm t Regular rhythm
t IVC diameter at end expiration is 2 cm This is most consistent with which of the fol-
t IVC diameter and end inspiration is 1 cm lowing conditions:
t Dyskinetic anterior wall of LV a. Pseudo PEA
Which of the following is the most appropriate b. True PEA
next step? c. Hypovolemia
d. Cardiac standstill
a. One liter normal saline bolus
b. Dobutamine infusion 13. Focused TTE during ACLS shows the
c. Increase norepinephrine infusion following:
d. Re-exploration t No wall motion
8. Which of the following echo findings is
t No pulse
most consistent with acute right heart
t Regular rhythm
failure following a massive PE? This is most consistent with which of the fol-
a. Severe pulmonic insufficiency lowing conditions:
b. RV free wall thickness >1 cm a. Pseudo PEA
c. Left ventricular end diastolic diameter of 8 cm b. True PEA
d. RV area > LV area c. Hypovolemia
9. A 56-year-old man is in the ICU intubated d. Cardiac standstill
and mechanically ventilated 2 hours after 14. A 42-year-old woman with a history of
an LVAD was placed. His SaO2 is 88% on a long standing hypertension is in the ICU
F1O2 of 1. His CXR is unremarkable. Which following CABG. Her CVP is 18 mm Hg
of the following TEE views would be most and her CI is 1.5 L/min/m2. HR is 90, BP is
helpful in determining the cause of his 90/60. Bedside echo shows the following:
hypoxia? t Left ventricular internal diameter (LVID) at
a. Midesophageal four-chamber end-diastole 4 cm
b. RV outflow t LVID end-systole 1 cm
c. Transgastric short axis t LV septal thickness at end-diastole 1.8 cm
d. Bicaval
Which of the following is the most appropriate
10. When performing a focused transthoracic next step?
echo examination during advanced cardiac
a. One liter normal saline
life support, which of the following is the
b. Norepinephrine infusion
preferred single view?
c. Vasopressin infusion
a. Subcostal four-chamber
d. Dobutamine infusion
b. Parasternal long axis
c. Parasternal short axis
d. Apical four-chamber

15. A 42-year-old woman with a history of 18. Which of the following findings is most
long standing hypertension is in the ICU consistent with severe aortic regurgitation
following CABG. Her CVP is 18 mm Hg (AR)?
and her CI is 1.5 L/min/m2. HR is 90, BP is a. Jet width/LVDT is 70%
90/60. Bedside echo shows the following: b. Vena contraction is 0.3 cm
t Left ventricular internal diameter (LVID) at c. Pressure half-time is 500 milliseconds
end-diastole 4 cm d. Regurgitant orifice area 0.1 cm2
t LVID end-systole 1 cm
19. Which of the following findings is most
t LV septal thickness at end-diastole 1.8 cm
consistent with severe central mitral
t Severe MR
regurgitation (MR)?
Which of the following is the most appropriate a. Jet area (percent of LA) 50%
next step? b. Vena contraction is 0.3 cm
a. One liter normal saline c. Regurgitation volume is 30 mL
b. Norepinephrine infusion d. Regurgitant orifice area is 2 cm2
c. Vasopressin infusion 20. A 65-year-old man in shock undergoes
d. Dobutamine infusion bedside echo. He is found to have severe
16. Which of the following findings is most mitral regurgitation (MR). Which of the
consistent with the diagnosis of severe following additional findings is most
aortic stenosis (AS)? consistent with acute severe MR?
a. Aortic jet velocity is 5 m/s a. Left ventricular internal diameter at end-
b. Mean gradient is 20 mm Hg diastole of 5 cm
c. Valve area is 1.2 cm2 b. Depressed LV function
d. A “late peaking” velocity curve c. Left atrial diameter of 6 cm
d. Mitral valve annulus of 3.5 cm
17. Which of the following findings is most
consistent with severe mitral stenosis (MS)?
a. Mean gradient is 12 mm Hg
b. Valve area is 1.5 cm2
c. PA systolic pressure is 35 mm Hg
d. Pressure half-time is 200 milliseconds

19 Transesophageal Echocardiography for Congenital
Heart Disease in the Adult
Pablo Motta and Wanda C. Miller-Hance
INTRODUCTION
The spectrum of congenital heart disease (CHD) seen in the adult varies widely. Malformations range from
mild anomalies requiring no intervention to extremely complex pathologies characterized by the presence
of multiple coexistent defects. Echocardiography represents the primary noninvasive imaging modality in
the assessment of these lesions. The transesophageal approach expands the applications of echocardiog-
raphy by allowing the acquisition of anatomic and functional information that may not be obtainable by
transthoracic imaging. This is of particular benefit to the adult individual with suboptimal transthoracic
windows as transesophageal echocardiography (TEE) significantly enhances the characterization of struc-
tural defects and evaluation of hemodynamics. Additional major contributions of TEE in CHD include
the intraoperative assessment of the surgical repair, detection of residual pathology, and guidance of the
intervention if an immediate revision is necessary. TEE also plays an important role in the cardiac catheter-
ization laboratory as an adjunct to therapeutic interventions in patients with CHD.
Until the last several years most of the TEE experience was limited to two-dimensional (2D) imaging
and complementary modalities; however, recent advances have resulted in three-dimensional TEE (3D-
TEE) being increasingly applied to all forms of heart disease. This includes the evaluation of congenital
lesions. The high-resolution spatial anatomic information provided, together with the demonstration of
salient features of the pathology from unique views, exceeds the capabilities of 2D-TEE imaging. This rep-
resents a distinct advantage in CHD. As the experience increases, 3D-TEE is likely to further facilitate
diagnostic and therapeutic strategies in patients affected by structural cardiovascular malformations.
This chapter focuses on selected anomalies in the adult with CHD and addresses corresponding applica-
tions of TEE. The role of this imaging modality in the intraoperative and cardiac catheterization settings is
highlighted. Although many of the defects can be fully characterized using the standard TEE views recom-
mended by the Society of Cardiovascular Anesthesiologists and American Society of Echocardiography in
the comprehensive guidelines, in some cases the detailed examination of the abnormalities, particularly in
the case of complex disease, requires modified planes of interrogation. Another important aspect of TEE
in CHD is the need not only for specific views but also sweeps that display the anatomic and spatial rela-
tionship among structures. As relevant to the pathology being considered, these modified cross sections/
sweeps will be described. The initial 3D-TEE experience in the adult with CHD is also briefly reviewed.
CONGENITAL HEART DISEASE IN THE ADULT: INCIDENCE,

PREVALENCE, AND SURVIVAL
The incidence of CHD in the United States is estimated to be 6.2 per 1,000 live births. This figure does
not include the bicuspid aortic valve (Bic AV), regarded as the most common form of CHD occurring in
2% to 3% of the general population. At birth, the most common cardiac structural abnormality is that of
a ventricular septal defect (VSD). Other relatively common congenital lesions include atrial septal defects
(ASDs), pulmonary stenosis (PS), and patent ductus arteriosus (PDA). Beyond these defects, other less
prevalent pathologies include tetralogy of Fallot (TOF), aortic stenosis (AS), coarctation of the aorta (CoA),
atrioventricular septal defects (AVSDs), and transposition of the great arteries (TGA).
Not surprisingly, the highest survival rate in CHD occurs among infants with milder forms of disease.
However, overall outcome in those with complex pathology has improved dramatically over the years. This
is attributed to factors such as prenatal diagnosis, advances in medical and surgical strategies, definitive 379

surgical repair at an earlier age, and improvements in intraoperative/postoperative care. The prevalence of
CHD is approximately 4 per 1,000 living adults, of which nearly 10% have complex CHD. Currently, there
are more adults than children with CHD in the United States accounting for an estimated population of
nearly 2 million adults. This group of patients is also referred to as the “Grown-Up with CHD (GUCH).”
It is anticipated that the number of adults with congenital cardiovascular malformations will continue to
increase worldwide, as well as the complexity of this patient group.
CARDIAC EMBRYOLOGY AND DEFECTS RESULTING

FROM ABNORMAL CARDIAC DEVELOPMENT
Familiarity with cardiac embryology and normal development facilitates the understanding of abnormal
cardiovascular anatomy and resultant pathology in CHD. Thus, a brief review is relevant to the discussion
of these lesions that follows.
The earliest developmental stage of the heart and vascular system is seen following the second week
of gestation. By the middle of the third week clusters of angiogenic cells develop and give rise to vascular
structures in the human embryo. Over time, these cells form two endothelial tubes that fuse to form a
single heart tube. This eventually differentiates into components that include the sinus venosus, atrium,
primitive ventricle, and bulbus cordis (Fig. 19.1A).
Initially a short and straight structure (single midline heart tube) undergoes a process of coordinated
rapid growth within the pericardial sac resulting in bending, rotation, and torsion, otherwise known as
looping. This leads to migration of the atria in a cephalad direction and orientation of the convex surface
of the heart to the right (Fig. 19.1B). The term “D-looping” is used to define this aspect of normal cardiac
development.
Following looping of the heart tube, the sinus venosus region undergoes many changes while developing
into the venous system of the heart. It begins as a paired structure and initially fuses to form a transverse
sinus with right and left “horns” (Fig. 19.2A). As development continues, the right horn enlarges due to
progressive shift of venous blood drainage to right-sided structures and the left horn becomes atretic.
Ultimately, the right sinus horn becomes incorporated into the right atrium (RA) as the vena cava and the
left sinus horn becomes the coronary sinus (Fig. 19.2B). The lack of regression of the left horn contributes
to the persistence of a left superior vena cava (L-SVC).
The primitive atrium is undivided and communicates with the primitive ventricle that connects to the
outlet bulbus cordis. Around the fourth week of human embryonic development, the process of cardiac
septation begins involving the atrium, ventricle, atrioventricular junction and valves, outflow tracts, and
semilunar valves. During atrial septation, the septum primum, formed by tissue ingrowth along the supe-
rior aspect of the primitive atria, extends inferiorly toward mesenchymal tissue swellings known as endo-
cardial cushions (future atrioventricular orifice) in a curtain-like fashion. Initially, the septum primum
leaves an inferior opening, the ostium primum, below its free edge. Subsequently, a second opening devel-
ops in the superior aspect of the septum primum referred to as ostium secundum. This provides for flow
of highly saturated placental blood across the interatrial septum during fetal life, from the RA to the left
atrium (LA). The septum primum then extends inferiorly, becoming continuous with developing endo-
cardial cushions of the atrioventricular junction and obliterates the ostium primum (Fig. 19.3A). Around
the fifth to sixth week of gestation, a second partition, the septum secundum, develops parallel and to the
right of the septum primum and similarly extends inferiorly (Fig. 19.3B). The septum secundum covers the
ostium secundum but forms an incomplete atrial partition. The formation of this incomplete atrial parti-
tion again ensures blood flow across the interatrial septum during fetal life. The remaining opening of the
septum secundum is the foramen ovale (Fig. 19.3C). Tissue from the septum primum overlies the foramen
ovale and forms a flap that closes when the left atrial pressure increases normally at birth. A patent foramen
ovale (PFO) does not represent a defect of atrial septal tissue as such but rather an incompetent flap valve
of the fossa, occurring in an estimated 25% of adults. The presence of a PFO has been implicated in the
etiology of migraines and strokes. ASDs can be the result of excessive resorption of septal tissue leading to
deficient septum primum (secundum defects), lack of fusion of the septum primum with absent endocar-
dial cushion (primum defects), or abnormal development of the sinus venosus portion of the atrial septum
(sinus venosus defects).

19. Transesophageal Echocardiography for Congenital Heart Disease in the Adult 381
Bulbus cordis
Primitive
ventricle
Atrium
Sinus venosus
Outflow tract
Primitive Primitive
right left atrium
atrium
Primitive
right
ventricle
Primitive
left ventricle
B
FIGURE 19.1 Heart tube. A: Left panel: The figure illustrates in graphical form the various components of the single
heart tube that include the sinus venosus, atrium, primitive ventricle, and bulbus cordis regions. Right panel: The early
stages of bending or looping of the heart tube within the pericardial sac are shown. The arrows note the usual direction
of looping. B: Graphic representation following completion of looping of the heart tube. Note the cephalad migration of
the atria, unseptated common outflow tract, and orientation of the convex surface of the heart toward the right.

Left
sinus horn Right
sinus horn
Transverse
sinus
Left
ventricle Right
ventricle
Aortic arch
Superior
Left vena cava
pulmonary
artery
Right
pulmonary artery
Left Right
pulmonary pulmonary
veins veins
Inferior
vena cava
Coronary
sinus
FIGURE 19.2 Development of systemic veins. A: Posterior view of the primitive heart depicting the prominent right
and left sinus horns and the transverse sinus. B: Posterior view of the developed heart. Note the coronary sinus, a rem-
nant of the left sinus horn. The enlarged right sinus horn is now incorporated into the right atrium as the superior and
inferior vena cavae.

Septum primum
Perforations in upper
Left atrium
Sinus septum primum
venosus Right
atrium
Right
atrium Septum primum
Ostium
primum
Ostium secundum
Ostium Endocardial cushion
primum
Ostium secundum
Septum
secundum
Septum primum
Primitive ventricle
B
Septum secundum
Septum secundum
Foramen ovale
Tissue from
septum primum
Primitive
right ventricle
C Foramen ovale
FIGURE 19.3 Stages of atrial septation. A: As the septum primum grows inferiorly toward the endocardial cushions, the
ostium secundum, labeled as perforations in upper septum primum, forms in the posterior portion of the septum pri-
mum. Once the ostium secundum is formed it ensures the flow of blood across the atrial septum. Thereafter, the septum
primum completes its growth and becomes continuous with the developing endocardial cushions of the atrioventricular
junction (see arrows). B: The septum secundum develops parallel and to the right of the septum primum. It forms an
incomplete partition. C: The remaining opening in the septum secundum is known as the foramen ovale. It is covered by
a flap valve formed from tissue from the septum primum. Normally this flap valve closes when pressure in the left atrium
increases, exceeding right atrial pressure, following birth.
Septation of the atrioventricular canal begins as the endocardial cushions enlarge and fuse. This occurs
concurrently with completion of the septum primum and expansion of the atrioventricular orifice. The
cushions, initially muscular in nature, perform a valve-like function and through a process of cellular dif-
ferentiation they become thin and membranous resulting in the formation of separate right and left atrio-
ventricular valves. Altered development during this process is thought to lead to persistence of a common
atrioventricular junction and contribute to atrioventricular valve abnormalities. Failure of normal fusion of
the endocardial cushions results in canal-type defects.

Right superior
conus swelling Left inferior
truncus swelling
Left ventral
conus swelling
Right dorsal
conus swelling
Endocardial
cushions
Muscular
interventricular
septum
FIGURE 19.4 Ventricular septation. The muscular interventricular septum grows in a dorsal direction toward the endo-
cardial cushions. Subsequently, the membranous interventricular septum occurs as an outgrowth of endocardial tissue
and portions derived from conus and truncal swellings.
Ventricular septation begins in the fifth week of gestation and is derived from a primordial muscular
interventricular septum, outgrowths of endocardial tissue, as well as tissue originating from conus and
truncal swellings (Fig. 19.4). Following fusion of these components, the ventricular septum is comprised
of a small membranous portion and a large muscular component that is divided into inlet, trabecular, and
outlet regions. Persistence of a small interventricular communication or incomplete formation of the sep-
tum can lead to VSDs.
The outflow tracts of the left ventricle (LV) and right ventricle (RV) are formed following septation or
partitioning of the bulbus cordis and single truncus arteriosus. This process includes the formation of bul-
bar and truncal ridges, spiraling, and resultant creation of a spiral aortopulmonary septum that separates
the future aorta (Ao) from the pulmonary artery (PA). The semilunar valves are derived from subendocar-
dial tissue swellings in the arterial trunks. Defects of conotruncal development, semilunar valve formation,
and aortopulmonary septation account for a large number of congenital defects (TOF, TGA, truncus arte-
riosus, and aortopulmonary window).
The coronary arteries appear relatively late during cardiac development. Subepicardial vascular net-
works during the fifth week of development are thought to give rise to the distal coronary vessels. The
origin of the proximal coronary vasculature is more controversial. The aortic sac, aortic arches, and dorsal
Ao contribute to the development of the mature aortic arch through an orchestrated series of events that if
altered can result in vascular anomalies.
CLASSIFICATION OF CONGENITAL HEART DISEASE

In view of the variable spectrum of pathology, several classification schemes have been proposed to facilitate
the understanding of CHD and the physiologic impact of these defects. Lesions can be characterized, among
many ways, according to severity of disease, presence or absence of cyanosis, or primary physiologic alteration.
Based on Severity of Disease

Defects have been stratified according to their severity or level of complexity into simple, moderate sever-
ity, or complex defects. This classification scheme has been utilized for recommendations regarding patient

care, anticipation of long-term problems, and expectation of potential outcomes. Intracardiac communica-
tions in their isolated forms represent in most cases simple defects. Complex pathology includes all forms
of cyanotic CHD, lesions associated with multiple concomitant defects, and malpositions of the heart/
viscera (heterotaxy syndromes).
Based on the Presence or Absence of Cyanosis

In this scheme, congenital cardiac malformations are divided into acyanotic or cyanotic lesions based on
whether the primary functional disorder results in cyanosis. Conditions associated with cyanosis are char-
acterized by restrictive pulmonary blood flow (in the presence of intracardiac shunting) or complete arte-
rial and venous admixture. Cyanosis is less likely to occur in individuals with pulmonary overcirculation
secondary to isolated intracardiac communications.
Based on Physiology of the Defect

The classification algorithm based on the physiologic spectrum of CHD comprises four major categories:
Shunts, obstructions to either pulmonary or systemic blood flow, regurgitant pathology, and mixed lesions.
Shunt lesions occur within the heart (intracardiac) or outside the heart (extracardiac). The direction and
magnitude of shunting depend on the size of the communication and the relative resistances of the pul-
monary and systemic circulations. Obstructive lesions can affect the inflow or outflow of blood and vary
widely in severity. Regurgitant disease is rarely found in isolation and is frequently secondary to the pri-
mary pathology. In mixed lesions, which account for a significant number of cyanotic heart defects, there
is mixing of the systemic and pulmonary venous returns.
SPECIFIC CONGENITAL HEART DEFECTS

The section that follows provides an overview of selected congenital heart defects. A brief discussion of
anatomy, pathophysiology, and management is presented followed by the detailed TEE evaluation of each
anomaly. This information is summarized in Tables 19.1 and 19.2.
ATRIAL SEPTAL DEFECT
Anatomy
The term ASD is used to refer to lesions that result in atrial level shunting. This may not necessarily imply
a deficiency of the atrial septum itself. Four main types include ostium secundum, ostium primum, sinus
venosus, and coronary sinus defects (Fig. 19.5). ASDs account for approximately 30% of all cases of CHD
detected in adults and in general are more common in females.
Ostium secundum defects are commonly located in the central portion of the interatrial septum in the
region of the fossa ovalis accounting for 70% of all atrial communications (Fig. 19.6, Video 19.1). Associated Video 19.1
abnormalities include mitral valve prolapse and mitral regurgitation.
Ostium primum defects (also known as partial AVSDs) are located in the inferior aspect of the inter-
atrial septum (Fig. 19.7, Video 19.2). They account for approximately 20% of ASDs and are associated with Video 19.2
a cleft in the anterior mitral leaflet and mitral regurgitation. This defect is considered within the spectrum
of AVSDs and may be seen in patients with Down syndrome, although the complete form of the defect is
more frequently the case.
Sinus venosus defects occur posteriorly adjacent to the entrance of the superior vena cava (SVC) or infe-
rior vena cava (IVC) into the RA (Fig. 19.8, Video 19.3). The superior defect is the most common type. They Video 19.3
account for 5% to 10% of ASDs. In this lesion, straddling of the caval vein over the atrial septum is com-
monly seen. These defects are often associated with partial anomalous pulmonary venous drainage from
the right lung due to deficiency of the wall that normally separates the veins and LA leading to pulmonary
vein unroofing.

386
TABLE 19.1 Congenital Heart Disease in the Adult: Physiology, Prevalence, Associated Lesions, Treatment, and Prognosis
Cardiac
pathology Physiology Epidemiology/prevalence Associated lesions Treatment/prognosis
Aortic stenosis t Obstruction to systemic blood flow t Bicuspid AV: Most common t VSD t For severe disease, surgical and
t Increased LV afterload congenital anomaly (2% of the t PDA transcatheter approaches available
t LVH and decreased diastolic population) and most common t Ascending aortopathy t Valvuloplasty high incidence of
compliance cause of AS in <65 y reintervention (>25% in the adult)
t Myocardial supply–demand
mismatch (possible ischemia)
Atrial septal t Left-to-right shunt t 30% of ACHD t Secundum: MV prolapse and/or t Surgical closure
defect t Right-sided volume load t PFO present in 25% of adults regurgitation t Secundum ASD may be amenable
t Late symptoms (CHF, atrial t Primum: Cleft MV ± regurgitation to device closure
arrhythmias, and rare PHTN) t Treated10-y survival 95%
Coarctation of t Obstruction to systemic blood t 5–8% of ACHD t Bicuspid AV t Surgical versus balloon dilation ±
the aorta flow t VSD stent placement
t Proximal hypertension t Mitral valve anomalies t If untreated, mortality 80% at 50 y
t Increased LV afterload t Left-sided obstructive lesions
t LVH and decreased diastolic
compliance
t Collateral circulation
Congenital t Potential coronary ischemia t Less than 1% t Isolated lesion t Coronary reimplantation and/or
coronary during exertion t Also seen in CHD (D-TGA, TOF, and unroofing
artery t CHF if large fistula other complex pathologies) t If occlusion of fistula indicated,
anomalies transcatheter and/or surgical

intervention
t No long-term follow-up reported
Congenitally t Asymptomatic or symptoms t Rare lesion in the adult patient t VSD t May require interventions
corrected related to intracardiac shunting or (accounts for ∼0.5% of all CHD) t Pulmonary outflow obstruction such as closure of intracardiac
transposition outflow obstruction t TV anomalies (Ebstein-like) communication, relief of
t Presence or absence of cyanosis t Atrioventricular block outflow obstruction, TV repair or
dependent on associated replacement, pacemaker insertion
pathology t Heart transplantation (RV or
t Adult symptoms: TR, RV failure, systemic ventricular failure)
and CHB t 15-y survival ∼60%
D-transposition t Parallel circulation requiring t Most common form of cyanotic CHD t VSD (20%) t Postatrial baffle repair (Mustard or
intercirculatory mixing (PFO, presenting in the neonatal period t LVOT obstruction Senning) may require interventions
ASD, VSD, or PDA) t High mortality if untreated early t Coronary artery anomalies for baffle leak/obstruction, TR,
t Cyanotic lesion in life atrial arrhythmias, or RV (systemic)
t Most adults have undergone a failure
surgical intervention t Post-ASO infrequent need for
reintervention
t 20-y survival after atrial switch
procedure ∼70%
Ebstein t Wide spectrum of disease t Occurs in 0.5% of all patients t PFO t Tricuspid valve repair/replacement
anomaly t Can be asymptomatic with CHD t ASD t ASD closure
t TR (variable severity) t 10-y survival ∼84%
t Right heart failure
t Atrial arrhythmias
t If associated PFO/ASD could
develop cyanosis
Patent ductus t Left-to-right shunt t 8% of ACHD t Isolated or in the context of t Surgical (open vs. VATS)
arteriosus t Left-sided volume load complex CHD t Percutaneous closure
t Symptoms and PHTN depends t Bicuspid AV t Treated 10-y survival ∼95%
on the size of the PDA
Pulmonary t Obstruction to pulmonary blood t 10% of ACHD t PFO t Balloon valvuloplasty
(pulmonic) flow t Most operated disease is mild t ASD (20%) t Surgical valvotomy is highly
stenosis t Increased RV afterload t VSD effective
t RVH with decreased diastolic t Obstructive subpulmonic t Treated 25-y survival ∼95%
compliance hypertrophy
t Acyanosis unless severe and
associated ASD/VSD
t If severe, may result in CHF

Single ventricle t Passive pulmonary circulation t Group includes a number of t Depends on the anatomy t Some patients require Fontan
t Single systemic ventricle (left or different pathologies revision (intracardiac to
right) t Survival beyond childhood extracardiac)
t Acyanosis after Fontan palliation requires intervention t Maze for arrhythmias/pacemaker
unless fenestrated for atrioventricular synchrony and
antiarrhythmia therapy
t Heart transplant
t Fontan revision inhospital
mortality ∼11%
(continued)
387
388
TABLE 19.1 Congenital Heart Disease in the Adult: Physiology, Prevalence, Associated Lesions, Treatment, and Prognosis (continued)
Cardiac
pathology Physiology Epidemiology/prevalence Associated lesions Treatment/prognosis
Tetralogy of t Obstructive lesion to RV outflow t Most common form of cyanotic t Right aortic arch (25%) t Long-term issues: Pulmonary
Fallot t Intracardiac shunting (left-to-right, congenital heart disease t PFO or ASD (Pentalogy of Fallot) regurgitation, RVOT problems,
right-to-left, and/or bidirectional) t Most surviving adults with prior t Coronary anomalies residual shunts
t Both above account for cyanosis palliative or definitive repair t Persistent L-SVC to coronary sinus t Interventions in the adult (e.g., RV-
t Increased RV afterload t Discontinuous PA to-PA conduit changes, pulmonary
t RVH decreased diastolic valve replacement)
compliance t Treated 30-y survival ∼86–90%
t Cyanotic spells associated with
infundibular spasm
Ventricular t Left-to-right shunt t Most common form of CHD in t Bicuspid AV t Surgical closure
septal defect t Left-sided volume load children t Coarctation of Ao t Muscular VSD may be amenable
t Early congestive symptoms and t High incidence of spontaneous t Occasionally RVOT obstruction to device closure
PHTN if defect large closure in childhood (double-chambered RV) t Residual defects associated with
t Isolated VSD rare in the adult complex CHD
(10–15% of ACHD) t Treated 10-y survival, no PHTN—
t Untreated defects in adults almost 96%
always small in size
ACHD, adult congenital heart disease; Ao, aorta; AS, aortic stenosis; ASD, atrial septal defect; ASO, arterial switch operation; AV, aortic valve; CHB, complete heart block; CHD, congenital heart

disease; CHF, congestive heart failure; D-TGA, d-transposition of the great arteries; L-SVC, left superior vena cava; LV, left ventricle; LVH, left ventricular hypertrophy; LVOT, left ventricular
outflow tract; MV, mitral valve; PA, pulmonary artery; PDA, patent ductus arteriosus; PFO, patent foramen ovale; PHTN, pulmonary hypertension; RV, right ventricle; RVH, right ventricular
hypertrophy; RVOT, right ventricular outflow tract; TOF, tetralogy of Fallot; TR, tricuspid regurgitation; TV, tricuspid valve; VATS, video assisted thoracoscopic surgery; VSD, ventricular septal
defect.
TABLE 19.2 Transesophageal Echocardiography in Congenital Heart Disease
Lesion TEE planes and information provided Postsurgical evaluation

Aortic stenosis ME AV SAX: AV morphology, valve motion Residual/recurrent obstruction, aortic
ME AV LAX and deep TG LAX: Valve morphology regurgitation, bioprosthetic/mechanical
and motion, valvar regurgitation, aortic root valve function, perivalvar leak (if prosthetic
size, subaortic and supra-aortic anatomy valve), ventricular function
TG LAX and deep TG LAX: Peak gradient across After Ross procedure: Neoaortic valve
obstruction obstruction/regurgitation, function of right
ME 4 CH: LV hypertrophy and function ventricular homograft, ventricular function
(global and segmental)
Atrial septal defect ME 4 CH: Secundum and primum defects, Residual shunts, ventricular function
pulmonary venous return, mitral valve Mitral regurgitation
anatomy (prolapse) Obstruction of pulmonary veins (sinus
ME bicaval: Sinus venosus defect and venosus ASD)
pulmonary veins
Coarctation of the UE Ao Arch SAX, ME Desc Ao SAX and LAX Residual gradient, recoarctation, aortic
aorta views (if visible): Posterior shelf, aliased flow aneurysm formation
by color Doppler and CW Doppler peak
velocity of >2.5 m/s
ME 4 CH, 2 CH, AV LAX and TG SAX: LV wall
thickness and function, mitral valve
morphology and function, aortic valve,
subvalvar and supravalvar obstruction
Congenital ME AV SAX and LAX views in diastole Assess repair (identify new coronary origin,
coronary artery unroofing, pathway from aorta to coronary
anomalies arteries)
Document flow in the vessels by color Doppler
Ventricular function—global and segmental
Congenitally ME 4 CH, 2 CH, TG mid-SAX: Ventricular Following double switch operation
corrected morphology and function, tricuspid valve Atrial baffle portion: Baffle leaks, obstruction
transposition function and associated lesions of venous pathways, AVV competence,
ME LAX: outflow obstruction function of systemic ventricle
Arterial switch portion: Outflow obstruction,
semilunar valve regurgitation
Residual intracardiac shunts
D-transposition ME 4 CH: AVV regurgitation, associated After Senning/Mustard procedure: Baffle
intracardiac shunts, ventricular function leaks, obstruction of venous pathways,
ME bicaval: Systemic and pulmonary venous function of systemic (right) ventricle, AVV
baffles competence
TG mid-SAX: Ventricular function and SWMA After arterial switch operation: Supravalvar
Deep TG LAX: Ventriculoarterial connections (aortic/pulmonary) stenosis or
and arterial anastomoses after arterial switch regurgitation, LV function, residual shunts
Ebstein anomaly ME 4 CH and the RV in-out: Evaluation of Residual TV insufficiency
tricuspid valve (apical displacement and RV size and function
leaflet anatomy/mobility)
Patent ductus May be difficult to visualize by TEE; however, Residual shunt, biventricular function
arteriosus ductal flow can be detected in the ME Asc
Ao SAX or RV in-out views by presence of
abnormal continuous flow into the PA
Pulmonary ME RV in-out and modified deep TG LAX: Residual pulmonary outflow tract
(pulmonic) Outflow tract evaluation and gradient obstruction, pulmonary regurgitation,
stenosis estimation RV size and function
ME Asc Ao SAX: Evaluation of pulmonic valve,
main pulmonary artery, and proximal
pulmonary artery branches
(continued)

TABLE 19.2 Transesophageal Echocardiography in Congenital Heart Disease (continued)
Lesion TEE planes and information provided Postsurgical evaluation

Single ventricle ME 4 CH, 2 CH, LAX, bicaval, RV in-out: AV Post Fontan: Cavopulmonary connection,
valve morphology and atrioventricular and Fontan baffle (patency/leak), aortic
ventriculoarterial connections regurgitation, systemic outflow tract
obstruction, AVV competence, ventricular
function, adequacy of ASD
Tetralogy of Fallot ME AV LAX and deep TG LAX: VSD and aortic Residual RVOT obstruction, pulmonic
override or conduit stenosis, residual shunts,
ME RV in-out: Evaluation of RVOT and ventricular function, aortic regurgitation
estimation of gradient
ME 4 CH: Location and extension of VSD and
other additional VSDs
Color Doppler in ME AV SAX and AV LAX:
Evaluation of coronary artery anomalies
Ventricular septal ME 4 CH and AV LAX: Perimembranous, inlet Residual shunts, AVV and semilunar valve
defect and muscular VSDs, chamber sizes, presence competence and ventricular function
of ventricular septal aneurysm
ME AV LAX and deep TG LAX: Evaluation of
aortic valve for regurgitation and herniation
Ao, aorta; Asc Ao, ascending aorta; ASD, atrial septal defect; AV, aortic valve; AVV, atrioventricular valve; CH, chamber; CW,
continuous wave; Desc Ao, descending aorta; in-out, inflow-outflow; LAX, long-axis; LV, left ventricle; ME, midesophageal;
PA, pulmonary artery; RV, right ventricle; RVOT, right ventricular outflow tract; SAX, short-axis; SWMA, segmental wall motion
abnormalities; TEE, Transesophageal echocardiography; TG, transgastric; TV, tricuspid valve; UE, upper esophageal; VSD,
ventricular septal defect.
Modified from: Russell IA, Rouine-Rapp K, Stratmann G, et al. Congenital heart disease in the adult: A review with internet-
accessible transesophageal echocardiographic images. Anesth Analg. 2006;102(3):694–723, with permission.
SVC
Ostium primum
Sinus
venosus
RA
Ostium
secundum
RV
Sinus
venosus
Coronary sinus
IVC
FIGURE 19.5 Atrial septal defects. The graphic representation depicts the typical location of the various interatrial
communications as follows: Centrally located ostium secundum defect, inferiorly located ostium primum defect, sinus
venosus defect near either the superior vena cava (SVC) or inferior vena cava (IVC) entrance and frequently associated
with anomalous pulmonary venous drainage (arrow), and coronary sinus defect. RA, right atrium; RV, right ventricle.
(From Perloff JK. The Clinical Recognition of Congenital Heart Disease. 4th ed. Philadelphia, PA: WB Saunders; 1994:293–
380, reproduced with permission.)

FIGURE 19.6 Secundum atrial septal defect. Left panel: Midesophageal four-chamber view depicting a moderate size
central defect in the atrial septum (arrow), typical of a secundum atrial septal defect. Right panel: Corresponding color
Doppler interrogation demonstrating left-to-right atrial level shunting (blue flow) across the defect. LA, left atrium; LV, left
ventricle; RA, right atrium; RV, right ventricle.
FIGURE 19.7 Primum atrial septal defect. Left panel: Midesophageal four-chamber view depicting a relatively small
defect in the inferior aspect of the atrial septum (arrow), location characteristic of a primum atrial septal defect. Right
panel: Corresponding color Doppler interrogation demonstrating left-to-right atrial level shunting across the defect.
An aneurysm, also known as a tricuspid pouch, is seen billowing into the right ventricle (RV) representing remnants of
endocardial cushion tissue. LA, left atrium; LV, left ventricle; RA, right atrium.
FIGURE 19.8 Sinus venosus atrial septal defect. Left panel: Midesophageal bicaval view depicting a communication
in the interatrial septum near the entrance of the superior vena cava (arrow). The findings are typical of a superior vena
cava-type sinus venosus atrial septal defect. Right panel: Corresponding color flow mapping demonstrating left-to-
right atrial level shunting across the communication. The superior vena cava frequently overrides this type of defect,
frequently associated with anomalous pulmonary venous drainage. LA, left atrium; RA, right atrium.

FIGURE 19.9 Atrial septal defect occluder device. Midesophageal aortic valve short-axis view with rightward trans-
ducer rotation demonstrating an atrial septal defect closure device straddling the interatrial septum. AO, aorta; LA, left
atrium; RA, right atrium; RV, right ventricle.
Coronary sinus defects result from a communication between the LA and the coronary sinus (coronary
sinus septum). These defects are relatively rare (less than 2% of ASDs) and frequently occur in association
with other malformations. They are typically seen within the context of a persistent L-SVC draining to an
unroofed coronary sinus. The orifice of the coronary sinus in this setting is usually large.
Pathophysiology
The physiologic consequence of an ASD is determined by the degree of shunting (predominant direction
is usually left to right). The defect size, ventricular compliances, and PA pressures determine the mag-
nitude of the shunt. A large defect leading to pulmonary overcirculation results in right-sided diastolic
volume overload manifested as RA, RV, and PA dilation. Over time, atrial arrhythmias and heart failure
can develop. Mild-to-moderate elevations of PA pressure can be seen in older patients; however, severe
pulmonary hypertension rarely occurs. Adults may remain asymptomatic and an ASD may represent an
incidental finding on echocardiography.
Management
Most patients with large defects undergo surgical closure. Selected ostium secundum defects may be ame-
Video 19.4 nable to percutaneous closure in the cardiac catheterization laboratory (Fig. 19.9, Video 19.4). Suitability
for transcatheter device occlusion of secundum ASDs includes size of the defect (<38 mm) and the pres-
ence of adequate rims of surrounding atrial septal tissue. Transcatheter device closure can also be consid-
ered in patients with a PFO and a history of cerebrovascular events in order to limit the risk of paradoxical
emboli. Device closure of other types of interatrial communications is not feasible due to the presence of
critically important structures surrounding the defects that may be compromised by the occluder.
Transesophageal Echocardiographic Evaluation

Suggested cross sections for a focused examination include midesophageal (ME) four-chamber (4 CH), ME
bicaval, and ME AV short-axis (SAX).
Goals of the two-dimensional examination are the following:
t Definition of defect location and size (detection of a PFO or small interatrial communication may require
the intravenous injection of agitated saline or other contrast material and a Valsalva maneuver to identify
right-to-left shunting)
t Determination of defect rims (5 mm ideally):
o Anterosuperior (aortic rim): ME AV SAX view, distance between aortic ring and defect (lack of rim
does not preclude device deployment)

o Posterior: ME 4 CH view, gap between coronary sinus and defect

o Inferoanterior: ME 4 CH, space between the defect and atrioventricular valves
o Superior-posterior: ME bicaval view, distance between the SVC and defect
o Inferoposterior: ME bicaval view, gap between the IVC and defect
t Assessment of mitral valve anatomy (evaluate for prolapse/cleft: Prolapse may occur in association with
secundum ASDs; a cleft in the anterior leaflet is commonly seen in partial AVSDs)
t Evaluation of pulmonary venous drainage (all cases, but particularly, sinus venosus ASDs)
t Examination of right-sided structures for dilation and motion of interventricular septum (flattened or
paradoxical motion related to volume load)
t Evaluation of RV wall thickness, suggestive of pulmonary hypertension
t Assessment of ventricular function
Goals of the Doppler examination are the following:
t Assessment of flow across defect: Nature, direction, and velocity
t Detection of tricuspid, mitral, and pulmonary valve (PV) regurgitation
t Measurement of tricuspid regurgitant jet velocity (V TR) for estimation of PA systolic pressure as follows:
RV systolic pressure = 4(V TR)2 + RA pressure
In the absence of RV outflow obstruction:
PA systolic pressure = RV systolic pressure
t Interrogate pulmonary venous flows
t Estimation of shunt magnitude (pulmonary and systemic blood flows) in the absence of significant
atrioventricular valve regurgitation
Goals of the examination during transcatheter device closure are the following:
t Determination of tissue rims (lack of inferior or posterior rim unfavorable)
t Assessment of relation of defect to surrounding anatomic structures
t Measurement of maximal defect diameter (balloon stretch sizing)
t Detection of leaks around the balloon
t Guidance for device deployment/device stability
t Assessment of residual shunting
FIGURE 19.10 Three-dimensional transesophageal echocardiographic image of atrial septal defect occluder device.
The image displays the right atrial disc and the delivery cable prior to release of the closure device.

Goals of the examination after surgical repair/catheter intervention are the following:
t Detection of residual interatrial shunting
t Evaluation of atrioventricular valve competence
t Evaluation of proper positioning of device during transcatheter closure (unobstructed flow in systemic
and adjacent pulmonary veins following device deployment)
t Exclusion of complications related to the intervention (for device: Embolization, erosion)
Applications of 3D imaging are the following:
t Enhances spatial details of the defect (size, location, rims, relationships between defect/device, and
adjacent anatomic structures)
t Facilitates continuous visualization of the 3D relations while monitoring ASD device deployment
Video 19.5 (Fig. 19.10, Video 19.5)
t Evaluates for appropriate ASD device position and entrapment of septal rims around the occluder
t Allows for acquisition of ventricular volumes, ejection fraction
VENTRICULAR SEPTAL DEFECT
Anatomy
VSDs are classified by location into four major groups: Perimembranous, muscular, doubly committed
outlet and inlet defects (Fig. 19.11). They can occur in isolation or as part of complex malformations. An
Doubly committed
outlet (subarterial)
Cusp of the
aortic valve
Perimembranous
Muscular
Inlet
FIGURE 19.11 Ventricular septal defects. Graphic rendering of interventricular septum as seen from the right ven-
tricular aspect. Ventricular septal defects are classified by location into four major groups: Perimembranous, mus-
cular, doubly committed (subarterial), and inlet defects. Muscular defects can occur anywhere in the trabecular or
inlet portion of the interventricular septum. In this figure, a portion of the aortic valve can be visualized through the
perimembranous defect.

FIGURE 19.12 Perimembranous ventricular septal defect. Left: Midesophageal four-chamber view depicting a large
defect in the membranous region partially covered by aneurysmal tissue (arrow). Right: Corresponding color Doppler
flow mapping demonstrating a significant amount of ventricular level left-to-right shunting across the defect. LA, left
atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.
isolated VSD is the most common congenital cardiac pathology diagnosed in infancy. Since 60% of smaller
defects close spontaneously and larger defects are usually repaired in childhood, VSDs account for only
10% to 15% of defects observed in adults with CHD.
Perimembranous defects account for approximately 70% of VSDs, involve most or all of the membranous
septum, and may extend into the muscular region. Associated findings can include an aneurysm of the mem-
branous septum that is composed of tricuspid valve tissue. On echocardiography this appears as a tissue
pouch and often limits shunting across the defect (Fig. 19.12, Video 19.6). Other pathology may consist of a Video 19.6
subaortic membrane or AV cusp herniation/prolapse (resulting in aortic regurgitation). A perimembranous
VSD may also be seen in the presence of obstruction within the RV cavity related to muscular band hyper-
trophy that divides the RV into two chambers (double-chambered right ventricle or DCRV).
Muscular defects are defined by their location in the muscular portion of the ventricular septum. They
account for 20% of VSDs, can be isolated or multiple (“Swiss cheese”-type) and are often located in the
central or apical portion of the trabecular septum (Fig. 19.13, Video 19.7). Video 19.7
Doubly committed outlet defects (also known as supracristal, subarterial, subpulmonary, infundibular,
or conal VSDs) are located in the infundibular septum immediately below the PV. They account for 5% of
VSDs and are frequently associated with AV prolapse resulting in regurgitation (Fig. 19.14, Video 19.8). Video 19.8
Inlet defects account for approximately 5% of VSDs and are located in close proximity to the atrioventric-
ular valves in the posterior or inlet portion of the ventricular septum (Fig. 19.15, Video 19.9). These defects Video 19.9
predominate in patients with Down syndrome. An associated primum ASD within the context of a common
atrioventricular valve annulus is part of the defect known as a complete AVSD (canal defect or endocardial
cushion defect). As previously noted, these are also commonly seen in individuals with Down syndrome.
FIGURE 19.13 Muscular ventricular septal defects. Image displays two muscular ventricular septal defects (VSDs) as
demonstrated in a transgastric left ventricular short-axis cross section. Two defects are seen, a larger one in the midmus-
cular region and a second, smaller one at the apex. LV, left ventricle; RV, right ventricle.

FIGURE 19.14 Supracristal (conal, subarterial) ventricular septal defect. Left panel: Midesophageal aortic valve long-
axis view demonstrates prolapse of the aortic valve (right coronary cusp) through a subarterial ventricular septal defect
(arrow). Right panel: Systolic frame demonstrating shunting across the ventricular communication. Ao, aorta; LA, left
atrium; LV, left ventricle; RVOT, right ventricular outflow tract.
Pathophysiology
The physiologic consequences of a VSD are determined by the size of the defect and the pulmonary vas-
cular resistance. Moderate-to-large defects are associated with significant left-to-right shunting, left heart
dilation, and symptoms of heart failure. Pulmonary vascular changes can occur leading to severe pulmo-
nary hypertension in patients with large, long-standing VSDs and substantial pulmonary overcirculation.
This in turn can lead to reversal in the direction of the shunt through the defect (right-to-left shunting) and
resultant cyanosis. Increased pulmonary vascular resistance secondary to irreversible vascular changes
leads to a condition known as Eisenmenger syndrome. Affected adults have a decreased survival rate and
generally are not considered candidates for surgical repair.
Management
Most symptomatic patients require intervention. Surgical closure of an isolated VSD is most frequently
accomplished through a transatrial or transpulmonary approach. Thus, the location of the communication
has important implications for surgical access to the defect. In selected cases transcatheter device occlu-
sion may be an option. This has been more commonly applied to muscular communications due to the
distant anatomic relationship of this type of defect to the atrioventricular valves/outflow tracts (Fig. 19.16,
Video 19.10 Video 19.10). In addition, these types of defects (particularly if multiple) can present significant challenges
FIGURE 19.15 Inlet ventricular septal defect. Midesophageal four-chamber view depicting a large ventricular septal
defect (VSD) in the inlet portion of the ventricular septum (arrow). Note the fact that both atrioventricular valves appear
to be at the same level in contrast to the normal offset where the tricuspid valve has a more apical insertion into the
ventricular septum as compared to the mitral valve. This is a typical finding in this type of defect. LA, left atrium; LV, left
ventricle; RA, right atrium; RV, right ventricle.

FIGURE 19.16 Muscular ventricular septal defect occluder device. A ventricular septal defect (VSD) occluder device is
seen (arrow) in the midmuscular portion of the ventricular septum in this transgastric short-axis view. LV, left ventricle;
RV, right ventricle.
for surgical closure. A catheter-based intervention can be accomplished either percutaneously in the car-
diac catheterization laboratory or in the operating room using a perventricular hybrid approach. The latter
strategy uses a combination of surgical and interventional techniques. During a typical procedure, follow-
ing a sternotomy, the free wall of the RV is punctured with a needle, a wire is introduced and a sheath is
placed across the wire. TEE guides placement of the device across the defect. Surgery for associated pathol-
ogy can then be performed using conventional techniques.

Suggested cross sections for a focused examination include ME 4 CH, ME AV long-axis (LAX), ME right
ventricular inflow–outflow (ME RV in–out), and deep transgastric (TG) LAX.
Goals of two-dimensional examination are the following:
t Assessment of defect location, size, and extension
t Inspection for associated abnormalities, including septal aneurysm
t Evaluation of AV for deformity (herniation and prolapse)
t Examination of PAs and left-sided cardiac structures for dilation
t Inspection for findings suggestive of pulmonary hypertension (RV wall thickness and configuration of
interventricular septum during systole)
t Confirmation of the presence of the defect, evaluation for additional defects
t Determination of the nature, magnitude, and direction of shunt flow
t Detection of tricuspid and/or aortic regurgitation (color Doppler)
t Estimation of PA systolic pressure by:
o Tricuspid regurgitant jet peak velocity (VTR)
o VSD jet peak velocity (VVSD):
RV systolic pressure = Systolic blood pressure − 4(VVSD)2
In the absence of RV outflow obstruction:
RV systolic pressure = PA systolic pressure
In the absence of LV outflow obstruction:
Systemic systolic blood pressure = LV systolic pressure
t Determination of flow restriction across VSD (high-velocity VSD jet suggests restriction vs. low-velocity
flow of a nonrestrictive defect)
t Estimation of the magnitude of the shunt (pulmonary to systemic blood flow ratio) in the absence of
significant atrioventricular valve regurgitation

Goals of the examination during transcatheter device closure are the following:
t Determination of VSD anatomy, size, and relationship to ventricular inflows and outflows
t Evaluation of valvar competence
t Detection of leaks around the balloon, if balloon sizing is performed
t Early detection of complications related to device positioning
t Guidance and monitoring during device deployment
t Assessment of leaks across device
t Detection of residual shunts
t Determination of potential changes in valvar regurgitation
t For percutaneous intervention: Evaluation of device position in septum and relative to adjacent structures
PATENT DUCTUS ARTERIOSUS
Anatomy
During fetal life, the arterial duct connects the PA to the descending Ao (Fig. 19.17) near the level of the left
subclavian artery. This communication allows for RV output into the Ao bypassing the lungs under normal
fetal conditions of increased pulmonary vascular resistance. Failure of closure of this communication in the
neonatal period results in persistent ductal patency. This lesion accounts for approximately 8% of cases of
CHD. As in many other defects, a PDA can be found in isolation or associated with additional cardiac defects.
Right common
carotid artery
Right Left common
subclavian artery carotid artery
Left
Right subclavian artery
pulmonary artery
Ductus arteriosus
Left
pulmonary
artery
Main
pulmonary
artery
FIGURE 19.17 Patent ductus arteriosus. Diagram depicting the ductus arteriosus as it connects the junction of the
main and left pulmonary arteries to the descending aorta in the region adjacent to the origin of the left subclavian artery.

Pathophysiology
The physiologic consequences of a PDA are determined by the size of the communication and the rela-
tive systemic and pulmonary vascular resistances. Although a small PDA may have little or no physiologic
consequences, hemodynamically significant left-to-right shunting in larger communications leads to pul-
monary overcirculation, congestive symptoms, and if chronic, may result in increased pulmonary vascular
resistance. Most individuals with a large shunt become symptomatic requiring medical attention. A PDA in
the adult patient, albeit rarely, can be associated with complications such as endarteritis, aneurysm forma-
tion, dissection, and rupture. Occasionally, in the older patient, left-to-right shunting and LV volume load
are limited by an increased pulmonary vascular resistance, a finding associated with the development of
Eisenmenger syndrome.
Management
Small communications may be suitable for percutaneous device occlusion. Surgical ligation of a PDA in
the adult may be complicated by calcification of ductal tissue increasing the risks of the procedure and
potential need for cardiopulmonary or ventricular bypass. In the setting of pulmonary vascular obstructive
disease, interventions to obliterate the communication are contraindicated.

Examination of a PDA is enhanced by color Doppler information superimposed on the 2D-TEE image.
This assessment may require nonstandard views that allow for visualization of the site of ductal insertion
into the main PA or for detection of flow (Fig. 19.18, Video 19.11). Suggested cross sections for focused Video 19.11
examination include ME ascending aorta (Asc Ao) SAX, upper esophageal aortic arch (UE Ao Arch) SAX,
and ME descending aortic (Desc Ao) LAX views.
Goals of two-dimensional examination are the following:
t Identification of the communication
t Evaluation of associated cardiac malformations
t Examination of the size of the PAs/left-sided cardiac chambers (to assess for the magnitude of the volume
overload)
t Evaluate RV wall thickness (as an indicator of pulmonary hypertension)
t Assessment of biventricular function
t Detection of presence and magnitude of ductal shunting
t Characterization of flow direction and velocity (flow typically continuous in nature into the PA)
FIGURE 19.18 Patent ductus arteriosus. Midesophageal right ventricular inflow–outflow view depicting blue flow
away from the transducer from a patent ductus arteriosus (PDA). AO, aorta; LA, left atrium; MPA, main pulmonary artery;
RA, right atrium; RV, right ventricle.

t Detection of retrograde flow in the thoracic Ao from ductal runoff

t Examination of valvar regurgitation
t Estimation of systolic PA pressure by tricuspid regurgitant jet and PDA jet (peak systolic velocity of
jet2 = systolic pressure gradient between the Ao and PA)
t Detection of residual ductal shunting
t Verification of unobstructed flow in adjacent structures
COARCTATION OF THE AORTA
Anatomy
CoA in the adolescent and adult patient is characterized by narrowing of the thoracic Ao immediately
opposite to the site of insertion of the ligamentum arteriosum (juxtaductal) (Fig. 19.19). Typically, this is
the result of a discrete obstructing shelf that projects into the aortic lumen. In some cases, diffuse aortic
arch and isthmic hypoplasia may be seen complicating the primary pathology, which in fact is the most
common finding during infancy. Associated defects include a Bic AV in up to 50% of patients, PDA, VSD,
and subaortic membrane. CoA accounts for approximately 6% of all CHD, is more common in males, and
20% of cases are diagnosed in adolescents or adults.
Pathophysiology
The main physiologic consequence of CoA is increased LV afterload due to obstruction to blood flow.
The systolic arterial blood pressure is increased proximal to the CoA and decreased distally. This gradient
Right common
carotid artery
Right Left common
subclavian artery carotid artery
Left
subclavian artery
Transverse aorta Coarctation of the aorta
Descending aorta
Ligamentum
arteriosum
Ascending aorta
Main
pulmonary
artery
FIGURE 19.19 Coarctation of the aorta. Graphic representation depicting the aortic narrowing in coarctation.

whether minimal or significant, is exacerbated by exercise. Systemic hypertension occurs frequently and
may result in hypertensive heart disease. The development of collaterals may be seen. Most adults with
CoA are asymptomatic, although recurrent epistaxis, headaches, claudication, dizziness, and palpitations
may occur. Major complications include aortic dissection, rupture or endarteritis of the Ao, cerebral aneu-
rysms/hemorrhage, infective endocarditis, and LV failure.
Management
The severity of the obstruction dictates the need for intervention. Options include surgical management
and balloon dilation with or without stent placement.

The surgical approach in uncomplicated CoA is via a thoracotomy incision. In this setting there is a lim-
ited role for TEE. The indications for TEE in most patients with CoA involve the evaluation of associated
defects that require cardiopulmonary bypass. The anterior position of the air-filled trachea relative to the
esophagus limits the TEE examination of the distal ascending Ao and proximal aortic arch, thereby mak-
ing this a difficult lesion to examine by TEE in detailed fashion. This pathology is most reliably assessed
comprehensively by other imaging modalities such as transthoracic echocardiography, magnetic resonance
imaging, and computed tomography. Suggested cross sections for focused TEE examination include UE Ao
Arch SAX and LAX and ME Desc Ao SAX and LAX (Video 19.12). Video 19.12
t Limited evaluation of the aortic arch/Ao (narrowing of descending Ao distal to left subclavian artery)
t Monitoring of LV function during aortic clamp application
t Evaluation of associated defects
t Determination of LV function and wall thickness
t Detection of turbulent, eccentric jets or flow acceleration in the descending Ao
t Determination of flow pattern (increased systolic velocity at region of obstruction and continuous
diastolic forward flow)
t Assessment of velocities across the area of narrowing and distally (this is complicated by the limited
ability to align the Doppler beam to the direction of blood flow)
t Characterization of aortic pulsations distal to the obstruction (blunted pattern with decreased systolic
upstroke in the presence of obstruction)
t Identification of flow in collateral vessels (color Doppler)
t As required for the assessment of associated pathology
t Detection of residual obstruction (difficult to assess due to suboptimal Doppler alignment with the
direction of flow)
t Identification of complications related to the intervention
t Evaluation of coexisting defects
AORTIC VALVE STENOSIS
Anatomy
Although the isolated Bic AV usually does not require treatment in infancy or childhood, it is a well-known
cause of morbidity in the adult. This represents the most common malformation of the normally tricuspid
AV and frequently results from commissural fusion. A “raphe” or false commissure may be present and the
resultant two leaflets or cusps may be equal or markedly different in size resulting in an eccentric line of
closure (Fig. 19.20, Video 19.13). A Bic AV can be associated with valvar stenosis or regurgitation and in Video 19.13
some cases, aortic root dilation. AS accounts for 6% of all CHDs. Among patients with symptomatic AS
who are younger than 65 years of age, a Bic AV is the most common finding. The mechanism of the valve

FIGURE 19.20 Bicuspid aortic valve. Midesophageal aortic valve short-axis view of a bicuspid aortic valve demon-
strates the “fish-mouth” appearance of the restrictive opening during systole. Note that there is fusion of the valve leaflets
at the intercoronary commissure.
obstruction is frequently related to leaflet calcification. Aortic regurgitation in most cases is the result of
cusp prolapse or redundancy. Weakness in the media of the ascending and transverse Ao may predispose
to aneurysm formation. Other associated defects include VSD, PDA, and CoA.
Pathophysiology
A Bic AV can thicken, calcify, and display decreased mobility over time. As valve stenosis progresses, the
LV systolic pressure increases and the wall hypertrophies. As the area of the valve orifice becomes more
restrictive and the stenosis becomes critical, LV systolic function decreases and heart failure occurs. Aortic
regurgitation may be seen leading to a volume load on the LV and resulting in chamber dilation.
Management
A number of strategies have been applied to patients with AV stenosis. Therapies, when necessary, include
catheter interventions and surgery. Transcatheter procedures consist of balloon valvuloplasty and most
recently, transcatheter AV implantation (discussed elsewhere in this textbook) for patients with severe AS
who are not candidates for surgery. Surgical valvotomy/valvuloplasty or valve replacement with a biopros-
thesis, mechanical valve, or pulmonary autograft (Ross procedure) represent alternate options.

Methods to determine AV area and the severity of obstruction are addressed elsewhere in this textbook. It
should be mentioned that the use of planimetry by 2D imaging to estimate AV area is unreliable in patients
with a Bic AV. Suggested cross sections for focused TEE examination include ME AV SAX and LAX, ME
LAX, ME 4 CH, TG LAX, deep TG LAX.
Goals of two-dimensional evaluation are the following:
t Determination of AV morphology (cusps, commissures, fish-mouth appearance of a Bic AV) and systolic
motion (systolic doming)
t Measurement of annular size (important in valve replacement and Ross procedure where near matching
of annular sizes is optimal)
t Identification of dilation of the ascending Ao (poststenotic or otherwise)
t Detection of LV hypertrophy or dilation
t Assessment of global and segmental LV function
t Evaluation of aortic root and ascending Ao
t Identification of associated pathology


t Identification of turbulent flow across the AV and/or aortic regurgitation
t Estimation of the gradient across the AV (TG LAX view or the deep TG LAX view suitable for spectral
Doppler interrogation; mean gradients have a better correlation with catheter-derived gradients)
t Examination of results depending on the type of intervention (residual obstruction, aortic regurgitation,
autograft, and pulmonary homograft function in the Ross procedure)
t Evaluation of prosthetic valve function and exclusion of paravalvar leak(s) following valve replacement
PULMONARY VALVE PULMONIC STENOSIS
Anatomy
A doming PV without clear leaflet separation is the most common pathology that causes congenital valvar
PS. The orifice of the valve ranges from pinhole to several millimeters in diameter (Fig. 19.21). Less com-
monly (10% of patients), valvar dysplasia and thickening are present with redundant leaflets that display
reduced systolic excursion. Pulmonic stenosis can occur as an isolated lesion and accounts for approximately
10% of CHD in adults. Associated defects include ASD, VSD, and obstructive subpulmonic hypertrophy.
Pathophysiology
The physiologic consequence of valvar PS is elevation of RV systolic pressure and subsequent RV hypertro-
phy, proportional to the degree of obstruction. Most severity grading systems rely on Doppler-derived peak
Post-stenotic dilation
of the main
pulmonary artery
Domed-shaped
pulmonary valve
with a small oriface
Hypertrophy of the
right ventricular muscle
FIGURE 19.21 Pulmonary (pulmonic) stenosis. Graphic representation of pulmonic stenosis. Typically in this pathology
the valve is domed-shaped with a small orifice. There is hypertrophy of the right ventricle and poststenotic dilation of the
main pulmonary artery. Arrows represent the direction of blood flow across the right side of the heart.

instantaneous transvalvar gradients (mild <36 mm Hg; moderate 36 to 64 mm Hg; severe >64 mm Hg). Mild
valvar obstruction is usually not associated with symptoms. Moderate stenosis may result in dyspnea and
fatigue during exertion. Patients with severe PS can manifest RV dilation and failure, although up to 25%
may be symptom-free. Typically, PS does not progress over time and decisions for intervention are based
on a combination of symptoms and valvar gradient. Patients with valvar dysplasia are more likely to develop
symptoms of fatigue, dyspnea, and RV failure. Occasionally, exertional chest pain and syncope are seen.
Management
Most symptomatic adults are treated with transcatheter balloon valvuloplasty. Pulmonary regurgitation
can occur after balloon valvuloplasty, but overall, the long-term results are excellent. Adults with a dysplas-
tic PV may require surgery and in some cases, valve replacement. Obstructive subpulmonic hypertrophy, if
present, can regress after either intervention.

Important aspects of the examination include evaluation not only of the PV itself but also the immediate
subvalvar and supravalvar regions. Suggested cross sections for focused TEE examination include ME Asc
Ao SAX, ME RV in–out, and UE Ao Arch SAX. A view of the RV outflow tract can be obtained from the
deep TG window after rotating the imaging plane to 90 degrees from the deep TG LAX view. This modified
view provides complementary anatomic information and facilitates gradient measurements.
Goals of two-dimensional evaluation are the following:
t Determination of PV morphology (number of cusps, thickening) and motion (doming)
t Measurement of annular size
t Evaluation of the subvalvar region, main PA, and proximal branches (to image the right PA: From the ME
Asc Ao SAX view, the transducer is slightly withdrawn to the upper esophagus and rotated rightward; to
display the left PA: From the UE Ao Arch SAX view, the transducer is slightly advanced and rotated leftward)
t Identification of poststenotic dilation of the PA
t Assessment of the RV including systolic function, wall hypertrophy, and dilation (position of
interventricular septum provides crude estimation of RV pressures)
t Identification of associated pathology (e.g., atrial communication)
t Identification of turbulent flow across the PV and/or pulmonary regurgitation
t Estimation of gradient across the PV (peak and mean) using spectral Doppler in views that allow for
optimal alignment with the direction of flow
t Evaluation of subvalvar and supravalvar regions to assess for associated obstruction
t Identification of tricuspid regurgitation and peak velocity assessment for RV pressure estimation
t Examination/quantitation of residual pathology depending on the intervention (residual obstruction,
pulmonary regurgitation)
t If valve replacement or RV-to-PA conduit placed, evaluation of patency, valvar regurgitation, perivalvar
leak as appropriate depending on the intervention
TETRALOGY OF FALLOT
Anatomy
The classic constellations of defects in TOF include a large nonrestrictive VSD, RV obstruction, aortic over-
ride, and RV wall hypertrophy (Fig. 19.22). The RV outflow obstruction is at any level or at a combination
of multiple levels. It is well recognized that this anomaly encompasses a morphologic spectrum. The mal-
formation represents the most common cyanotic cardiac defect (accounting for 10% of all CHD) and is one
of the most prevalent lesions of moderate severity seen in adults. Associated defects include a PFO/ASD,
PDA, additional VSDs, vascular anomalies (aortic arch, coronary arteries, and systemic veins), aortic root

Muscle obstructing the

right ventricular
outflow tract Small
pulmonary
valve
Aorta above the

ventricular
Ventricular septal defect
septal defect
Hypertrophy
of the right
ventricular wall
FIGURE 19.22 Tetralogy of Fallot. Classic features of this lesion include a ventricular septal defect, right ventricular
outflow tract obstruction, right ventricular hypertrophy, and aortic override over the ventricular septal defect. The right
ventricular outflow tract obstruction frequently occurs at multiple levels.
dilation, as well as other pathologies. Variants of tetralogy display, in addition to the typical features of TOF,
other defects such as a complete AVSD in “tet-canal” patients. Pulmonary atresia with VSD is considered
to represent an extreme form of TOF.
Pathophysiology
The clinical manifestations in patients with TOF relate primarily to the severity of RV outflow obstruc-
tion. This, along with the magnitude of ventricular level right-to-left shunting, accounts for the degree of
cyanosis. Although in the vast majority this diagnosis is made in infancy and childhood, this pathology
may occasionally present in adulthood when the RV outflow obstruction is minimal to mild in severity. The
unrestrictive VSD and RV pressure at systemic levels result in RV hypertrophy.
Management
Most adults have undergone prior palliative or “corrective” procedures. Definitive surgery in TOF consists of
relief of the RV outflow obstruction and closure of the VSD. When the size of the pulmonary annulus is restric-
tive, the repair requires placement of a patch across this region (transannular patch). This disrupts PV integrity
and results in some degree of pulmonary regurgitation that is likely to increase over time. On occasion, place-
ment of a RV-to-PA extracardiac conduit is necessary to establish RV outflow tract continuity. Reintervention,
either surgical or in the catheterization laboratory, may be required for increasing pulmonary regurgitation,
residual or recurrent RV outflow tract obstruction, or residual VSD. In some cases, indications for reopera-
tion include severe aneurysmal dilation of the RV outflow/false aneurysm, significant aortic regurgitation, and
progressive root dilation. Recent advances now allow for percutaneous PV implantation in selected patients.

FIGURE 19.23 Tetralogy of Fallot. Midesophageal right ventricular inflow–outflow view displaying two of the features
of tetralogy of Fallot: A large ventricular septal defect (arrow) and anterior deviation of the conal septum (asterisk) result-
ing in narrowing across the right ventricular outflow tract (RVOT). AO, aorta; MPA, main pulmonary artery; VSD, ventricu-
lar septal defect.

The characteristic echocardiographic finding in TOF is that of anterior, superior, and leftward deviation
of the conal (infundibular or outlet) septum. This is optimally seen in the ME LAX, ME RV in–out, and
Video 19.14 modified deep TG LAX view described previously that displays the RV outflow (Fig. 19.23, Video 19.14).
The ventricular communication is usually a large subaortic defect best demonstrated in the ME AV SAX
and LAX, and ME 4 CH views. Additional communications at the atrial and ventricular levels should be
explored. Aortic override is best appreciated in the ME LAX, ME AV LAX, TG LAX, and deep TG LAX
Video 19.15 views (Fig. 19.24, Video 19.15). Evaluation of the RV outflow and PAs requires a combination of scanning
planes that define the subvalvalvar, valvar, and supravalvar regions. TEE interrogation of the distal pulmo-
nary bed and aortopulmonary collaterals, if suspected or present, is suboptimal at best because of limited
views of these structures. Suggested cross sections for focused TEE examination include ME 4 CH, ME
LAX, ME AV SAX and LAX, ME RV in–out, ME Asc Ao SAX, TG LAX, and deep TG views.
As mentioned, reoperation in the adult patient with TOF is frequently related to pulmonary regurgita-
Video 19.16 tion resulting in RV dilation and in some cases, RV dysfunction (Figs. 19.25 and 19.26, Videos 19.16 and
Video 19.17 19.17). This may also impair LV myocardial performance. Residual or recurrent obstruction at the level of
the pulmonary outflow tract, main PA/branches, or a residual intracardiac shunt may require reinterven-
Video 19.18 tion (Fig. 19.27, Video 19.18). The same TEE views previously suggested for the initial repair can also be
applied to this assessment.
FIGURE 19.24 Tetralogy of Fallot, aortic override. Midesophageal long-axis view displays aortic override over the ven-
tricular septal defect (VSD) in tetralogy. AO, aorta; LA, left atrium; LV, left ventricle; RV, right ventricle.

FIGURE 19.25 Tetralogy of Fallot, pulmonary regurgitation. Midesophageal aortic valve short-axis view depicts a dia-
stolic color Doppler jet of pulmonary regurgitation (blue signal) in a patient with a history of tetralogy repair. AO, aorta;
MPA, main pulmonary artery; RVOT, right ventricular outflow tract.
FIGURE 19.26 Tetralogy of Fallot, right ventricular dilation. Midesophageal four-chamber view demonstrating a
volume-loaded, dilated right ventricle (RV) in a patient post-tetralogy repair undergoing pulmonary valve replacement
for severe regurgitation. LA, left atrium; LV, left ventricle; RA, right atrium.
FIGURE 19.27 Tetralogy of Fallot, outflow obstruction, recurrent obstruction. Midesophageal right ventricular inflow–
outflow view displaying muscular right ventricular outflow tract obstruction in a patient with a history of tetralogy repair.
The bright area noted by the asterisk indicates the ventricular septal defect patch. AO, aorta; MPA, main pulmonary
artery; LA, left atrium; RA, right atrium; RV, right ventricle.


t Characterization of RV outflow tract obstruction (distinguish from double-chamberered RV, where
there is also a VSD; however, anomalous muscle bundles account for midcavitary obstruction and no
infundibular obstruction is present)
t Evaluation of PA annular dimensions, MPA, and branch PA sizes
t Definition of VSD (size and location)
t Evaluation of degree of aortic override, ventriculoarterial connection (distinguish from double-outlet
RV, where mitral–aortic fibrous continuity is lacking)
t Determination of aortic root dimension
t Exclusion/evaluation of associated pathology
t Confirmation of coronary artery anatomy
t Assessment of RV hypertrophy, biventricular function
t Characterization of flow across VSD (direction and velocity) and other intracardiac communications
t Definition of level/severity of the RV outflow obstruction
t Evaluation of AV competence
t Detection of tricuspid regurgitation and assessment of peak regurgitant velocity for RV systolic pressure
estimate
t Evaluation for residual pathology such as RV outflow obstruction and intracardiac shunts
t Assessment of tricuspid, pulmonary, and AV competence
t Evaluation of tricuspid regurgitation and peak regurgitant velocity for estimation of RV systolic pressure
t In the patient undergoing reintervention following TOF repair: Evaluation for pulmonary/conduit
obstruction and/or regurgitation, the presence of residual intracardiac shunts or other pathologies,
configuration of interventricular septum, tricuspid and AV competence, and biventricular size and
systolic function
TRANSPOSITION OF THE GREAT ARTERIES
Anatomy
Dextro-transposition of the great vessels (D-TGA) is characterized by concordance of the atrioventricular
connections and discordance of the ventriculoarterial connections. A morphologic RA is connected to a
morphologic RV; however, the RV ejects into the Ao. A morphologic LA drains into a morphologic LV that
gives rise to the PA (Fig. 19.28). The abnormal origin of the great arteries results in a parallel relation of
these structures rather than the normal crossover between the two. D-transposition accounts for 4% of all
cases of CHD. Associated pathology may include PDA, ASD, VSD, obstruction to pulmonary blood flow,
AV abnormalities, variation in the origin and course of the coronary arteries, and aortic arch anomalies.
Pathophysiology
In D-TGA, the systemic and pulmonary circulations function in parallel rather than in series, leading to
cyanosis in the neonatal period. Mixing of the parallel circuits at the atrial, ventricular, or great artery level
is essential for survival.
Management
The surgical management of this lesion has evolved dramatically over the years. In the past, most patients
underwent either palliation or an atrial baffle procedure (Mustard or Senning operation; Fig. 19.29, Video
Video 19.19 19.19). This is also referred to as an “atrial switch procedure.” This intervention consists of rerouting the
systemic venous blood through the mitral valve, LV, and PA, while the pulmonary venous return is diverted
across the tricuspid valve, RV, and Ao. This allows for separation of pulmonary and systemic circulations

Left atrium
Pulmonary
Superior
artery
vena cava
Aorta
Right atrium
Left
Right ventricle
ventricle
Inferior
vena cava
FIGURE 19.28 Transposition of the great arteries. The graphic representation depicts the anatomic features in
D-transposition of the great arteries. In this lesion the right atrium is connected to the right ventricle that gives rise to the
aorta. The left atrium is connected to the left ventricle that gives rise to the pulmonary artery. This relationship is defined
as atrioventricular concordance and ventriculoarterial discordance.
SVC
Pulmonary
veins
SVA
PVA
LV
RV
IVC
A B
FIGURE 19.29 Transposition of the great arteries, atrial redirection procedure. A: Midesophageal four-chamber view
illustrates the features of an atrial redirection procedure. In this procedure, venous returns from the systemic and pul-
monary circulations are redirected using a baffle. This results in drainage of deoxygenated blood from the superior and
inferior vena cavae into the systemic atrium (SVA), then through the mitral valve into the left ventricle (LV), being ejected
into the pulmonary artery. Oxygenated blood from the pulmonary veins drains into the pulmonary atrium (PVA), then
through the tricuspid valve into the right ventricle (RV), then into the aorta. The RV remains the systemic ventricle. B: This
sketch depicts the direction of blood flow following an atrial redirection procedure. The atrial baffle is noted in yellow.
SVC, superior vena cava; IVC, inferior vena cava.

Aorta Pulmonary artery
Ventricular
Right and left septal defect Translocated
coronary arteries coronary arteries
FIGURE 19.30 Transposition of the great arteries, arterial switch procedure. In this surgical procedure, the aorta and pul-
monary arteries are transected and anastomosed to their appropriate respective ventricular outflows. The coronary arteries
are translocated to the systemic outflow tract. In this diagrammatic representation a ventricular septal defect is depicted.
and physiologic correction, but maintains the RV as the systemic pump. Most adult patients are likely to have
undergone this type of repair. Long-term concerns following atrial switch procedures include function of the
systemic RV, tricuspid (systemic) valve competence, obstruction of venous pathways/baffle leaks, arrhyth-
mias, the late development of pulmonary vascular disease, and sudden cardiac death. Currently, the favored
approach for infants with D-TGA is anatomic correction or arterial switch surgery (Jatene procedure) (Fig.
19.30). This involves transection of the great arteries above the valve sinuses and anastomoses to their appro-
priate respective ventricular outflows, in addition to translocation of the coronary arteries to the systemic
outflow tract. At the time of this intervention additional defects are also addressed. Problems at follow-up
are primarily related to supravalvar or branch PA stenosis, neoaortic root dilation/regurgitation, and issues
related to the coronary arteries. Catheter-based interventions and/or reoperation may be required for pro-
gression of the primary pathology, recurrent disease, or sequelae associated with prior surgical procedures.

The echocardiographic evaluation should include 2D imaging, spectral Doppler examination, color-flow
mapping, and possibly contrast echocardiography. Suggested cross sections for focused TEE examination
include ME 4 CH, ME bicaval, ME LAX, TG mid-SAX, and deep TG LAX.
t Assessment of atrioventricular and ventriculoarterial connections
t Evaluation of associated pathology such as intracardiac communications and outflow tract obstruction
t Estimation of ventricular dimensions and systolic function
t Characterization of flow across intracardiac communications
t Assessment of outflow tract gradients
t Evaluation of valvar competence
t For atrial baffle (atrial switch procedures):
o Visualization of systemic and pulmonary venous pathways to assess for obstruction; the administra-
tion of contrast (agitated saline or albumin) through an arm vein facilitates this assessment (in the

absence of obstruction, contrast rapidly courses from the SVC into the systemic venous atrium and
no contrast is seen in the IVC aspect of the baffle; if severe obstruction of superior limb, contrast is
diverted through collaterals to the lower aspect of the systemic venous baffle)
o Monitoring during transcatheter balloon dilation and possible stenting of venous pathway obstruction
o Assessment of baffle leaks (administration of agitated saline solution through a peripheral or central
vein may assist in the identification of baffle leaks)
o Monitoring during transcatheter occlusion of baffle leaks
o Evaluation of systemic RV function and tricuspid valve (systemic atrioventricular valve) for regurgitation
t For arterial switch procedures:
o Evaluation of semilunar valves for regurgitation
o Evaluation of outflow tract obstruction/arterial root dimensions
o Assessment of residual shunts
o Assessment of global and segmental left ventricular function
CONGENITALLY CORRECTED TRANSPOSITION OF THE GREAT ARTERIES
Anatomy
Congenitally corrected transposition of the great arteries (CCTGA) is characterized by discordance
between the atrioventricular and ventriculoarterial connections (double discordance). The RA connects to
a morphologic LV that ejects into the PA, while the LA connects to a morphologic RV that ejects into the
Ao (Fig. 19.31). This defect is relatively rare, accounting for less than 0.5% of all forms of CHD. Corrected
Pulmonary
artery
Superior
vena cava
Right
atrium Left atrium
Aorta
Right
ventricle
Inferior
vena cava
Left ventricle
FIGURE 19.31 Congenitally corrected transposition. Diagrammatic representation of the abnormal connections of the
cardiac segments in this lesion. Note the “doubly discordant” atrioventricular and ventriculoarterial connections.

transposition is also referred to as levo-transposition of the great arteries (L-TGA) due to the abnormal
looping pattern of the heart tube during development (L-loop) in this lesion. This results in the Ao being
oriented to the left (levo) rather than to the right (D-loop) as is normally the case. This defect is frequently
associated with cardiac anomalies such as VSD, obstruction to pulmonary blood flow, and left atrioven-
tricular (tricuspid) valve abnormalities such as Ebstein-like malformation or dysplasia.
Pathophysiology
In this lesion, the systemic venous return enters the PA being ejected by a morphologic LV; the pulmonary
venous blood exits into the Ao as ejected by a morphologic RV. The serial arrangement of the systemic
and pulmonary circulations results in normal physiology—hence the term “corrected.” Cyanosis occurs in
nearly half of the patients with CCTGA because of associated lesions. However, in the absence of concomi-
tant pathology, a small number of individuals can have relatively normal lives and even survive into the
seventh and eighth decades. Unfortunately, in the majority, progressive systolic impairment of the systemic
RV ensues, frequently associated with concomitant systemic (tricuspid) atrioventricular valve regurgita-
tion, overt heart failure, and/or conduction defects prompting medical care.
Management
Most patients require surgery to address associated defects. Interventions include closure of intracardiac
communications, relief of pulmonary outflow tract obstruction, and tricuspid valve repair/replacement
(so-called “classic repairs”). In view of late problems that usually include ventricular dysfunction and tricus-
pid regurgitation, in addition to the high incidence of reoperation, alternate strategies have been proposed.
In some cases, more complex interventions such as “double switch procedures” (atrial redirection and
arterial switch) or modifications thereof may be advised. Under circumstances where the LV pressure is
subsystemic and the chamber is not able to assume the role of a systemic pump following this type of inter-
vention (absent or restrictive VSD, or no pulmonary outflow obstruction), preliminary PA banding may
be performed to train the LV over a period of time. This approach may not be successful past adolescence.
A high incidence of atrioventricular block is seen in this lesion and therefore there is a frequent need for
pacemaker placement/replacement in this patient group.

Definition of atrioventricular connections by echocardiography requires identification of the characteristic
features that establish cardiac chamber morphology. The atrioventricular valves are associated with their
corresponding ventricles, thus the morphologic tricuspid valve will identify the RV and the morphologic
mitral valve the LV. In the ME 4 CH view, the morphologic RV is characterized by inferior insertion of the
septal leaflet of the tricuspid valve to the ventricular septum (relative to the mitral valve) and by the presence
Video 19.20 of the moderator band (Fig. 19.32, Video 19.20). The tricuspid valve characteristically displays attachments
to the ventricular septum (septophilic) in contrast to the mitral valve (septophobic). The LV is identified
by two distinct papillary muscles in the TG mid-SAX view. Typically, in CCTGA the Ao is anterior and to
the left relative to the PA. Suggested cross sections for focused TEE examination include ME 4 CH, ME 2
CH, ME LAX, TG mid-SAX, TG LAX, and deep TG views (standard and modified).
t Determination of atrial arrangement, ventricular and great artery morphologies
t Evaluation of associated defects
t Estimation of ventricular dimensions and systolic function
t Characterization of flow across intracardiac communications
t Assessment of outflow tracts for presence and severity of obstruction
t Evaluation of atrioventricular valve regurgitation

FIGURE 19.32 Congenitally corrected transposition. Midesophageal four-chamber view displays the abnormal (dis-
cordant) atrioventricular connection of this lesion. The right atrium (RA) empties into the morphologic left ventricle (LV)
through the mitral valve, and the left atrium (LA) empties into the morphologic right ventricle (RV) through a tricuspid
valve. Note the apical displacement of the tricuspid valve, frequently seen in this lesion.
t Evaluation of residual shunts, outflow obstruction, systemic atrioventricular valve regurgitation
t Assessment of systolic function of a morphologic RV in the systemic circulation/LV segmental function
important in double switch operation because of coronary translocation
t Interrogation of atrial baffle in double switch procedures
t Determination of adequacy of PA banding if training strategy (band gradient, septal configuration, wall
thickness)
EBSTEIN ANOMALY
Anatomy
The hallmark of Ebstein anomaly is apical displacement of the septal and often, posterior tricuspid valve
leaflets (Fig. 19.33, Video 19.21). Classic findings include abnormal tricuspid leaflet morphology/dysplasia, Video 19.21
a redundant sail-like anterior leaflet associated with varying degrees of regurgitation, and an atrialized
inlet portion of the RV resulting in a reduction in the functional components of this chamber. This lesion
accounts for less than 1% of CHD. Frequent associated defects are atrial communications and RV outflow
tract anomalies.
FIGURE 19.33 Ebstein anomaly of the tricuspid valve. Midesophageal four-chamber view with rightward transducer
rotation. Note the severe apical displacement of the tricuspid valve septal leaflet with respect to the annulus (arrows).
This results in an atrialized portion of the right ventricle (aRV). LV, left ventricle; RV, right ventricle.

Pathophysiology
The wide anatomic spectrum in this lesion together with the concomitant presence of associated
defects accounts for the variable hemodynamic abnormalities and clinical manifestations. The severity
of tricuspid regurgitation plays a major role resulting in RA dilation and the development of arrhyth-
mias, enlargement of an atrial communication, concomitant shunting, and heart failure symptoms.
Associated atrial level right-to-left shunting and/or pulmonary outflow tract obstruction account for
the presence of cyanosis in some cases. Various degrees of RV hypoplasia and systolic dysfunction may
be seen.
Management
The adult with Ebstein anomaly may only require medical surveillance. Supraventricular arrhythmias
and/or with severe tricuspid regurgitation represent the most common indications for intervention
in this patient group. Tricuspid valve repair or replacement may be necessary with the closure of an
existing interatrial communication. Atrial plication and/or a maze procedure may also be indicated.
In some cases, a bidirectional cavopulmonary connection is created in an effort to decrease the vol-
ume load to the RV and optimize LV preload, particularly within the context of a small or severely
dilated chamber and/or decreased systolic function. This is referred to as “one-and-a-half ” ventricle
approach.

The tricuspid valve pathology and degree of valvar regurgitation is best assessed in the ME 4 CH, ME
RV in–out, and TG RV inflow views. Important aspects to be examined include septal leaflet displace-
ment, leaflet motion, adherence or tethering of septal and posterior leaflets to underlying myocardium, and
chordal support apparatus. These may impact the feasibility of a successful repair.
t Assessment of tricuspid valve leaflet morphology, mobility, attachments, coaptation point (favorable
factors for repair are a large mobile anterior leaflet with a free leading edge)
t Determination of apical tricuspid septal leaflet displacement (>8 mm/m2 distance from anterior mitral
leaflet abnormal) (Fig. 19.34)
t Assessment of RA, tricuspid annulus, and RV sizes; evaluation of atrialized portion of RV
t Evaluation of associated defects such as intracardiac communications, RV outflow obstruction, and
mitral valve prolapse
t Assessment of biventricular function (for RV: Atrialized, trabecular, and outlet portions)
FIGURE 19.34 Ebstein anomaly of the tricuspid valve, leaflet displacement. Midesophageal four-chamber view in a
patient with Ebstein anomaly illustrating the measurement of apical tricuspid septal leaflet displacement relative to the
septal insertion of the anterior mitral leaflet (asterisk).


t Interrogation of tricuspid valve for regurgitation (presence, origin, severity, peak regurgitant jet velocity);
in most cases, the regurgitant jet originates below the level of the annulus
t Inspection of RV outflow for obstruction and if present, determination of gradient (severe leaflet dis-
placement can lead to RV outflow obstruction)
t Interrogation of atrial septum (presence of communication, size, direction of shunting)
Goals of the examination after surgical repair or during/after catheter intervention are the following:
t Evaluation of tricuspid valve for stenosis and regurgitation
t Examination of prosthetic valve function as indicated
t Exclusion of residual intracardiac shunting (contrast study with agitated saline)
Applications of 3D imaging are the following:
t Visualization of tricuspid valve leaflet morphology and coaptation (3D-TEE observations have been
shown to correlate with intraoperative findings)
SINGLE VENTRICLE LESIONS OR UNIVENTRICULAR HEART
Anatomy
The spectrum of single ventricle or univentricular heart encompasses a wide variety of anatomic arrangements.
In most cases there is a degree of ventricular hypoplasia. Some patients with a biventricular heart are not able
to undergo surgery that allows for a two-ventricle repair, thus a single ventricle management strategy is under-
taken. This group of patients is functionally considered within the univentricular heart category. The major ana-
tomic variants of single ventricle include tricuspid atresia, hypoplastic left heart syndrome, and double-inlet LV.
Pathophysiology
A common feature among these lesions is complete admixture of systemic and pulmonary venous blood
at the atrial or ventricular level. Another frequent finding is systemic or pulmonary outflow obstruction.
Management
Surgical procedures initially attempt to protect the integrity of the pulmonary vascular bed and myocar-
dium. Specific goals are to prevent pulmonary overcirculation, which may lead to elevation of PA pressure/
pulmonary vascular resistance, ventricular volume overload, and myocardial dysfunction.
Norwood procedure: In infants with LV hypoplasia (hypoplastic left heart syndrome) and ductal-depen-
dent systemic blood flow, the initial surgical intervention is a Norwood procedure. This consists of recon-
struction of the hypoplastic Ao/arch, creation of a systemic-to-PA connection to provide a reliable source
of pulmonary blood flow, and atrial septectomy to ensure unrestricted egress of pulmonary venous blood
into the systemic RV. Either a modified Blalock–Taussig (see below) or Sano connection (Gore-Tex tube
from the single ventricle to PA) is created (Fig. 19.35).
Modified Blalock–Taussig shunt: In patients with anatomical substrates associated with restricted or
ductal-dependent pulmonary blood flow, a systemic-to-pulmonary connection is created as a reliable
source of pulmonary blood flow. This typically consists of a Gore-Tex graft between the subclavian artery
and a branch PA. In some cases, ductal stent placement is considered instead of a surgically created shunt.
PA band: In patients with excessive pulmonary blood flow, mechanical limitation of pulmonary over-
circulation is accomplished by placement of a PA band. This aims to prevent the development of pulmo-
nary hypertension/vascular changes. The adequacy of the intervention can be assessed by estimation of
the peak systolic pressure gradient across the PA band. This requires spectral Doppler interrogation and
application of the simplified Bernoulli equation (pressure gradient = 4V 2; where V = PA band peak velocity)
(Fig. 19.36). Ideally, the band reduces the PA systolic pressure to at least one-third of the systemic arterial
blood pressure.

Neoaorta
Pulmonary
artery
Right ventricular
to pulmonary
artery conduit
FIGURE 19.35 Norwood procedure with Sano modification. The graphic representation depicts the reconstructed
aorta (neoaorta) and the conduit from the right ventricle to the pulmonary artery to allow for pulmonary blood flow.
There is complete mixing of the systemic and pulmonary venous returns resulting in cyanosis.
FIGURE 19.36 Pulmonary artery band. Spectral Doppler interrogation across a pulmonary artery band. The peak veloc-
ity obtained by continuous wave Doppler can be applied to estimate the band gradient using the modified Bernoulli
equation.

FIGURE 19.37 Fontan procedure. Midesophageal four-chamber view in a patient post atriopulmonary Fontan connec-
tion. There is severe dilation of the right atrium (RA). The atretic right ventricular inflow and hypoplastic right ventricle
(RV) are seen. LA, left atrium; LV, Left ventricle.
Glenn anastomosis and Fontan procedure: The eventual goal of surgical palliation in a patient with sin-
gle ventricle physiology is separation of the pulmonary and systemic circulations. At present, the favored
approach is sequential diversion of the systemic venous blood directly into the pulmonary vascular bed.
This consists of an initial Glenn anastomosis and a subsequent Fontan procedure. In the Glenn operation, a
cavopulmonary connection is created allowing for blood flow from the SVC into both PAs (bidirectional).
This is a modification of the classic Glenn operation where the PAs were divided and the flow was only into
a single branch PA. The eventual separation of the pulmonary and systemic circulations in patients with
single ventricle physiology requires a Fontan procedure to direct blood from the IVC into the PAs. This
completes the total cavopulmonary connection.
The Fontan operation has been modified over the years. It is likely that many adult patients have under-
gone procedures in the past that are no longer favored as these have been associated with significant
long-term morbidity such as atrial arrhythmias, liver dysfunction, congestive heart failure, progressive
ventricular dysfunction, protein losing enteropathy, and stroke (Fig. 19.37, Video 19.22). These patients Video 19.22
may need reoperation(s) to improve their physiologic condition including revision of the cavopulmonary
connection to what is now considered a more favorable modification, optimization of cardiac rhythm, fen-
estration along the systemic venous pathway, and ultimately, if necessary, transplantation.

Diagnostic assessment of the functional single ventricle requires a combination of imaging planes, includ-
ing nonstandard views depending on the anatomy and information of interest. In most cases, the exami-
nation addresses the nature of the interatrial communication, atrioventricular valve competence, outflow
tract patency, and ventricular function. The ME 4 CH view is particularly helpful in characterizing the
atrioventricular connections (Fig. 19.38, Video 19.23). Additional views contribute to the segmental analy- Video 19.23
sis of the anatomy by defining the ventriculoarterial connections, ventricular morphology, and location of
hypoplastic or rudimentary chambers. Color flow and spectral Doppler interrogation is essential to deter-
mine valve competence and inflow/outflow tract obstruction. Suggested cross sections for focused TEE
examination include ME 4 CH, ME 2 CH, ME LAX, ME bicaval, and ME RV in–out. The TG and deep TG
views complement the anatomic details obtained in other windows.
t Evaluation of adequacy of the interatrial communication and systemic outflow tract patency
t Characterization of associated defects
t Estimation of ventricular chamber sizes and ventricular function
t Assessment of atrioventricular and semilunar valves for obstruction/regurgitation
t Estimation of gradient if outflow tract obstruction is present

FIGURE 19.38 Single ventricle. Midesophageal four-chamber view depicting the echocardiographic findings in tricus-
pid atresia. Note the absent right atrioventricular connection and the severely hypoplastic right ventricle in this patient.
LA, left atrium; LV, left ventricle; RA, right atrium.
t Evaluation of the adequacy of the intervention (imaging of a modified Blalock–Taussig shunt or Glenn
connection is not always possible by TEE because of limited imaging planes)
t Determination of flow through the Sano (RV to PA) connection if performed as part of the Norwood
procedure
t Exclusion of obstruction of blood flow at the atrial level
t Assessment of patency across Fontan connection, characterization of flow across IVC pathway to PA,
evaluation of fenestration (if present), and exclusion of thrombi
t Evaluation of valvar competence and ventricular function
t Monitoring during catheter interventions that may either create or obliterate a Fontan fenestration (this
represents a pop off allowing for right-to-left shunting to provide for maintenance of cardiac output)
t Evaluate for compression of the right pulmonary veins
CONGENITAL CORONARY ARTERY ANOMALIES
Anatomy
Anomalies of the coronary arteries of a congenital nature represent a diverse group of malformations.
These are rare collectively. The most common are anomalies of origination and course (i.e., anomalous
origin of the coronary artery from the PA and aberrant origin from the incorrect sinus potentially associ-
ated with an abnormal intramural or intra-arterial course), anomalies of intrinsic vessel anatomy (i.e., ostial
atresia and coronary aneurysm), and anomalies of coronary termination (i.e., coronary fistula draining into
a cardiac chamber/vascular structure).
Pathophysiology
The physiology and clinical manifestation of these congenital pathologies are extremely variable. These
anomalies may present as an incidental finding on echocardiography. In some cases, these are identified
in the evaluation of a heart murmur or congestive symptoms (coronary fistula), or myocardial dysfunction
(anomalous origin from PA). Chest pain, ventricular arrhythmias, syncope, and near sudden death events
are the main presentations of an aberrant origin of a coronary artery from the aortic root in adolescents
and adults. Ischemia in patients with these lesions is considered the result of impaired myocardial oxygen
delivery either at rest or during conditions of increased demands. This may be due to either an abnormal
coronary ostium, acute angulation of a coronary artery origin, extrinsic compression along an anoma-
lous course, or alterations in coronary blood flow related to a low diastolic pressure (as is the case when
the coronary artery originates from the pulmonary root).

FIGURE 19.39 Coronary arteries. Midesophageal aortic short-axis view depicting normal origin of the coronary arter-
ies from the aortic root as shown by the two arrows (left panel); anomalous origin of the left coronary artery from the
right sinus as indicated by the arrow (middle panel); and anomalous origin of the right coronary artery from the left sinus
as indicated by the arrow (right panel).
Management
The presentation in the adult patient of anomalies involving origination/course and intrinsic vessel anat-
omy is usually related to myocardial ischemia during exercise as mentioned. Therefore, this entity is part
of the differential diagnosis of sudden death in athletes. For patients with symptoms related to origin of
a coronary artery from the opposite sinus, options include medical management/surveillance, coronary
angioplasty with stent placement, and surgical intervention.

The coronary arteries are best visualized in the ME AV SAX and LAX views (Fig. 19.39). Most of the
coronary flow occurs during diastole and assessment should focus on this portion of the cardiac cycle. For
anomalous origin of the left coronary artery from the PA, views that display the MPA (i.e., ME RV in–out)
are essential. The TEE examination of coronary anomalies that involve origin from a controlateral sinus of
Valsalva requires views that display the aortic root (Fig. 19.39, Videos 19.24 and 19.25). For the evaluation Video 19.24
of fistulous connections, the examination should focus on views that allow for the coronary flow to be fol- Video 19.25
lowed into the site(s) of drainage.
t Evaluation of the origin of the coronary arteries
t Assessment of vessel course (evaluate for interarterial/intramural path)
t Determination of ventricular size and systolic function (global and segmental)
t Interrogation with pulsed and color flow Doppler to visualize the origin and course of the coronary
arteries (this may require adjustment in the echocardiographic settings to detect low velocity flow signals)
t Assessment of the intervention (revision of coronary origin, unroofing of intramural segment, successful
occlusion of coronary fistula)
t Documentation of flow in the coronary vessels by color Doppler
t Evaluation of ventricular function
TRANSESOPHAGEAL ECHOCARDIOGRAPHY IN THE CARDIAC

CATHETERIZATION LABORATORY FOR ADULTS WITH
CONGENITAL HEART DISEASE
The main indications for catheter-based interventions in the adult with CHD are related to valve disease,
closure of communications (intracardiac/vascular), and relief of vascular obstruction. The use of TEE is
well documented in these settings. Benefits include the acquisition of detailed anatomic and hemodynamic

data before and during interventions, real-time evaluation of catheter placement across valves and vessels,
immediate assessment of the procedure, and monitoring for catheter-related complications. As the appli-
cations of 3D-TEE continue to evolve, this technology is likely to provide further benefits to the care of
adults with CHD undergoing catheter-based interventions by enhancing the characterization of the defects
and providing guidance and monitoring during the procedures.
TRANSESOPHAGEAL ECHOCARDIOGRAPHY FOR NONCARDIAC

SURGERY IN ADULTS WITH CONGENITAL HEART DISEASE
The use of TEE during noncardiac surgery in the adult with CHD has not been explored to the same extent
as in atherosclerotic heart disease. However, TEE in this patient group can be applied similarly in the evalu-
ation of ventricular volume, function, and myocardial ischemia in order to optimize care. Patients with
intracardiac shunts may benefit from TEE given the potential for paradoxical emboli associated with cer-
tain interventions. This may also be the case for those with CHD and associated elevations in PA pressures/
vascular resistance under certain circumstances. Intraoperative TEE should be considered for patients with
CHD and limited cardiac reserve, poor exercise tolerance, and anyone with significant potential risk of
perioperative morbidity during noncardiac procedures. It should be emphasized that adults with CHD
may have concurrent acquired heart disease, increasing their risks for hemodynamic disturbances during
noncardiac surgery and thus the potential benefits of intraoperative TEE.
LIMITATIONS OF TRANSESOPHAGEAL ECHOCARDIOGRAPHY

IN CONGENITAL HEART DISEASE
Despite the significant contributions of TEE in CHD some limitations should be acknowledged. Optimal
interrogation of far-field structures may not be feasible, such as may be the case of right ventricular outflow
tract connections. Other anatomic structures of interest may not be amenable to imaging through the
transesophageal approach (i.e., the distal branch PAs, aortic arch).
With respect to the perioperative setting, it is recognized that a variety of factors (level of inotropic
support, catecholamine state immediately after bypass, loading conditions, myocardial functional state)
can impact the echocardiographic findings. These variables may underestimate or overestimate the hemo-
dynamic severity of the condition in question. Therefore, decisions regarding return to bypass to address
residual congenital pathology need to consider TEE findings within the context of many other factors.
SUMMARY
TEE has been shown to provide anatomic and hemodynamic information beyond that acquired with con-
ventional transthoracic imaging. This imaging modality is particularly relevant to the characterization of
structural cardiovascular abnormalities and pathology of a congenital nature. In the operating room, TEE
allows for confirmation of preoperative diagnoses and modification of the surgical strategy if necessary.
This technology facilitates perioperative care by assisting in the formulation of anesthetic plans, guiding
fluid management and the selection of inotropes/vasoactive agents. Allowing for continuous monitoring of
myocardial function and the detection of intracavitary/intravascular air and myocardial ischemia are well-
known benefits of TEE, also applicable to the congenital cardiac patient. Evaluation of the repair in CHD
and assessment of residual pathology in an effort to improve overall patient outcome represents one of the
main attributes of this imaging approach. TEE is well-known to be extremely valuable in the assessment
of factors that may lead to difficulties during weaning from cardiopulmonary bypass. The contributions of
TEE have also been documented in the cardiac catheterization laboratory during monitoring of interven-
tions, increasing the safety of these procedures while reducing exposure to ionizing radiation, and allowing
for the immediate identification of complications. The number of adults with CHD is likely to increase and
with that the overall complexity of this population. It is anticipated that further advancements in the imag-
ing technology, including that of 3D TEE, will continue to play a major role in the care of these patients.

ACKNOWLEDGMENT
The authors would like to recognize the contributions of Dr. Kathryn Rouine-Rapp to this chapter in prior
editions. Portions of the previously published material were incorporated in this revised and updated
chapter.
SUGGESTED READINGS
Attenhofer Jost CH, Connolly HM, Dearani JA, et al. Ebstein's anomaly. Circulation. 2007;115:277–285.
Baker GH, Shirali G, Ringewald JM, et al. Usefulness of live three-dimensional transesophageal echocardiography in a congenital
heart disease center. Am J Cardiol. 2009;103:1025–1028.
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.
Brickner ME, Hillis LD, Lange RA. Congenital heart disease in adults. First of two parts. N Engl J Med. 2000;342:256–263.
Brickner ME, Hillis LD, Lange RA. Congenital heart disease in adults. Second of two parts. N Engl J Med. 2000;342:334–342.
Bashore TM. Adult congenital heart disease: Right ventricular outflow tract lesions. Circulation. 2007;115:1933–1947.
Gatzoulis MA, Webb GD, Daubeney PEF. Diagnosis and Management of Adult Congenital Heart Disease. 2nd ed. Philadelphia,
PA: Elsevier-Saunders; 2011.
Inglessis I, Landzberg MJ. Interventional catheterization in adult congenital heart disease. Circulation. 2007;115:1622–1633.
Khairy P, Poirier N, Mercier LA. Univentricular heart. Circulation. 2007;115:800–812.
Kovacs AH, Verstappen A. The whole adult congenital heart disease patient. Prog Cardiovasc Dis. 2011;53:247–253.
Le Gloan L, Mercier LA, Dore A, et al. Recent advances in adult congenital heart disease. Circ J. 2011;75:2287–2295.
Meadows J, Landzberg MJ. Advances in transcatheter interventions in adults with congenital heart disease. Prog Cardiovasc Dis.
2011;53:265–273.
Miller-Hance WC, Silverman NH. Transesophageal echocardiography (TEE) in congenital heart disease with focus on the adult.
Cardiol Clin. 2000;18:861–892.
Moodie D. Adult congenital heart disease: Past, present, and future. Tex Heart Inst J. 2011;38:705–706.
Russell IA, Rouine-Rapp K, Stratmann G, et al. Congenital heart disease in the adult: A review with internet-accessible trans-
esophageal echocardiographic images. Anesth Analg. 2006;102:694–723.
Shanewise JS, Cheung AT, Aronson S, et al. ASE/SCA guidelines for performing a comprehensive intraoperative multiplane
Silvilairat S, Cabalka AK, Cetta F, et al. Echocardiographic assessment of isolated pulmonary valve stenosis: Which outpatient
Doppler gradient has the most clinical validity? J Am Soc Echocardiogr. 2005;18:1137–1142.
Vaidyanathan B, Simpson JM, Kumar RK. Transesophageal echocardiography for device closure of atrial septal defects: Case selec-
tion, planning, and procedural guidance. JACC Cardiovasc Imaging. 2009;2:1238–1242.
Warnes CA, Liberthson R, Danielson GK, et al. Task force 1: The changing profile of congenital heart disease in adult life. J Am
Coll Cardiol. 2001;37:1170–1175.
Warnes CA. Transposition of the great arteries. Circulation. 2006;114:2699–2709.
Webb G. The future of adult congenital heart disease care in the United States. Prog Cardiovasc Dis. 2011;53:324–326.

QUESTIONS
1. Most frequently performed surgical c. Midesophageal aortic valve short-axis view
procedure in the adult patient with d. Midesophageal aortic valve long-axis view
congenital heart disease: e. Midesophageal bicaval view
a. Pulmonary (pulmonic) valve replacement
7. Type of ventricular septal defect most
b. Placement of ventricular assist device
amenable to percutaneous device closure
c. Arterial switch operation
due to its anatomic characteristics:
d. Closure of ventricular septal defect
a. Perimembranous defect
e. Heart transplantation
b. Muscular defect
2. Anomalous pulmonary venous drainage is c. Supracristal defect
most frequently seen in association with: d. Inlet defect
a. Secundum atrial septal defect e. Conal
b. Primum atrial septal defect
8. Type of ventricular septal defect seen in
c. Sinus venosus atrial septal defect
association with complete atrioventricular
d. Patent foramen ovale
canal (atrioventricular septal defect):
e. The type of atrial septal defect seen in an
a. Perimembranous defect
atrioventricular canal defect
b. Muscular defect
3. Lesion least likely to be associated with a c. Supracristal defect
ventricular septal defect: d. Subarterial defect
a. Right ventricular outflow tract obstruction e. Inlet defect
b. Tetralogy of Fallot
9. A peak velocity of 4 m/s across a ventricular
c. Bicuspid aortic valve
septal defect given optimal Doppler
d. Partial anomalous pulmonary venous return
alignment, a systemic blood pressure of
e. Coarctation of the aorta
100/56 mm Hg, and no right ventricular
4. Regarding a bicuspid aortic valve all the outflow tract obstruction, would predict a
following are true EXCEPT for: systolic pulmonary artery pressure of:
a. It represents the most common form of a. Suprasystemic levels
congenital heart disease b. Systemic levels
b. It displays a “fish-mouth” appearance in the c. A fourth of the systemic pressure
midesophageal aortic short-axis view d. 36 mm Hg
c. It is found in a significant number of e. 46 mm Hg
patients with coarctation
10. In which aortic valve intervention is it
d. It may be associated with aortic root dilation
particularly important to evaluate the
e. It invariably results in severe aortic stenosis
pulmonary (pulmonic) valve?
5. The presence of a persistent left superior a. Aortic balloon valvuloplasty
vena cava should be suspected if the TEE b. Aortic valve replacement
displays: c. Ross procedure
a. Dilated left atrium d. Subaortic resection
b. Enlarged coronary sinus e. Aortic valvotomy
c. An interatrial shunt by injection of agitated
11. Pulmonary (pulmonic) stenosis is
saline into a right arm vein
considered moderate if:
d. Ebstein anomaly
a. Estimated gradient across the valve exceeds
e. Pulmonary (pulmonic) stenosis
>64 mm Hg
6. Optimal TEE view to assess the b. Right ventricular pressure is suprasystemic
anterosuperior rim of a secundum atrial c. The patient presents with chest pain symp-
septal defect during device closure: toms
a. Midesophageal four-chamber view d. Doppler-derived peak instantaneous trans-
b. Midesophageal two-chamber view valvar gradient is between 36 and 64 mm Hg
e. There is an associated atrial septal defect

12. In a patient with tetralogy of Fallot, TEE 17. Regarding univentricular palliation during
imaging in the midesophageal short-axis the Fontan procedure which statement is
view is useful to detect which potentially true?
associated lesion: a. There is mixing of the oxygenated and deox-
a. Coronary artery anomalies ygenated blood with an average systemic
b. Systemic venous anomalies arterial oxygen saturation of ∼80%
c. Right aortic arch b. The pulmonary and systemic circulations
d. Left ventricular outflow tract obstruction are separated
e. Persistent left superior vena cava to the cor- c. The physiology varies depending on
onary sinus whether the single ventricle has a left or
right ventricular morphology
13. In tetralogy of Fallot, placement of an
d. An arterial shunt is necessary to maintain
extensive transannular patch during the
pulmonary blood flow
definitive repair invariably results in:
e. Increases in the pulmonary artery pressures
a. Residual right ventricular outflow tract
have no effect on Fontan physiology
obstruction
b. Free pulmonary regurgitation 18. The origin of the coronary arteries from
c. Cyanosis the sinuses of Valsalva is best interrogated
d. Syncope in the:
e. Branch pulmonary artery stenosis a. Deep transgastric views
b. Midesophageal short-axis view during sys-
14. Long-term problems associated with
tole
an atrial switch procedure (Mustard or
c. Midesophageal short-axis view during dias-
Senning operation) for D-transposition
tole
of the great arteries include all of the
d. Midesophageal four-chamber during dias-
following EXCEPT for:
tole
a. Baffle stenoses
e. Midesophageal long-axis view during sys-
b. Right ventricular dilation
tole
c. Right ventricular systolic dysfunction
d. Tricuspid regurgitation 19. Regarding congenital coronary artery
e. Supravalvar pulmonary (pulmonic) stenosis anomalies the following are true EXCEPT
for:
15. Regarding congenitally corrected
a. May be seen in association with congenital
transposition and features that facilitate
heart disease
echocardiographic diagnosis, which of the
b. May present as an incidental finding
following is correct:
c. Always present as a manifestation of isch-
a. A ventricular septal defect is rarely seen
emia
b. The spatial orientation of the great arteries
d. Upon diagnosis surgical intervention may
is abnormal
or may not be indicated
c. The systemic ventricle is the left ventricle
e. Should be evaluated by two-dimensional
d. The tricuspid valve insertion in the septum
echocardiography as well as color Doppler
is more superior than that of the mitral
imaging
valve
e. Mitral regurgitation is a frequent finding 20. Regarding the use of TEE in the
catheterization laboratory in congenital
16. The apical displacement index used as
heart disease:
a criterion for the diagnosis of Ebstein
a. It can be used as a diagnostic tool prior to
anomaly is defined as:
the procedure
a. >8 mm/m2 body surface area
b. It serves to monitor interventional proce-
b. <8 mm/m2 body surface area
dures
c. =8 mm/m2 body surface area
c. It can detect procedural complications early
d. 12 mm/m2 body surface area
d. It can limit radiation exposure
e. All the statements are correct

20 Cardiac Masses and Embolic Sources
Farid Jadbabaie
TRANSESOPHAGEAL ECHOCARDIOGRAPHY (TEE) IS AN extremely useful imaging modality for the

assessment of cardiac masses and sources of emboli. Enhanced resolution of TEE and proximity of the
transducer to posterior cardiac structures enable visualization of small masses or thrombi in the left
atrium or the left atrial appendage (LAA) that would otherwise be missed on transthoracic echocar-
diography. Moreover, additional techniques such as contrast echocardiography and three-dimensional
(3D) imaging can provide further information on vascularity of the mass and its spatial relationship
to neighboring cardiac structures. In evaluation of cardiac masses, it is essential to identify normal
cardiac structures and recognize image artifacts that can be mistaken for a cardiac mass or throm-
bus (1,2). Normal structures such as pectinate muscle in the LAA or the tissue fold between LAA
and left upper pulmonary vein (Coumadin ridge) can be mistaken for a thrombus or a small tumor
(Fig. 20.1). Similarly, a prominent Chiari network in the right atrium can be mistaken for a right atrial
mass.
A B
FIGURE 20.1 Normal cardiac structures can often be mistaken for cardiac masses or thrombus. Panel A shows a promi-
nent pectinate muscle in the left atrial appendage mimicking a thrombus. An example of a prominent Coumadin ridge
is shown in panel B and an example of a prominent Chiari network is shown in panel C. LAA, left atrial appendage;
LA, left atrium; PV, pulmonary vein; LV, left ventricle; RA, right atrium; asterisk, shows the posterior horn of left atrial
appendage.
424

20. Cardiac Masses and Embolic Sources 425
A B
FIGURE 20.2 Example of a large myxoma in the left atrium (asterisk) with a stalk (arrow) attached to the atrial septum
(panel A). Tumor prolapses into left ventricle during diastole (panel B). LA, left atrium; RA, right atrium; SVC, superior
vena cava.
CARDIAC TUMORS
Primary cardiac tumors are very rare and account for 25% of all cardiac neoplasms in pathologic stud-
ies (3). Majority of primary cardiac tumors are benign without local invasion or metastatic spread. In
contrast, malignant tumors often appear as large masses with invasion into the surrounding cardiac
structures.
Myxoma
Myxoma is the most common primary cardiac tumor in adults and accounts for 30% of all primary car-
diac neoplasms. Cardiac myxomas commonly arise from the left atrium but can also originate from the
right atrium or the ventricles. These tumors are usually pedunculated and have a smooth surface. The
most common attachment site is the fossa ovalis on the left side of the atrial septum. Myxoma is a slow-
growing tumor and can remain asymptomatic for a long period of time. If undetected, myxomas can
grow in size and occupy a significant portion of the left atrium, causing obstruction of the flow across the
mitral valve (Fig. 20.2, Videos 20.1, 20.2). Cardiac myxomas are friable and can often result in systemic Video 20.1
embolization. Video 20.2
Lipoma
Lipomas are the second most common cardiac tumors in adults and account for 10% of all benign car-
diac neoplasms (3). These tumors usually originate from ventricular myocardium and less commonly from
atrial myocardium. These tumors are often sessile with increased echogenicity and have a smooth surface.
Lipomas are slow-growing tumors and can become large and cause blood flow obstruction (Fig. 20.3,
Video 20.3). Cardiac lipomas should be distinguished from lipomatous hypertrophy of interatrial septum, Video 20.3
which is hallmarked by the infiltration of mature fat cells and a characteristic appearance of the dumbbell-
shaped thickening of atrial septum with the sparing of fossa ovalis (4) (Fig. 20.4, Video 20.4). Lipomatous Video 20.4
hypertrophy is more commonly seen in older adults, especially older women, and usually has a benign
clinical course.
Papillary Fibroelastoma
Papillary fibroelastoma is the third most common primary cardiac tumor in adults. Fibroelastomas are
small mobile tumors that commonly originate from the valvular leaflets but can also arise from other
endocardial surfaces. Aortic valve is the most common site of origin followed by the mitral valve. These
tumors often appear as a small (0.5 to 2 cm) pedunculated echo density, with multiple mobile fibrillar
projections, that is attached to the valve leaflets (5–7) (Fig. 20.5, Video 20.5). Fibroblastomas have a high Video 20.5

FIGURE 20.3 Example of a large lipoma (asterisk) involving the interatrial septum. Note the echogenicity of the tumor
and acoustic shadowing. LA, left atrium; IVC, inferior vena cava; RA, right atrium; SVC, superior vena cava.
FIGURE 20.4 Example of lipomatous hypertrophy of interatrial septum (asterisks) is depicted. Note the characteristic
“dumbbell-shape” appearance and sparing of fossa ovalis. LA, left atrium; RA, right atrium; SVC, superior vena cava.
A B
FIGURE 20.5 A: Example of a papillary fibroelastoma on aortic valve (arrow). B: Example of a papillary fibroelastoma
arising from the chordae tendineae in the left ventricle (arrow). LA, left atrium; LV, left ventricle.

FIGURE 20.6 Example of a Lambl’s excrescence on the aortic valve leaflets (arrow).
potential for embolization, which is thought to be from the embolization of tumor fragments or associ-
ated thrombi. Risk of embolization is higher as the tumor grows larger. Valvular fibroelastomas are fre-
quently confused with vegetations given the size, location, and potential for embolization. In contrast to
vegetations, fibroelastomas mostly arise from the aortic side of the aortic valve leaflets (5,6) and are not
associated with significant valvular abnormalities (7). Prominent valvular (Lambl’s) excrescences are the
other condition that can also be confused with fibroelastomas (6). Valvular excrescences are commonly
seen on commissural edges of the valve leaflets and comprise a small fibrous core covered by endothe-
lial cells. These densities are commonly seen on TEE in all groups and are not associated with embolic
events (8). An example of a prominent Lambl’s excrescence on the aortic valve is shown in Figure 20.6,
(Video 20.6). Video 20.6
Rhabdomyoma
Rhabdomyomas are the most common primary cardiac tumor in children (2,3). Rhabdomyomas are
almost always associated with tuberous sclerosis. They usually originate from either ventricle and
are often multiple. These tumors can become large and cause valvular or outflow tract obstruction.
Asymptomatic rhabdomyomas are usually followed over time, as some of these tumors can spontane-
ously resolve.
Fibroma
Fibromas are the second most common benign cardiac tumor in children. Fibromas usually originate from
the ventricles or the atrioventricular grove. A characteristic feature of fibromas is the presence of central
calcification. Fibromas usually appear as a large single intramural mass with multiple central densities.
Singularity and presence of central calcification are key factors in differentiating fibromas from rhabdo-
myomas (Fig. 20.7).
Cardiac Sarcomas
Malignant tumors such as sarcomas are rare causes of cardiac tumors and usually originate from the
ventricular myocardium. These tumors can become large and invade into any cavity and surrounding struc-
tures with protruding mobile components and an attached thrombus (Fig. 20.8). One of the distinguish-
ing features of malignant cardiac tumors is enhancement with ultrasound contrast given their extensive
vascularity.

FIGURE 20.7 Example of a fibroma involving the medial left atrial wall and the atrial septum (arrow). LA, left atrium;
SVC, superior vena cava; RA, right atrium.
Metastatic Tumors
Metastatic tumors involve the heart or the pericardium through local invasion (such as breast or lung Ca)
or hematogenous spread (melanoma). Tumors that invade the heart locally can at times be seen on TEE as
Video 20.7 an external mass compressing or invading the cardiac chambers (Fig. 20.9, Video 20.7).
Embolization
Most cardiac tumors have the potential for embolization. Emboli can be from tumor fragments or dis-
sociation of attached thrombi. Certain tumors, such as fibroelastoma and myxoma, are associated with
higher rates of embolization. In one study, 30% of patients with an incidental finding of fibroelastoma had
symptoms consistent with systemic embolization on clinical follow-up (5). In rare instances, large tumor
fragments from distant sites can be seen in transit through the inferior vena cava and the right heart.
Renal cell carcinoma is commonly associated with embolization and transit of tumor fragments through
the right heart.
Tumor
A B
FIGURE 20.8 Mid esophageal bicaval view of an angiosarcoma of the right atrium. In this image, a large mass is occu-
pying the entire right atrium (panel A). Tumor fragments (asterisks) prolapse across the tricuspid valve (arrow heads) into
the right ventricle and right ventricular outflow tract (panel B). LA, left atrium; RA, right atrium; SVC, superior vena cava;
RVOT, right ventricular outflow tract.

FIGURE 20.9 Example of a large extracardiac tumor manifesting as a heterogenous mass anterior to the superior vena
cava. RA, right atrium; LA, left atrium; SVC, superior vena cava; RV, right ventricle.
INTRACARDIAC THROMBUS
Thrombi can be formed within any cardiac chamber and are mostly associated with an underlying wall
motion abnormality or low flow state leading to stasis of blood. The most common sites for intracardiac
thrombus are the left atrial appendage and the left atrium and are commonly seen in patients with atrial
fibrillation or rheumatic mitral disease (Fig. 20.10, Videos 20.8, 20.9). Thrombus can also be formed Video 20.8
on intracardiac devices such as pacemaker wires or septal closure devices or be attached to indwelling Video 20.9
catheters in the right heart (Fig. 20.11, Videos 20.10, 20.11). Thrombus in the ventricles is almost always Video 20.10
associated with an underlying wall motion abnormality. Fresh thrombi tend to be round and mobile, Video 20.11
whereas chronic thrombi appear flat and laminated and are less mobile. Size and mobility are important
predictors of systemic embolization (Fig. 20.12, Video 20.12). Video 20.12
FIGURE 20.10 Midesophageal image of the left atrial appendage at 30 degrees is depicted. A large thrombus (arrow)
is seen in the left atrial appendage.

FIGURE 20.11 Example of a large thrombus (Th) in the right atrium (RA) is shown in a patient with indwelling hemodi-
alysis catheter (arrow). LA, left atrium; SVC, superior vena cava.
Technical Considerations in Evaluation of Cardiac Masses

Current echocardiographic techniques are limited in the assessment of histology of cardiac masses.
However, size, shape, mobility, and anatomic location as well as associated clinical history and response
to therapy may offer clues to the origin and type of the mass; for example, resolution of a mass after a few
weeks of anticoagulation is suggestive of thrombus (Fig. 20.13). In addition, use of ultrasound contrast
agents can provide further information on the vascularity of the suspected mass. Malignant tumors are
usually highly vascular and appear highly enhanced with ultrasound contrast, whereas benign stromal
tumors with low vascularity or organized thrombus will show low enhancement; fresh clots will appear
Video 20.13 as filling defects (Video 20.13). Echocardiographic characteristics of different cardiac masses are sum-
marized in Table 20.1.
FIGURE 20.12 Midesophageal commissural view of the left ventricle in systole showing a large apical thrombus
(arrow) in a patient with apical hypokinesis. LA, left atrium; LV, left ventricle.

FIGURE 20.13 Example of a small thrombus (Th) in the oblique pericardial sinus adjacent to the right upper pulmo-
nary vein. (RUPV) and left atrial appendage (App) in a patient with recent pulmonary vein ablation procedure for atrial
fibrillation. Thrombus was resolved on repeat TEE after four weeks of anticoagulation. Small amount of fluid is seen in
the pericardial space (P).
TEE in the Assessment of Cardiac Sources of Emboli

Emboli originating from the heart or great vessels are common etiologic factors in stroke and peripheral
arterial occlusions. More than 20% of all cases of ischemic stroke are embolic in origin. In as many as 40%
of stroke patients, despite intense clinical workup, the etiology is not identified. These patients with cryp-
togenic stroke are younger, with less evidence of generalized atherosclerosis (10,11). It has been shown that
the incidence of a patent foramen ovale (PFO) is higher in this population, suggesting a potential role of
paradoxical embolism as the etiologic factor. Atherosclerotic disease of the ascending aorta and aortic arch
are other potential sources of emboli in older patients.
Cardiac sources of emboli can be further divided into probable and possible sources based on the
strength of association.
Probable Sources of Emboli

Left Atrial Appendage Thrombus
Thrombus in the left atrium or LAA is a common source of systemic embolization especially in patients
with atrial fibrillation (Fig. 20.10, Videos 20.8, 20.9). Left atrial clot is usually an extension of existing Video 20.8
Video 20.9
TABLE 20.1 Echocardiographic Characteristics of Common Cardiac Masses
Mass type Appearance Size and location Other

Myxoma Large, smooth surface, Left atrium, right atrium Minimal enhancement
mobile and pedunculated with echo contrast
Papillary fibroelastoma Mobile pedunculated, Small (<1 cm), attached to No significant valvular
multiple fibrillar valvular structures/cords regurgitation
projections
Lipoma Smooth surface, large, Ventricular and atrial Minimal enhancement
increased echogenicity myocardium with ultrasound contrast
Thrombus Stagnation, prior Any size, commonly in low No enhancement with
instrumentation, often flow areas such as atrial contrast. Resolution
mobile appendage or apex with after anticoagulation
wall motion abnormalities

A B
FIGURE 20.14 Example of a prominent pectinate muscle in the left atrial appendage mimicking a thrombus is depicted
(panel A). Images obtained at an orthogonal plane from the same patient demonstrate that the density is a septation
between lobes of the left atrial appendage (panel B) (arrow).
thrombus in the left atrial appendage (LAA). The LAA is an extension of the left atrial cavity and originates
from the superior aspect of the left atrium anterior to the insertion site of the left upper pulmonary vein.
The LAA is usually comprised of two or more lobes and is lined with pectinate muscle. The LAA is best
visualized in the midesophageal position with the transducer at 30- to 60-degree rotation. With gradual
increase in the transducer rotation up to 150 degrees, detailed views of the wall structure and the number
of lobes can be obtained. It is essential to image the appendage in orthogonal views to be able to identify the
pectinate muscle and distinguish it from a potential thrombus (Fig. 20.14). In addition to two-dimensional
(2D) images, a detailed examination of the atrial appendage should include an assessment of blood flow
velocity by pulse wave Doppler. Decreased blood flow velocity (<40 cm/s) in the LAA has been shown to be
associated with an increased risk of thromboembolic events.
Thrombus in Left Ventricle

Thrombus in the left ventricle is usually associated with regional wall motion abnormalities. The majority
Video 20.12 of thrombi in the left ventricle (LV) are located in the apex (Fig. 20.12, Video 20.12). TEE is often limited
in visualizing the apex, given its anterior location and relative distance from the transducer. The LV apex
is best seen in the ME LAX view with slight retroflexion of the probe. In contrast to TEE, transthoracic
echocardiography is a better technique to assess the LV apex.
Endocarditis
Vegetation on any cardiac valve can also be a source of embolic events. Vegetation size (size >10 mm) and
mobility on TEE are independent risk factors for embolic events (12).
Possible Sources of Emboli

Spontaneous Echo Contrast (Smoke)
Spontaneous echo contrast (SEC) or smoke is an echogenic swirling pattern of blood flow in the left atrium
Video 20.13 associated with stagnation (Fig. 20.15, Video 20.13). The exact mechanism of SEC is not well understood
but it is thought to be due to aggregation of red blood cells. The presence of SEC in the left atrium or LAA
is associated with an increased risk of thromboembolism (13). It should be noted that gain settings on the
echocardiography equipment should be optimized before any diagnosis of SEC is made, since an increased
gain setting can mimic SEC.

FIGURE 20.15 Midesophageal image of the left atrium demonstrating increased left atrial size and spontaneous echo
contrast.
Paradoxical Embolus Through a Patent Foramen Ovale (PFO)

Transit of a venous embolus through a PFO across the atrial septum can lead to systemic embolization.
This theory is further supported by anecdotal reports of paradoxical embolus caught in transit across the
septum (Video 20.14) and the higher incidence of PFOs in young patients with cryptogenic stroke (10,14). Video 20.14
Therefore, a TEE for the evaluation of sources of embolus should include a detailed evaluation of the atrial
septum for the presence of a PFO including color flow Doppler (CFD) interrogation and performance of
an agitated saline bubble study. The atrial septum is best seen in the midesophagus with a transducer angle
of 100 to 120 degrees (ME bicaval view). A PFO can be seen by CFD demonstrating flow across the fora-
men ovale or by an early appearance of agitated saline bubbles in the left atrium after intravenous injection Video 20.15
of agitated saline contrast (Fig. 20.16, Videos 20.15, 20.16). PFO’s can be easily closed via a percutaneous Video 20.16
approach using an Amplatzer occluder device. (Videos 20.17–20.19). It is important to recognize correct Video 20.17
implantation as these devices can migrate and embolize requiring surgical intervention. Video 20.18
Video 20.19
FIGURE 20.16 Midesophageal bicaval view after intravenous injection of agitated saline demonstrating passage of
saline bubbles across a patent foramen ovale into the left atrium. LA, left atrium; RA, right atrium; SVC, superior vena cava.

REFERENCES
1. Peters PJ, Reinhardt S. The echocardiographic evaluation of intracardiac masses: A review. J Am Soc Echocardiogr. 2006;19(2):
230–240.
2. Goldman JH, Foster E. Transesophageal echocardiographic (TEE) evaluation of intracardiac and pericardial masses. Cardiol
Clin. 2000;18(4):849–860.
3. Armstrong WF, Ryan T. (Chapter 23) Masses, tumors, and source of embolus. In: Feigenbaum’s Echocardiography. 7th ed.
Philadelphia, PA: Lippincott Williams & Wilkins; 2010.
4. O’Connor S, Recavarren R, Nichols LC, et al. Lipomatous hypertrophy of the interatrial septum: An overview. Arch Pathol Lab
Med. 2006;130(3):397–399.
5. Sun JP, Asher CR, Yang XS, et al. Clinical and echocardiographic characteristics of papillary fibroelastomas: A retrospective
and prospective study in 162 patients. Circulation. 2001;103:2687–2693.
6. Gowda RM, Khan IA, Nair CK, et al. Cardiac papillary fibroelastoma: A comprehensive analysis of 725 cases. Am Heart J.
2003;146(3):404–410.
7. Klarich KW, Enriquez-Sarano M, Gura GM, et al. Papillary fibroelastoma: Echocardiographic characteristics for diagnosis and
pathologic correlation. J Am Coll Cardiol. 1997;30:784–790.
8. Roldan CA, Shively BK, Crawford MH. Valve excrescences: Prevalence, evolution and risk for cardioembolism. J Am Coll
Cardiol. 1997;30(5):1308–1314.
9. Kirkpatrick JN, Wong T, Bednarz JE, et al. Differential diagnosis of cardiac masses using contrast echocardiographic perfusion
imaging. J Am Coll Cardiol. 2004;43:1412–1419.
10. Kizer JR, Devereux RB. Clinical practice. Patent foramen ovale in young adults with unexplained stroke. N Engl J Med.
2005;353:2361–2372.
11. Wu LA, Malouf JF, Dearani JA, et al. Patent foramen ovale in cryptogenic stroke: Current understanding and management
options. Arch Intern Med. 2004;164(9):950–956.
12. Thuny F, Di Salvo G, Belliard O, et al. Risk of embolism and death in infective endocarditis: Prognostic value of echocardiog-
raphy: A prospective multicenter study. Circulation. 2005;112(1):69–75.
13. Bernhardt P, Schmidt H, Hammerstingl C, et al. Patients with atrial fibrillation and dense spontaneous echo contrast at high
risk a prospective and serial follow-up over 12 months with transesophageal echocardiography and cerebral magnetic reso-
nance imaging. J Am Coll Cardiol. 2005;45(11):1807–1812.
14. Cramer SC. Patent foramen ovale and its relationship to stroke. Cardiol Clin. 2005;23(1):7–11.

QUESTIONS
For the following questions 1 to 10, please select 12. All of the following statements are true
true or false. EXCEPT:
a. Primary cardiac tumors are very rare and
1. The Coumadin ridge is the tissue fold
comprise a minority of all cardiac neo-
between left atrial appendage and left
plasms
upper pulmonary vein that can often be
b. Metastatic tumors involve the heart or peri-
mistaken for a thrombus or a small tumor.
cardium through local invasion or hema-
2. The Chiari network is a remnant of fetal togenous spread
circulation which appears as a mobile c. Locally invading tumors are often seen as a
density in the left atrium and can be mass invading the chambers or pericardium
confused with a left atrial mass. d. Echocardiography is an effective technique
in identifying the tissue origin of cardiac
3. Lipomatous hypertrophy of the intra-atrial masses
septum is commonly seen in older women
and usually has a benign clinical course. 13. All of the following statements are true
EXCEPT:
4. Myxoma is a highly vascular tumor a. A myxoma is the most common primary
that will appear highly enhanced after cardiac tumor in adults
administration of echo contrast. b. Cardiac myxomas are pedunculated masses
5. Benign stromal tumors with low vascularity that commonly arise from the atrioventric-
appear as filling defects on contrast ular valves
echocardiography. c. A myxoma is a slow-growing tumor and can
remain asymptomatic for a long period of
6. Renal cell carcinoma is commonly time
associated with transit of tumor fragments d. A myxoma can grow in size and occupy a
through the IVC to the right heart. significant portion of the cardiac chambers
7. Decreased blood flow velocity (<40 cm/s) 14. All of the following statements are true
in the left atrial appendage is associated EXCEPT:
with an increased risk of thromboembolic a. Fibroelastomas are small mobile tumors
events. that appear as a small (0.5 to 2 cm) pedun-
8. The presence of a PFO in an otherwise culated echo density on valvular structures
healthy patient is a strong predictor of b. Fibroelastomas are often associated with
stroke. valvular calcifications
c. Fibroblastomas have high potential for
9. Increased gain setting on echo machines embolization
can mimic spontaneous echo contrast. d. In contrast to vegetations, fibroelastomas
10. In endocarditis, the vegetation size is not a are not associated with significant valvular
predictor of embolic events. regurgitations
11. All of the following statements regarding an 15. All of the following statements are true
intracardiac thrombus are true EXCEPT: EXCEPT:
a. A left ventricular apical thrombus is almost a. Rhabdomyomas are the most common pri-
always associated with apical wall motion mary cardiac tumor in children
abnormality b. Rhabdomyomas are almost always associ-
b. The left ventricular apex is best seen from a ated with tuberous sclerosis
transgastric TEE view c. Rhabdomyomas are single tumors that usu-
c. A thrombus will appear as a filling defect ally originate from the atrial myocardium
with administration of echo contrast d. Asymptomatic rhabdomyomas are usually
d. Size and mobility are predictors of systemic followed over time, as some of these tumors
embolization can spontaneously resolve

16. All of the following statements are true c. The presence of SEC in the left atrium
EXCEPT: appendage is associated with increased risk
a. Fibromas are the second most common of thromboembolism
benign cardiac tumor in children d. Spontaneous echo contrast is only seen in
b. Fibromas usually originate from the intra- atrial fibrillation
atrial septum
19. All of the following statements are true
c. Singularity is a key factor in differentiating
EXCEPT:
fibromas from rhabdomyomas
a. Lambl’s excrescences are commonly seen
d. The presence of central calcification adds in
on commissural edges of the valve leaflets
differentiating fibromas from rhabdomyo-
b. Larger Lambl’s excrescences are often con-
mas
fused with valvular vegetations
17. All of the following statements are true c. Similar to vegetations, Lambl’s excrescences
EXCEPT: are associated with valvular regurgitations
a. Intracardiac thrombi are associated with d. Lambl’s excrescences are not associated
stasis of blood with embolic events
b. Thrombus can be formed on intracardiac
20. All of the following statements are true
devices such as pacemaker wires
EXCEPT:
c. Thrombus in the ventricles is almost always
a. Fibroblastomas have high potential for
associated with underlying wall motion
embolization
abnormality
b. Emboli are from tumor fragments or associ-
d. Thrombus size is not a predictor of systemic
ated thrombi
embolization
c. Tumor size is not a predictor of emboliza-
18. All of the following statements are true tion
EXCEPT: d. Valvular fibroelastomas are frequently con-
a. Spontaneous echo contrast (SEC) or smoke fused with vegetations given the size, loca-
is an echogenic swirling pattern of blood tion, and potential for embolization
flow in the left atrium
b. The presence of SEC in the left atrium or
LAA is associated with increased risk of
thromboembolism

V MAN AND MACHINE
21 3D TEE Imaging
Annette Vegas
INTRODUCTION
Real-time (RT) three-dimensional (3D) TEE is being increasingly used in the perioperative period to assess
cardiac anatomy and function. Ease of acquisition with rapid online display of detailed dynamic 3D images
has overcome some of the early limitations associated with 3D echocardiography. A basic understanding
of evolving 3D technology enables the echocardiographer to master the new skills necessary to acquire,
manipulate, and interpret 3D datasets (1–3). Cardiac structures can be shown from any perspective includ-
ing a virtual surgical orientation. This single display of a dynamic image is an invaluable visual aid to the
echocardiographer and surgeon to better communicate and understand individual patient anatomy. In addi-
tion, exportation of 3D datasets to analytical software permits prompt off-line reconstruction of 3D models
to accurately quantify cardiac anatomy and ventricular function. This chapter presents key features of the
emerging 3D technology used in echocardiography and reviews the current applications of RT 3D TEE.
3D TECHNOLOGY
A fundamental difference between two-dimensional (2D) and 3D echocardiographic imaging is how the
image is acquired and displayed. Volume scanning is used in RT 3D echocardiography as compared with
the standard sector planes in 2D (4). This requires the use of special ultrasound probes to acquire raw data
and integrated ultrasound machine software to process 3D datasets.
TEE Probes
The modern adult 2D TEE multiplane transducer comprises a linear phased array of 64 to 128 piezoelectric
crystals arranged to cover a circular transducer face. Sequential activation of the crystals generate a 2D,
sector-shaped, flat, ultrasound plane that can be mechanically or electronically rotated in 1-degree incre-
ment through 180° to scan a conical-shaped area. Three-dimensional images can be created using a stan-
dard 2D multiplane TEE probe but this is time-consuming and requires off-line reconstruction.
RT 3D echocardiography uses transthoracic echocardiography (TTE) and transesophageal echocardiog-
raphy probes with special matrix array transducers. In a similarly sized 5 to 7 MHz 3D TEE probe (X7-2t,
Philips Healthcare, Andover, MA), extreme miniaturization assembles 2,500 piezoelectric crystals arranged in
50 rows by 50 columns to cover the entire square transducer face. Each crystal can be independently activated
(fully sampled), focused, and steered. This generates an ultrasound beam that can be steered in the azimuthal
(x-y) and the elevational plane (x-z) to cover a 3D pyramidal scanning volume (Fig. 21.1). In addition, these
probes can also perform all the standard 2D functions including M-mode, Doppler (spectral, color, and tis-
sue) modes and are also able to simultaneously display two independent 2D scanning planes (xPlane mode).
3D Imaging
Creation of a 3D ultrasound image of the heart involves four basic steps: Data acquisition, data storage, data
processing, and image display (Fig. 21.1A). 437

438 V. Man and Machine
A D E F
FIGURE 21.1 3D imaging. A: 3D echocardiographic imaging includes four stages: Data acquisition, data storage, data
processing, and data display. B: A matrix array probe comprising 2,500 piezoelectric crystals is used to volume scan and
acquire raw 3D data. C: Data processing involves creation of a 3D dataset comprising voxels through conversion (white)
and interpolation (purple). D–F: 3D data can be displayed as (D) wireframe, (E) surface, or (F) volume rendered as shown
here for the left ventricle. Images (B) and (C) used with permission of M. Corrin, (D–F) from: Vegas A, Meineri M. Three-
dimensional transesophageal echocardiography is a major advance for intraoperative clinical management of patients
Video 21.1 undergoing cardiac surgery: A core review. Anesth Analg. 2010;110:1548–1573, with permission. Video 21.1.
Data Acquisition
Initial 3D data acquisition obtains echocardiographic characteristics of many single points within a volume
of tissue. The matrix array probe is held immobile while the transducer automatically steers the ultrasound
beam to scan a pyramidal volume of tissue in three dimensions.
Data Storage
Data storage maintains data flow from the initial raw data acquisition to the next step of data process-
ing. During the volume scanning technique, data is streamed through the onboard computer, allowing
for immediate concurrent data storage and processing (online) within the ultrasound machine. Off-line
exportation and reconstruction of the 3D dataset is no longer required.
Data Processing
Data processing consists of two integrated steps: Conversion and interpolation that transform the scanned
raw data for a specific volume into a 3D dataset used to create a 3D object (Fig. 21.1C).
Conversion positions and assigns x-y-z coordinates (Cartesian volume) to each of the scanned raw data
points identifying their echogenic characteristics with a known position in space. Interpolation fills the
gaps between all the known points in space to generate a 3D dataset comprising voxels or volume elements.
A voxel is a (vo)lume of pi(xel)s that encrypts the physical characteristics and location of the smallest cube
in a dataset, which is used for 3D display. Resolution of the 3D image depends on voxel size. Larger voxels

21. 3D TEE Imaging 439
resulting in poorer resolution are generated when raw data is available for fewer points in the scanned
volume and interpolation has to fill wider gaps.
3D Display
The process of making a 3D dataset visible is termed 3D display which can be either as multiple 2D image
planes or a 3D graphic reproduction.
Graphic rendering is a computer graphics process that creates a 3D object or image. Segmentation is the
first step in graphic rendering during which the object to be rendered is identified and separated from sur-
rounding structures in the 3D dataset. This consists of differentiating cardiac tissue from blood, pericardial
fluid, and air which is facilitated by their dissimilar ability to reflect ultrasound. It is achieved by setting
the threshold of echo density for blood thus excluding any point with a lower echo density from further
processing. This step delineates the 3D surfaces of cardiac tissue.
Following segmentation, the 3D dataset undergoes one of the three increasingly complex graphic
rendering techniques: Wireframe, surface, or volume rendering (Fig. 21.1D–F) to display the 3D
object.
Wireframe rendering is the simplest and fastest way of creating a visible 3D object. A series of equidis-
tant points on the surface of a 3D object are defined and connected with lines (wires) to form a mesh of
small polygonal tiles. Smoothing algorithms can refine the narrow angles and make the object appear more
real. In clinical practice this technique is used for structures with relatively flat surfaces such as the left
ventricular (LV) and the atrial cavities (Fig. 21.1D).
Surface rendering extends the wireframe technique by defining more points on the surface of a 3D
object making the lines joining them invisible. It generates 3D objects with detailed solid surfaces but an
empty hollow inner core (Fig. 21.1E). This makes morphologic assessment of the corresponding anatomical
structure (e.g., cardiac valves) and determination of cavity volume (e.g., LV volume) feasible.
Volume rendering retains all the 3D data and displays a 3D object with full details of the surface and
inner structure. This enables the potential display of every voxel of the 3D dataset permitting a “virtual dis-
section” of the 3D object (Fig. 21.1F).
Despite being composed of voxels, these 3D objects are seen on the screen as pixels of a 2D image.
Perspective, light casting, and depth color coding are used to give a visual sense of depth and reality. Any
rendered 3D object can be freely rotated in the display and shown from any orientation. Furthermore the
3D datasets can be displayed as a static or a moving object. A moving (dynamic) 3D object is often referred
to as four dimensional (4D), with time considered as the fourth dimension.
3D IMAGE ACQUISITION
The acquisition of 3D-TEE images can occur instantaneously either in (a) RT (live) or (b) gated that is timed
to the electrocardiogram (ECG) over multiple heartbeats. Currently the term “real time” refers to any 3D
image that changes on the display with probe movement. Gated images are created as a loop by stitch-
ing together subvolumes acquired from consecutive heartbeats. Over a fixed number of cardiac cycles,
the same portion of the ECG wave (usually the R wave) triggers the recording of each subvolume and
allows rapid, within seconds, data reconstruction synchronous with the ECG. It works best for a regular
rhythm. Arrhythmias, electrocautery artifacts, and probe movement will affect the ability to seamlessly
stitch together the subvolumes. A demarcation line, termed a stitch artifact, appears between the subvol-
umes distorting the anatomical structures potentially affecting analysis.
All forms of ultrasound imaging are limited by the speed of sound (1,500 m/s). RT 3D TEE has a com-
plex interdependence of temporal resolution, sector size, and image resolution. In 3D echocardiography,
temporal resolution can be described in terms of volume rate or frame rate (FR) as shown on the display.
There is insufficient time for sound to traverse large tissue volumes in the RT scanning modes. For instance,
at a depth of 12 cm, scanning in 2D (90 scan lines) requires 14.8 milliseconds giving a 62 Hz FR with 3D
(2,400 scan lines), it requires 396 milliseconds resulting in a 1 to 11 Hz FR. Current-gated acquisition and
evolving 3D technology is being developed to produce large 3D volumes in RT with good temporal and
spatial resolution.

A,B D
C E
FIGURE 21.2 3D imaging modes. The various 3D imaging modes display assorted volumes of information at different
frame rates; (A) Live (up to 30° × 60°) of a rotated midesophageal four-chamber (ME 4-C) view (inset); (B) Zoom (90° × 90°)
of an unrotated en face view of the mitral valve; (C) Full Volume (90° × 90°) of an ME 4-C view as four segments joined
together and rotated. A mitral regurgitation jet is shown in (D) 2D using xPlane and (E) 3D color Doppler Full Volume
which has the smallest volume (40° × 40°) and a 19-Hz FR despite containing seven consecutive segments. (Modified
from: Vegas A, Meineri M. Three-dimensional transesophageal echocardiography is a major advance for intraoperative
Video 21.2 clinical management of patients undergoing cardiac surgery: A core review. Anesth Analg. 2010;110:1548–1573, with
Video 21.3 permission.) Videos 21.2, 21.3, 21.4.
Video 21.4
Imaging Modes
Single button activation of specific 3D imaging modes (iE33 machine, Philips Healthcare) for both
TEE and TTE matrix array probes include (a) Live, (b) Zoom, (c) Full Volume (FV), and (d) color Doppler
FV (Fig. 21.2). Choosing between modes for specific structures is a balance between selecting pyramidal
image size, volume or FR, and RT imaging (Table 21.1).
TABLE 21.1 3D Imaging Modes
Color Doppler
Live Zoom Full Volume Full Volume
Dimensions 60° × 30° by image 20° × 20° to 100° × 90° × 90° by image 40° × 40° by
depth 100° by a variable depth limited height
height
Real time (RT)a Yes Yes No/yes No/yes
Frame rate (FR)/ 20–30 Hz 5–15 Hz 20–50 Hz 15–25 Hz
temporal resolution High Low High Mid
Spatial resolution Mid High High Low
Cardiac structures Any cardiac structure MV, LAA, IAS LV, RV, MV Regurgitant jets,
imaged heart defects
a
The ability to image in RT depends on ultrasound machine software.
MV, mitral valve; LAA, left atrial appendage; IAS, interatrial septum; LV, left ventricle; RV, right ventricle.

A D
B E
C F
FIGURE 21.3 3D image optimization and artifacts. Postprocessing image optimization of displayed 3D datasets
involves adjusting (A) gain, (B) brightness, and (C) smoothing. Artifacts in 3D images include (D) stitch artifact (arrow)
between adjacent segments in a full volume en face MV view. E: Overgain appears as brown speckles (arrow) which may
be mistaken for a mass in the left atrium in this Zoom en face MV view. F: Dropout from shadowing (arrow) is similar to a
2D image as shown for a calcified bicuspid aortic valve in SAX using live mode. (From: Vegas A, Meineri M, Jerath A. Real-
time three-dimensional transesophageal echocardiography. A Step-by-Step Guide. New York, NY: Springer; 2012, with
kind permission of Springer Science + Business Media.) Video 21.5. Video 21.5
Depending on the ultrasound machine software, 3D datasets for the same-sized volume in all 3D modes
can be acquired and displayed in RT over multiple heartbeats (1,2,4,5) increasing temporal resolution. The
acquisition time is longer for more beats. The single beat acquisition has the lowest FR and is useful with
arrhythmias as it does not require an ECG.
(a) Live displays a RT narrow angle 3D pyramidal volume with fixed dimensions of 60° × 30° by the same
depth of the initial 2D view for one or multiple heartbeats. Cardiac structures are imaged in 3D using
the familiar 2D scanning planes. Rotation of this 3D image can be used as a quick test of the general 3D
image settings (Figs. 21.2A and 21.3A). The limited sector size necessitates physical probe movement
to image entire structures.
(b) Zoom displays a RT magnified subsection of 3D pyramidal volume that can vary in dimensions from
20° × 20° to 100° × 100° by a variable height of the 2D view. The 3D pyramidal volume is centered to a
specific region of interest (e.g., the mitral valve [MV]) and kept as small as possible in order to improve
the FR and image definition (Fig. 21.2B).
(c) Full Volume is an ECG-gated or RT acquisition of a large 3D pyramidal volume with dimensions up to
90° × 90° by the height of the 2D view. Individual wedge-shaped subvolumes created over consecutive
heartbeats are stitched together and synchronized to the same cardiac cycle (Fig. 21.2C). Different FV
acquisition options can be chosen to optimize (a) volume size (seven beats over large sector), (b) ECG
(four beats over large sector), or (c) FR (seven beats over small sector). A machine preset (auto crop
50%) initially displays only half of the volume-rendered image revealing its inner details (Fig. 21.1F).
(d) Color Doppler FV is a gated or an RT acquisition of a small 3D pyramidal volume with superimposed 3D
representation of color Doppler flow. Similar to Zoom, color sectors with an appropriate Nyquist are
centered on two orthogonal 2D color Doppler views to represent the 3D volume. Stitching artifacts are

common as acquisition involves multiple subvolumes. Given the amount of information (3D volume
and 3D flow), the current technology only creates a small (up to 40° × 40°) 3D volume at a low
FR <20 Hz (Fig. 21.2D).
POSTPROCESSING
Image Optimization
Important determinants of 3D image quality and size during image acquisition are line density and trans-
ducer frequency. Line density is the number of scan lines per volume and affects the sector size and spatial
resolution. A low line density results in a larger sector size but poorer spatial resolution. Transducer fre-
quency is determined by the selection of options such as (a) penetration (low frequency), (b) general (inter-
mediate frequency), or (c) resolution (high frequency), and like in 2D imaging, can dramatically affect the
image appearance. The quality of the 3D image starts with adjustment of gain and compression to optimize
the 2D image. Gain, brightness (increasing whiteness), and smoothing (reducing image coarseness) are
adjustable 3D settings in RT or on any stored 3D datasets (Fig. 21.3A–C).
Image Artifacts
As previously described, a stitch artifact occurs between subvolumes in an FV-rendered image (Fig. 21.3D). Exces-
sive gain in a 3D image results in noise that appears as brown speckles and may obscure structures (Fig. 21.3E).
Dropout is an absence of echoes and appears black on the display (Fig. 21.3F). It may result from insufficient gain,
shadowing, or ultrasound attenuation. Thin (interatrial septum [IAS]) and distant structures (aortic and pulmonic
valves) remain difficult to image by 3D TEE. Most artifacts present in a 2D image will also appear in the 3D image.
Cropping and Orientation

Any 3D volume can be cropped, rotated, and displayed from any perspective (Fig. 21.4). It is possible now
to present intraoperative RT 3D TEE images in the surgeon’s orientation. The easily recognized aortic valve
B C
FIGURE 21.4 Cropping and rotation. All 3D datasets can be cropped along any plane and freely rotated to be displayed
in any orientation. A: Shown here is a prolapsed P1 scallop of the mitral valve (MV) in an en face view from the left atrium
(LA), cropped along the red dotted line and rotated 90° to a sagittal plane. B: Cropping can utilize a crop box to cut along
predefined planes or a mobile plane (purple). C: Cropping in real-time positions and adjusts a crop box to a region of inter-
est with simultaneous display of any side of the crop box. Shown here is a 3D en face view of the MV from the LA which
corresponds to the top of the crop box with reference 2D multiplanar reconstruction (MPR) images. Ba, back; Bo, bottom; F,
front; L, left; R, right; T, top. (From: Vegas A, Meineri M, Jerath A. Real-time three-dimensional transesophageal echocardiog-
raphy. A Step-by-Step Guide. New York, NY: Springer; 2012, used with kind permission of Springer Science + Business Media.)

(AV) is often used as a reference to orient the 3D volume in space. Alternatively, the reference 2D orthogo-
nal planes can be displayed to guide orientation (Fig. 21.4C).
Cropping can be performed online without employing analytical software, in RT or on stored
3D images. A crop box with six standard orthogonal planes or an arbitrary cropping plane can be
freely oriented in space and aligned to any anatomical structure of interest (Fig. 21.4B) to crop stored
images.
Measurements
Current 3D technology does not allow even simple online measurement of length or area within
the 3D image. A grid can be overlaid in RT and used to estimate dimensions within the 3D image.
Quantitative assessment of the 3D image requires exporting the 3D dataset into dedicated analytical
software (see below). Thus analyzed 3D datasets can accurately quantify anatomic and physiologic
information comparable to other imaging techniques (2D TEE, cardiac magnetic resonance imaging
[MRI]).
QUANTIFICATION ANALYSIS MODELS

Proprietary software programs are currently available for postacquisition off-line analysis of 3D datasets:
QLAB (Philips Healthcare, Andover, MA), TomTec (TomTec, Munich, Germany), and eSie Valves® (Siemens
Medical Solutions, Malvern, PA). TomTec and eSie Valves® can read 3D TTE and TEE datasets generated
A C
FIGURE 21.5 LV function. Quantification of left ventricular (LV) function requires exportation of an LV Full Volume data-
set to analytical software (QLAB Advanced, Philips Healthcare). A: Initial analysis uses multiplanar reconstruction (G,
green; R, red; B, blue) to align the planes through the LV apex. B: Following identification of the LV walls, a semiautomated
algorithm generates a surface-rendered endocardial cast and calculates the LV volume for each frame in the cardiac
cycle. Ejection fraction (EF) is determined from the end-diastolic volume (EDV) and end-systolic volume (ESV). C: The
endocardial cast can be divided according to the 17-segment ASE LV model. The subvolume of each LV segment can
be displayed over time for the entire cardiac cycle. (A, B) from: Vegas A, Meineri M, Jerath A. Real-time three-dimensional
transesophageal echocardiography. A Step-by-Step Guide. New York, NY: Springer; 2012. used with kind permission of
Springer Science + Business Media. Video 21.6. Video 21.6

A B
FIGURE 21.6 RV function. Specific software (4D RV Function, TomTec, Munich, Germany) can be used to create
a dynamic 3D model for the right ventricle (RV). A: Analysis uses multiplanar reconstruction of an RV 3D dataset.
B: A surface-rendered endocardial cast of the RV is displayed with its volume throughout the cardiac cycle. Ejection
fraction (EF) and stroke volume (SV) are calculated from the RV end-diastolic volume (EDV) and end-systolic volume
Video 21.7 (ESV). Video 21.7.
by different ultrasound systems while QLAB is manufacturer specific. All use a semiautomated method to
create dynamic or static models of cardiac structures.
QLAB combines three applications (MV quantification [MVQ], 3D quantification [3DQ], and 3DQ
Advanced) and is available on the Phillips iE33 ultrasound machine for processing of 3D datasets. QLAB uses
multiplanar reconstruction (MPR) to display the 3D volume in three color-coded orthogonal 2D planes: Green:
x/y elevation plane; red: y/z lateral plane; blue: x/z depth plane. These planes can be adjusted independently
or locked together to cut the 3D dataset in an infinite number of planes, each displayed in a separate window
(Fig. 21.5A).
MVQ creates a static 3D MV model from Zoom and FV datasets for comprehensive quantification
and identification of MV pathology (Fig. 21.6A). The basic 3DQ application analyzes any FV dataset of
the LV for quick accurate measurements of area, length, volume, and calculation of ejection fraction
(EF). The advanced 3DQ (3DQ Advanced, QLAB) application constructs a dynamic 3D endocardial
cast of the LV cavity from an FV dataset (Fig. 21.5B) which can also be divided into 17 LV segments
(Fig. 21.5C).
The TomTec package includes MV analysis (4D MV Assessment©), 3D volume quantification (4D
Cardio-View™), LV (4D LV analysis©), and RV (4D RV Function©) using semiautomated 3D volume
reconstruction. The user interface is similar to QLAB and displays the 3D volume dataset together with
three MPRs. It can perform 17-segment analysis of LV function and assess LV synchronicity although its
unique feature is a dynamic 3D RV model (Fig. 21.7).
eSie Valves® (Siemens Medical Solutions, Malvern PA) is a freestanding software in development for
MV and AV analysis (6). It takes 5 to 10 minutes to create a dynamic 3D MV model of a complete heart
cycle. A comprehensive biometric and kinematic measurement suite is available in a numerical, graphical
output as well as mapped to the model. It is the only software that constructs patient-specific physiologic
dynamic 3D AV and aortic root model with simultaneous analysis and display of the aortic-mitral complex
(Fig. 21.6C).

A C
FIGURE 21.7 Valve analysis software. There is vendor-specific software available to analyze 3D valve datasets. A: QLAB
mitral valve quantification (MVQ, Philips Healthcare, Andover, MA) creates a static 3D model for the mitral valve with
multiple measurements. B: TomTec 4D MV Assessment© (Munich, Germany) analyzes any MV 3D datasets acquired from
multiple vendors to provide a dynamic MV model. C: eSie Valves® (Siemens Medical Solutions, Malvern PA) also analyzes
3D datasets from any vendor to uniquely display a dynamic model of both the mitral and aortic valves. Video 21.8. Video 21.8
CLINICAL APPLICATIONS
Similar to 2D TEE, structures closest to the TEE probe are easily imaged in 3D (Table 21.2), thus allowing assess-
ment of clinical relevant issues in RT (5). In some instances 3D echocardiography has proven superior to 2D
echocardiography particularly for the assessment of the LV (volume, EF, mass, and dyssynchrony) and the MV.
Despite recent recommendations for 3D echocardiographic image acquisition and display (1), there remains a
lack of a standardized protocol for the use of intraoperative RT 3D TEE in everyday practice (Table 21.3). Acqui-
sition of 3D images is fast but manipulating and analyzing the 3D datasets takes time. This is problematic as a
real advantage of 3D datasets is the ability to quantify LV function and MV structure using analytical software.
Time constraints, limitations with simple measurements, and low temporal resolution restrict the use of RT 3D
TEE to its current role as a complement to 2D TEE studies in the hectic intraoperative environment.
TABLE 21.2 Structures Visualized with RT 3D TEE
Structure Adequate 3D viewsa (%)

Mitral valve (MV) 85–91
Left atrial appendage (LAA) 86
Interatrial septum (IAS) 84
Left ventricle (LV) 77
Aortic valve (AV) 18
Tricuspid valve (TV) 11
a
3D Zoom, except full volume for LV.
Adapted from: Sugeng L, Shernan SK, Salgo IS, et al. Live 3-dimensional
transesophageal echocardiography initial experience using the fully-sampled
matrix array probe. J Am Coll Cardiol. 2008;52:446–449.

TABLE 21.3 Protocol for RT 3D TEE
Structure View 3D mode Clinical Utility

Mitral valve 0°–120° ME Zoom, FV Morphology, function, quantify
views ± CD (EROA in MR, MVA in MS)
Aortic valve 60° ME SAX ± CD Zoom AV area, TAVI
120° ME LAX ± CD
Tricuspid valve 0°–30° ME 4-C ± CD Zoom Unstudied
40° TG ± CD
Pulmonic valve 90° UE ± CD Zoom TEE limited visualization
120° ME 3-C ± CD
Interatrial septum 0° ME view Zoom, FV Atrial septal defect
Left ventricle 0°–120° ME FV Volume, mass, EF, dyssynchrony
Right ventricle 0°–120° ME FV Volume, EF
Left atrial appendage 0°, 45°, 60°, 90° ME Live, Zoom Thrombus
Left atrium TG view FV Volume
ME, midesophageal; CD, color Doppler; FV, Full Volume; EROA, effective regurgitant orifice area; MR, mitral regurgitation; MVA,
mitral valve area; MS, mitral stenosis; SAX, short axis; LAX, long axis; AV, aortic valve; TAVI, transcatheter aortic valve implantation;
C, chamber; TG, transgastric; UE, upper esophageal; EF, ejection fraction.
Adapted from: Lang RM, Badano LP, Tsang W, et al. EAE/ASE recommendations for image acquisition and display using three-
dimensional echocardiography. J Am Soc Echocardiogr. 2012;25(1):3–46.
Mitral Valve
The native MV is easily imaged by TEE using standard 2D planes as well as various 3D modes including
Live, Zoom, and FV (7). A simple live acquisition from the midesophagus can be rotated to be viewed from
the left atrium (LA), but yields only part of the MV. Imaging of the entire MV is best performed using the
Zoom mode (Fig. 21.8) with excellent spatial but low temporal resolution (2). FV acquisition of the MV
improves temporal resolution for assessment of MV leaflet motion but may contain stitch artifacts which
can complicate image interpretation.
Where previously multiple 2D views were used to assess MV pathology, the entire MV can now be seen
on a single screen display with good spatial resolution. Any 3D image of the MV can be rotated and cropped
to examine discrete pathology. In addition, 3D TEE can readily assess normal and abnormal prosthetic MV
function including the size and location of paravalvular leaks (8).
3D Assessment of the Mitral Valve

The en face view of the MV in the surgeon’s orientation as viewed from the LA with the AV at the top of
the image (12 o’clock) and the left atrial appendage to the left (Fig. 21.8) is widely used to display the MV
in 3D. In this image detailed anatomy of the MV can be appreciated including the individual scallops of the
posterior leaflet. Manipulation of the 3D image can better define complex MV pathology involving clefts,
perforations, and both commissures (7).
Planimeter of MV area (MVA) by RT TTE better correlates with invasive catheter measurement and
2D pressure half-time. Planimetry can be performed using the xPlane mode or MV analytical software by
more accurately aligning 2D planes through the narrowest valve orifice.
Angled Views
The en face MV view using Zoom and FV datasets can foreshorten the extent of mitral leaflet motion
and may underestimate mitral valve prolapse (MVP). Rotating the en face view through 360° (Fig.
21.9A) provides additional perspectives from ‘angled views’; anterolateral commissure, posterior scal-
lops, and posteromedial commissure views (9). Systematic use of these views is less time-consuming

A C
B D
FIGURE 21.8 3D Zoom of the mitral valve. A: Acquisition of a Zoom dataset for the mitral valve (MV) begins with
positioning two boxes to encompass the MV. It is useful to include a portion of the aortic valve (AV) to aid orientation of
the 3D image. B: The initial 3D volume needs to be rotated and optimized by reducing the gain to display (C) an enface
view of the MV. This orientation is comparable to (D) the surgeon’s intraoperative view of the MV through the left atrium.
The commissures (anterior, AC and posterior, PC) and individual scallops of the posterior MV leaflet (P1, P2, P3) are easily
identifiable. AMVL, anterior mitral valve leaflet; LAA, left atrial appendage. (Reprinted from: Vegas A, Meineri M. Three-
dimensional transesophageal echocardiography is a major advance for intraoperative clinical management of patients
undergoing cardiac surgery: A core review. Anesth Analg. 2010;110:1548–1573, with permission.) Video 21.9. Video 21.9
than off-line processing and enables accurate RT identification of prolapsed segments involving both
commissures and the posterior leaflet.
3D Quantification
Using a proprietary software package (3DQ, Philips Healthcare) a Zoom or FV dataset of the MV can be
analyzed for mitral leaflet motion in relation to the annulus. An en face 2D view is displayed on the screen
as a guide to orientating 2D planes in MPR (Fig. 21.9B). Frame by frame motion of the MV can be analyzed
in different planes to assess leaflet motion.
Mitral Valve Quantification

The off-line construction of dynamic or static 3D MV models using proprietary software (Philips QLAB
MVQ, TomTec 4D MV Assessment©, and Siemens eSie Valves®) yields detailed quantitative information
about the MV (Figs. 21.6 and 21.9C). The preoperative use of 3D TEE may provide surgeons with additional
information about MV pathology to guide individual patient management.
Color Doppler
3D color Doppler assessment of the MV is limited by a small sector size which may not fully encom-
pass pathologic flow. The frequent presence of arrhythmias results in stitch artifacts which can complicate
interpretation of flow. The poor temporal resolution may be incapable of capturing the optimal frame for
quantitative assessment of lesions. Despite these limitations the 3D color Doppler mode offers improved

A
C
FIGURE 21.9 Mitral valve assessment. Currently, 3D TEE can assess the MV using multiple real-time and off-line ana-
lytic techniques. A: In addition to the enface view, angled views obtained from manipulating a Zoom of Full Volume MV
dataset can improve visualization of pathology. The anterolateral, scallop, and posteromedial orientations for the MV
demonstrate a flail P2 segment (red arrows) with multiple torn chordae. B: Analysis using QLAB (3DQ, Philips Healthcare)
multiplanar views can precisely identify prolapse of individual MV segments. C: MV models as previously mentioned in
Figure 21.7 can be constructed using analytical software to provide quantitative details of the MV. Illustrations in (A)
are used with permission of Frances Yeung and images from: Vegas A, Meineri M, Jerath A. Real-time three-dimensional
transesophageal echocardiography. A Step-by-Step Guide. New York, NY: Springer; 2012, used with kind permission of
Video 21.10 Springer Science + Business Media. Video 21.10.
insight into the variable geometry of the mitral regurgitation (MR) jet associated with different MV pathol-
ogies. The more accurate measurement of an irregular-shaped proximal isovelocity area (PISA) and vena
contracta (VC) width may better quantify MR severity (10).
Left and Right Ventricles

Left ventricular volume, global and regional wall motion, mass and synchronicity can be accurately assessed
using 3D echocardiography (1). FV acquisition is the only 3D imaging modality that can capture the entire
LV volume at sufficient FR (25 Hz) for dynamic assessment. Left ventricular volumes can be measured with
RT 3D TEE using two methods: 3D-guided biplanes or direct volumetric analysis.
The 3D-guided biplane method more easily positions two perpendicular 2D planes to accurately cut the
LV along its long axis at the true apex (Fig. 21.5A). Ideal midesophageal (ME) four-chamber and two-chamber
2D views are simultaneously displayed and the LV volume, EF, and mass are calculated by applying the
modified Simpson’s biplane method of the disks to the end-systolic and end-diastolic frames. This method
minimizes foreshortening of the LV using TEE but still relies on geometric assumptions.
Direct volumetric analysis measures LV volume throughout the cardiac cycle from a surface-rendered
cast of the LV cavity (Fig. 21.5B). The end-diastolic volume (EDV) and end-systolic volume (ESV) are mea-
sured and the stroke volume (SV) and EF are calculated. This method more accurately quantifies LV vol-
umes particularly in patients with an abnormal ventricular shape or regional wall motion abnormalities.
This in part relates to better alignment through the cardiac apex, inclusion of more endocardial surface
during analysis, and the lack of geometric shape assumption.

A C
FIGURE 21.10 Transcatheter aortic valve implantation (TAVI). A: Shown is a Full Volume dataset of a calcified aortic
valve (AV) from the aorta with 2D AV LAX and AV SAX views for reference. Measurement of the calcific AV annulus is more
easily performed in 2D. B: During TAVI procedures, 3D TEE can provide real-time information about positioning of various
wires, catheters, and the prosthetic valve (arrow). Correct alignment of the prosthetic valve equator is slightly below the
native AV annulus. C: Post valve deployment in Zoom of a well-functioning Edwards Sapien transcatheter heart valve
(THV) from the aorta during diastole. Video 21.11. Video 21.11
The RT 3D TEE assessment of regional LV wall motion is based on a change in LV chamber subvolume
over time from altered segmental myocardial contractility (Fig. 21.5C). Unlike standard 2D TEE there is no
direct measurement of myocardial thickening or displacement of individual segments.
The unusual geometric shape of the RV is well suited for 3D echocardiographic assessment of size,
volume, and EF (11). Off-line measurement of RV volume and function can be determined using special
analytical software from FV datasets of the RV (Fig. 21.6).
The accuracy of 3D TTE in measuring LV and RV volume is comparable to 2D TTE, MRI, and CT
techniques (1). There are no established normal values for LV EDV and ESV determined by 3D echocar-
diography. There is currently no study validating the use of 3D LV volume reconstructions from 3D TEE
datasets to assess LV volume.
Aortic Valve
The normal thin pliable AV cusps and heavily calcified AV are difficult to image by RT 3D TEE, though 3D
AV modeling may overcome this (6). Live, Zoom, or FV 3D en face AV views from the aorta or left ven-
tricular outflow tract (LVOT) are orientated with the right coronary cusp positioned inferiorly at 6 o’clock.
Three-dimensional echocardiography can better assess AV area by planimetry or the continuity equation
(1). TEE has proven a useful adjunct (12) during positioning and in assessing the function of transcatheter
AV implantation (Fig. 21.10).
Aorta
Three-dimensional TEE can image the entire aorta, excluding the blind spot, to assess aortic pathology
(13). Details of complex aortic root pathology including aortic aneurysm, aortic dissection, pseudoaneu-
rysm of the intravalvular fibrosa, and sinus of Valsalva aneurysm can be well imaged (Fig. 21.11). Better
topographic definition of atheromatous disease can be obtained using 3D TEE and epiaortic scanning.

FIGURE 21.11 Aortic root pathology. A: A patient with an aortic root abscess (arrow) is shown in 2D xPlane and in 3D Full
Volume. The patient had a previous mechanical mitral valve replacement (MVR) and the abscess that involved the intervalvular
fibrosa (arrow) between the aortic valve and prosthetic MV. B: Shown is a patient with an aortic root dissection with the dissec-
Video 21.12 tion flap (arrow) prolapsing through the aortic valve in 2D xPlane (AV SAX and AV LAX) and 3D Full Volume (AV LAX). Video 21.12.
A C
FIGURE 21.12 Patent foramen ovale (PFO) and atrial septal defect (ASD) closure. A: The intra-atrial septum can be interro-
gated using a Full Volume dataset orientated to be viewed from the right atrium. Shown is a patient with a PFO compared with
the surgical findings. B: Size and location of this ASD secundum is assessed using QLAB (3DQ, Philips Healthcare) by positioning
planes parallel (B, blue) and through the center of the defect (G, green and R, red). C: 3D Zoom from left atrium of the deployed
Amplatzer® device used to close the ASD. A, anterior; I, inferior; IVC, inferior vena cava; P, posterior; S, superior; SVC, superior vena
cava. (A) from: Vegas A, Meineri M, Jerath A. Real-time three-dimensional transesophageal echocardiography. A Step-by-Step
Video 21.13 Guide. New York, NY: Springer; 2012, used with kind permission of Springer Science + Business Media. Video 21.13.

A B
FIGURE 21.13 Masses. RT 3D TEE can better assess the location and attachments of masses. Size is more easily mea-
sured in 2D as there is no simple way to measure size without exporting the 3D dataset to analytical software. A: A
thrombus (arrow) is shown at the orifice of the left atrial appendage (LAA) in a 2D ME LAA view and Zoom from the left
atrium. B: A patient with a lipoma of the left ventricle that measures 4.48 cm × 1.97 cm in a 2D ME LAX view. A Full Vol-
ume of the left ventricular outflow tract shows its slender attachment to the interventricular septum (arrows) below the
aortic valve (AV). MV, mitral valve. (B) from: Vegas A, Meineri M, Jerath A. Real-time three-dimensional transesophageal
echocardiography. A Step-by-Step Guide. New York, NY: Springer; 2012, used with kind permission of Springer Science +
Business Media. Videos 21.14, 21.15. Video 21.14
Video 21.15
Interatrial Septum
The IAS is well imaged using 3D TEE either with Zoom or FV modes (14). The IAS can be orientated to
be shown from the LA or right atrium (RA) and facilitates demonstration of common pathology such as a
patent foramen ovale (PFO) or atrial septal defect (ASD) (Fig. 21.12). The use of TEE to guide placement
of percutaneous device closure (Fig. 21.12) of holes in the heart including ASD, ventricular septal defect
(VSD), and paravalvular leaks of prosthetic valves has been well described (15).
Masses
The location and attachment of intracardiac masses (Fig. 21.13) can be accurately assessed using RT 3D
TEE to facilitate surgical planning (16). The entire left atrial appendage can also be imaged for thrombus
(Fig. 21.13). Measurement of any mass size is performed in 2D or 3D with analytical software.
Hypertrophic Obstructive Cardiomyopathy

Hypertrophic obstructive cardiomyopathy (HOCM) presents with an asymmetric interventricular sep-
tum (IVS) and narrowing of the LVOT. Surgical resection of the IVS is a therapeutic option that results
in relief of LVOT obstruction, improving symptoms and patient outcome. TEE has been successfully
used to guide surgical septal myectomy. As the LVOT is a tubular structure that is difficult to image
using 2D images, 3D TEE is a useful tool to better understand LVOT anatomy and guide surgical inter-
vention (Fig. 21.14).

B C
FIGURE 21.14 Hypertrophic obstructive cardiomyopathy. A: This pathology is readily identifiable in the 2D ME
AV LAX view as septal thickening and systolic subvalvular obstruction with posterior-directed mitral regurgitation.
B: Measurement of septal thickness is performed at end-diastole from a 2D ME AV LAX view. C: 3D TEE Full Volume of the
AV LAX view may prove useful to provide more accurate information about septal thickness by better positioning a plane
Video 21.16 perpendicular to the septum. Video 21.16.
ACKNOWLEDGMENTS
Many thanks to Dr. Massimiliano Meineri for his help in creating the video clips and Ms. Willa Bradshaw
for preparing the figures.
REFERENCES
echocardiography. J Am Soc Echocardiogr. 2012;25(1):3–46.
2. Vegas A, Meineri M. Three-dimensional transesophageal echocardiography is a major advance for intraoperative clinical man-
agement of patients undergoing cardiac surgery: A core review. Anesth Analg. 2010;110:1548–1573.
3. Vegas A, Meineri M, Jerath A. Real-time three-dimensional transesophageal echocardiography. A Step-by-Step Guide.
New York, NY: Springer; 2012.
4. Salgo IS. Three-dimensional echocardiographic technology. Cardiol Clin. 2007;25:231–239.
5. Sugeng L, Shernan SK, Salgo IS, et al. Live 3-dimensional transesophageal echocardiography initial experience using the fully-
sampled matrix array probe. J Am Coll Cardiol. 2008;52:446–449.
6. Ionasec RI, Voigt I, Georgescu B, et al. Patient-specific modeling and quantification of the aortic and mitral valves from 4-D
cardiac CT and TEE. IEEE Trans Med Imaging. 2010;29:1636–1651.
7. Salcedo EE, Quaife RA, Seres T, et al. A framework for systematic characterization of the mitral valve by real-time three-
dimensional transesophageal echocardiography. J Am Soc Echocardiogr. 2009;22:1087–1099.
8. Sugeng L, Shernan SK, Weinert L, et al. Real-time three-dimensional transesophageal echocardiography in valve disease:
Comparison with surgical findings and evaluation of prosthetic valves. J Am Soc Echocardiogr. 2008;21:1347–1354.
9. Biaggi P, Gruner C, Jedrzkiewicz S, et al. Assessment of mitral valve prolapse by 3D TEE angled views are key. JACC Cardiovasc
Imaging. 2011;4:94–97.
10. Sugeng L, Weinert L, Lang RM. Real-time 3-dimensional color Doppler flow of mitral and tricuspid regurgitation: Feasibility
and initial quantitative comparison with 2-dimensional methods. J Am Soc Echocardiogr. 2007;20:1050–1057.

11. Horton KD, Meece RW, Hill JC. Assessment of the right ventricle by echocardiography: A primer for cardiac sonographers.
12. Jayasuriya C, Moss RR, Munt B. Transcatheter aortic valve implantation in aortic stenosis: The role of echocardiography. J Am
Soc Echocardiogr. 2011;24:15–27.
13. Evangelista A, Aguilar R, Cuellar H, et al. Usefulness of real-time three-dimensional transoesophageal echocardiography in the
assessment of chronic aortic dissection. Eur J Echocardiogr. 2011;12:272–277.
14. Saric M, Perk G, Purgess JR, et al. Imaging atrial septal defects by real-time three-dimensional transesophageal echocardiog-
raphy: Step-by-step approach. J Am Soc Echocardiogr. 2010;23:1128–1135.
15. Perk G, Lang RM, Garcia-Fernandez MA, et al. Use of real time three-dimensional transesophageal echocardiography in
intracardiac catheter based interventions. J Am Soc Echocardiogr. 2009;22:865–882.
16. Muller S, Feuchtner G, Bonatti J, et al. Value of transesophageal 3D echocardiography as an adjunct to conventional 2D imag-
ing in preoperative evaluation of cardiac masses. Echocardiography. 2008;25:624–631.

QUESTIONS
1. Real-time 3D TEE acquires raw data by: 9. Structures are most difficult to image using
a. Volume scanning 3D if they are:
b. Sector scanning a. In the near field
c. Off-line reconstruction b. Thickened
d. Planar scanning c. Heavily calcified
d. Mobile
2. An RT 3D echo probe comprises a:
a. Linear phased array of 250 crystals 10. 3D color Doppler is least affected by:
b. Fully sampled matrix array of 2,500 crystals a. Sector size
c. Nonlinear phased array of 250 crystals b. Stitch artifacts
d. Partly sampled matrix array probe of 1,100 c. Frame rate
crystals d. Nyquist limit
3. Which is not a step in creating a 3D image? 11. Which 3D mode is best to obtain an en face
a. Segmentation view of the entire mitral valve?
b. Rendering a. 3D Live
c. Conversion b. 3D Zoom
d. Interpretation c. 3D Full Volume
d. 3D color Doppler
4. Which form of rendering allows a virtual
dissection of a structure? 12. Which structure should be included to help
a. Wireframe orientate the mitral valve in 3D space?
b. Sector a. Tricuspid valve
c. Surface b. Aortic valve
d. Volume c. Pulmonic valve
d. Left upper pulmonary vein
5. Which 3D mode has the largest sized 3D
dataset? 13. Angled views to assess mitral valve prolapse
a. 3D Live does not include the:
b. 3D Zoom a. Left ventricular view
c. 3D Full Volume b. Posteromedial view
d. 3D color Doppler c. Scallop view
d. Anterolateral view
6. Which 3D mode has the lowest frame rate?
a. 3D Live 14. Mitral valve area in mitral stenosis
b. 3D Zoom is most accurately assessed using 3D
c. 3D Full Volume echocardiography by:
d. 3D color Doppler a. Direct planimetry in real time
b. Creation of 3D model
7. Postprocessing to optimize a 3D image does
c. Off-line measurement using multiplanar
not include adjusting:
reconstruction
a. Gain
d. Superimposing a 3D grid
b. Color
c. Brightness 15. 3D assessment of global left ventricular
d. Smoothing function using a surface-rendered model
does not overcome the limitation of:
8. Which is not an artifact in 3D images?
a. Poor endocardial definition
a. Overgain
b. Ventricular size
b. Dropout
c. Ventricular shape
c. Stitch
d. Wall motion abnormalities
d. Inversion

16. 3D TTE assessment of LV global function is 19. During transcatheter aortic valve
not comparable to: implantation procedures, 3D TEE is least
a. 2D TTE useful to:
b. Computed tomography (CT) a. Measure aortic valve diameter
c. Magnetic resonance imaging (MRI) b. Position valve
d. 3D TEE c. Assess paravalvular leak
d. Assess valve function
17. Assessment of LV regional wall motion
abnormalities using 3D TEE involves: 20. Real-time 3D TEE assessment of masses
a. Measuring wall thickening cannot be easily used to determine:
b. Measuring wall motion a. Location
c. Assessing segmental timing b. Size
d. Measuring segmental volume c. Attachment
d. Functional effect
18. During assessment of aortic root dissection
3D TEE poorly interrogates:
a. Flap location and movement
b. Aortic insufficiency severity
c. Aortic arch involvement
d. Coronary blood flow

22 Common Artifacts and Pitfalls of Clinical
Echocardiography
Fabio Guarracino and Albert C. Perrino, Jr.
C LINICALLY IMPORTANT IMAGING AR TIFACTS RESULT from the interplay of the ultrasound system,
the patient, and the interpreting echocardiographer. Knowledge of the types of artifacts that occur during a
standard TEE examination is of paramount importance for the correct interpretation of the echo data. The
most common artifacts seen in clinical practice are the result of (a) normal or variant anatomic structures
that are misdiagnosed, (b) the physical limitations of ultrasound imaging, and (c) undesirable interactions
of ultrasound with tissues or medical devices. In this chapter we first review the common false interpre-
tations of normal anatomy. Second, we discuss the artifacts commonly encountered in two-dimensional
imaging and three-dimensional imaging, and finally, we discuss the artifacts commonly encountered in
Doppler examinations.
NORMAL ANATOMIC VARIANTS IN TWODIMENSIONAL IMAGING

Both novice and experienced echocardiographers may call normal structures abnormal. These normal vari-
ants can affect the intraoperative diagnosis and lead to an inappropriate surgery, which can have a devastat-
ing impact on the outcome. Careful evaluation and a consideration of the common variants discussed in
the subsequent text can help limit problems related to misdiagnosis.
Crista Terminalis
The crista terminalis has been misinterpreted as a right atrial tumor or thrombus. This prominent
muscular ridge can be differentiated from an anomaly by its characteristic appearance and position.
The crista terminalis originates at the junction of the right atrium and superior vena cava and runs
longitudinally toward the inferior vena cava. The crista terminalis separates the trabeculated appendage
of the atrium from the smooth tubular portion. The structure is best visualized in the midesophageal
(ME) bicaval view (Fig. 22.1).
Eustachian Valve or Chiari Network

The Eustachian valve is often misdiagnosed as an intra-atrial thrombus. The Eustachian valve (called a
Chiari network when fenestrated) is the remnant of the embryologic right venous valve, which is important
in utero to direct inferior vena cava blood flow across the fossa ovalis. The filamentous structures can be
differentiated from thrombus by their characteristic “insertion” into the atrial wall. They are best visualized
in the ME bicaval view, in which they can be seen originating from the junction of the right atrium and
inferior vena cava (Fig. 22.1).
Lipomatous Hypertrophy of the Atrial Septum

Myxomas, the most common cardiac tumors, often originate from the interatrial septum and typically
involve the fossa ovalis. Lipomatous hypertrophy of the atrial septum can mimic atrial masses such as
myxomas. The characteristic “dumbbell” shape seen in the ME four-chamber or ME bicaval view differen-
tiates lipomatous hypertrophy from other structures. The appearance is caused by fatty infiltration of the
atrial septum with sparing of the fossa ovalis (Fig. 22.2).
456

22. Common Artifacts and Pitfalls of Clinical Echocardiography 457
CT
FIGURE 22.1 A: The Eustachian valve is easily seen in this midesophageal bicaval view. B: A prominent Chiari network
(arrows). LA, left atrium; RA, right atrium; CT, crista terminalis.
FIGURE 22.2 The characteristic dumbbell shape of a lipomatous atrial septum with sparing of the fossa ovalis is seen
in this midesophageal bicaval view. LA, left atrium; RA, right atrium; SVC, superior vena cava.

FIGURE 22.3 A Coumadin ridge is seen between the left atrial appendage and the left upper pulmonary vein (LUPV).
LA, left atrium; LV, left ventricle.
Coumadin Ridge
A prominent muscle ridge is formed between the left atrial appendage and the atrial insertion of the
left upper pulmonary vein. This prominence is often misdiagnosed as thrombus and is referred to as the
Coumadin ridge or “Q-tip” sign. The lack of mobility and characteristic location, best seen in the ME two-
chamber view, help distinguish it from an abnormal structure (Fig. 22.3).
Pericardial Sinuses
Pericardial sinuses (or folds) between the atria and great vessels can give rise to echolucent spaces despite
only minimal amounts of pericardial fluid. The transverse and oblique sinuses of the pericardium can easily
mimic pericardial cysts or abscesses. Pericardial fat seen in these extracardiac structures can also mimic
intracardiac thrombus (Fig. 22.4).
FIGURE 22.4 Transverse sinus filled with pericardial fluid can be seen in this midesophageal view at 60 degrees. LAA,
left atrial appendage.

FIGURE 22.5 A Lambl excrescence is seen on the aortic valve (arrow).
Lambl Excrescences
Fine filamentous strands, Lambl excrescences, can be seen originating from the aortic valve of elderly
patients. These structures can be differentiated from valvular vegetations by their characteristic “delicate”
appearance in the absence of any clinical evidence of endocarditis (Fig. 22.5).
Moderator Band and False Tendon

The moderator band of the right ventricle has been misinterpreted as an intracardiac mass. This specialized
cardiac trabeculation runs from the right ventricular free wall to the interventricular septum. It is often
best seen in the ME four-chamber view (Fig. 22.6A). In contrast, a false tendon is an anatomic variant of the
left ventricle consisting of fibromuscular string(s) coursing from the interventricular septum to the region
about the papillary muscles (Fig. 22.6B and Video 22.1). They are best detected in ME longitudinal views Video 22.1
and can be mistaken for subaortic membranes and pseudoaneurysm.
Pleural Effusion
Pleural effusions of the left side of the chest can mimic aortic dissection. In the descending aorta long-axis
view, a pleural effusion will parallel the course of the aorta and have the appearance of a true lumen–false
lumen dissection. Changing to the descending aorta short-axis view and identifying the characteristic tri-
angular shape of a left-sided pleural effusion easily confirm the diagnosis of effusion versus dissection
(Fig. 22.7). To inspect for a right-sided pleural effusion the probe is turned progressively leftward from the
descending aortic views to examine the right posterior chest.
TWODIMENSIONAL ECHOCARDIOGRAPHIC IMAGING ARTIFACTS
Suboptimal Image Quality

The inability to visualize cardiac structures because of suboptimal image quality remains a challenge in
transesophageal echocardiographic diagnosis. Most commonly, improper settings of the ultrasound unit
are to blame, but patient anatomy, acoustic interfaces (e.g., air between the probe and the stomach or
esophageal wall, hiatal hernia), and sonographer skill play a definite role. Adjustments in machine settings
coupled with minor manipulations of the ultrasound probe can lead to substantial improvement in to low
quality images. This topic is discussed further in Chapter 23.

FIGURE 22.6 A: The moderator band of the right ventricle is seen in this midesophageal four-chamber view. B: In
contrast, a left ventricular false tendon. LV, left ventricle; RV, right ventricle; LA, left atrium.
FIGURE 22.7 A pleural effusion is seen in a transverse plane.

FIGURE 22.8 Transgastric mid short-axis view demonstrating septal and lateral wall dropout.
FIGURE 22.9 A: Mitral valve and apparatus imaged with chordae tendineae parallel to the ultrasound beam (mide-
sophageal five-chamber view). B: Markedly improved delineation of the chordae tendineae with the ultrasound beam
perpendicular to the chordae tendineae (transgastric long-axis view). LA, left atrium; MV, mitral valve; LV, left ventricle.

Air between the transducer surface and tissue, encountered in transgastric views more often than in
transesophageal views, causes severe image degradation to the point of complete inability to image. Gastric
suctioning before the transesophageal echocardiographic examination can rectify the poor acoustic trans-
mission caused by an air–tissue interface.
Imaging is also frequently suboptimal when the cardiac structure of interest lies parallel to the ultra-
sound beam. A common example of this artifact is “dropout” of the lateral and septal walls in the TG short-
axis and ME four-chamber views (Fig. 22.8). As specular reflections are maximized when tissue interfaces
lie perpendicular to the ultrasound beam, this artifact is best overcome by repositioning the ultrasound
probe to a more favorable vantage point. Another example of this phenomenon is the impaired ability to
visualize thin linear structures, such as the chordae tendineae of the mitral valve, when they are parallel
to the ultrasound beam (ME five-chamber view) (Fig. 22.9A). However, when these structures are interro-
gated perpendicular to the beam (TG two-chamber view), they are easily visualized (Fig. 22.9B).
Acoustic Shadowing
Acoustic shadowing occurs when the ultrasound beam meets an interface of two structures with marked
differences in acoustic impedance. Common examples include structures with a high level of acoustic
impedance, such as calcific aortic or mitral valves (Fig. 22.10A).
Such structures strongly reflect and scatter the ultrasound signal, thereby limiting distal penetration
of the sound waves. Similarly, mechanical prostheses and the struts of bioprosthetic valves produce shad-
owing. The resultant image reveals an echo-dense structure with a lack of signal in the sector beyond the
structure (Fig. 22.10B).
FIGURE 22.10 A: In this view a broad area of the distal scan is not visible due to shadowing from a calcific aortic valve
(arrows). B: Acoustic shadowing caused by a prosthetic mitral valve ring imaged in the midesophageal four chamber
view. The arrows point to the long axial shadows. LA, left atrium; MV, mitral valve; LV, left ventricle.

FIGURE 22.11 Discrepancy between axial and lateral sizes of microbubbles as a consequence of resolution artifact.
Dist A and Dist B indicate lateral and axial dimensions, respectively.
Lateral Resolution
The two-dimensional image is created from a series of individual ultrasound beams or scan lines. Since struc-
tures lying between any two beams are not interrogated, the machine creates their display by averaging infor-
mation received from the adjacent beams. This causes two problems. First, determinations of the size of a
structure between beams (lateral resolution) are never as precise as measurements made along the beam’s
path (axial resolution). Consequently, most system’s axial resolution is at least twice the lateral resolution.
Second, with sector scans, the ultrasound scan lines are closest to each other in the near field and the length
between them increases with increasing depth. Since this results in decreasing lateral resolution with increas-
ing depth, while axial resolution remains constant, shape distortion artifact occurs. This typically appears as
lateral stretching of small, strongly echogenic objects, such as intracardiac catheters, bubbles, or wires. Round
structures, such as intracardiac contrast agents or air, appear markedly elongated as seen in Figure 22.11.
Side Lobe and Beam Width

Side lobes are weak beams emitted outside the path of the main ultrasound beam. Although weak, when
they encounter an echo-dense structure such as a calcified aorta, mitral valve ring, or any prosthetic
material or catheter (Fig. 22.12A), the resulting reflection can be strong enough to be detected. When
this occurs the scanner misplaces these echoes in the image, incorrectly assuming they were generated by
structures lying in the path of the main beam. The artifact is displayed at the appropriate distance from the
transducer but at the wrong lateral position. Since the ultrasound beam sweeps the entire scan sector, side
lobe artifacts often appear as narrow, curvilinear densities smeared over the entire scan sector.
Beam width artifacts differ from side lobe artifacts in that they are produced by the main ultrasound
beam itself. They occur because each display pixel is generated from the data produced by a three-
dimensional, cone-shaped ultrasound wave. Thus structures adjacent the beam’s center (in the lateral or
elevational planes) that lie within the cone-shaped main beam are displayed. This creates artifacts that
appear as structures or catheters in the wrong position, flaps in the aorta (Fig. 22.12B), or elongated struc-
tures. Beam width artifacts also occur with spectral Doppler and are discussed later.
Reverberation and Mirroring

Reverberations are caused by the repeated back-and-forth reflection of an ultrasound wave between two
strong specular reflectors. This phenomenon leads to two types of imaging artifacts. In the first, multiple
linear densities are produced in the area of the imaging sector distal to the reflecting structures (Fig. 22.13).

PA catheter and sidelobes
AoV
FIGURE 22.12 A: Side lobe artifact from a pulmonary artery catheter appearing as an echo-dense bright linear struc-
ture. B: A Beam Width artifact of aortic wall imaged in the ascending aorta. LA, left atrium; LV, left ventricle; RV, right
ventricle; RA, right atrium; AoV, aortic valve.
The second type of artifact occurs when the strong echoes are reflected from the transducer itself. The
reflection then travels back to the same target, where it is echoed a second time toward the detecting trans-
ducer. As a result, an artifact is produced that appears as a duplication or “mirror image” of the structure in
the far field. Since this second trip doubles the travel time, the target structure is imaged once at the correct
distance and a second time at twice the distance from the transducer. The descending thoracic aorta in both
the transverse and longitudinal scans is a common source of this type of reverberation artifact. The vessel is
imaged correctly in the near field and falsely duplicated immediately below. The duplicating reverberation
artifact also extends in this case to color flow imaging (Fig. 22.14).
FIGURE 22.13 Reverberation artifact resulting from a mechanical mitral valve is easily seen distal to the valve. LA, left
atrium.

FIGURE 22.14 A mirror image of the true aortic arch is seen in the far field. Note that the false arch is the same size as
the true structure. The color flow Doppler signals are also duplicated. Ao, aorta.
FIGURE 22.15 A: Electrocautery artifacts in the midesophageal five-chamber view. B: Electrocautery interference with
color Doppler shown in a midesophageal long-axis view.

Electronic Noise
Electronic noise, of which electrocautery is the major source, causes an imaging artifact that resembles a
“snowed image” pattern. Viewing cardiac anatomy through this snowstorm is an annoying reality of echo-
cardiographic imaging during surgery (Fig. 22.15).
ARTIFACTS IN SPECTRAL AND COLOR FLOW DOPPLER

Spectral and color flow Doppler are susceptible to several of the mechanisms of artifact production that
occur in two-dimensional imaging; however, the appearance of the artifacts is quite different. In addition,
the Doppler examinations are susceptible to a number of artifacts unique to this method such as aliasing
and artifacts that result from incorrect alignment between the ultrasound beam and blood flow.
Aliasing
A shortcoming of pulsed wave Doppler systems, which includes color flow Doppler, is that the maximal blood
velocities that can be accurately quantified are limited by the pulse repetition frequency. Specifically, any
Doppler frequency shift greater than one-half of the pulse repetition frequency, known as the Nyquist limit,
results in a distorted spectral signal. The distortion in the Doppler signal, called aliasing, causes several types
of artifacts in the pulse wave spectral signal or color flow map. Common examples include “wraparound” of
the spectral signal (see Figure 5.10) and red–blue stippling on the color flow map (see Figure 5.14).
Acoustic Shadowing in Color Flow

Strong specular reflectors result in acoustic shadowing not only with two-dimensional imaging but also
with Doppler modes. This artifact can be misinterpreted as a lack of blood flow in the shadowed region and
is commonly seen during the interrogation of prosthetic or heavily calcified valves (Fig. 22.16).
Nonparallel Beam Angle

Since the Doppler shift is proportional to the cosine of the angle between the path of the ultrasound beam
and that of the blood flow, blood flow velocities are underestimated when the orientation of the ultrasound
beam is not parallel to the blood flow. With color flow Doppler, this artifact typically occurs when the course
of a vessel is oblique to the ultrasound beam. The blood flow perpendicular to the path of the Doppler beam
FIGURE 22.16 Acoustic shadowing in color flow Doppler caused by a prosthetic mitral valve ring in the midesophageal
aortic valve long-axis view. The arrow points to the long axial shadow. LA, left atrium; MV, mitral valve; Ao, aorta; LV, left
ventricle.

FIGURE 22.17 Nonparallel beam angle color flow Doppler artifact in the aortic arch. The direction of blood flow is
indicated by the horizontal arrow. The angled arrows indicate the direction of the Doppler ultrasound interrogating beam.
is color-coded black (i.e., no flow). Also, as the Doppler beam sweeps across the imaging sector, it intersects
the blood path at varying angles, causing a peculiar artifact in the color flow map. For example, if the blood
flow in an artery is directed from left to right across the ultrasound sector, the color mapper will character-
ize the flow in the left side of the sector red (i.e., directed toward the transducer) and the blood flow in the
right side of the sector blue (i.e., moving away from the transducer). Therefore, an image is created in which
it appears as if the blood were colliding in the middle portion of the vessel (Fig. 22.17).
Mirroring
This artifact appears in the spectral display as a symmetric duplication of the actual flow signal, but in
the opposite direction (Fig. 22.18). It is related to a process known as quadrature phase demodulation,
which allows the echo system to separate the Doppler-shifted signal from the complex returning signal.
The demodulation procedure uses a second, weaker signal that is generated out of phase with the broadcast
FIGURE 22.18 Pulsed wave Doppler mirroring artifact. Transmitral flow and its weaker mirrored signal.

FIGURE 22.19 Color flow Doppler reverberations are seen distal to a mechanical mitral valve in this midesophageal
commissural view. LA, left atrium; LV, left ventricle.
signal. However, excessive gain in the system causes the weak but incompletely canceled signal to be dis-
played as a mirror image of the actual flow signal.
Color Flow Reverberation and Gain-related Anomalies

As discussed previously, reverberations are secondary reflections that occur when ultrasound is reflected a
second time, typically from the transducer, highly reflective tissue, or intracardiac materials (e.g., a pulmo-
nary artery catheter). In the case of secondary reflections from the transducer face a ghost of the primary
image often appears at twice the distance of the actual target from the transducer hence the term “mirror
image.” With Doppler reverberation, the reflected signal from a moving target is stronger than the original
signal, so that the color intensity of the ghost is increased in comparison with that of the primary target
(Figs. 22.14 and 22.19).
FIGURE 22.20 A: From the transgastric (TG) mid short-axis view, the pulsed wave sample volume is shown placed on the
interventricular septum. Spectral signals show high-velocity flow during systole. This is not caused by an interventricular sep-
tal defect; rather, it is an artifact of blood flow from the adjacent left ventricular outflow tract (LVOT), which lies just anterior to
the imaged plane. B: With slight anteroflexion of the probe, the LVOT is visualized in the deep TG long-axis view.

FIGURE 22.20 (continued)
Beam Width Flow Artifacts

Although the heart is typically presented in two dimensions with echocardiography, the image is actually
created by three-dimensional ultrasound signals. Just as beam width flow artifacts can occur in the 2D
image, it also becomes possible to detect blood flow lying outside the displayed two-dimensional image.
An example of this phenomenon is shown in Figure 22.20A, in which interrogation of the interventricular
septum reveals high-velocity flow. This is not the result of a ventricular septal defect but an artifact caused
by blood flow in the left ventricular outflow tract, which lies in a plane just anterior to the TG short-axis
view seen in Figure 22.20B.
Range Ambiguity with Pulsed Wave Doppler

One of the main advantages of pulsed wave Doppler is the ability to range gate a sample volume. However,
strongly reflected signals originating from blood flow at two or three times the depth of the pulsed wave
FIGURE 22.21 Top: In the deep transgastric long axis, the pulsed wave Doppler sample volume is positioned at the
tips of the mitral valve leaflets. Note that the left ventricular outflow tract and ascending aorta lie in the path of the beam
in the far field. Bottom: The displayed pulsed wave spectral signal shows not only the diastolic flow through the mitral
valve but also the left ventricular outflow tract and aortic blood flow velocities during systole. These measurements of
the far field velocities are at exactly two and three times the distance to the primary measurement.

sample volume arrive at the transducer simultaneously with those produced from subsequent pulse signals
reflected from the target. This artifact is particularly problematic when high pulse repetition frequency
Doppler is employed. These signals are displayed and can be misinterpreted as blood flow within the target
volume (Fig. 22.21).
SUMMARY
An appreciation of cardiac embryology and anatomy will enable the echocardiographer to interpret cardiac
structures with an unusual appearance accurately, so that unnecessary surgical intervention is prevented.
A thorough understanding of two-dimensional and Doppler technologies is required to minimize misin-
terpretation.
REFERENCES
1. Prabhu M, Raju D, Pauli H. Transesophageal echocardiography: Instrumentation and system controls. Ann Card Anaesth.
2012;15(2):144–155.
2. Maltagliati A, Pepi M, Tamborini G, et al. Usefulness of multiplane transesophageal echocardiography in the recognition of
artifacts and normal anatomical variants that may mimic left atrial thrombi in patients with atrial fibrillation. Ital Heart J.
2003;4(11):797–802.
3. Badano L, Piazza R, Bisignani G, et al. Echocardiographic features of left ventricular aneurysm and false tendon in a patient
with postinfarction pseudoaneurysm after aneurysmectomy. G Ital Cardiol. 1993;23(3):295–299.
4. Vignon P, Spencer KT, Rambaud G, et al. Differential transesophageal echocardiographic diagnosis between linear artifacts
and intraluminal flap of aortic dissection or disruption. Chest. 2001;119(6):1778–1790.
5. Burwash IG, Chan KL. Transoesophageal echocardiography. In: Otto CM, ed. The Practize of Clinical Echocardiography. 3rd
ed. Philadelphia, PA: Elsevier Saunders; 2007:5–25.
6. Bolognesi M, Bolognesi D. A prominent crista terminalis associated with atrial septal aneurysm that mimics right atrial mass
leading to atrial arrhythmias: A case report. J Med Case Rep. 2012;6(1):403.
7. Akcay M, Bilen ES, Bilge M, et al. Prominent crista terminalis: As an anatomic structure leading to atrial arrhythmias and
mimicking right atrial mass. J Am Soc Echocardiogr. 2007;20(2):197.e9–e10.
8. Spieker LE, Hufschmid U, Oechslin E, et al. Double aortic and pulmonary valves: An artifact generated by ultrasound refrac-
tion. J Am Soc Echocardiogr. 2004;17(7):786–787.
9. Rittgers SE. Signal processing of Doppler information. Echocardiography. 1987;4(1):7–14.
10. Abu-Zidan FM, Hefny AF, Corr P. Clinical ultrasound physics. J Emerg Trauma Shock. 2011;4(4):501–503. doi: 10.4103/0974-
2700.86646.

QUESTIONS
1. What is the most common type of imaging c. Axial resolution
artifact? d. Lateral resolution
a. Acoustic shadowing
8. The artifacts correlated to the lateral
b. Reverberation
resolution are:
c. Suboptimal image quality
a. A double image of the object of interest
d. Mirroring
b. A single image of two objects orientated
2. Which of the following assumptions of the perpendicular to the main beam
US imaging system can be disrupted when c. Multiple equidistance bright signals
artifacts occur? d. None of the above
a. The echoes travel in straight lines from the
9. Range ambiguity depends on the failure
transducer
of which of the following fundamental
b. The echoes come back to the transducer
assumptions?
after a single reflection
a. The time that a single reflection employs to
c. The time that the US wave employs to return
return back to the transducer only depends
to the transducer provides the distance
on the distance between the reflector and
between the transducer and the reflective
the transducer itself
structure
b. The echoes detected by the system are those
d. All of the above
generated by the most recent pulse emitted
3. Acoustic shadowing can result from: by the transducer
a. High attenuation c. a and b
b. Refraction d. All the echoes are generated by the US main
c. Enhancement beam
10. Aliasing artifacts are typical of:
4. Acoustic shadowing will produce a dark a. 2D US
area: b. Color Doppler and pulsed Doppler
a. Proximal to the strong reflector c. Continuous wave Doppler
b. Distal to the strong reflector d. None of the above
c. Left of the strong reflector
11. Which of the following factors is not related
d. Right of the strong reflector
to aliasing in spectral Doppler imaging?
5. Axial resolution artifacts occur when: a. Pulse repetition frequency
a. Two objects lying perpendicular to the main b. Nyquist limit
US beam are displayed as a single structure c. “Wraparound”
b. Two objects lying parallel to the main US d. Lateral resolution
beam are displayed as a single structure
12. The crista terminalis is located in the:
c. The US system employs longer spatial pulse
a. Right atrium
length
b. Left atrium
d. The US system employs shorter pulse dura-
c. Right ventricle
tion
d. Left ventricle
6. In most imaging systems, axial resolution is
13. The moderator band is located in the:
at least:
a. Right atrium
a. Equal to lateral resolution
b. Left atrium
b. Twice the lateral resolution
c. Right ventricle
c. Ten times the lateral resolution
d. Left ventricle
d. Half of the lateral resolution
14. The Eustachian valve is located in the:
7. The diameter of the US main beam
a. Right atrium
impacts:
b. Right ventricle
a. Temporal resolution
c. Left atrium
b. The number of scan lines
d. Left ventricle

15. The Coumadin ridge is located in the: 18. Side lobe artifacts:
a. Right atrium a. Are true structures outside the path of the
b. Right ventricle main beam
c. Left atrium b. Are true structures in the path of the main
d. Left ventricle beam
c. Are incorrectly displayed in the two-
16. Which of the following statements is NOT
dimensional sector
true of a lipomatous atrial septum?
d. a and c
a. It has a dumbbell shape
b. The fatty infiltration is echo-dense 19. Reverberation artifacts will not produce:
c. The fossa ovalis is thickened a. Multiple linear densities
d. The fossa ovalis is spared b. Dual structures in an axial orientation
c. Dual structures in a left–right orientation
17. In an interrogation of flow with
d. A duplication that is the same size as the
spectral Doppler, a nonparallel beam
original
angle will:
a. Overestimate the true velocity 20. The comet tails are an atypical examples of:
b. Underestimate the true velocity a. Reverberation
c. Correctly measure the velocity b. Ringdown
d. Spectral Doppler does not measure c. Multipath
velocities d. Mirroring

23 Techniques and Tricks for Optimizing
Transesophageal Images
Alan C. Finley and Scott T. Reeves
INTRODUCTION
The accuracy and diagnostic confidence of a transesophageal echocardiographic (TEE) study depends
greatly on the quality of the ultrasound image. Image quality is affected by several factors, including patient
anatomy, the quality of the ultrasound system, and the skill of the echocardiographer. This chapter dis-
cusses the controls on the echocardiography machine and the process of optimizing their settings to obtain
images of the highest quality.
TWODIMENSIONAL CONTROLS
Preprocessing Versus Postprocessing Controls

Preprocessing controls adjust the transmission and acquisition of the ultrasound signals. Preprocessing set-
tings control the formatting of the ultrasound signal for conversion into an electric signal. Changes in the
preprocessing controls affect the information that the scanner will access to create an image (1), and this
formatted information is the basis on which an image is created. Postprocessing settings affect the manner
in which the formatted information is displayed on the monitor. Simply put, postprocessing defines the
“cosmetic appearance” of the ultrasound data displayed on the monitor.
Transmit Power
Transmit power controls the amplitude (acoustic power) of the transmitted ultrasound signal. Modern echo-
cardiography systems default to a high power setting to maximize the signal-to-noise ratio. A theoretic con-
cern is that high power ultrasound can have deleterious effects on tissue, particularly in fetal echocardiogra-
phy. Federal standards restrict the maximal intensities allowed for transmit power settings on commercially
available ultrasound systems. Typically, echocardiography systems default to the maximum transmit power;
however, proper adjustment of transmit power becomes critical when echo contrast studies are performed.
Gain
Increasing the gain increases the amplitude of the electric signal generated by returning ultrasound signals
received at all depths. Unfortunately, any noise present is also amplified. Setting the gain too high or too
low affects the ability to read the image correctly. When the gain is set too high, the image appears bright,
and linear structures, such as the mitral valve, appear thickened. Increases in the gain also increase the
amount of visible noise. For instance, with moderately excessive gain settings, the left ventricular (LV)
cavity acquires a speckled appearance, which can make it difficult to differentiate the LV cavity from the
myocardium. With further increases in the gain, the entire LV takes on a whitened appearance and the
ability to differentiate structures is lost.
When the gain is set too low, only bright signals, such as those from the pericardium, are visible, and
very low-amplitude signals, such as the signal from an LV thrombus or “smoke” in the LV, are lost (2). Video 23.1a
Therefore, the gain should be adjusted to obtain an image with a gray scale ranging from low-amplitude Video 23.1b
(dark gray) to high-amplitude (white) signals. The gray scale, displayed as a bar graph on the right side of Video 23.1c
the image, is useful for guiding adjustments. Figure 23.1 (Video 23.1a–c) demonstrates the effect of three
separate gain settings on the same midesophageal two-chamber view.
473

A B
C
Video 23.1a
Video 23.1b FIGURE 23.1 The midesophageal two-chamber view with the gain setting normal (A), too low (B), and too high (C).
Video 23.1c (Video 23.1a–c).
Clinical Pearl
The bright ambient lighting of the operating room often misleads the echocardiographer to use excessive
gain settings. This problem can be overcome by eliminating the operating room lights briefly during the
examination or shielding the screen with a hood.
Time Gain Compensation

Attenuation results in the signals returning from the far field being weaker than signals from the near field.
Therefore, the ability to selectively adjust the gain setting at each depth is essential to optimize the image
and is commonly referred to time gain compensation (3). For example, the echocardiographer can use the
time gain compensation to amplify the weaker signals returning from the far field more than the signals
returning from shallower depths (near field). The echocardiographer should be careful when adjusting the
time gain compensation. If it is set too low, the elimination of true tissue signals is a risk. The time gain com-
Video 23.2b pensation should be used to eliminate gain-related artifacts and optimize far-field structures. The effects of
Video 23.2c time gain compensation settings on image quality are shown in Figure 23.2 (Video 23.2b, c).
Clinical Pearl
In a normal examination, the time gain compensation controls are set lower in the near field and higher in
the far field. However, for imaging pathology in the near field with low echogenicity (e.g., thrombus in the
aorta or left atrium), the near-field time gain compensation should be increased.
Lateral Gain Compensation

Ultrasound beams transmitted through tissue side by side can be subject to different levels of attenuation.
Lateral gain compensation is used to counter this effect by amplifying the weaker signals to a greater extent

23. Techniques and Tricks for Optimizing Transesophageal Images 475
A B
FIGURE 23.2 A: The time gain compensation is determined by a series of sliding controls. The upper controls affect the
near field and the lower controls the far field. Note the high setting of the second control and its effect on the midfield
Video 23.2b
in (B). B: The mitral valve apparatus is obscured by specular noise. C: The time gain compensation controls were subse-
quently reduced, after which the image quality improved markedly. Video 23.2b, c. Video 23.2c
and ensures brightness is uniform across the entire width of the image display. The effects of lateral gain
compensation can be used to amplify weaker lateral signals and aid in detection of endocardial borders. The
effects of lateral gain compensation on image quality are shown in Figure 23.3 (Video 23.3b, c).
Depth
This control selects the maximal distance to be displayed. Increasing depth beyond the structure of interest
has several negative consequences.
1. The image size is reduced. The most obvious consequence is that the image size is reduced because a
larger area of the cardiac anatomy must be displayed on a screen of fixed size. The display of the cardiac
structure of interest will be smaller and therefore more difficult to evaluate.
2. The frame rate is lower. In addition, as the depth is increased, the frame rate of the two-dimensional
ultrasound is slowed because the system must wait longer for signals to be received. Doubling the depth
of penetration doubles the wait time before another pulse can be sent, so that the pulse repetition
frequency and subsequently the frame rate are decreased (4).
Therefore, to optimize image display and temporal resolution, the depth should be set just beyond the
structure of interest, as shown in Figure 23.4.
It must also be appreciated that the lateral resolution of the ultrasound system is inversely proportional
to the depth. Therefore, it is practical to have the position of the probe as close as possible to the structure
of interest. For example, when the leaflets of the aortic valve are being evaluated, the ME aortic valve short-
axis view is preferable to the deep transgastric (TG) long-axis view because the probe is closer to the aortic
valve and lateral resolution is improved.

A B
FIGURE 23.3 A: The lateral gain compensation is determined by a series of sliding controls. The left controls affect the
left of the image sector while the right controls affect the right. Note the high setting on the second control from the
Video 23.3b right and its effect on visualizing the anterior wall in (B). B: The anterior wall is obscured by specular noise. C: The lateral
Video 23.3c gain compensation controls were subsequently reduced, after which the image quality improved. Video 23.3b, c.
Clinical Pearl
Resist increasing the depth beyond the setting that displays the structure of interest.
Focus
The focus control enables the operator to focus the ultrasound beam at a selected distance from the trans-
ducer. This is achieved by altering the sequences of electric impulses sent to the transducer elements. The
A B
FIGURE 23.4 The transgastric mid short-axis view with too much depth (A) and with the depth correctly set (B). Note
the focal point in image (B) is located at 6 cm, exactly in the center of the left ventricle. The focal point is marked by a bar
Video 23.4a with a green circle in the middle. Also note the frame rate has decreased from 50 Hz to 47 Hz (shown in upper left hand
Video 23.4b corner) with increasing the depth. Video 23.4a, b.

goal of focusing is to have the beam narrowest at the location of the structure being evaluated because a
thinner beam improves lateral resolution (5). The user must be cognizant of the focus depth of the system,
which is typically marked on the edge of the sector (Fig. 23.4).
If the focal zone is located too far from the area of interest, the image resolution may not be sufficient for
proper evaluation. When the atrial septum is being evaluated for a patent foramen ovale, the focus should
be placed at this level. Remember that structures distal to the focal point lie in the far field and may appear
“fuzzy” or abnormally thick. Avoid evaluating small structures distal to the focal point until the focal point
is moved to that level.
Clinical Pearl
Adjust the focus point to the level of the structure of interest for high-resolution imaging.
Frequency
A feature of modern TEE systems is that they are capable of multiple frequencies, so that the transmitted
ultrasound frequency can be adjusted. This can be especially important in TEE applications. The basic
principle is that higher frequency beams maximize the length of the near field. When the structures being
evaluated are in close proximity to the transducer (atria, aorta), higher frequencies are used to optimize
resolution (6). When the structures being evaluated are farther from the transducer (deep TG views),
higher frequencies may not be adequate because penetration is poor and attenuation is greater. In these
situations, the frequency should be reduced until a satisfactory image is produced.
Clinical Pearl
Use higher frequencies when evaluating shallow structures and lower frequencies when evaluating deep
structures (i.e., TG views).
Dynamic Range
Modern ultrasound transducers are capable of detecting reflected ultrasound signals with amplitudes
over a range of approximately 100 dB (7). Unfortunately, the monitors used in these systems are capable
of displaying only a much smaller range (∼30 dB). Therefore, to display the range of ultrasound signals
detected by the transducer, the dynamic range control allows the wide spectrum of ultrasound ampli-
tudes to be compressed. The compressed signals are then displayed on the monitor as varying shades
of gray.
Ultrasound systems have both a fixed dynamic range, which is limited by the hardware of the system,
and a selectable dynamic range, which can be changed according to the echocardiographer’s preference.
Increasing the dynamic range of the system increases the number of shades of gray between black and
white within the image and therefore increases image detail, so that a smoother image appears on the
display screen. Decreasing the dynamic range of the system increases the contrast of the image, with
more black and white areas than shades of gray. The effect of dynamic range on image quality is shown
in Figure 23.5.
Compression
Compression is a postprocessing tool that in conjunction with the preprocessing dynamic range con-
trol setting alters the range of the displayed gray scale (8). The compression control changes how
the given dynamic range of ultrasound data is displayed. When the compression control is reduced,
the given dynamic range is displayed with the largest range of allowable shades of gray. The lowest
intensity signal is displayed as black, and the highest intensity signal is displayed as white. As the
compression control is increased, the range of shades of gray used to produce the image is reduced to
produce a softer, smoother image. The gray scale is therefore compressed by eliminating the display
of shades of gray at each end of the spectrum. Compression settings are a personal preference of the
echocardiographer.

A B
Video 23.5a FIGURE 23.5 A midesophageal four-chamber view concentrating on the left atrium and left ventricle. With the
Video 23.5b dynamic range too low (A), normal (B), and too high (C). Note the increasing shades of gray as the dynamic range is
Video 23.5c increased. Video 23.5a–c.
Reject
In the early stages of ultrasound development, it was discovered that ultrasound transducers detect many
sources of low-level interference from within the body. Examples include movement artifacts, the elec-
tronic noise of equipment, such as ventilators, and aberrant ultrasound resulting from refraction of the
ultrasound signal. These low-level signals are detected by the scanner and displayed in the image as “noise.”
To eliminate such signals, all ultrasound systems have a fixed or default “filter” that removes any signal
below a certain amplitude threshold (the lower limit of the displayed dynamic range) (3). Sometimes, the
default filter is not enough to remove the noise in an image. The reject control is an adjustable control that
enables the user to eliminate a greater number of low-intensity signals. The reject control is used to elimi-
nate signals that are usually located in blood pools and are a result of artifacts. When the reject control
is adjusted, care must be taken not to eliminate important low-intensity echoes from certain pathologic
conditions. Specifically, fresh thrombi within a cardiac chamber or vessel have a low-intensity (dark) signal
that may be eliminated from the image if the reject is set too high.
Clinical Pearl
Increase the reject control to eliminate noise (random echoes often found in blood pools and other low-
intensity areas). Do not use excessive reject because low-intensity echoes such as thrombi may be removed
from the image.
Persistence
Persistence is a postprocessing control that can best be described as signal averaging or image blending.
The term is derived from earlier ultrasound systems that used cathode ray tubes for display. After the

A B
FIGURE 23.6 A midesophageal aortic valve long-axis view with a normal sector width (A) and one that has been
narrowed (B). Note the increase in frame rate from 50 Hz to 86 Hz (shown in upper left hand corner) with narrowing Video 23.6a
the sector. Video 23.6a, b. Video 23.6b
phosphor elements in the tube were illuminated to form an image, rather than disappearing instantly, the
luminescence faded gradually (or persisted).
As a result, new images were displayed while the old, dimmer image was still on the screen (9). With
the advent of digital scan converters and the replacement of cathode ray tubes with modern monitors,
the term persistence is now used for frame averaging in the digital scan converter. As incoming signals are
processed by the system, images are displayed as they are created in their purest form (no persistence),
or the system can average one image with the next and display the averaged image. Persistence is used to
smooth the appearance of the heart in motion. As the persistence control is increased, more images are
used to create the averaged image, and temporal and spatial resolution is decreased. If the persistence is set
too high, the image is often described as appearing to be in “slow motion.” Since valvular structures move
rapidly, persistence is usually set low in echocardiographic applications to retain temporal resolution and
a real-time appearance.
Sector Size
Sector size controls the angle of the sector displayed on the monitor. Most ultrasound scanners can display
sectors with angles ranging from 15 to 90 degrees. Wide angles allow the operator to survey a broad array
of cardiac structures in a single view. The most important effect of the sector size is on the frame rate. The
wider the sector size, the lower the frame rate and the temporal resolution (Fig. 23.6, Video 23.6a, b). For a Video 23.6a
proper evaluation of fast-moving structures, the sector size should be kept small to allow for higher frame Video 23.6b
rates. Some scanning systems do not depend on sector size for high frame rates and can achieve adequate
frame rates with a full 90-degree sector.
Clinical Pearl
Larger sector sizes result in lower frame rates and a lower level of temporal resolution. When valvular
structures are evaluated, it is helpful to decrease the sector size (or use motion mode [M-mode]) to improve
the frame rates.
Harmonics
With standard echocardiography, ultrasound waves are received at the same frequency that they were
transmitted. This frequency is commonly referred to as the fundamental frequency. During the course
of propagation, the ultrasound waves interact with tissue and this interaction results in the tissues oscil-
lating to create a low-amplitude, high-frequency ultrasound wave referred to as the harmonic frequency.
With harmonics, the fundamental frequency is filtered out and only the harmonic frequency is used
to create an image. The main advantage of using the harmonic frequency to create an image is that it

A B
FIGURE 23.7 A midesophageal two-chamber view with a color sector size that is set to cover only the region of interest
Video 23.7a (A) and one that covers an area that is larger than the area of interest (B). Note the decrease in frame rate from 16 Hz to
Video 23.7b 10 Hz (shown in the upper left hand corner) with narrowing the sector. Video 23.7a, b.
disproportionately reduces weak signals that result in artifacts. Eliminating the “noise” provides better
contrast and may result in improved ability to detect endocardial border definition.
COLOR CONTROLS
Region of Interest
The region of interest is the area that defines where the color will be displayed. There are certain limi-
tations to setting the size of the region of interest. As the size of the region of interest increases, the
Video 23.7a
frame rate decreases (Fig. 23.7, Video 23.7a, b) (10). The goal is to optimize the frame rate to improve
Video 23.7b
temporal resolution and the assessment of blood flow. The depth also affects the color frame rate. As
the depth increases, the system must wait longer for the returning signal; therefore, the frame rate
is slower.
Clinical Pearl
Resist increasing the size of color sector beyond that which displays the region of interest.
Color Gain
Color gain is similar to two-dimensional gain in that it increases or amplifies the signal generated by
the returning echoes. It is very important to have the color gain set properly. If the gain is set too low,
a small jet, such as a small atrial septal defect or patent foramen ovale, can be missed. If the gain is set
too high, the size of a regurgitant jet is frequently overestimated. The color gain is adjusted simply by
increasing the color gain control until speckles of color lay outside the blood pools and then decreasing
Video 23.8 the gain one to two settings until the speckles go away. Figure 23.8 (Video 23.8) shows different color
gain settings.
Color Scale
The color scale is the range of color velocities displayed. To optimize the color scale, one must be cog-
nizant of the general velocities of the blood flow being evaluated. For example, when lower flow veloci-
ties in the pulmonary veins are evaluated, one must decrease the color scale. Adjusting the scale will
affect the Nyquist limit. Velocities sampled outside this range cause aliasing within the color display. In
certain applications, such as when the proximal isovelocity surface area (PISA) is calculated, adjusting
the color scale to produce aliasing is required to create an adequate flow convergence hemisphere for
measurement.

FIGURE 23.8 A midesophageal aortic valve long-axis view with the color gain too high. To appropriately set the color
gain setting, the gain should be decreased until the speckles go away.
Variance
The variance color flow map displays the range of velocities in any given sample volume. The variance
in flow is displayed as shades of green, whereas normal flows are displayed with the standard red–blue
color flow map. In laminar flow, the range of velocities in a given sample volume is relatively small, and
laminar flow appears color-coded as red or blue. In turbulent flow, the number of velocities is increased
(i.e., increased variance) such that turbulent flow is color-coded as green (11). A variance map may help to
identify a small turbulent jet by tagging it with a different (i.e., green) color.
STORAGE SYSTEMS: ANALOG VIDEOTAPE VERSUS DIGITAL STORAGE

The advantages of videotape storage are its availability and reasonable cost. A patient’s study can be
reviewed anywhere a videocassette recorder is available. A shortcoming is that it is difficult to archive and
retrieve studies, and to directly compare different studies of the same patient. For example, if a patient
has an LV ejection fraction of 40% on one examination and on a subsequent examination a value of 30%
is reported, it is essential to determine whether this represents deterioration in function or differences in
interpretation. With digital technology, a direct side-by-side comparison can be performed.
Current digital technology also allows the study data to be manipulated. The reviewer can adjust
the postprocessing controls, including contrast, brightness, and two-dimensional and Doppler gain.
It is also possible to make measurements from stored images without having to recalibrate the system.
Finally, optical storage media make it practical to house large databases in minimal space. In sum,
digital storage offers major advantages for archiving, retrieving, and sharing echocardiographic
studies.
SUMMARY
The extensive control options of modern full-platform echocardiography systems provide the echocardiog-
rapher with tools for reliably obtaining high-quality images under a broad range of conditions. With a firm
understanding of the control settings available, the examiner can optimize image acquisition and display
and detect pathology that might otherwise be missed.

REFERENCES
1. Marcus ML, Schelbert HR, Skorton DJ, et al. Cardiac Imaging—A Companion to Braunwald’s “Heart Disease”. Philadelphia,
PA: WB Saunders; 1991:363.
2. Feigenbaum H. Echocardiography. Philadelphia, PA: Lippincott Williams & Wilkins; 2010:17.
4. Weyman AE. Principles and Practice of Echocardiography. Philadelphia, PA: Lea & Febiger; 1994:219.
5. Thrush A, Hartshorne T. Peripheral Vascular Ultrasound: How, Why, and When. London: Churchill Livingstone; 1999:17–18.
7. Weyman AE. Principles and Practice of Echocardiography. Philadelphia, PA: Lea & Febiger; 1994:49–50.
8. Hagen-Ansert SL. Textbook of Diagnostic Ultrasonography. St. Louis, MO: Mosby; 1989:38–39.
9. Weyman AE. Cross-sectional Echocardiography. Philadelphia, PA: Lea & Febiger; 1982:55.
10. Thrush A, Hartshorne T. Peripheral Vascular Ultrasound: How, Why, and When. London: Churchill Livingstone; 1999:42.
11. Weyman AE. Principles and Practice of Echocardiography. Philadelphia, PA: Lea & Febiger; 1994:225–226.

QUESTIONS
1. Smoothing of a two-dimensional image is 8. As the number of velocities in a color sector
referred to as: increase, the ______ is said to increase
a. Reject a. Dynamic range
b. Compression b. Variance
c. Dynamic range c. Nyquist limit
d. Variance d. None of the above
2. Time gain compensation allows the 9. The amplitude of the transmitted
echocardiographer to overcome: ultrasound signal is controlled by:
a. Attenuation a. The transmit power
b. Low frame rate b. Adjusting the gain
c. Poor lateral resolution c. Adjusting the time gain compensation
d. Image artifacts d. All of the above
3. Increasing the size of the color flow 10. Decreasing the depth of the image results in:
Doppler sector will: a. A lower frame rate
a. Decrease axial resolution b. Lower temporal resolution
b. Improve temporal resolution c. A higher pulse repetition frequency
c. Decrease temporal resolution d. Lower axial resolution
11. By lowering the Nyquist limit:
4. Increasing the dynamic range results in: a. Lower velocity blood will be displayed
a. An increase in the number of shades of gray b. A jet will appear smaller
between black and white c. Pulse repetition frequency will increase
b. An increase in the shades of gray at each d. All of the above
end of the spectrum
12. To optimize color gain settings:
c. An elimination of a greater number of low-
a. The gain should be increased until color
intensity signals
pixels appear within the tissues
d. An elimination of a greater number of high-
b. Settings should be changed to the echocar-
intensity signals
diographer’s preference
5. Higher frequency ultrasound beams have c. The gain should be increased until color
all of the following properties EXCEPT: pixels appear within the tissues and then
a. Improved resolution in the near field reduced slightly
b. Less penetration d. None of the above
c. Subject to greater attenuation
13. Postprocessing controls include:
d. Improved lateral resolution
a. Doppler gain
6. Focusing an ultrasound beam on an object b. Brightness
results in: c. Contrast
a. Improved lateral resolution in the far field d. All of the above
b. Increased frame rate
14. The filtering of low-intensity signals is
c. Improved axial resolution in the near field
performed with which control:
d. Improved lateral resolution in the near field
a. Reject
7. Techniques to improve image quality b. Compression
include: c. Dynamic range
a. Using lower frequencies when visualizing d. Persistence
structures in the far field
15. To optimize image quality of the aortic valve
b. Adjust the depth so as not to include struc-
in the deep transgastric view, one could:
tures beyond the structure of interest
a. Increase the frequency
c. Adjust the color flow Doppler sector to
b. Adjust the focus to the level of the aortic
include only the region of interest
valve
d. All of the above
c. Increase the transmit power
d. Set the time gain compensation higher in
the near field

16. To optimize the image quality of the mitral 18. High gain settings result in:
valve in the mitral commissural view, one a. Increased lateral resolution
could: b. Increased temporal resolution
a. Increase the sector size c. Decreased temporal resolution
b. Increase the frequency d. The image appearing brighter
c. Increase the gain
19. Frame rate is affected by:
d. Increase the image depth to encompass the
a. Sector size
entire left ventricle
b. Image depth
17. When applying color flow to the aortic valve c. Color sector size
in the midesophageal aortic valve long- d. All of the above
axis view, the temporal resolution will be
20. Excessive reject may result in the inability
increased by:
to image:
a. Increasing the area which color is displayed
a. An intracardiac thrombus
b. Decreasing the image depth
b. Valvular motion
c. Adjust the Nyquist limit so aliasing does not
c. Turbulent blood flow across a stenotic
occur
aortic valve
d. All of the above
d. Lower flow velocities in the pulmonary
veins

II
APPENDICES
A Transesophageal Echocardiographic Anatomy
ME Asc aortic SAX Probe adjustment: neutral Sector depth: ∼6 cm

Primary diagnostic issues Required structures
Aortic atherosclerosis Aorta in cross section in transverse
Aortic dissection plane (0 degree)
Pulmonary artery pathology (emboli, Pulmonary artery (main and
dilation, other) proximal right)
ME Asc aortic LAX Probe adjustment: neutral Sector depth: ∼6 cm
Aortic atherosclerosis Ascending aorta in long axis
Aortic dissection Right pulmonary artery in cross section
UE aortic arch SAX Probe adjustment: neutral Sector depth: ∼6 cm

Aortic atherosclerosis Aortic arch in cross section
Aortic dissection Main pulmonary artery (often not
Pulmonic valve well seen)
UE aortic arch LAX Probe adjustment: rightward Sector depth: ∼6 cm

Aortic atherosclerosis Distal ascending aortal/aortic arch
Aortic dissection
Visualization of aortic cannulation site
Desc aortic SAX Probe adjustment: neutral Sector depth: ∼6 cm

Primary diagnostic issue Required structures
Aortic atherosclerosis Descending aorta in cross section
Aortic dissection in transverse plane (0 degree)
Desc aortic LAX Probe adjustment: neutral Sector depth: ∼6 cm

Aortic atherosclerosis Descending aorta in long axis in
Aortic dissection longitudinal plane (90 degrees)
ME AV SAX Probe adjustment: neutral Sector depth: ∼10 cm

Primary diagnostic issue Required structures
Aortic stenosis Three leaflets
Valvular morphology Commissures
Coaptation point
(continued)
485

486 Appendices
ME RV inflow–outflow Probe adjustment: neutral Sector depth: ∼10 cm

Pulmonic valve disease Pulmonic valve
Pulmonary artery pathology Tricuspid valve
RVOT pathology Main pulmonary artery (at least 1 cm
Doppler evaluation of tricuspid valve distal to the pulmonic valve)
RVOT (at least 1 cm proximal to the
pulmonic valve)
ME AV LAX Probe adjustment: neutral Sector depth: ∼10 cm
Aortic valve pathology LVOT (at least 1 cm proximal to
Aortic pathology (ascending and root) the aortic valve)
LVOT pathology Aortic valve (visualized cusps
Anterior leaflet mitral valve approximately equal in size)
Ascending aorta (at least 1 cm distal
to the sinotubular junction)
ME bicaval Probe adjustment: neutral Sector depth: ∼10 cm
Atrial septal defect RA free wall (or appendage)
Tumor Superior vena cava (at least its
Retrograde venous cannula positioning entry into the RA)
Interatrial septum
ME four-chamber Probe adjustment: neutral-retroflex Sector depth: ∼14 cm
Atrial septal defect LA
Chamber enlargement dysfunction LV
Mitral disease Mitral valve
Tricuspid disease Tricuspid valve (maximal annular
Detection of intracardiac air dimension)
ME two-chamber Probe adjustment: neutral Sector depth: ∼14 cm
LA appendage LA appendage
Mass/thrombus Mitral valve
LV apex pathology LV apex (i.e., maximal LV length)
LV systolic dysfunction (apical segments)
ME LAX Probe adjustment: neutral Sector depth: ∼12 cm
Mitral valve pathology LV
LVOT pathology Mitral valve
LVOT
ME mitral commissural Probe adjustment: neutral Sector depth: ∼12 cm

Localization of mitral valve pathology Mitral valve (P1, P3, and A2 scallops)
Papillary muscles/chordae tendineae
LA
LV
TG mid-SAX Probe adjustment: neutral Sector depth: ∼12 cm
Hemodynamic instability LV cavity
LV enlargement LV walls (at least 50% of circumference
LV hypertrophy with visible endocardium)
LV systolic dysfunction Papillary muscles (approximately
(global and regional) equal in size and distinct from
ventricular wall)

A. Transesophageal Echocardiographic Anatomy 487
TG two-chamber Probe adjustment: neutral Sector depth: ∼12 cm

LV systolic dysfunction (anterior Mitral leaflets
and inferior basal segments) Mitral subvalvular apparatus
LV (anterior and inferior: basal
plus mild segments)
TG RV inflow Probe adjustment: neutral-rightward Sector depth: ∼12 cm
RV systolic dysfunction Tricuspid leaflets
Tricuspid valve pathology Tricuspid subvalvular apparatus
TG RV inflow–outflow Probe adjustment: neutral-rightward Sector depth: ∼14 cm

RV systolic dysfunction RA
RVOT pathology RV
Pulmonary artery pathology Main pulmonary artery
Pulmonic valve evaluation Pulmonic valve
TG basal SAX Probe adjustment: neutral Sector depth: ∼12 cm
LV systolic dysfunction (basal segments) Mitral leaflets
Mitral valve pathology Mitral subvalvular apparatus
LV (basal segments)
TG LAX Probe adjustment: neutral-leftward Sector depth: ∼12 cm

LV systolic dysfunction (anteroseptal and Mitral leaflets
posterior: basal segments) Mitral subvalvular apparatus
Doppler evaluation of aortic valve LV (anteroseptal and posterior:
basal plus midsegments)
Aortic valve
Deep TG LAX Probe adjustment: neutral Sector depth: ∼16 cm
Aortic valve pathology LV
LVOT pathology Aortic valve
Doppler evaluation of aortic valve Aorta
ME, midesophageal; Asc, ascending; SAX, short axis; LAX, long axis; UE, upper esophageal; Desc, descending; AV, aortic valve; RV,
right ventricular; LVOT, left ventricular outflow tract; RA, right atrium; LA, left atrium; LV, left ventricular; RVOT, right ventricular
outflow tract; TG, transgastric.
Modified from Miller JP, Lambert SA, Shapiro WA, et al. The adequacy of basic intraoperative transesophageal echocardiography
performed by experienced anesthesiologists. Anesth Analg 2001;92:1103–1110, with permission.

B Cardiac Dimensions
TABLE B.1 Reference Values for Normal Adult TEE Measurements
Parameter Mean ± SD (mm) Range (mm)

Right pulmonary artery diametera 17 ± 3 12–22
Left upper pulmonary vein diameter 11 ± 2 7–16
Left atrial appendage Length 28 ± 5 15–43
Diameter 16 ± 5 10–28
Superior vena cava diameter 15 ± 3 8–20
Right ventricular outflow tract diameterb 27 ± 4 16–36
Left atriumc Anteroposterior diameter 38 ± 6 20–52
Medial-lateral diameter 39 ± 7 24–52
Right atriumc Anteroposterior diameter 38 ± 5 28–52
Medial-lateral diameter 38 ± 6 29–53
Tricuspid annular diameterc 28 ± 5 20–40
Mitral annular diameterc 29 ± 4 20–38
Coronary sinus diameter 6.6 ± 1.5 4–10
Left ventricled Anteroposterior diameter (diastole) 43 ± 7 33–55
Medial-lateral diameter (diastole) 42 ± 7 23–54
Anteroposterior diameter (systole) 28 ± 6 18–40
Medial-lateral diameter (systole) 27 ± 6 18–42
Aortic root diameterb 28 ± 3 21–34
Descending thoracic Proximal 21 ± 4 14–30
aorta diameter Distal 20 ± 4 13–28
a
Right pulmonary artery diameter measured in midesophageal ascending aorta short-axis view.
b
Aortic root and right ventricular outflow tract diameters measured in the midesophageal right ventricular inflow/outflow tract
view.
c
Atrial (end-systole) and both mitral and tricuspid annular (mid-diastole) diameters measured in the midesophageal
four-chamber view.
d
Left ventricular dimensions measured in transgastric mid short-axis view.
SD, standard deviation.
Adapted from Cohen G, White M, Sochowski R, et al. Reference values for normal transesophageal measurements. J Am Soc
Echocardiogr 1995;8:221–230.
488

C Hemodynamic Calculations
TABLE C.1 Estimation of Hemodynamic Pressures
Normal values
Pressure estimated Required measurement Formula (mm Hg)
CVP Respiratory IVC collapse ≥40% <10 mm Hg
(spontaneously breathing)
Right ventricular Peak velocityTR RVSP = 4(vTR)2 + CVP (No PS) 16–30 mm Hg
systolic pressure CVP estimated or measured
(RVSP)
RV systolic pressure Systemic systolic blood RVSP = SBP – 4(vLV – RV )2 Usually >50 mm Hg
(with VSD) pressure (SBP) (No AS or LVOT obstruction)
Peak vLV–RV
Pulmonary artery Peak velocityTR PASP = 4(vTR)2 + CVP (no PS) 16–30 mm Hg
systolic (PASP) CVP estimated or measured)
Pulmonary artery End diastolic PAEDP = 4(vPR ED)2 + CVP 0–8 mm Hg
diastolic (PAD) VelocityPR
CVP estimated or measured
Pulmonary artery Acceleration time (AT) to peak PAM = (–0.45) AT + 79 10–16 mm Hg
mean (PAM) VPA (in m/s)
RV dP/dt TR spectral envelope RV dP = 4v2TR (2 m/s) – 4v2TR (1 m/s) >150 mm Hg/ms
T TR (2 m/s) – T TR (1 m/s) RV dP/dt =
dP/T TR (2 m/s) – T TR (1 m/s)
Left atrial systolic Peak vMR LASP = SBP – 4(vMR)2 (No AS or 3–15 mm Hg
(LASP) SBP LVOT obstruction)
LA (PFO) VelocityPFO LAP = 4(vPFO)2 + CVP 3–15 mm Hg
CVP estimated or measured
LV diastolic (LVEDP) End diastolic LVEDP = DBP – 4(vAR)2 3–12 mm Hg
VelocityAR
Diastolic blood pressure (DBP)
LV dP/dt MR spectral envelope LV dP = 4v2MR (3 m/s) – 4v2MR (1 m/s) >1000 mm Hg/ms
TMR (3 m/s) – TMR (1 m/s) LV dP/dt =
dP/TMR (3 m/s) – TMR (1 m/s)
CVP, central venous pressure; IVC, inferior vena cava; RV, right ventricle; Dysfx, dysfunction; TR, tricuspid regurgitation; PS,
pulmonary stenosis; VSD, ventricular septal defect; LV, left ventricle; AS, atrial stenosis; LVOT, left ventricular outflow tract;
PAEDP, pulmonary artery end-diastolic pressure; PR ED, pulmonary regurgitation end diastolic; PA, pulmonary artery; MR, mitral
regurgitation; LA, left atrium; PFO, patent foramen ovale; AR, aortic regurgitation.
489

D Valve Prostheses
TABLE D.1 Normal Doppler Echocardiographic Values of Aortic Valve Prosthesis
Peak gradient Mean gradient Peak velocity Effective orifice

Valve Size n (mm Hg) (mm Hg) (m/s) area (cm2)
ATS open pivot AP 16 6 47.7 ± 12 27 ± 7.3 3.44 ± 0.47 0.61 ± 0.09
ATS open pivot 19 9 47 ± 12.6 26.2 ± 7.9 3.41 ± 0.43 0.96 ± 0.18
(bileaflet) 21 15 25.5 ± 6.1 14.4 ± 3.5 2.4 ± 0.39 1.58 ± 0.37
23 8 19 ± 7 12 ± 4 1.8 ± 0.2
25 12 17 ± 8 11 ± 4 2.2 ± 0.4
27 10 14 ± 4 9±2 2.5 ± 0.3
29 5 11 ± 3 8±2 3.1 ± 0.3
Biocor stentless 21 45 35.97 ± 4.06 18 ± 4
(stentless 23 115 29.15 ± 8.28 18.64 ± 7.14 3 ± 0.6 1.4 ± 0.5
bioprosthesis) 25 100 28.65 ± 6.6 17.72 ± 6.99 2.8 ± 0.5 1.6 ± 0.38
27 55 25.87 ± 2.81 18 ± 2.8 2.7 ± 0.2 1.9 ± 0.46
≥29 16 24 ± 2
Biocor extended 19–21 12 17.5 ± 5.8 9.7 ± 3.5 1.3 ± 0.4
stentless (stentless 23 18 14.8 ± 5.9 8.1 ± 3.1 1.6 ± 0.3
bioprosthesis) 25 20 14.2 ± 3.5 7.7 ± 1.9 1.8 ± 0.3
Bioflo pericardial 19 16 37.25 ± 8.65 24.15 ± 5.1 0.77 ± 0.11
(stented 21 9 28.7 ± 6.2 18.7 ± 5.5 1.1 ± 0.1
bioprosthesis) 23 4 20.7 ± 4 12.5 ± 3 1.3 ± 0.09
Björk-Shiley 19 37 46.0 26.67 ± 7.87 3.3 ± 0.6 0.94 ± 0.19
monostrut (tilting 21 161 32.41 ± 9.73 18.64 ± 6.09 2.9 ± 0.4
disk) 23 153 26.52 ± 9.67 14.5 ± 6.2 2.7 ± 0.5
25 89 22.33 ± 7 13.3 ± 4.96 2.5 ± 0.4
27 61 18.31 ± 8 10.41 ± 4.38 2.1 ± 0.4
29 9 12 ± 8 7.67 ± 4.36 1.9 ± 0.2
Björk-Shiley spherical 17 1 4.1
(tilting disk) or not 19 2 27.0 21.8 ± 3.4 3.8 1.1
specified 21 18 38.94 ± 11.93 17.34 ± 6.86 2.92 ± 0.88 1.1 ± 0.25
23 41 33.86 ± 11 11.5 ± 4.55 2.42 ± 0.4 1.22 ± 0.23
25 39 20.39 ± 7.07 10.67 ± 4.31 2.06 ± 0.28 1.8 ± 0.32
27 23 19.44 ± 7.99 1.77 ± 0.12 2.6
29 5 21.1 ± 7.1 1.87 ± 0.18 2.52 ± 0.69
31 2 2.1 ± 0.14
Carbomedics 17 7 33.4 ± 13.2 20.1 ± 7.1 1.02 ± 0.2
(bileaflet) 19 63 33.3 ± 11.19 11.61 ± 5.08 3.09 ± 0.38 1.25 ± 0.36
21 111 26.31 ± 10.25 12.68 ± 4.29 2.61 ± 0.51 1.42 ± 0.36
23 120 24.61 ± 6.93 11.33 ± 3.8 2.42 ± 0.37 1.69 ± 0.29
25 103 20.25 ± 8.69 9.34 ± 4.65 2.25 ± 0.34 2.04 ± 0.37
27 57 19.05 ± 7.04 8.41 ± 2.83 2.18 ± 0.36 2.55 ± 0.34
29 6 12.53 ± 4.69 5.8 ± 3.2 1.93 ± 0.25 2.63 ± 0.38
Carbomedics 19 10 43.4 ± 1.8 24.4 ± 1.2 1.22 ± 0.08
reduced (bileaflet)
Carbomedics 19 4 29.04 ± 10.1 19.5 ± 2.12 1.8 1 ± 0.18
supraannular top 21 30 29.61 ± 8.93 16.59 ± 5.79 2.62 ± 0.35 1.18 ± 0.33
hat (bileaflet) 23 30 24.38 ± 7.53 13.29 ± 3.73 2.36 ± 0.55 1.37 ± 0.37
25 1 22.0 11.0 2.4
490
(continued)

D. Valve Prostheses 491
TABLE D.1 Normal Doppler Echocardiographic Values of Aortic Valve Prosthesis (continued )

Carpentier-Edwards 19 56 43.48 ± 12.72 25.6 ± 8.02 0.85 ± 0.17
(stented 21 73 27.73 ± 7.6 17.25 ± 6.24 2.37 ± 0.54 1.48 ± 0.3
bioprosthesis) 23 100 28.93 ± 7.49 15.92 ± 6.43 2.76 ± 0.4 1.69 ± 0.45
25 85 23.95 ± 7.05 12.76 ± 4.43 2.38 ± 0.47 1.94 ± 0.45
27 50 22.14 ± 8.24 12.33 ± 5.59 2.31 ± 0.39 2.25 ± 0.55
29 24 22.0 9.92 ± 2.9 2.44 ± 0.43 2.84 ± 0.51
31 4 2.41 ± 0.13
Carpentier-Edwards 19 14 32.13 ± 3.35 24.19 ± 8.6 2.83 ± 0.14 1.21 ± 0.31
pericardial 21 34 25.69 ± 9.9 20.3 ± 9.08 2.59 ± 0.42 1.47 ± 0.36
(stented prothesis) 23 20 21.72 ± 8.57 13.01 ± 5.27 2.29 ± 0.45 1.75 ± 0.28
25 5 16.46 ± 5.41 9.04 ± 2.27 2.02 ± 0.31
27 1 19.2 5.6 1.6
29 1 17.6 11.6 2.1
Carpentier-Edwards 19 15 34.1 ± 2.7 1.1 ± 0.09
supraannular 21 8 25 ± 8 14 ± 5 1.06 ± 0.16
AV (stented
bioprosthesis)
CryoLife O'Brien 19 47 12 ± 4.8 1.25 ± 0.1
stentless (stentless 21 163 10.33 ± 2 1.57 ± 0.6
prothesis) 23 40 8.5 2.2
25 40 7.9 2.3
27 39 7.4 2.7
Duromedics (Tekna; 19 1 3.6
bileaflet) 21 3 19.08 ± 16 8.98 ± 5 1.3
23 12 19.87 ± 7 7±2 2.64 ± 0.27
25 18 21 ± 9 5±2 2.34 ± 0.38
27 15 22.5 ± 12 6±3 1.88 ± 0.6
29 1 13.0 3.4 2.1
Edwards Prima 19 7 30.9 ± 11.7 15.4 ± 7.4 1 ± 0.3
stentless (stentless 21 30 31.22 ± 17.35 16.36 ± 11.36 1.25 ± 0.29
bioprosthesis) 23 62 23.39 ± 10.17 11.52 ± 5.26 2.8 ± 0.4 1.49 ± 0.46
25 97 19.74 ± 10.36 10.77 ± 9.32 2.7 ± 0.3 1.7 ± 0.55
27 46 15.9 ± 7.3 7.1 ± 3.7 2 ± 0.6
29 11 11.21 ± 8.6 5.03 ± 4.53 2.49 ± 0.52
Hancock I (stented 21 1 3.5
bioprosthesis) 23 14 19.09 ± 4.35 12.36 ± 3.82 2.94 ± 0.24
25 26 17.61 ± 3.13 11 ± 2.85 2.36 ± 0.37
27 20 18.11 ± 6.92 10 ± 3.46 2.4 ± 0.36
29 2 2.23 ± 0.04
31 1 2.0
Hancock II (stented 21 39 20 ± 4 14.8 ± 4.1 1.23 ± 0.27
bioprosthesis) 23 119 24.72 ± 5.73 16.64 ± 6.91 1.39 ± 0.23
25 114 20 ± 2 10.7 ± 3 1.47 ± 0.19
27 133 14 ± 3 1.55 ± 0.18
29 35 15 ± 3 1.6 ± 0.15
Ionescu-Shiley 17 11 42.0 21.1 ± 3.21 0.86 ± 0.1
(stented 19 63 23.17 ± 6.58 20.44 ± 8.47 2.63 ± 0.32 1.15 ± 0.18
bioprosthesis) 21 11 27.63 ± 8.34 15.1 ± 1.56 2.75 ± 0.25
23 5 18.09 ± 6.49 9.9 ± 2.85 2.1 ± 0.38
25 1 18.0
27 3 14.75 ± 2.17 8.97 ± 0.57 1.92 ± 0.14
29 1 16.0 7.3 2.0

492 Appendices

Jyros bileaflet 22 4 17.3 10.8 1.5
(bileaflet) 24 7 18.6 11.4 1.5
26 8 14.4 8.4 1.7
28 3 10.0 5.7 1.9
30 1 8.0 6.0 1.6
Lillehei-Kaster 14 1 2.7
(tilting disk) 16 2 3.43 ± 0.39
18 2 2.85 ± 0.21
20 1 1.7
Medtronic Freestyle 19 11 13.0
stentless (stentless 21 85 7.99 ± 2.6 1.6 ± 0.32
bioprosthesis) 23 141 7.24 ± 2.5 1.9 ± 0.5
25 164 5.35 ± 1.5 2.03 ± 0.41
27 105 4.72 ± 1.6 2.5 ± 0.47
Medtronic-Hall 20 24 34.37 ± 13.06 17.08 ± 5.28 2.9 ± 0.4 1.21 ± 0.45
(tilting disk) 21 30 26.86 ± 10.54 14.1 ± 5.93 2.42 ± 0.36 1.08 ± 0.17
23 27 26.85 ± 8.85 13.5 ± 4.79 2.43 ± 0.59 1.36 ± 0.39
25 17 17.13 ± 7.04 9.53 ± 4.26 2.29 ± 0.5 1.9 ± 0.47
27 8 18.66 ± 9.71 8.66 ± 5.56 2.07 ± 0.53 1.9 ± 0.16
29 1 1.6
Medtronic intact 19 16 39.43 ± 15.4 23.71 ± 9.3 2.5
(stented 21 55 33.9 ± 12.69 18.74 ± 8.03 2.73 ± 0.44 1.55 ± 0.39
bioprosthesis) 23 110 31.27 ± 9.62 18.88 ± 6.17 2.74 ± 0.37 1.64 ± 0.37
25 41 27.34 ± 10.59 16.4 ± 6.05 2.6 ± 0.44 1.85 ± 0.25
27 16 25.27 ± 7.58 15 ± 3.94 2.51 ± 0.38 2.2 ± 0.17
29 5 31.0 15.6 ± 2.1 2.8 2.38 ± 0.54
Medtronic Mosaic, 21 51 12.43 ± 7.3 1.6 ± 0.7
porcine (stented 23 121 12.47 ± 7.4 2.1 ± 0.8
bioprosthesis) 25 71 10.08 ± 5.1 2.1 ± 1.6
27 30 9.0
29 6 9.0
Mitroflow (stented 19 4 18.7 ± 5.1 10.3 ± 3 1.13 ± 0.17
bioprosthesis) 21 7 20.2 15.4 2.3
23 5 14.04 ± 4.91 7.56 ± 3.38 1.85 ± 0.34
25 2 17 ± 11.31 10.8 ± 6.51 2 ± 0.71
27 3 13 ± 3 6.57 ± 1.7 1.8 ± 0.2
O’Brien-Angell 23 14.5 ± 7.77 1.15 ± 0.07
stentless (annular 25 50 19 ± 12.72 1.12 ± 0.25
position; stentless 27 18 ± 12.72 1.55 ± 0.21
bioprosthesis) 29 12 ± 7.07 2.05 ± 1.2
O’Brien-Angell 23 9 ± 1.4 1.58 ± 0.58
stentless 25 50 7.5 ± 0.7 2.37 ± 0.18
(supraannular 27 8.5 ± 0.7 2.85 ± 0.87
position; stentless 29 7 ± 1.4 2.7 ± 0.42
bioprosthesis)
Omnicarbon 21 71 36.79 ± 12.59 19.41 ± 5.46 2.93 ± 0.47 1.25 ± 0.43
(tilting disk) 23 83 29.33 ± 9.67 17.98 ± 6.06 2.66 ± 0.44 1.49 ± 0.34
25 81 24.29 ± 7.71 13.51 ± 3.85 2.32 ± 0.38 1.94 ± 0.52
27 40 19.63 ± 4.34 12.06 ± 2.98 2.08 ± 0.35 2.11 ± 0.46
29 5 17.12 ± 1.53 10 ± 1.53 1.9 ± 0.06 2.27 ± 0.23
Omniscience 19 2 47.5 ± 3.5 28 ± 1.4 0.81 ± 0.01
(tilting disk) 21 5 50.8 ± 2.8 28.2 ± 2.17 0.87 ± 0.13
23 8 39.8 ± 8.7 20.1 ± 5.1 0.98 ± 0.07
(continued)


On-X (bileaflet) 19 6 21.3 ± 10.8 11.8 ± 3.4 1.5 ± 0.2
21 11 16.4 ± 5.9 9.9 ± 3.6 1.7 ± 0.4
23 23 15.9 ± 6.4 8.5 ± 3.3 2 ± 0.6
25 12 16.5 ± 10.2 9 ± 5.3 2.4 ± 0.8
27–29 8 11.4 ± 4.6 5.6 ± 2.7 3.2 ± 0.6
Sorin Allcarbon 19 7 44 ± 7 29 ± 8 3.3 ± 0.3 0.9 ± 0.1
(tilting disk) 21 25 36.52 ± 9.61 21.07 ± 6.72 2.93 ± 0.2 1.08 ± 0.19
23 37 34.97 ± 10.97 18.72 ± 6.49 2.9 ± 0.41 1.31 ± 0.2
25 23 22 ± 4.68 13.85 ± 3.97 2.37 ± 0.23 1.96 ± 0.71
27 13 16.3 ± 3.3 10.15 ± 3.76 2 ± 0.25 2.51 ± 0.57
29 4 13 ± 4 8±2 1.8 ± 0.3 4.1 ± 0.7
Sorin Bicarbon 19 19 29.53 ± 4.46 16.35 ± 1.99 2.5 ± 0.1 1.36 ± 0.13
(bileaflet) 21 70 24.52 ± 7.1 12.54 ± 3.3 2.46 ± 0.31 1.46 ± 0.2
23 71 17.79 ± 6.1 9.61 ± 3.3 2.11 ± 0.24 1.98 ± 0.23
25 40 18.46 ± 3.1 10.05 ± 1.6 2.25 ± 0.19 2.39 ± 0.29
27 8 12 ± 3.25 7 ± 1.5 1.73 ± 0.21 3.06 ± 0.47
29 4 9 ± 1.25 5 ± 0.5 1.51 ± 0.1 3.45 ± 0.02
Sorin Pericarbon 23 15 39 ± 13 25 ± 8 2.0
(stentless
bioprosthesis)
St. Jude Medical 19 100 35.17 ± 11.16 18.96 ± 6.27 2.86 ± 0.48 1.01 ± 0.24
(bileaflet) 21 207 28.34 ± 9.94 15.82 ± 5.67 2.63 ± 0.48 1.33 ± 0.32
23 236 25.28 ± 7.89 13.77 ± 5.33 2.57 ± 0.44 1.6 ± 0.43
25 169 22.57 ± 7.68 12.65 ± 5.14 2.4 ± 0.45 1.93 ± 0.45
27 82 19.85 ± 7.55 11.18 ± 4.82 2.24 ± 0.42 2.35 ± 0.59
29 18 17.72 ± 6.42 9.86 ± 2.9 2 ± 0.1 2.81 ± 0.57
31 4 16.0 10 ± 6 2.1 ± 0.6 3.08 ± 1.09
St. Jude Medical 19 19 25.81 ± 7.52 16.44 ± 3.57 1.65 ± 0.2
Hemodynamic 21 30 18.9 ± 7.31 9.62 ± 3.37 2.15 ± 0.29
Plus (bileaflet)
Starr-Edwards 21 5 29.0 1.0
(ball-and-cage) 22 2 4
23 22 32.6 ± 12.79 21.98 ± 8.8 3.5 ± 0.5 1.1
24 43 34.13 ± 10.33 22.09 ± 7.54 3.35 ± 0.48
26 29 31.83 ± 9.01 19.69 ± 6.05 3.18 ± 0.35
27 14 30.82 ± 6.3 18.5± 3.7 1.8
29 8 29 ± 9.3 16.3 ± 5.5
Stentless porcine 21 3 14 ± 5 8.7 ± 3.5 1.33 ± 0.38
xenograft 22 3 16 ± 5.6 9.7 ± 3.7 1.32 ± 0.48
(stentless 23 4 13 ± 4.8 7.7 ± 2.3 1.59 ± 0.6
bioprosthesis) 24 3 13 ± 3.8 7.7 ± 2.2 1.4 ± 0.01
25 6 11.5 ± 7.1 7.4 ± 4.5 2.13 ± 0.7
26 3 10.7 7 ± 2.1 2.15 ± 0.2
27 1 9.2 5.5 3.2
28 1 7.5 4.1 2.3
Toronto stentless, 20 1 10.9 4.6 1.3
porcine (stentless 21 9 18.64 ± 11.8 7.56 ± 4.4 1.21 ± 0.7
bioprosthesis) 22 1 23.0 1.2
23 84 13.55 ± 7.28 7.08 ± 4.33 1.59 ± 0.84
25 190 12.17 ± 5.75 6.2 ± 3.05 1.62 ± 0.4
27 240 9.96 ± 4.56 4.8 ± 2.33 1.95 ± 0.42
29 200 7.91 ± 4.17 3.94 ± 2.15 2.37 ± 0.67

494 Appendices
TABLE D.2 Normal Doppler Echocardiographic Values for Mitral Valve Prosthesis
Peak Mean Peak Pressure Effective

gradient gradient velocity half-time orifice area
Valve Size n (mm Hg) (mm Hg) (m/s) (ms) (cm2)
Biocor (stentless 27 3 13 ± 1
bioprosthesis) 29 3 14 ± 2.5
31 8 11.5 ± 0.5
33 9 12 ± 0.5
Bioflo pericardial 25 3 10 ± 2 6.3 ± 1.5 2 ± 0.1
(stented 27 7 9.5 ± 2.6 5.4 ± 1.2 2 ± 0.3
bioprosthesis) 29 8 5 ± 2.8 3.6 ± 1 2.4 ± 0.2
31 1 4.0 2.0 2.3
Björk-Shiley (tilting disk) 23 1 1.7 115
25 14 12 ± 4 6±2 1.75 ± 0.38 99 ± 27 1.72 ± 0.6
27 34 10 ± 4 5±2 1.6 ± 0.49 89 ± 28 1.81 ± 0.54
29 21 7.83 ± 2.93 2.83 ± 1.27 1.37 ± 0.25 79 ± 17 2.1 ± 0.43
31 21 6±3 2 ± 1.9 1.41 ± 0.26 70 ± 14 2.2 ± 0.3
Björk-Shiley monostrut 23 1 5.0 1.9
(tilting disk) 25 102 13 ± 2.5 5.57 ± 2.3 1.8 ± 0.3
27 83 12 ± 2.5 4.53 ± 2.2 1.7 ± 0.4
29 26 13 ± 3 4.26 ± 1.6 1.6 ± 0.3
31 25 14 ± 4.5 4.9 ± 1.6 1.7 ± 0.3
Carbomedics (bileaflet) 23 2 1.9 ± 0.1 126 ± 7
25 12 10.3 ± 2.3 3.6 ± 0.6 1.3 ± 0.1 93 ± 8 2.9 ± 0.8
27 78 8.79 ± 3.46 3.46 ± 1.03 1.61 ± 0.3 89 ± 20 2.9 ± 0.75
29 46 8.78 ± 2.9 3.39 ± 0.97 1.52 ± 0.3 88 ± 17 2.3 ± 0.4
31 57 8.87 ± 2.34 3.32 ± 0.87 1.61 ± 0.29 92 ± 24 2.8 ± 1.14
33 33 8.8 ± 2.2 4.8 ± 2.5 1.5 ± 0.2 93 ± 12
Carpentier-Edwards 27 16 6±2 1.7 ± 0.3 98 ± 28
(stented 29 22 4.7 ± 2 1.76 ± 0.27 92 ± 14
bioprosthesis) 31 22 4.4 ± 2 1.54 ± 0.15 92 ± 19
33 6 6±3 93 ± 12
Carpentier-Edwards 27 1 3.6 1.6 100
pericardial (stented 29 6 5.25 ± 2.36 1.67 ± 0.3 110 ± 15
bioprosthesis) 31 4 4.05 ± 0.83 1.53 ± 0.1 90 ± 11
33 1 1.0 0.8 80
Duromedics (bileaflet) 27 8 13 ± 6 5±3 75 ± 12
29 14 10 ± 4 3±1 161 ± 40 85 ± 22
31 21 10.5 ± 4.37 3.3 ± 1.36 140 ± 25 81 ± 12
33 1 11.2 2.5 138 ± 27 85
Hancock I or not 27 3 10 ± 4 5±2 1.3 ± 0.8
specified (stented 29 13 7±3 2.46 ± 0.79 115 ± 20 1.5 ± 0.2
bioprosthesis) 31 22 4 ± 0.86 4.86 ± 1.69 95 ± 17 1.6 ± 0.2
33 8 3±2 3.87 ± 2 90 ± 12 1.9 ± 0.2
Hancock II (stented 27 16 2.21 ± 0.14
bioprosthesis) 29 64 2.77 ± 0.11
31 90 2.84 ± 0.1
33 25 3.15 ± 0.22
Hancock pericardial 29 14 2.61 ± 1.39 1.42 ± 0.14 105 ± 36
(stented bioprosthesis) 31 8 3.57 ± 1.02 1.51 ± 0.27 81 ± 23
(continued)

TABLE D.2 Normal Doppler Echocardiographic Values for Mitral Valve Prosthesis (continued)

Ionescu-Shiley (stented 25 3 4.87 ± 1.08 1.43 ± 0.15 93 ± 11
bioprosthesis) 27 4 3.21 ± 0.82 1.31 ± 0.24 100 ± 28
29 6 3.22 ± 0.57 1.38 ± 0.2 85 ± 8
31 4 3.63 ± 0.9 1.45 ± 0.06 100 ± 36
Ionescu-Shiley lowprofile 29 13 3.31 ± 0.96 1.36 ± 0.25 80 ± 30
(stented bioprosthesis) 31 10 2.74 ± 0.37 1.33 ± 0.14 79 ± 15
Labcor-Santiago 25 1 8.7 4.5 97 2.2
pericardial (stented 27 16 5.6 ± 2.3 2.8 ± 1.5 85 ± 18 2.12 ± 0.48
bioprosthesis) 29 20 6.2 ± 2.1 3 ± 1.3 80 ± 34 2.11 ± 0.73
Lillehei- Kaster 18 1 1.7 140
(tilting disk) 20 1 1.7 67
22 4 1.56 ± 0.09 94 ± 22
25 5 1.38 ± 0.27 124 ± 46
Medtronic-Hall 27 1 1.4 78
(tilting disk) 29 5 1.57 ± 0.1 69 ± 15
31 7 1.45 ± 0.12 77 ± 17
Medtronic Intact, porcine 29 3 3.5 ± 0.51 1.6 ± 0.22
(stented prosthesis) 31 14 4.2 ± 1.44 1.6 ± 0.26
33 13 4 ± 1.3 1.4 ± 0.24
35 2 3.2 ± 1.77 1.3 ± 0.5
Mitroflow (stented 25 1 6.9 2.0 90
bioprosthesis) 27 3 3.07 ± 0.91 1.5 90 ± 20
29 15 3.5 ± 1.65 1.43 ± 0.29 102 ± 21
31 5 3.85 ± 0.81 1.32 ± 0.26 91 ± 22
Omnicarbon (tilting disk) 23 1 8.0
25 16 6.05 ± 1.81 1.77 ± 0.24 102 ± 16
27 29 4.89 ± 2.05 1.63 ± 0.36 105 ± 33
29 34 4.93 ± 2.16 1.56 ± 0.27 120 ± 40
31 58 4.18 ± 1.4 1.3 ± 0.23 134 ± 31
33 2 4±2
On-X (bileaflet) 25 3 11.5 ± 3.2 5.3 ± 2.1 1.9 ± 1.1
27–29 16 10.3 ± 4.5 4.5 ± 1.6 2.2 ± 0.5
31–33 14 9.8 ± 3.8 4.8 ± 2.4 2.5 ± 1.1
Sorin Allcarbon 25 8 15 ± 3 5±1 2 ± 0.2 105 ± 29 2.2 ± 0.6
(tilting disk) 27 20 13 ± 2 4±1 1.8 ± 0.1 89 ± 14 2.5 ± 0.5
29 34 10 ± 2 4±1 1.6 ± 0.2 85 ± 23 2.8 ± 0.7
31 11 9±1 4±1 1.6 ± 0.1 88 ± 27 2.8 ± 0.9
Sorin Bicarbon (bileaflet) 25 3 15 ± 0.25 4 ± 0.5 1.95 ± 0.02 70 ± 1
27 25 11 ± 2.75 4 ± 0.5 1.65 ± 0.21 82 ± 20
29 30 12 ± 3 4 ± 1.25 1.73 ± 0.22 80 ± 14
31 9 10 ± 1.5 4±1 1.66 ± 0.11 83 ± 14
St Jude Medical 23 1 4.0 1.5 160 1.0
(bileaflet) 25 4 2.5 ± 1 1.34 ± 1.12 75 ± 4 1.35 ± 0.17
27 16 11 ± 4 5 ± 1.82 1.61 ± 0.29 75 ± 10 1.67 ± 0.17
29 40 10 ± 3 4.15 ± 1.8 1.57 ± 0.29 85 ± 10 1.75 ± 0.24
31 41 12 ± 6 4.46 ± 2.22 1.59 ± 0.33 74 ± 13 2.03 ± 0.32

496 Appendices
TABLE D.2 Normal Doppler Echocardiographic Values for Mitral Valve Prosthesis (continued)

Starr-Edwards 26 1 10.0 1.4
(ball-and-cage) 28 27 7 ± 2.75 1.9 ± 0.57
30 25 12.2 ± 4.6 6.99 ± 2.5 1.7 ± 0.3 125 ± 25 1.65 ± 0.4
32 17 11.5 ± 4.2 5.08 ± 2.5 1.7 ± 0.3 110 ± 25 1.98 ± 0.4
34 1 5.0 2.6
Stentless quadrileaflet 26 2 2.2 ± 1.7 1.6 103 ± 31 1.7
bovine pericardial 28 14 1.58 ± 0.25 1.7 ± 0.6
(stentless bioprosthesis) 30 6 1.42 ± 0.32 2.3 ± 0.4
Wessex (stented 29 9 3.69 ± 0.61 1.66 ± 0.17 83 ± 19
bioprosthesis) 31 22 3.31 ± 0.83 1.41 ± 0.25 80 ± 21
TABLE D.3 Normal Doppler Echocardiographic Values for Tricuspid Prosthesis
Valve type Examples Peak velocity (m/s) Mean pressure gradient (mm Hg)
Caged ball Starr-Edwards 1.3 ± 0.2 3.2 ± 0.8
Tilting disk Björk-Shiley 1.3 2.2
Bileaflet St. Jude 1.2 ± 0.3 2.7 ± 1.1
Porcine Carpentier-Edwards 1.3 ± 0.2 3.2 ± 0.8
Adapted from Rosenhek R, Binder T, Maurer G, et al. Normal values for Doppler echocardiographic assessment of heart valve
prostheses. J Am Soc Echocardiogr 2003;16:116.

E Classification of the Severity of Valvular Disease
TABLE E.1 Grading Severity of Aortic Regurgitation

2D imaging of LV at end Enlarged in other conditions Normal Variable Dilated (chronic)
diastole:
(Normal <5.6 cm or 3.2 cm/M2) Normal in acute AR
2D aortic leaflets Inaccurate Variable Variable Possible flail, coaptation
defect, variable
a
Color Doppler:
Jet height/LVOT height % Inaccurate with eccentric jets <25% 25–64% ≥65%
% jet diameter in LVOT/ Inaccurate with eccentric jets <5% 5–20% (mild to 21–59% (mod to severe);
Area of LVOT moderate) >59% severe
a
Vena contracta width (cm) Accuracy with multiple jets <0.3 cm 0.3–0.6 cm >0.6 cm
Diastolic flow reversal in Stiff aorta, brief is normal Brief, early Holodiastolic, Holodiastolic, increased
descending aorta (Nl) variable amplitude
height
Slope of the regurgitant jet Onset velocity ⬃ to diastolic/ Slow ≥2 m/s ≥3 m/s
LV by 4V 2
Pressure half-time of Effected by aorta and LV >500 ms 200–500 ms <200 ms
regurgitant jet compliance
Regurgitant volume Maximum <30 mL 30–44 mL 45–59 mL (mod to
(mL/beat) (mild to severe); ≥60 mL
moderate) severe
Regurgitant fraction (%) Maximum <30% 30–39% 40–49% (mod to
(mild to severe); ≥50 mL
moderate) severe
EROA (cm2) Maximum; good with <0.10 cm2 0.10–0.29 cm2 ≥0.30 cm2
eccentric jets
CW Doppler spectral density Qualitative; mod to severe Faint Variable Dense
overlap
a
Aliasing velocity set at 50–60 cm/s.
LV, left ventricle; AR, aortic regurgitation; LVOT, left ventricular outflow tract; Mod, moderate; EROA, effective regurgitant orifice
area; CW, continuous wave.
TABLE E.2 Grading Severity of Aortic Stenosis
Aortic sclerosis Mild Moderate Severe

Aortic jet velocity (m/s) ≤2.5 m/s 2.6–2.9 3–4 >4
Mean gradient (mm Hg) — <20 20–40 >40
AVA (cm2) — >1.5 1–1.5 <1
Indexed AVA (cm2/m2) — >0.85 0.60–0.85 <0.6
Velocity ratio >0.50 0.25–0.50 <0.25
AVA, aortic value area.
Adapted from: Baumgartner H, Hung J, Bermejo J, et al. Echocardiographic assessment of valve stenosis: EAE/ASE 497

498 Appendices
TABLE E.3 Grading Severity of Mitral Regurgitation

2D imaging LA size LAE may be caused Usually Variable LA enlargement
by other conditions normal
Acute MR may have
normal LA size
LV size — Usually Variable Often enlarged
normal (chronic MR)
MV apparatus May have severe Normal or Normal or Often visible
MR with structurally abnormal abnormal coaptation
normal MV defect
Color flow Maximum jet Technical (power, <4 cm2 — >8 cm2
Doppler (CFD) area aliasing velocity, Wall jet
color gain, Circumferential
frequency) LA jet
Load dependent
Wall impingement
Jet area/LA area — — — >40%
Visible flow Dependent on gain Rarely present Sometimes Often present
convergence and aliasing present
area velocity
Vena contracta Not useful for <0.3 0.3–0.69 ≥0.7
width (cm) multiple jets
Cannot add
diameters
Spectral Doppler PW mitral Dependent on A dominant Variable Restrictive
inflow load, diastolic fx, pattern
MVA, AF
PW PV flow Increased LAP, AF — Often systolic Systolic flow
blunting reversal
CW spectral — Faint — Dense
density
Regurgitant — <30 30–59 ≥60
volume
(mL/beat)
Regurgitant — <30 30–49 ≥50
fraction (%)
EROA (cm2) — <0.20 0.20–0.39 ≥0.40
LA, left atrium; LAE, left atrial enlargement; MR, mitral regurgitation; LV, left ventricle; MV, mitral valve; PW, pulse wave; fx, function;
MVA, mitral valve area; AF, atrial fibrillation; PV, pulmonary valve; CW, continuous wave; EROA, effective regurgitant orifice area;
left atrial pressure.
Adapted from: 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. J Am Soc Echocardiogr. 2003;16(7):777–802.
TABLE E.4 Grading Severity of Mitral Stenosis
Grade
Specific findings:
MVA (cm2) >1.5 1–1.5 <1
Supportive findings:
Mean gradient (mm Hg)a <5 5–10 >10
Pulmonary artery pressure (mm Hg) <30 30–50 >50
a
Patients in normal sinus rhythm with a heart rate between 60–80 bpm.
MVA, mitral valve area.

E. Classification of the Severity of Valvular Disease 499
TABLE E.5 Grading Severity of Tricuspid Regurgitation

2D imaging RA/RV/IVC size Not specific Normal Variable Usually dilated
RA diameter <4.6 cm Normal in acute TR
RV diameter <4.3 cm
Tricuspid valve Nonspecific Normal Variable Flail poor
structure coaptation/flail
leaflet
Doppler Maximum jet area Technical factors <5 cm2 5–10 cm2 >10 cm2
(Nyquist limit Loading
50–60 cm/s) Underestimates
(eccentric jets)
Hepatic vein flow Blunting multiple Systolic Systolic Systolic reversal
causes dominance blunting
Jet density-contour Qualitative, Soft parabolic Dense variable Dense triangular
CW complimentary contour with early
data peaking
Vena contracta Directs need of Not defined <0.7 >0.7
diameter (VCD) further
(cm) confirmation
PISA radius (cm) Validation lacking <0.5 0.6–0.9 >0.9
baseline shift with
(Nyquist 28 cm/s)
RA, right atrium; RV, right ventricle; IVC, inferior vena cava; CW, continuous wave; PISA, proximal isovelocity surface area;
TR, tricuspid regurgitation.
regurgitation with two-dimensional and Doppler echocardiography. J Am Soc Echocardiogr. 2003;16(7):777–802.
TABLE E.6 Findings Indicative of Hemodynamically Significant Tricuspid Stenosis
Specific findings
Mean pressure gradient ≥5 mm Hg
Inflow time–velocity integral >60 cm
T½ ≥190 ms
Valve area by continuity equation ≤1 cm2
Supportive findings
Enlarged right atrium ≥ moderate
Dilated inferior vena cava
Adapted from: 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.

500 Appendices
TABLE E.7 Grading Severity of Pulmonary Regurgitation

2D imaging Pulmonic valve Normal Variable Abnormal
RV size
RV diameter Nonspecific Normal Variable Dilated (except
<4.3 cm acute)
RVED area
= 35.5 cm2
Paradoxical septal Not specific Normal Variable Flail and poor
motion (volume for PR coaptation
overload pattern)
Doppler Color flow Poor correlation Small Variable Large
Doppler with severity <10 mm
Jet size of PR length
Vena contracta Not validated <small Variable Wide origin
(Nyquist limit
50–60 cm/s)
Jet density and Qualitative Faint Dense; variable Dense
deceleration CW Slow deceleration deceleration Steep deceleration
Short
Pulmonic systolic Time-consuming Slight increase Intermediate Great increase
flow compared to
systemic
RV, right ventricle; RVED, right ventricular end diastolic; CW, continuous wave; PR, pulmonic regurgitation.
regurgitation with two-dimensional and Doppler echocardiography. J Am Soc Echocardiogr. 2003;16(7):777–802; Bonow RO,
Carabello BA, Chatterjee K, et al. ACC/AHA 2006 guidelines for the management of patients with valvular heart disease: A report
of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (writing Committee to
Revise the 1998 guidelines for the management of patients with valvular heart disease) developed in collaboration with the
Society of Cardiovascular Anesthesiologists endorsed by the Society for Cardiovascular Angiography and Interventions and
the Society of Thoracic Surgeons. J Am Coll Cardiol. 2006;48(3):e1–148; Hatle L. Noninvasive assessment of valve lesions with
Doppler ultrasound. Herz. 1984;9:213–221 and Fawzy ME, Mercer EN, Dunn B, et al. Doppler echocardiography in the evaluation
of tricuspid stenosis. Eur Heart J. 1989;10(11):985–990.
TABLE E.8 Grading Severity of Pulmonary Stenosis

Peak velocity (m/s) <3 3–4 >4
Peak gradient (mm Hg) <36 36–64 >64

F Answers to End-of-Chapter Questions
Chapter 1 7. a 14. c
1. c 8. d 15. c
2. a 9. b 16. b
3. b 10. b 17. d
4. d 11. c 18. a
5. a 12. b 19. c
6. a 13. b 20. a
Chapter 2
1. c. Figure 2.1 outlines the standard terminology for probe manipulation. Turning the probe in a leftward
or counterclockwise direction will place more left-sided structures in the center of the imaging sector.
Rotation refers to the angle of the imaging plane.
2. a. Using the right hand analogy described in the text and Figures 2.2 and 2.3, at 45 degrees, right hand is
rotated 45 degrees clockwise so that the right thumb is toward the left shoulder and the right little finger
is toward the right hip. This is the approximate orientation of the probe when viewing the ME AV SAX.
3. e. Although the majority of views with have the aorta, left atrium, or left ventricle at the apex of
the imaging sector. In the TG RV inflow view the right ventricle is seen at the apex of the imaging
sector.
4. a. Although the cusps of the AV can be seen in the ME AV LAX, it is difficult, if not impossible, to
truly identify the near-field cusp as left or noncoronary cusp. The only view where all the three cusps
can be clearly seen and identified is the ME AV SAX. The valve cusps should not be visible in either of
the ascending aortic views.
5. b. The AV annulus is best seen in the ME AV LAX view. It is important to get the largest diameter
when making the measure; otherwise the plan is off the midline and not the true diameter. In the ME
AV SAX it is difficult to determine the correct level to make the measurement. The ME ascending
aortic views image the aorta above the level of the annulus.
6. a. The tip of a correctly placed intra-aortic balloon pump should be in the proximal descending aortic
distal to the takeoff of the great vessels. This area of the aorta is only seen in the ME descending aortic
short- and long-axis views.
7. e. All of the views can be helpful with the placement of a pulmonary artery catheter. The ME bicaval
view can be used to steer the catheter into the tricuspid valve (seen at approximately 7 o’clock). This
view is especially useful when refloating a PA catheter following CPB. The RV inflow–outflow view
and the ascending aortic short axis can confirm that the catheter has passed into the main pulmonary
artery. The ascending aortic long- and short-axis views can identify if the catheter is in the right
pulmonary artery.
8. d. All the listed views except the ME two-chamber provide views of the tricuspid valve. The RV
inflow–outflow and the ME two-chamber views are most commonly used to evaluate the tricuspid
valve, especially with color flow Doppler. The ME two-chamber view allows evaluation of the mitral
valve not the tricuspid.
9. b. At 0 degrees, left-sided structures are visible on the right, and right-sided structures are visible on
the left side of the imaging display. At 180 degrees, the imaging plane has rotated a full 180 degrees
and the image is reversed so that right-sided structures are now visible on the right side of the screen.
501

502 Appendices
10. a. The TG basal SAX allows for assessment of mitral valve and LV basal segment regional function.
The papillary muscles, mid, and apical LV segments should not be seen in the TG basal SAX view.
11. a. The ME four-chamber view looks at the septal and lateral walls of the left ventricle. The TG RV
inflow view does not look at any of the left ventricle. As discussed in the Physics and Doppler Chapter,
axial resolution is far superior to lateral resolution. Even though the anterior wall of the left ventricle
is seen in the TG mid-SAX and in the ME two-chamber views, whenever possible, measurements
should be performed in an axial direction as in the TG mid-SAX view and not a lateral direction as in
the ME two-chamber view.
12. d. The UE aortic arch LAX view looks at the distal ascending aorta and aortic arch. Aortic athero-
sclerosis and dissection pathology may be seen in this view. Depending on the surgical technique, the
aortic cannulation site may be seen in this view. The tip of an intra-aortic balloon pump should be
seen in the proximal portion of the descending aorta and is not visible in the UE aortic arch LAX view.
13. a. Pulmonary veins are seen emptying into the left atrium so any view of the left atrium may reveal the
pulmonary veins. The pulmonary veins are most commonly seen in modifications of the ME bicaval
and two-chamber views. The left atrium is seen in the ME AV short axis and can potentially show the
left sided pulmonary veins. The term ME midshort axis is not commonly used nomenclature for a
standard view. This will be discussed in depth in the subsequent chapters.
14. a. As described in Figure 2.1, the large knob controls ante- and retroflexion. The small knob controls
left–right flexion. A button controls image rotation. Advancing or withdrawing the probe controls
probe depth.
15. a. The femoral cannula will not be visible in the femoral artery. However, TEE is especially useful for
placement of the venous cannula. The cannula is advanced up the IVC through the right atrium and
into the proximal SVC. Using the ME bicaval view, the cannula can be precisely placed in the correct
position.
16. d. Both the ME RV inflow–outflow and the UE aortic arch SAX views allow inspection of the
pulmonary valve. The ME RV inflow–outflow view allows for inspection of the RV outflow tract
and the UE aortic arch SAX view provides the proper angle for spectral Doppler interrogation of the
outflow tract and the pulmonic valve.
17. d. Depending on the view obtained, the aorta, the left atrium, and the left ventricle may be seen at
the apex of the imaging sector and hence in the near field. By increasing the near-field gain, pathology
present near the apex may be better defined. Evaluation of the mitral valve is not as dependent on
near-field gain changes.
18. b. The left atrial appendage is best viewed in the ME two-chamber view. The ME bicaval, four-
chamber, and the TG two-chamber views show portions of the left atrium but not the appendage.
19. a. As discussed in the Physics Chapter, spectral Doppler (both PW and CW) measures flow in an axial
direction from the probe head. In the TG LAX and deep TG LAX aortic flow is aligned in an axial
direction. In the ME AV LAX, flow is perpendicular to the axial direction and spectral Doppler is not
useful.
20. a. Papillary muscles should not be visible in the TG basal SAX. This view is at the level of the chordae
tendineae/mitral valve and above the papillary muscles.
Chapter 3 7. c 14. (a) i, (b) ii

1. d 8. d 15. a
2. c 9. d 16. c
3. d 10. b 17. b
4. c 11. d 18. c
5. a 12. b 19. c
6. c 13. c 20. c

F. Answers to End-of-Chapter Questions 503
Chapter 4 7. d 14. a
1. a 8. c 15. b
2. c 9. d 16. c
3. b 10. b 17. d
4. b 11. a 18. d
5. d 12. c 19. d
6. b 13. d 20. b
Chapter 5 7. c 14. b
1. c 8. a 15. d
2. b 9. b 16. b
3. d 10. d 17. d
4. c 11. b 18. a
5. a 12. b 19. b
6. c 13. a 20. d
Chapter 6 7. c 14. d
1. a 8. d 15. a
2. d 9. a 16. b
3. b 10. b 17. b
4. b 11. b 18. c
5. b 12. d 19. c
6. b 13. b 20. a
Chapter 7
1. d. Changes in LV relaxation and compliance contribute to the spectrum of Doppler LV filling patterns
that are observed with progressive diastolic dysfunction. The initial abnormality of diastolic filling in
most disorders of cardiac physiology is impaired myocardial relaxation exceeding that expected with
aging alone. Impaired LV relaxation occurs with myocardial ischemia/infarction, LV hypertrophy,
hypertrophic cardiomyopathy, and in the early stages of infiltrative disorders (12).
2. a. The diagnosis of pericardial tamponade includes identification of significant respiratory variation in
atrial and ventricular Doppler inflow profiles. Normally during spontaneous respiration, intrathoracic
pressures are transmitted equally to the pericardial space and intracardiac chambers. The transmission
of intrathoracic pressure, however, is shielded by significant pericardial effusions. Consequently, LA
and LV filling pressure gradients are decreased during spontaneous inspiration, resulting in diminished
pulmonary venous forward diastolic velocities, delayed MV opening, prolonged IVRT, and decreased
mitral E-wave velocity (23,48). Reciprocal changes occur in the transtricuspid valve velocities.
3. a. The TMDF profile associated with impaired relaxation is typically characterized by a prolonged
IVRT and a decreased initial TMPG (Fig. 7.4) (13). Consequently, the peak E-wave velocity decreases
relative to the peak A-wave velocity when LV relaxation is impaired (E/A < 1), since the MV tends to
open before relaxation is complete. In addition, the duration of LV relaxation is prolonged resulting
in a prolonged DT (5) since the LA–LV pressure gradient takes longer to equilibrate.
4. c. The normal PVAR (≈90 to 115 milliseconds) duration is the same or less than the transmitral A-wave
duration (≈120 to 140 milliseconds) (11). In general, LA contraction should result in a greater net
forward blood volume and flow toward a normal, compliant LV compared with any retrograde flow
back toward the PV. A PVAR velocity that exceeds the mitral A-wave by >35 cm/s or PVAR duration
>30 milliseconds longer than the transmitral A-wave duration usually indicates an age-independent
elevation in LVEDP (18).

504 Appendices
5. a. A typical pulmonary venous Doppler flow (PVDF) profile consists of an antegrade systolic velocity
which may appear monophasic, or biphasic especially in the presence of low LAP probably owing to
temporal dissociation of atrial relaxation and mitral annular motion (Fig. 7.5) (16). The first systolic
component, PVS1, is dependent upon LA relaxation and the subsequent decrease in pressure. The
later peaking PVS2, reflects right ventricular (RV) stroke volume, LA compliance, the effects of early
ventricular systole on LAP, and any concomitant MR.
6. e. A typical pulmonary venous Doppler flow (PVDF) profile consists of an antegrade systolic velocity
which may appear monophasic, or biphasic especially in the presence of low LAP probably owing to
temporal dissociation of atrial relaxation and mitral annular motion (Fig. 7.5) (16). The first systolic
component, PVS1, is dependent upon LA relaxation and the subsequent decrease in pressure. The
later peaking PVS2, reflects right ventricular (RV) stroke volume, LA compliance, the effects of early
ventricular systole on LAP, and any concomitant MR.
7. b. (Table 7.2)
8. d. In patients with atrial fibrillation (AF), the transmitral and PVAR-waves are absent and the E-wave
peak velocity and DT vary with the length of the cardiac cycle. AF may also be associated with a loss
of PVS1, and a decreased PVS2 relative to the dominant PVD (23). Peak acceleration rate of the E-wave
velocity (24), transmitral E-wave DT shortening, and the duration and initial deceleration slope time
of PVD may still correlate with increased LV filling pressure in the presence of AF (23).
9. c. The intermediate, pseudonormalized stage of diastolic dysfunction is therefore characterized by
normal values for peak E-wave and A-wave velocities, IVRT, and DT. Reducing preload by utilizing
reverse Trendelenburg positioning, partial cardiopulmonary bypass (CPB), a Valsalva maneuver (14),
or by administering nitroglycerin may also reveal underlying impaired LV relaxation in a patient with
pseudonormalized transmitral inflow (15).
10. a. In contrast to standard Doppler filling indices, Vp is relatively independent of preload, yet responds
to changes in lusitropic conditions (32) and systolic performance (33). Consequently, while TMDF
and PVDF tend to show a parabolic distribution from normal through progressive. Furthermore,
altering preload by utilizing various techniques (partial CPB, inferior vena cava occlusion, intravenous
nitroglycerin, amyl nitrate inhalation, Valsalva maneuver, Trendelenburg positioning, leg lifting)
is associated with changes in transmitral peak E-wave velocity, E/A-wave velocity, and E-wave
deceleration, but has little affect on Vp (33–35).
11. b. Both strain rate (SR) and strain (S) imaging are angle dependent. However, they are generally used
in long-axis views to measure longitudinal shortening (systolic function) or lengthening (diastolic
function) of the LV along the ultrasound beam. Consequently, unlike Doppler tissue imaging (DTI),
both S and SR are relatively independent of translational or rotational movement. Thus strain imaging
may have additional advantages over conventional echocardiography techniques for evaluating
diastolic function in the perioperative period.
12. b. Diastolic RV dysfunction can manifest with the same relative changes in transtricuspid peak E- and
A-wave velocities, E/A-wave ratios, and DT that occur with TMDF profiles associated with alterations
in LV relaxation and compliance (43,44). The ratio of the total hepatic reverse flow integral to total
forward flow integral (TVIA + TVIV/TVIS + TVID) increases with either RV diastolic dysfunction or
significant TR, but appears to be more affected by the former (45). In addition, a marked shortening
of the transtricuspid DT and diastolic predominance of HV flow with prominent V- and A-wave
reversals during spontaneous inspiration, indicates significant decreases in RV compliance and
increased diastolic filling pressures (Fig. 7.11C) (10).
13. c. Congestive heart failure (CHF) is the most common diagnosis amongst inpatients in the United
States and accounts for 720,000 hospital admissions annually (54). Nearly half of the patients with
CHF have diastolic dysfunction and normal ejection fraction (55). Diastolic dysfunction increases
with age, especially amongst elderly patients with hypertensive heart disease (55).
14. c. Preoperative diastolic dysfunction has also been reported in 30% to 60% of cardiac surgical patients
and independently associated with difficult weaning from cardiopulmonary bypass (CPB), more
frequent inotropic support, and increased morbidity.
15. e. While more complex algorithms for evaluating diastolic dysfunction may be considered impractical
to obtain in the perioperative period, simpler echocardiographic measures of diastolic dysfunction

including the tissue Doppler-derived surrogate for LV diastolic pressure E/e′, have also been shown
to be prognostic of adverse postoperative outcomes after cardiac surgery (60,61).
16. d. Diastolic deformation of the LV can also be analyzed with strain imaging and Vp to describe both
early and late filling. Pixel velocity values obtained by color DTI can be processed to velocity gradients
as a measure of longitudinal strain rate with a technique termed strain rate imaging (SRI), which can
show the spatial–temporal relations of the diastolic phases. The phases of early and late filling can
be seen to consist of a stretch wave in the myocardium, propagating from the base to the apex (Vp).
Diastolic function is characterized by both peak strain rate and propagation velocity of this wave
(41) (Fig. 7.10). In a series of 26 patients with hypertension, normal systolic function, and impaired
diastolic function, Stoylen et al. (41) demonstrated that both the peak diastolic SR and Vp are reduced.
17. d. Preoperative diastolic dysfunction has also been reported in 30% to 70% of cardiac surgical patients
and independently associated with difficult weaning from cardiopulmonary bypass (CPB), more
frequent inotropic support, and increased morbidity (3,37). Merello et al. (59) evaluated diastolic
dysfunction in 191 CABG patients. Mortality and complications through 30 days postoperatively
were compared with that predicted by the EuroSCORE and Parsonnet score. Increasing degrees of
diastolic dysfunction correlated well with survival. However, mortality was not predicted by either
the EuroSCORE or Parsonnet score suggesting the potential values adding a measure of diastolic
dysfunction to these widely used risk stratification schemes (59).
18. a. The concordance between mitral annular motion assessed by DTI and mitral inflow velocities,
however, is disrupted with progressive diastolic dysfunction when poor relaxation coexists with an
elevated filling pressure. In patients with elevated LVEDP who present with a pseudonormal (27) or
restrictive transmitral Doppler inflow velocity profile (28), E′ remains reduced suggesting relative
preload independence (Fig. 7.7). In fact, E′ has actually been shown to be the best discriminator
between normal and pseudonormal patients when compared to any single or combined index of
TMDF or PVDF profiles (25).
19. a. The LA contribution to LV diastolic filling is usually <20% in young healthy patients, yet may
approach 50% in patients with decreased LV filling associated with early diastolic dysfunction.
20. d. The pseudonormalized filling pattern represents a moderate stage of diastolic dysfunction where a
“normal” early TMPG is generated by the balance between compromised LV relaxation and gradually
increasing filling pressures as LV compliance decreases. The pseudonormalized PV Doppler flow
velocity profile is often characterized by a pattern of relative systolic blunting and a prolonged PVAR
duration and velocity compared with the transmitral A-wave duration depending upon the LAP and
degree of reduced LV compliance (Fig. 7.4). In this scenario, the PVDF pattern may be helpful in
distinguishing a pseudonormal from normal TMDF profile.
Chapter 8 7. e 14. b
1. d 8. c 15. c
2. c 9. d 16. a
3. c 10. e 17. a
4. a 11. e 18. d
5. d 12. d 19. a
6. b 13. e 20. b
1. d 8. c 15. a
2. c 9. c 16. b
3. d 10. a 17. d
4. d 11. c 18. b
5. a 12. d 19. d
6. d 13. b 20. d

506 Appendices
1. d 8. b 15. c
2. c 9. b 16. a
3. a 10. d 17. d
4. c 11. d 18. b
5. a 12. d 19. c
6. d 13. a 20. b
Chapter 11 7. e 14. d
1. d 8. a 15. f
2. d 9. e 16. a
3. e 10. a 17. c
4. d 11. a, b 18. c
5. e 12. a, b 19. a
6. b 13. c, d 20. c
Chapter 12 7. c 14. a
1. c 8. d 15. e
2. c 9. d 16. c
3. d 10. b 17. a
4. b 11. b 18. a
5. a 12. d 19. c
6. b 13. c 20. d
Chapter 13
1. c. The simplified Bernoulli equation, ΔP = 4 × V 22, is often used to estimate the transvalvular pressure
gradient across a prosthetic aortic valve. When the proximal flow velocity in the left ventricular
outflow tract is close to or exceeds 1.5 m/s, the nonsimplified Bernoulli equation, ΔP = 4 × (V 22 − V 12)
provides a more accurate estimate of the transvalvular pressure gradient across the prosthetic valve in
the aortic position. Using the nonsimplified Bernoulli equation, ΔP = 4 × (2.312 − 1.542) = 11.9 mm Hg.
2. c. Moderate prosthetic–patient mismatching. The estimated orifice area (EOA) of the prosthetic
valve is calculated by EOA = LVOTarea × (VTILVOT/VTIAoV). The LVOT area is determined by the
formula, LVOTarea = π × (LVOTdiameter/2)2. The EOA indexed to body surface area, EOAi = EOA/BSA.
In the above case, the calculated EOAi for the patient is (π × [LVOTdiameter/2]2 × [30 cm/60 cm])/1.68 =
0.76 cm2/m2. An EOAi ≤ 0.65 cm2/m2 is consistent with severe prosthetic–patient mismatch,
EOAi > 0.65 cm2/m2 and ≤0.85 cm2/m2 is consistent with moderate prosthetic–patient mismatch, and
EOAi > 0.85 cm2/m2 is consistent with no or mild prosthetic–patient mismatch.
3. e. Combining qualitative and quantitative echocardiographic parameters of regurgitation in an
integrative approach is typically necessary to provide an estimate of the severity of prosthetic
regurgitation because grading the severity of prosthetic aortic regurgitation is more difficult than grading
native aortic regurgitation. Standard echocardiographic parameters to grade the severity of native aortic
valve regurgitation do not always provide an accurate assessment of the severity of prosthetic aortic
regurgitation.
4. a. A normally functioning prosthetic valve in the mitral position has a peak velocity <1.9 m/s, mean
gradient ≤5 mm Hg, and pressure half-time of <130 milliseconds. A peak velocity 2.5 m/s, mean
gradient >10 mm Hg, and pressure half-time >200 milliseconds suggest significant prosthetic mitral
stenosis.

5. e. A prosthetic valve with an estimated orifice area (EOA) greater than 1.3 cm2 would yield an indexed
estimated orifice area (EOAi = EOA/BSA) of >0.65 cm2/m2. An EOAi greater than 0.65 cm2/m2 would
avoid severe prosthetic–patient mismatch. Severe prosthetic–patient mismatch is defined as an
EOAi ≤ 0.65 cm2/m2.
6. d. Leakage at the proximal anastomotic suture line would cause cardiac tamponade in the acute
setting because blood would extravasate into the pericardial space. Paravalvular regurgitation is not
possible with composite aortic root replacement because the prosthetic valve is fused to the vascular
graft used to replace the aortic root and ascending aorta. A delayed dehiscence of the proximal aortic
suture line would lead to an aortic pseudoaneurysm.
7. d. The TEE transgastric long-axis view provides an image of the prosthetic valve in the aortic position
in the far field where the motion of both occluders can often be imaged. The individual motion of each
occluder of a mechanical bileaflet prosthesis in the aortic position cannot be reliably determined from
the midesophageal imaging planes because of acoustic shadowing caused by the annular stent or the
occluders.
8. a. The TEE midesophageal view provides an image plane through the prosthetic valve in the mitral
position where the motion of both occluders can usually be discerned without interference from
acoustic shadowing. Depending on the orientation of the hinge points of the prosthetic valve at the
time of implantation, adjusting the TEE multiplane angle from the midesophageal window to provide
a cross section perpendicular to the motion of the occluders permits the motion of both occluders to
be imaged simultaneously.
9. c. The severity of paravalvular regurgitation, if present can be detected and estimated by the TEE
examination. The TEE examination cannot accurately estimate the transvalvular pressure gradient
or effective orifice area for a caged-disc prosthetic valve because blood flow through the orifice is not
central.
10. d. The TEE upper esophageal aortic arch short-axis view provides a cross section through the pulmonic
valve and pulmonary artery in long axis that permits blood flow velocity across the pulmonic valve to
be measured using continuous wave Doppler. The mean pulmonary artery pressure and pulmonary
artery diastolic pressure can be estimated from the velocity profile of the transvalvular regurgitant jet.
11. e. The prosthetic valve type must be a pericardial bioprosthetic valve because the bioprosthetic valve
leaflets constructed from pericardium are mounted onto stents or struts that can be imaged within
the aortic root in the TEE midesophageal aortic valve short-axis imaging plane. Stents or struts are
absent in porcine stentless bioprosthetic valves that are constructed from the porcine aortic root and
reinforced by a fabric cuff. Mechanical prosthetic valves can be identified by the acoustic shadowing
produced by the pyrolytic carbon valve occluders.
12. a. Bileaflet mechanical prosthetic valves produce characteristic specular acoustic artifacts in the
spectral display of flow through the valve upon leaflet opening and closure. The native mitral valve,
bioprosthetic valves in the mitral position, or mitral valve after repair with a prosthetic annular ring
do not produce specular acoustic artifacts in the spectral display that mark the opening and closure
of the valve leaflets.
13. a. Although the caged-ball valve was the first prosthetic heart valve to be successfully implanted, it is
no longer manufactured for clinical implantation. The present generation of prosthetic valves has a
more favorable hemodynamic performance in relation to their annular diameter as compared to the
first generation caged-ball prosthetic valves.
14. e. Paravalvular regurgitation, vegetation, transvalvular regurgitation, and motion or “rocking” of the
prosthetic valve stent indicating annular dehiscence can all be signs of prosthetic endocarditis on the
echocardiographic examination.
15. d. Regurgitation occurring at a site between the native valve annulus and the sewing ring is defined
a paravalvular regurgitation and is always considered pathologic. Physiologic, nonpathologic
regurgitation can be detected by Color Doppler flow imaging at the coaptation of the leaflets, the
hinge points, through cloth-covered regions of the valve stent, and even through suture holes in the
sewing ring of prosthetic valves immediately after implantation.

508 Appendices
16. e. Leaflet prolapse, calcification, perforation, and restriction are all signs of structural valvular
degeneration that eventually affect bioprosthetic valves.
17. c. A Doppler velocity index (DVI) less than 0.25 indicates prosthetic valve stenosis. Pannus ingrowth
is the most common cause of stenosis in a patient with a mechanical prosthetic valve. Pannus is
difficult to image even with TEE and must be diagnosed based on indirect evidence of the effect of
pannus causing valve stenosis, pannus impeding the range of motion of the occluders, or transvalvular
regurgitation from pannus impairing leaflet closure.
18. a. The Doppler velocity index (DVI) is a ratio of the blood flow velocity in the left ventricular outflow
tract, proximal to the prosthetic valve to the transvalvular blood flow velocity across the prosthetic
valve. The DVI provides a measure of the prosthetic valve orifice area relative to the cross-sectional
area of the left ventricular outflow tract. Using the DVI to quantify the severity of prosthetic aortic
valve stenosis is independent of the area of the left ventricular outflow tract, cardiac rhythm, or
cardiac output.
19. b. Transesophageal echocardiography (TEE) has a high sensitivity (86% to 94%) and specificity (88%
to 100%) for detecting vegetations, paravalvular regurgitation, or abscess associated with prosthetic
endocarditis. TEE is superior to transthoracic echocardiography (TTE) for diagnosis of prosthetic
endocarditis.
20. c. The Medtronic Hall mechanical tilting disk valve has a central orifice through which a large central
regurgitant washing jet arises when the valve is in the closed position in systole. A Starr–Edwards
(caged-ball valve) has no washing jet. The Bjork–Shiley (single tilting disk) valve has two laterally
directed regurgitant jets that originate from the site where the occluder contacts the annular stent,
but no central jet. A St. Jude Medical bileaflet mechanical valve has regurgitant washing jets that
originate from the hinge points of the occluder or from the site where the occluder contacts the
annular stent, but never produces a large central regurgitant jet. The Sorin Mitroflow valve is a
pericardial bioprosthetic valve which is approved in the United States for implantation only in the
aortic position. Only a mechanical prosthetic valve produces the degree of acoustic shadowing and
comet tail artifact seen on the far side of the prosthetic valve in the TEE image above.
Chapter 14 7. b 14. d
1. c 8. c 15. b
2. c 9. a 16. c
3. c 10. c 17. c
4. c 11. c 18. d
5. d 12. d 19. c
6. a 13. d 20. b
Chapter 15
1. e. Compression of the recurrent laryngeal nerve can occur between the TEE probe and an endotra-
cheal tube when in situ for prolonged periods. Midesophageal views can be safely obtained in
patients with a hiatus hernia.
2. b. Stitching artifacts occur with full-volume acquisition.
3. b
4. b
5. c. Transgastric views are often lost. The development of mitral regurgitation may result in conversion
to on-pump but is not a contraindication.
6. d
7. a
8. d

9. a
10. d. Turbulence in the inflow cannula is detected by CFD.
11. a. RV failure occurs in 30% of LVAD patients. It is usually temporary in nature.
12. b 15. b 18. c

13. a 16. b 19. c
14. d 17. c 20. d
Chapter 16 7. b 14. b
1. c 8. c 15. d
2. d 9. b 16. b
3. a 10. b 17. d
4. c 11. b 18. d
5. d 12. c 19. c
6. a 13. c 20. b
Chapter 17
1. a. Zones 3 and 4 cannot be reliably imaged due to bronchial interposition.
2. c. An intimal flap is seen due to the separation of that layer from the medial or adventitial layer of
the aorta. Aortic regurgitation, effusions, and regional wall motion abnormalities are often seen in
association with aortic dissections, but do not make the diagnosis.
3. b. Unlike the ascending or descending aorta, the aortic arch is typically seen in long axis around 0
degrees and short axis at 90 degrees due to its horizontal nature.
4. a. DeBakey Type III, also called Stanford Type B, dissections only involve the descending aorta. They
are generally medically managed initially, unless there are signs of visceral malperfusion, such as
bowel ischemia.
5. b. The TRUE lumen typically expands during systole. Statements A, C, and D are correct regarding
the false lumen.
6. c. Ascending aortic aneurysms typically develop over a long time period and are not considered an
acute aortic syndrome.
7. a. The arrow is pointing to the distal end of an elephant trunk graft. It can be identified as a graft
material versus a cannula by the serrated appearance.
8. d. Intramural hematomas (IMHs) are part of the acute aortic syndromes, with Type A considered a
surgical emergency because they can progress to flap formation or frank aortic rupture. The etiology
is thought to be rupture of the vasa vasorum in the medial layer as opposed to a tear in the intimal
layer. Medial thickening of 7 mm or more is consistent with ascending IMHs. Atherosclerotic plaques,
not IMHs, typically protrude into the lumen of the aorta above the intimal layer.
9. b. The maximum aortic root diameter is within normal limits, but the ascending aorta (5.1 cm) is
clearly dilated. Since the sinotubular junction can be discerned (i.e., it is not effaced), this is best
classified as a supracoronary or tubular aneurysm. “Type A” is a dissection classification, and there
does not appear to be any flap present.
10. c. A dissection flap can usually be distinguished from artifact by its rapid, oscillatory movements
within the lumen of the aorta. Objects with indistinct borders that cross anatomical boundaries (i.e.,
seen outside of the aorta) are typically artifacts.

510 Appendices
11. b. According to 2010 guidelines on thoracic aortic disease, patients undergoing cardiac surgery with
dilation of the ascending aorta measuring 4.5 cm or greater should be considered for concomitant
aortic repair. It is important to note, however, that exactly what type of surgical intervention (i.e.,
replacement vs. plication vs. external wrapping) is not addressed.
12. a. This image shows the descending aorta in short axis, not the aortic arch since the omniplane angle
is at 0 degrees. The color Doppler shows flow from the lumen where the “X” is located into the other
lumen during systole. The “X” is therefore within the true lumen.
13. c. Unlike a linear (i.e., vascular) probe, a phased-array transducer can typically visualize all walls of
the aorta at once. However, a phased-array probe cannot be placed directly on the aorta. Both types
of probes are available in high frequencies (>7 MHz) and can be placed in sterile sheaths for use on
the surgical field.
14. b. The Crawford system of thoracoabdominal aneurysm (TAA) classification was developed
in order to help standardize the reporting of the extent of the aneurysm. Type I TAAs involve
most of the descending thoracic aorta, but typically terminate prior to the renal arteries in the
abdomen. Type II TAAs have the greatest extent, involving all of the thoracic descending aorta and
reach below the renal arteries, often into the inguinal area. Type III TAAs involve the distal half
or less of the descending thoracic aorta, and Type IV TAAs may only involve the upper abdominal
aorta.
15. c. This is a Type A intramural hematoma, as evidenced by the medial thickening of 10 mm. No
dissection flap is present. Atherosclerotic disease would typically protrude irregularly into the
lumen of the aorta and be seen as intimal thickening. Seen in more than one view, this is not an
artifact.
16. a. This is an epiaortic scan (note lack of an omniplane angle) showing the midascending aorta in short
axis, making C incorrect. Thickening of >3 mm is present, making this a grade 3 plaque. The intimal
layer is intact in this patient, whereas a penetrating atherosclerotic plaque would disrupt it and erode
into the media. The white line in the center of the aorta is an artifact, likely caused by either the
catheter in the right PA or in the superior vena cava.
17. d. Since the risk of rupture increases dramatically at 7 cm in the descending aorta, it is recommended
that asymptomatic patients undergo stent or open repair at diameters ≥6 cm. The cutoff for ascending
aortic repair is 5.5 cm, and 4.5 cm if the patient is already undergoing cardiac surgery.
18. d. The size of a patient's aorta most closely correlates with age and body surface area, which is
dependent upon height and weight.
19. d. This patient should go directly to the operating rooms since the TEE images clearly show a
dissection flap. Other imaging tests are not necessary. Although some aortic regurgitation is present,
a new aortic valve alone will not appropriately treat this condition.
20. b. Any plaque with a mobile component would be a Grade V lesion on the Katz grading system. There
is no grade M. Type A is the Stanford classification of acute aortic dissection. Type IV refers to the
Crawford classification system of thoracoabdominal aneurysms.
Chapter 18
1. a. Her ventricular dimensions are small, and fractional shortening is elevated (3.5 − 0.5/3.5 × 100 =
85.7%). This is most consistent with hypovolemia.
2. c. Her LV dimensions are all in the upper limit of normal and her fractional shortening is normal
(6 − 4/6 × 100 = 33.33%). This is most consistent with vasodilatory shock due to urosepsis.
3. b. Her LV dimensions show an enlarged LV, and her fractional shortening is decreased (8 − 7/8 × 100 =
12.5%). This is most consistent with myocardial dysfunction.
4. d. She has dilated RV with TR, this is most consistent with an acute pulmonary embolus.
5. a. Although her LV size and fractional shortening are normal, she has a small IVC with marked
collapse on inspiration. This implies fluid responsiveness and a bolus should be given then the
measurements should be repeated.

6. d. TTE cannot rule out postoperative tamponade, because postop tamponade can be localized—as
opposed to the usual medical tamponade. TEE showed an isolated clot posterior to the left atrium
that was impairing LV filling.
7. d. A new regional wall motion abnormality may mean the bypass graft to the LAD is down. This
requires urgent intervention—either in the operating room or cath lab.
8. d. The normal response to acute RV failure is dilation, that can also result in TR.
9. d. With a normal CXR, a right to left shunt needs to be ruled out. The bicaval view is the best view to
rule out an ASD/PFO.
10. a. In supine patients undergoing CPR this is often the easiest and fastest four-chamber view to obtain.
11. d. The key is to minimize interruptions of CPR, so the best time to perform a limited echo is after
shock and 2 minutes of CPR during the rhythm and pulse check.
12. a. Patients with wall motion on echo, but no pulse may have a better outcome. This finding would
support continuation of ACLS.
13. b. This describes true PEA. True PEA has a worse prognosis than pseudo PEA.
14. a. Her ventricle is small, and fractional shortening is normal (4 − 1/4 × 100 = 75%), but she has severe
LV hypertrophy, which makes CVP very unreliable as a marker of fluid responsiveness.
15. a. She most likely has severe MR due to systolic anterior motion of the MR. This process is worsened
by hypovolemia, small LV size, and increased contractility. The first step would be to optimize LV
volume and size.
16. a. Severe AS is defined by:
t Jet velocity >4 m/s
t Mean gradient >40 to 50 mm Hg
t Valve area <1 cm2
t The shape of the curves do not correspond with severity.
17. a. Severe MS is defined by:
t Mean gradient >10 mm Hg
t Valve area <1 cm2
t PA systolic pressure >50 mm Hg
t Pressure half-time >220 milliseconds
18. a. Severe AR is defined by:
t Jet width/LVDT of >65%
t Vena contraction of >0.6 cm
t Pressure half-time of <200 milliseconds
t Regurgitant orifice area of >0.3 cm2
19. a. Severe MR is defined by:
t Jet area (percent of LA) of >40%
t Vena contraction of >0.7 cm
t Regurgitation volume of >60 mL
t Regurgitant orifice area of >0.4 cm2
20. a. Acute MR (endocarditis, papillary/chordal rupture) is associated with normal LV size and function,
normal LA size, and normal annulus. Chronic MR (myxomatous, annular dilation) is associated with
LV and LA dilation. LV function may be normal or depressed.
Chapter 19
1. a. The most frequently performed surgical procedures in adults with congenital heart disease include
pulmonary valve replacement, closure of secundum atrial septal defect, aortic valve replacement, and
right ventricle to pulmonary artery conduit placement.

512 Appendices
2. c. Among atrial septal defects, those involving the sinus venosus region are most commonly associated
with anomalous pulmonary venous drainage.
3. d. Congenital lesions associated with a ventricular septal defect include a bicuspid aortic valve, aortic
coarctation, and right ventricular outflow tract obstruction. One of the components of the “tetrad” in
tetralogy of Fallot is a conoventricular septal defect.
4. e. A bicuspid aortic valve represents the most common form of congenital pathology. The characteristic
feature on echocardiography is a “fish-mouth” appearance of the valve in systole. Some patients can
develop aortic stenosis, aortic regurgitation, and/or aortic root dilation.
5. b. A persistent left superior vena cava is associated with an enlarged coronary sinus. The presence of
this systemic venous connection is confirmed by the appearance of right atrial contrast upon injection
of agitated saline into a left arm or left neck vein. This is characterized by contrast draining across the
coronary sinus into the right atrium.
6. c. The anterosuperior rim of an atrial septal defect is best imaged in the midesophageal aortic valve
short-axis view and represents the distance between the aortic ring and the defect. The lack of this
rim does not necessarily preclude device deployment.
7. b. Muscular ventricular septal defects may be suitable for percutaneous device closure due to their
favorable location as they are relatively distant from the aortic and atrioventricular valves. These
defects oftentimes are difficult to identify by the surgeon due to their location in the trabecular
portion of the ventricular septum.
8. e. Inlet defects are located in close proximity to the atrioventricular valves in the posterior or inlet
portion of ventricular septum. A common atrioventricular valve annulus and associated primum
atrial septal defect are also part of a complete atrioventricular canal defect.
9. d. The right ventricular (or pulmonary artery) systolic pressure can be estimated using the formula: RV
systolic pressure = Systolic blood pressure − 4(VVSD)2. In this case, RV systolic pressure = 100 − 4(4)2 or
would be equal to 36 mm Hg.
10. c. During a Ross procedure a pulmonary autograft is harvested and used to replace the aortic root.
An assessment of the pulmonic valve in terms of patency/competency is thus essential before this
intervention is undertaken. The right ventricular outflow tract is reconstructed using a homograft or
alternate material.
11. d. Severity grading systems for pulmonary (pulmonic) stenosis rely on Doppler-derived peak
instantaneous transvalvar gradients. Moderate stenosis is characterized by a gradient of 36 to 64
mm Hg. Symptoms associated with moderate obstruction include dyspnea and fatigue. Systemic and
suprasystemic right ventricular pressures imply severe disease.
12. a. Associated lesions in tetralogy of Fallot include anomalies of the systemic veins, aortic arch,
and coronary arteries. The midesophageal aortic valve short-axis view facilitates the assessment of
anomalous origin of the coronary arteries in tetralogy of Fallot.
13. b. Extensive patching across the pulmonary (pulmonic) valve, also referred to as transannular
patching in patients with tetralogy of Fallot, results in free pulmonary regurgitation. In addition
to this indication, other causes of surgical reintervention include right ventricular outflow
tract obstruction, aneurysmal dilation of the right ventricular outflow, and significant residual
intracardiac shunts.
14. e. Long-term problems in patients with D-transposition of the great arteries depend on the type of
initial repair. Patients who underwent an atrial switch procedure (Mustard or Senning operation),
which leaves the morphologic right ventricle (RV) supporting the systemic circulation, have a high
likelihood of developing RV failure and tricuspid regurgitation over time. Conversely, patients who
undergo an arterial switch operation have significantly less morbidity in the current surgical era.
15. b. Atrioventricular valves are associated with their corresponding ventricle. A septophilic tricuspid
valve will identify a right ventricle and a septophobic valve a left ventricle. In corrected transposition
the discordant atrioventricular connection implies that the right ventricle functions as the systemic
chamber. This defect is frequently associated with a ventricular septal defect, obstruction to pulmonary

blood flow, and left atrioventricular (tricuspid) valve dysplasia (Ebstein-like malformation). There is
abnormal spatial orientation of the great arteries relative to that present in the normal heart.
16. a. An apical displacement index that exceeds 8 mm/m2 relative to the mitral hinge point on the
ventricular septum is consistent with the diagnosis of Ebstein anomaly.
17. b. The separation of the pulmonary and systemic circulations in patients with single ventricle
physiology is achieved with the Fontan procedure, which directs blood from the inferior vena cava
into the pulmonary artery without intervening pumping chamber.
18. c. The coronary arteries are best visualized in the midesophageal aortic short- and long-axis views.
Most of the coronary perfusion occurs during diastole; thus, in that portion of the cardiac cycle, the
vessels are easier to be identified.
19. c. Congenital coronary artery anomalies can be seen as isolated lesions or within the context of
congenital or acquired heart disease. They can be recognized as an incidental finding, present with
nonspecific symptoms, or manifest as myocardial ischemia.
20. e. All the statements are correct. The use of TEE in the cardiac catheterization laboratory to
acquire detailed anatomic and hemodynamic data before and during interventions has been well
documented. TEE provides for real-time evaluation of catheter placement across valves and vessels
and immediate assessment of interventional procedures. It is also valuable in monitoring for catheter-
induced complications, such as cardiac tamponade. This modality also limits radiation exposure by
complementing the information obtained by fluoroscopy and angiography.
Chapter 20 7. True 14. b

1. True 8. False 15. c
2. False 9. True 16. b
3. True 10. False 17. d
4. False 11. b 18. d
5. True 12. d 19. c
6. True 13. b 20. c
Chapter 21
1. a. Acquisition of raw 3D data involves volume scanning with online processing. Planar or sector
scanning is used for 2D imaging and may be processed off-line to create 3D images.
2. b. Current technology uses a fully sampled matrix array probe which comprises 2,500 crystals all of
which can be fully activated or sampled.
3. d. Processing of raw 3D data includes the initial steps of segmentation, conversion, and interpolation
followed by rendering to display the 3D dataset.
4. d. Volume rendering includes all the data points and recreates the inner details of a structure. Surface
and wireframe rendering show only the outer parts of structures.
5. c. 3D full volume dataset is the largest. The other modes can be adjusted but are limited in width and
depth.
6. b. 3D zoom has good spatial resolution but often has a low frame rate of <10 Hz. 3D color Doppler
also may have a low frame rate but gating and the small sector size improves the frame rate to over 10
Hz.
7. b. All the others can be adjusted on all 3D datasets.
8. b. All the others can appear in 3D datasets. Stitch artifacts occur in full volume acquisitions between
adjacent segments.
9. c. Like in 2D imaging, heavily calcified structures create dropout in the far field from shadowing
making it difficult to image them completely.

514 Appendices
10. d. The Nyquist limit is set in the 2D image prior to the 3D color Doppler FV acquisition and cannot
be adjusted in the 3D dataset.
11. b. The Zoom mode is the easiest and most reliable to show the entire MV in a single display. Full
Volume can achieve an en face view but is often subject to stitch artifacts making interpretation
difficult.
12. b. The aortic valve is easily incorporated into 3D MV datasets and helps orientate the MV with the AV
often positioned at the top of the display.
13. a. All the angled views are displayed from the left atrium, not the LV, and orientated to emphasize
different regions of the MV.
14. c. Off-line processing using analytical software that aligns planes through the narrowest orifice allows
accurate planimetry of the MV orifice. It is considered the gold standard for assessing MV area in
mitral stenosis. Creation of an MV model can assess other dimensions of the MV.
15. a. Assessment of LV function using analytical software to create the surface-rendered model requires
good endocardial definition to semiautomatically trace the endocardial border. Poor endocardial
definition makes assessment difficult.
16. d. There have been no studies to date that have looked at the reliability of assessing LV global function
using 3D TEE.
17. d. Individual LV segmental volumes are graphed against time to show wall motion abnormalities.
Unlike 2D imaging, wall motion thickening and motion are not directly assessed. Timing of wall
motion abnormalities is an important determinant of ventricular dyssynchrony.
18. c. Like 2D imaging the aortic arch may be obscured by the trachea (blind spot), so obtaining good-
quality arch images may be difficult.
19. a. Shadowing in calcific aortic stenosis makes the aortic annulus difficult to measure in both 2D and
3D images. This cannot be overcome even by exporting 3D datasets to analytical software.
20. b. A current limitation of RT 3D echocardiography is the inability to perform even simple area or
length measurements without exporting the 3D dataset to analytical software. The other answers are
easily obtained using 3D TEE.
1. c 8. b 15. c
2. d 9. c 16. c
3. a 10. b 17. b
4. b 11. d 18. d
5. b 12. a 19. c
6. b 13. c 20. a
1. b 8. b 15. b
2. a 9. a 16. b
3. c 10. c 17. b
4. a 11. a 18. d
5. d 12. c 19. d
6. d 13. d 20. a

Index
Note: Page numbers followed by f and t indicate figure and table respectively.
A regurgitant volume calculation,

Absorption, 5 233–234
Acoustic impedance, 4, 4t vena contracta mapping, 230–232, 231f
Acoustic shadowing, 462, 462f recommended views, 226–227
Acurate valve, 327 regurgitant jet, 230, 230f
Acute hypoxia, in ICU, 372–373, 373f severity of, 229t, 232–233, 497
Acute Mitral Regurgitation, 93, 94f TEE evaluation, 225, 226, 235
ALARA (As Little As Reasonably Achievable) Aortic root, 348
principle, 2 Aortic stenosis (AS), 240, 327
Alfieri stitch, 213, 214f in aortic regurgitation, 251
Alias artifact, 111f pathophysiology, 240–241
Aliasing, 110, 466 planimetry of aortic orifice, 247–248, 248f
Allograft valves, 261t, 274 pre- and postoperative subaortic obstruction,
American Society of Echocardiography, 267 251–153, 252f
Amplitude, 1–2 quantitative Doppler assessment, 241–248
A-mode, 4, 14 continuity equation, 244–247, 244f–247f,
Amyloid restrictive cardiomyopathy, 74f 244t
Aneursym modified Bernoulli equation, 242–244,
left ventricular, 76f 242t, 243f
pseudoaneurysm, 77 TEE Doppler views, 241–242
true severity of, 240t, 497
associated findings, 76 special considerations in assessment of
two-dimensional characteristics, 76, 76f dimensionless index, 251
Annuloplasty, 212 dobutamine stress testing, 251
Aorta low gradient, low stroke volume critical
descending AS, 250–251
long-axis view, 44, 46f pressure recovery, 249, 250f
short-axis view, 42, 43f systemic hypertension and arterial
midesophageal ascending compliance, 249–250
long-axis view, 25, 27f technical considerations in assessment of,
short-axis view, 26, 27f 249
upper esophageal aortic arch Aortic valve (AV)
long-axis view, 42, 44f echocardiographic evaluation, 226, 241
short-axis view, 42, 45f midesophageal aortic valve long-axis view,
Aortic dissection, in ICU, 372 27–29, 29f
Aortic grafts, evaluation of, 355, 356f, 357, midesophageal aortic valve short-axis view,
357f 26, 28f
Aortic regurgitation (AR), 224 midesophageal bicaval view, 28, 30f
color M-mode assessment of, 228f midesophageal four-chamber view, 32–33,
hemodynamics of, 225–226 30f
mechanisms of, 224–225 midesophageal right ventricular inflow-
pseudosevere, 230f outflow view, 26–27, 29f
quantitative assessment prosthesis, normal Doppler
aortic diastolic flow reversal, 232–233, echocardiographic values, 490–493
232f replacement, 310
aortic regurgitant jet decay slope, 233 Aortic valve stenosis
color flow mapping, 227–230, 228f–230f, anatomy, 401–402, 402f
234–235 management, 402
Doppler signal characteristics in, 235 pathophysiology, 402
pressure half-time measurement, 233 TEE evaluation, 402–403
515

516 Index
AR. See Aortic regurgitation (AR) Axial resolution, 10

Artifacts, 456 Azimuth (lateral) resolution, 10
alias, 111f
normal anatomic variants in 2D imaging, 456 B
Coumadin ridge, 458, 458f Backing, 7
crista terminalis, 456 Barlow’s disease, 210–211, 211f
eustachian valve/Chiari network, 456, Beam orientation implications, Doppler analysis,
457f 105
false tendon, 459, 460f Bernoulli equation, 124–125
Lambl excrescences, 459, 459f calculation, 123f
lipomatous hypertrophy of atrial modified, for aortic transvalvular gradients,
septum, 456, 457f 242–244, 242t, 243f
moderator band, 459, 460f Bileaflet valves, 262, 261t, 262f–266f, 268t
pericardial sinuses, 458, 458f TEE examination, 262
pleural effusion, 459, 460f blood flow patterns, 264–265
in spectral and color flow Doppler, 466 leaflet motion, 262, 263f, 264f
acoustic shadowing in color flow, 466, paravalvular regurgitation, 265
466f proper valve seating, 264, 265f
aliasing, 466 transvalvular regurgitation, 265, 266f
beam width flow artifacts, 469, 469f valve gradient and effective orifice area,
color flow reverberation and gain-related 265, 266f, 267, 267t
anomalies, 468 Billowing, 161, 163f, 207, 208f
mirroring, 467–468, 467f Biologic valves, 261t, 271–274
nonparallel beam angle, 466–467, 467f Biventricular assist devices (BIVADs), 315
range ambiguity with pulsed wave Bjork–Shiley valve, 269f
Doppler, 469–470 Blood flow
two-dimensional echocardiographic calculation, 118–121, 121f
acoustic shadowing, 462, 462f common profiles, 120f
electronic noise, 465f, 466 detection, 102, 103f
lateral resolution, 463, 463f velocity, 103–104, 104f
mirroring, 464, 465f Blunt, 119, 120f
reverberations, 463–464, 464f B-mode (brightness mode), 14
septal and lateral wall dropout, 461f Bull’s eye, 305f
side lobe and beam width, 463, 464f
suboptimal image quality, 459, 461f, 462 C
AS. See Aortic stenosis (AS) Caged-ball valves, 261t, 268, 269f
ASD. See Atrial septal defect (ASD) Carbomedics R-series mechanical bileaflet
ASE (American Society of Echocardiography), 58t prosthetic aortic valve, 262, 262f
Asymmetric septal hypertrophy (ASH), 70 Carcinoid syndrome, 294
Atheroma of aorta, 357–358 Cardiac arrest ultrasound examination
aortic plaque measurement, 357f (CAUSE), 372
epiaortic imaging of aorta, 358f Cardiac chamber collapse, 372
five-point TEE grading system for, 358t Cardiac dimensions, 488
Atrial septal defect (ASD), 385, 390f Cardiac dysfunction, assessment and management
anatomy, 385 of, 308, 308t
coronary sinus defects, 392 atrial septal defect, 309
management, 392 dynamic mitral regurgitation, 308
occluder device, 392f, 393f hypovolemia, 308
ostium primum defects, 385, 391f intracardiac shunt, 309
ostium secundum defects, 385, 391f low ejection fraction, 309
pathophysiology, 392 patent foramen ovale, 309
sinus venosus defects, 385, 391f pleural effusions, 309
TEE evaluation, 392–394 previously unknown AV disease, 310
Attenuation, 6f right ventricular dysfunction, 308–309
Attenuation coefficient, 5 unexpected findings, 309

Index 517
Cardiac resynchronization therapy (CRT), 67 region of interest, 480, 480f

Cardiac sarcomas, 427, 428f variance, 481
Cardiac tamponade, in ICU, 372 Color gain, 480, 481f
Cardiac tumors, 424, 425 Color scale, 480
echocardiographic characteristics, 431t Compression controls, 477
embolization, 428 Congenital heart disease (CHD), 379
fibroma, 427, 428f cardiac embryology and defects, abnormal
lipomas, 425, 426f development and, 380–384
myxomas, 425, 426f atrial septation, stages of, 383f
normal cardiac structures mistaken for, 424f heart tube, 380, 381f
papillary fibroelastoma, 425–427, 426f looping of heart tube, 380, 381f
rhabdomyomas, 427 systemic veins, development of, 382f
technical consideration in evaluation of, ventricular septation, 384, 384f
430, 431f catheter-based interventions in adult with,
Cardiomyopathies 419–420
acquired primary, 72–73 classification of, 384
amyloid restrictive, 74f on physiology of defect, 385
dilated, 69f on presence/absence of cyanosis, 385
echocardiography in, 73–75 on severity of disease, 384–385
hypertrophic, 68–70, 70f incidence of, 379
myocarditis, 72 prevalence of, 380
peripartum, 73 specific, 385, 386f–390f
primary genetic, 68–71 aortic valve stenosis, 401–403, 402f
primary mixed, 71–72 atrial septal defect, 385, 390f–391f,
primary restrictive, 72 392–394
recent classification, 68 coarctation of aorta, 400–401, 400f
restrictive, 74t congenital coronary artery anomalies,
secondary, 73 418–419
tako-tsubo, 72f congenitally corrected transposition of
Cardioplegia, 312–313, 313f great arteries, 411–413, 411f, 413f
Cardiopulmonary resuscitation (CPR), 369 Ebstein anomaly, 413–415, 413f, 414f
Carpentier–Edwards model 6900 bovine patent ductus arteriosus, 398–400,
pericardial bioprosthetic mitral valve, 272f 398f, 399f
Carpentier–Edwards model 6625 porcine pulmonic stenosis, 403–404, 403f
bioprosthetic mitral valve, 271f single ventricle or univentricular heart,
Carpentier’s classification of MV, on leaflet 415–418, 416f–418f
motion, 161, 162f, 205–208, 206f–209f tetralogy of Fallot, 404–408, 405f–408f
Central venous pressure (CVP), 302 transposition of great vessels, 408–411,
CHD. See Congenital heart disease (CHD) 409f, 410f
Chiari network, 290, 456, 457f ventricular septal defect, 394–398,
Chordae, artificial, implantation of, 212–213 394f–397f
Chordae tendineae, 160 survival rate in, 379–380
Chordal transfer, 213 TEE in, 379
Circumflex coronary artery, visualization of, limitations of, 420
209, 210f noncardiac surgery in adult with CHD,
Cleft mitral valve, 214 420
Closure backflow, 264 Congenitally corrected transposition of the great
Coarctation of aorta (CoA) arteries (CCTGA)
anatomy, 400, 400f anatomy, 411–412, 411f
management, 401 management, 412
pathophysiology, 400–401 pathophysiology, 412
TEE evaluation, 401 TEE evaluation, 412–413, 413f
Color controls Constrictive pericarditis (CP), 152
color gain, 480, 481f Continuity equation, for aortic valve area
color scale, 480 calculation, 244–247, 244f–247f, 244t

518 Index
CoreValve, 327, 328f follow-up and device dysfunction,

Coronary arteries 320–321
echocardiographic assessment of, 84, 85f inflow cannula, 317–319, 317f, 318f
congenital anomalies of intracardiac shunts, 315
anatomy, 418 intracardiac thrombus, 315, 316f
management, 419 outflow cannula, 319–320, 319f, 320f
Pathophysiology, 418 post-VAD implantation checks and
TEE evaluation, 419 complications, 320t
Doppler evaluation, 85 right ventricular function, 316
detection, 86–87 valvular abnormalities, 315–316
Coronary artery bypass graft (CABG), 302 weaning from, 321
Coronary revascularization, TEE for, 302 Coumadin ridge, 458, 458f
advantages of use of, 302 Crawford classification, of thoracoabdominal
cardiac dysfunction assessment and aneurysms, 356f
management, 308, 308t Crista terminalis, 456
atrial septal defect, 309 Critical care echocardiography, 364
dynamic mitral regurgitation, 308 and advance cardiac life support, 369
hypovolemia, 308 cardiac arrest, causes of, 369t
intracardiac shunt, 309 focused goal-directed TEE, 369
low ejection fraction, 309 bilateral pleural space views, 370
patent foramen ovale, 309 ME bicaval view, 370
pleural effusions, 309 ME four- and five-chamber views, 370
previously unknown AV disease, 310 ME RV inflow–outflow view, 370
right ventricular dysfunction, miniaturized TEE probe, 370, 371f
308–309 TG LAX view, 370
unexpected findings, 309 TG midpap SAX view, 370
combined CABG and MVR, 310 focused goal-directed TTE, 364, 365f
3D echo, use of, 311 apical four-chamber view, 366, 366f
endoscopic vein harvesting, 314–315 apical two-chamber view, 366, 367f
extra corporeal membrane oxygenation, parasternal long axis, 364, 365f
321–322 parasternal short axis, 365, 366f
new RWMAs after bypass, 305–306 pleural ultrasound, 368, 368f
management of, strategy for, 307, 307t subcostal four-chamber, 366, 367f
prebypass examination, 303 ICU complications, findings in, 370
ischemia monitoring, 304–305 acute hypoxia, 372–373, 373f
new advances in cardiac function aortic dissection, 372
assessment, 304, 305f, 306f cardiac tamponade, 372
ventricular function assessment, 303–304, hypotension, 370
304t hypovolemia, 371
role in patients undergoing CABG, 303t left ventricular failure, 371
safety and complications, 302 pulmonary embolism, 373
shortcomings, 305 right ventricular failure, 371–372, 372f
specific surgical situations protocols for echocardiography, in critically
off-pump CABG, 311–312 ill patients, 364
redo sternotomy, 311 Critical care ultrasound (CCUS). See Critical
vascular cannulations, role in, 312 care echocardiography
aortic cannula, 312 Crux of heart, 160
cardioplegia, 312–313, 313f, 314f
femoral vascular cannulation, 314 D
IABP, 313 Density, scan line, 17
port access surgery, 314, 315f Depth controls, 475–476, 476f
ventricular assist devices, 315–321 Dextro-transposition of the great vessels (D-TGA),
aortic atheroma, 317 408–411, 409f, 410f
cannulas positioning, 317–320 Dial-a-jet phenomenon, 227

Index 519
Diastolic dysfunction, 138 limitations of, 110

clinical definition, 138 low-amplitude, low-frequency signal, 107f
clinical relevance of, 152–153 Nyquist limit, 110
diastolic physiology and, 138, 139f presentation, 107–109
Doppler echocardiographic measures of, pulsed wave, baseline setting effect on, 112f
153f, 154t quantitative Doppler and hemodynamics,
Diastolic function, assessment of 118–133
left ventricle, 139 quantitative Doppler characteristics, 77
color M-mode transmitral propagation system processing, 110
velocity for, 147–148, 148f techniques, 109–113
mitral annular Doppler tissue imaging TEE Doppler examinations, 106
for, 146–147, 146f two-dimensional versus Doppler flow
physiologic variables influence on measurement, 106f
TMDF and PVDF profiles, 145 velocity measurements, maximizing,
pulmonary venous flow, 144–145, 144f 110–111
strain and strain rate, 149 Doppler indicators, 93
transmitral blood flow, 139–144, 141f, Doppler velocity index (DVI), 267, 267t
142t, 143f Dynamic motion and image quality, 17
two-dimensional and M-mode Dynamic range controls, 477, 478f
echocardiography, 139 Dysrhythmias, 145
right ventricle, 149–152, 151f
Diffuse myxomatous degeneration. See Barlow’s E
disease Ebstein’s anomaly, 294
Digital scan conversion, 13 anatomy, 413, 413f
Dimensionless index, 251 management, 414
Dispersion, 5 pathophysiology, 414
Dobutamine stress testing, 251 TEE evaluation, 414–415, 414f
Doppler of tricuspid valve, 413f, 414f
analysis, 103–106 Eccentric mitral regurgitation (MR) jet,
beam orientation implications, 105, 105f 163, 164f
blood supply, 82 Echo dropout, 5
clinical caveats, 110 Echocardiography, three-dimensional, 93–94
color flow mapping, 114 Edge-to-edge repair, 213, 214f
color tissue, 64 Edwards SAPIEN valve, 328f
continuous wave, 113 Effective orifice area (EOA), 267t
cosine relationship, 104f Effective regurgitant orifice area (EROA), 169
data presentation Electric connector, 7f
audible broadcast, 107–108 Electrical processing, 13
spectral display, 108–109 Electrodes, 7
echocardiography heart rhythm, 133 Electronic noise, 465f, 466
evaluation of coronary artery blood flow, 85–86 Elephant trunk, for staged aortic repairs,
frequency shift, 102–103 355, 356f
blood velocity, 104 Elevational resolution, 12
demodulation process, 106 Emboli, 431
Doppler effect, 102 cardiac sources, 431
Doppler equation, 103 possible sources
fast Fourier technique, 106 paradoxical embolus through PFO, 433,
indicators, 93 433f
isolation, 106 spontaneous echo contrast, 432, 433f
quadrature demodulation, 106 probable sources
signal frequency and blood flow, endocarditis, 432
102–103 left atrial appendage thrombus, 431–432,
high-frequency pulsed, 113 432f
left ventricular pseudoaneurysm, 77, 77f thrombi in left ventricle, 430f, 432

520 Index
Endocardial fractional shortening, 52 Left atrial appendage (LAA), thrombus in,

Endoscopic vein harvesting (EVH), 314–315 431–432, 432f
Epoxy filler, 7f Left ventricular assist device (LVAD), 309, 315, 316
eSie Valves (3D datasets software program), Left ventricular ejection fraction (LVEF), 309, 311
443, 444 Left ventricular failure, in ICU, 371
EuroSCORE score, 153 Left ventricular systolic function
Eustachian valve, 456, 457f color tissue Doppler, 64
Extra corporeal membrane oxygenation (ECMO), defined, 51–53
echo in Doppler strain and strain rate, 64–65, 65t
cannulation placement, 321–322, 321f echocardiographic modalities for
complications, 322 factor, 63t
weaning from, 322 three-dimensional echocardiography, 59–61
tissue Doppler imaging, 62–63, 62f
F left ventricular synchrony, 67–68, 68f
Faceplate, 7 quantitative evaluation of, 53–58
False tendon, 459, 460f relative wall thickness, 53
Far field (Fraunhofer), 9 speckle tracking echocardiography, 66–67, 66f
Fast Fourier technique, 106 ventricular wall thickness, 53
Femoral vascular cannulation, 314 Lipomas, 425, 426f
Fibroma, 427, 428f Lipomatous hypertrophy of atrial septum, 456, 457f
Flail, 161, 163f, 208, 209f LVAD. See Left ventricular assist device (LVAD)
Focus controls, 476–477
Focused echocardiographic evaluation in M
resuscitation (FEER), 372 McConnell sign, 373
Frequency controls, 477 Mechanical heart valves, 261–270, 261t
Medtronic ATS, 3f, 274
G Medtronic Hall valve, 269f
Gliding/sliding sign, 373 Metastatic tumors, 428, 429f
Mirroring, 464, 465f, 467–468, 467f
H Mitral annulus, 159
Harmonics controls, 479–480 Mitral apparatus, preoperative structural
Heart cycle, phases of, 150f assessment of, 196–204, 196f–201f
Hemodyamic calculations, 489 anterior leaflet length, 202, 202f
Hypertrophic obstructive cardiomyopathy calcification, 201, 201f
(HOCM), 451, 452f coaptation length, 204, 205f
Hypotension, in ICU, 370 C-sept distance, 202, 203f
Hypovolemia, 308, 371 left ventricular end-diastolic internal
diameter, 204
I left ventricular end-systolic internal diameter,
International Registry of Acute Aortic 203–204, 203f
Dissection (IRAD) database, 349 ME four-chamber view, 198, 198f
Intra-aortic balloon pumps (IABPs), 302, 312, 313 ME LAX view, 198, 199f
Intracardiac shunts, 309 midesophageal (ME) four-chamber view, 197,
Intracardiac thrombus, 429, 429f, 430f 197f
Intramural hematoma (IMH), 352, 353f mitral annulus, size of, 202, 202f
Ischemia, monitoring of, 304–305, 306f posterior leaflet length, 202, 202f
tenting area, 204, 205f
J tenting height, 204, 204f
JenaValve, 327 TG basal SAX view, 199, 200f
TG two-chamber view, 199, 199f
L three-dimensional view, 199, 200f, 201f
Lambl excrescences, 421, 421f, 459, 459f Mitral clip intervention, 337–338
Lateral gain compensation controls, 474–475, 476f delivery system, 338, 338f
Leakage backflow, 264–265 exclusion criteria, 338

Index 521
inclusion criteria, 338 TEE evaluation of, 180–188

procedure three-dimensional echocardiographic
clip implantation, 340–341, 340f, 341f evaluation of, 189–190, 189f, 190t
device orientation and catheter positioning, Mitral valve (MV)
339–340, 340f anatomy, 159–160, 159f, 179
postintervention assessment, 341, 342f, 343, estimated regurgitant orifice area,
343f 169f
transseptal puncture, 338–339, 339f nomenclatures of, 160–161, 160f
Mitral regurgitation (MR), 159, 194, 308 prolapse, 210
Carpentier’s classification of, on leaflet prosthesis, normal Doppler
motion, 161, 162f echocardiographic values, 494–496
chronic severe, 194, 195f quantitative evaluation of, 168–170, 169f
Doppler and quantitative values in, 166t three-dimensional examination, 171–173,
eccentric jets, 163, 164f 172f, 173f, 174f
etiology and mechanism of, 161, 161t Mitral valve repair, 194
evaluation pitfalls, 170 echocardiographic evaluation, 195
functional, 170–171, 194 goals of, 212
ischemic, 161 postrepair TEE examination, 215
leaflet motion, excessive, 163f aortic dissection, 219
PW Doppler of pulmonary artery vein flow, aortic valve insufficiency, 219
165, 165f circumflex coronary artery perfusion, 215
severity of, 498 complete deairing of left ventricle, 215
structural, 194 global/regional ventricular dysfunction,
TEE evaluation of, 163–167 218
mechanism of MR and location of lesion, mitral stenosis, 218
167–168, 167f potential complications, 218–219
severity of MR, 163–164, 164f, 165f, 166t residual mitral regurgitation, 216–217, 217f
two-dimensional examination, 163 SAM and dynamic LV outflow tract
vena contracta, measurement of, 163, 164f obstruction, 218–219, 219f
wall-hugging jets, 164 ventricular rupture, 219
Mitral stenosis (MS), 179 prerepair evaluation, 195–196
continuity equation, for valve area calculation, circumflex coronary artery, visualization of,
187 209, 210f
2D echocardiographic examination, 181–183, MV apparatus, 196–204 (see also Mitral
181f apparatus, preoperative structural
echocardiographic scoring system, assessment of )
181–182, 182t MV leaflets, function of, 205–208
doming/hockey stick deformity, 181, 181f for planning surgical procedure,
etiology of, 179–180, 180f 210–211, 211t, 212f
grading severity of, 184t secondary and coexisting abnormalities,
LA spontaneous echo contrast and, 182, 182f identification of, 209–210
left atrial myxoma and, 180f severity of MV regurgitation, 208
physiologic assessments surgical techniques for, 212
deceleration time, 186, 186f annuloplasty, 212
planimetry valve area, 184–185, 184f artificial chordae implantation, 212–213
pressure gradient, determination of, 183, 183f chordal shortening/papillary muscle
pressure half-time, 185–186, 185f, 185t shortening, 213
valve area calculations, 184 chordal transfer, 213
PISA method, and MV area calculation, edge-to-edge repair, 213, 214f
187–188, 187f leaflet resection, 213
practical approach to evaluation of, type III dysfunction, 214–215
188–189 type I MV dysfunction, 214
rheumatic, 180 Moderator band, 286, 286f, 459, 460f
severity of, 498 MR. See Mitral regurgitation (MR)

522 Index
MS. See Mitral stenosis (MS) Pleural effusions, 309, 459, 460f
Multiplane reconstruction (MPR), of mitral Polytetrafluoroethylene (PTFE) chordae,
plane, 172–173, 173f 212
MV leaflets, resection of, 213 Port access surgery, 314
Myocardial ischemia Pressure half-time method
characteristics, 88t and mitral stenosis, 185, 185f, 185t
clinical syndrome, 88 MV area calculation from, 186
complications, 95–98, 95f–97f Pressure recovery (PR), 249, 250f
diagnosis, clinical applications, 82 Prolapse, 161, 163f, 207, 208f
echocardiographic assessment, 88–91 Prosthetic aortic stenosis, Doppler parameters
echocardiographic detection, 91–93 for diagnosis of, 268t
physiological basis for detection of, 87 Prosthetic endocarditis, 280, 280f
Myocardial stunning, 305–306 Prosthetic valves, 258
Myxomas, 425, 426f allograft valves, 274
bileaflet valves, 261t, 262–267, 262f–266f,
N 267t, 268t
Near and far fields, 8–9 biologic valves, 271–274
Near field (Fresnel), 9 caged-ball valves, 268, 269f
Nonparallel beam angle, 466–467, 467f dysfunction, echocardiographic diagnosis,
275–280
O endocarditis, 280, 280f
Off-pump coronary artery bypass (OPCAB) hemolysis, 280
conversion to CPB during, 312 LVOT obstruction, 280
graft patency during, 312 prosthesis–patient mismatch, 279
IABP insertion, 312 prosthetic valve regurgitation, 275–278
MR during, 312 prosthetic valve stenosis, 278–279,
preload assessment during, 312 279t
RWMA during, 311 thrombosis and pannus, 279–280
TEE intraoperative evaluation, 311 echocardiographic features, 260 (see also
specific types)
P mechanical heart valves, 261–270
Pannus formation on a Bjork–Shiley valve, 270, stented pericardial valve, 271–272,
270f 272f–273f
Papillary fibroelastoma, 425–427, 426f stented porcine heterografts, 271, 271f
Papillary muscles, 159–160 stentless valves, 272, 274, 274f
anterolateral, 160 TEE evaluation of, 258
posteromedial, 160 advantages of, 258
shortening, 213 bileaflet mechanical prosthesis in aortic
Paravalvular regurgitation, 265 position and, 260f, 261f
Parsonnet score, 153 indications for, 259t
Patent ductus arteriosus, 399f technical considerations in, 259–260, 260f,
anatomy, 398, 398f 261f
management, 399 tilting disc valves, 268–270, 269f, 270f
pathophysiology, 399 types, 261t
TEE evaluation, 399–400 Proximal isovelocity surface area (PISA) method,
Patent foramen ovale (PFO), 309, 315, 431 169, 169f, 187–188, 187f
Penetrating atherosclerotic ulcer (PAU), 353, PS. See Pulmonic stenosis (PS)
353f Pulmonary artery band, 415, 416f
Pericardial sinuses, 458, 458f Pulmonary artery pressure, 302
Pericardial tamponade (PT), 152 Pulmonary embolism, in ICU, 373
Persistence controls, 478–479 Pulmonary regurgitation, 500
Planimetry Pulmonary stenosis, 500
of aortic orifice, 247–248, 248f Pulmonary venous Doppler flow velocity
for MV area calculation, 184–185, 184f (PVDF) profile, 144–145, 144f

Index 523
Pulmonic regurgitation (PR), 295 and 2D imaging, difference between, 437

Pulmonic stenosis (PS), 296 image acquisition, 439
anatomy, 403, 403f imaging modes, 440–441, 440f, 440t
Doppler echocardiography, 296 image optimization and artifacts, 440f
management, 404 LV function, 443f
pathophysiology, 403–404 postprocessing, 442
Ross procedure, 296 cropping and orientation, 442–443, 442f
TEE evaluation, 404 image artifacts, 442
two-dimensional echocardiography, image optimization, 442
296 measurements, 443
Pulmonic valve (PV) protocol for, 446t
anatomy, 295 quantification analysis models, 443–444
pulmonic regurgitation, 295 RV function, 444f
pulmonic stenosis, 296 structures visualized with, 445t
TEE views, 295, 295f, 296f technology, 438f
Pulsed wave Doppler data acquisition, 438
baseline setting effect on, 112f data processing, 438–439
clinical caveats, 110 data storage, 438
echocardiography heart rhythm, 133 3D display, 439
high-frequency, 113 TEE probes, 437
interpretation, 109 valve analysis software, 445f
limitations, 110 Regional wall motion abnormalities (RWMAs),
Nyquist limit, 110 302, 304, 305
system processing, 110 new, after cardiopulmonary bypass, 305–307,
velocity measurements, maximizing, 307t
110–111 OPCABG and, 311
Pulseless electrical activity (PEA), 369 Region of interest, 480, 480f
Pulse repetition frequency, 16, 110 Regurgitant fraction (RF), 168
Regurgitant volume (RV), 122–123, 168
Q Reject controls, 478
QLAB (3D datasets software program), Reverberation artifacts, 463–464, 464f
443–444 Rhabdomyomas, 427
“Q-tip” sign, 458 Right atrium (RA)
Quadrature demodulation anatomy, 290, 291f
Doppler frequency shift, 106 TEE views, 290
phase demodulation, 467 Right ventricular assist device (RVAD), 315
Right ventricular (RV), 286
R anatomy, 286, 286f
Real-time three-dimensional transesophageal dilation, 288, 288f
echocardiography (RT-3D TEE), dysfunction, 308–309
296–297, 297f, 304, 311, 336–337 failure in ICU, 371–372, 372f
clinical applications, 445, 445t hepatic venous flow patterns, 289, 289f
aorta, 449, 450f hypertrophy, 288
aortic valve, 449 ischemia, 94–95
atrial septal defect closure, 450f regional function assessment, 290
hypertrophic obstructive cardiomyopathy, interventricular septum, 290
451, 452f RV pressure overload, 290
interatrial septum, 450f, 451 RV volume overload, 290
intracardiac masses, 451, 451f systolic function, 288
left and right ventricles, 448–449 TEE views, 287, 287f
mitral valve, 446–448, 447f, 448f tricuspid annular plane systolic excursion,
patent foramen ovale, 450f 288–289
transcatheter aortic valve implantation, RWMAs. See Regional wall motion
449f abnormalities (RWMAs)

524 Index
S Tetralogy of Fallot (TOF)

Sand blasting effect, 312, 313f anatomy, 404–405, 405f
SAPIEN valve, 327, 328f management, 406
Sector size controls, 479, 479f pathophysiology, 405
Segmental scores, 307t TEE evaluation, 406, 406f–407f, 408
Segmental wall motion, 89t Thoracic aorta, 347
Side lobe artifacts, 463, 464f acute aortic syndromes, 349
Single ventricle/univentricular heart aortic dissection, 349–350, 350f–352f,
anatomy, 415 350t
Glenn anastomosis and Fontan procedure, intramural hematoma, 352, 353f
417 penetrating atherosclerotic ulcer, 353,
management, 415 353f
modified Blalock–Taussig shunt, 415 anatomy, 347–348, 347f
Norwood procedure, 415, 416f aneurysms, 354–355, 354f, 354t, 355f
PA band, 415, 416f aortic atheroma, 357–358, 357f, 358f, 358t
pathophysiology, 415 aortic grafts, evaluation of, 355–357, 356f,
TEE evaluation, 417–418, 418f 357f
Sinotubular junction (STJ), 348, 354 esophagus and aorta switches, relationship
Sound and tissue interactions between, 348, 348f
attenuation, 5–6 TEE imaging, 348–349, 348f
reflection, 4 Thoracic aortic aneurysms, 354–355, 354t,
refraction, 5 355f, 356f
Sound waves Thoracic aortic dissections, 349–350
amplitude, 1 entry point, identification of, 350, 352f
frequency, 2 flap, 350f
physical properties, 1–4 intraoperative TEE in, role of, 350t
ultrasound, 3 irregularly shaped dissection flap, 351f
vibrations, 1, 2f pulmonary artery catheter mimicking
wavelength, 2 flap, 352f
Spontaneous echo contrast (SEC), 432, 433f Stanford and DeBakey classification systems
Starr–Edwards caged-ball mechanical valve, for, 351f
269f Thoracic endovascular aortic repair (TEVAR), 355
Stented pericardial valve, 261t, 271–272, Three-dimensional regional wall motion map,
272f–273f 306f
Stented porcine heterografts, 261t, 271, 271f Three-dimensional transesophageal
Stentless valves, 261t, 272, 274, 274f echocardiography (3D TEE). See Real-
St. Jude Medical Trifecta porcine pericardial time three-dimensional transesophageal
bioprosthetic aortic valve, 272f echocardiography (RT-3D TEE)
Storage systems, 481 Thrombus
Strain rate imaging (SRI), 149 intracardiac, 429, 429f, 430f
Strain (S), 149 in left atrium, 431–432, 432f
Strut fracture, 270 in left ventricle, 432
Systolic anterior motion (SAM), of anterior MV Tilting disc valves, 261t, 268–270, 269f, 270f
leaflet, 211 Time constant of relaxation, 138
Systolic blunting, 145 Time gain compensation controls, 474, 475f
Systolic dyssynchrony index (SDI), 311 Tissue Doppler imaging (TDI), 94, 304
Systolic predominance, 145 TomTec (3D datasets software program), 443,
444, 445f
T Transesophageal echocardiography (TEE)
Tachycardia, 145 Doppler examinations, 106
TAVI. See Transcatheter aortic valve examination goals, 23–24
implantation (TAVI) probe
TEE. See Transesophageal echocardiography advancement, 23f
(TEE) insertion, 20

Index 525
manipulation, 20, 21f diseases of

multiplane imaging angle, 21–23 tricuspid regurgitation, 292, 293f, 294f
schematic representation, 23f tricuspid stenosis, 292
TR. See Tricuspid regurgitation (TR) etiology of diseases of
Transcatheter aortic valve implantation (TAVI), annular dilation, 292
327, 449f carcinoid syndrome, 294
aortic stenosis and, 327 Ebstein’s anomaly, 294
3D echocardiography, role of, 336–337 endocarditis, 294
procedural performance rheumatic disease, 294
transaortic approach, 329 RT-3D TEE for, 296–297, 297f
transapical approach, 329 TEE views, 291
transfemoral approach, 329 TS. See Tricuspid stenosis (TS)
TEE guidance for, 329–330, 337 Tumors
annulus measurement, 330–331, 330f cardiac, 425–427
balloon valvuloplasty, 331–332, 332f malignant, 427
guidewire placement, 331 metastatic, 428, 429f
limitations of, 337 Two-dimensional controls, 473
postimplantation aortic valve assessment, compression, 477
334–336, 334f–336f depth, 475–476, 476f
valve implantation, 332–333, 333f dynamic range, 477, 478f
valves and delivery systems, 327, 328f focus, 476–477
Transesophageal echocardiography (TEE) frequency, 477
anatomy, 485–487 gain, 473–474, 474f
Transmit power controls, 473 harmonics, 479–480
Transmitral blood flow (TMDF) velocity profile, lateral gain compensation, 474–475, 476f
139–144, 141f, 142t, 143f persistence, 478–479
Transmitral pressure gradient (TMPG), preprocessing versus postprocessing controls,
140 473
Transposition of great arteries reject, 478
anatomy, 408, 409f sector size, 479, 479f
arterial switch procedure, 410f time gain compensation, 474, 475f
atrial redirection procedure, 409f transmit power, 473
management, 408, 409f, 410, 410f Two-dimensional image
pathophysiology, 408 dynamic motion, 16–17
TEE evaluation, 410–411 image quality, 16–17
Transtricuspid Doppler flow (TTDF) velocities, sector imaging, 16
149 Two-dimensional scan systems, 15–16
Transvalvular regurgitation, pathologic, 265,
266f U
Tricuspid prosthesis, normal Doppler Ultrasound
echocardiographic values of, 496 attenuation, 6f
Tricuspid regurgitation (TR), 292 beam
Doppler echocardiography electronic beam focusing, phased
color flow Doppler, 292, 293f array, 10
pulsed wave Doppler, 292, 294f focusing, 10
pulmonary artery systolic pressure near and far fields, 8–9
estimation, 292 resolution, 10–12
severity of, 499 three-dimensional, 8–9
two-dimensional echocardiography, 292 formation of ultrasound waves, 7
Tricuspid stenosis (TS), 292, 499
Doppler echocardiography, 292 V
two-dimensional echocardiography, 292 Valve area, 123
Tricuspid valve (TV) Valve prostheses, 490–496
anatomy, 291, 291f Valvular disease, severity of, 497–500

526 Index
Valvular fibroelastomas, 427 restrictive, 74t

Variance color flow map, 481 secondary, 73
Vascular cannulations, TEE role in, 312–314 takotsubo, 72
Vascular resistance, 129–131 Ventricular septal defect (VSD)
Velocity anatomy, 394–395, 394f
blood flow, 104f, 105f inlet, 395, 396f
pulsed wave measurements, 110–111, 113 management, 396–397
Vena contracta, measurement of, 163, 164f muscular, 395, 395f
Veno-venous (V-V) ECMO, 321–322 occluder device, 397f
Ventricular assist devices (VADs), 315–321 pathophysiology, 396
Ventricular pathology perimembranous, 395, 395f
cardiomyopathies supracristal, 395, 396f
acquired primary, 72–73 TEE evaluation, 397–398
amyloid restrictive, 74f Ventricular septal dyskinesia, 307
cardiomyopathies, 68–69, 69f Ventricular septal hypokinesis, 307
dilated, 69f, 71–72 Vibrations, 1, 2f
echocardiography in, 73–74 Videotape storage, 481
hypertrophic, 68–70, 70f VSD. See Ventricular septal defect (VSD)
myocarditis, 72–73
peripartum, 73 W
primary genetic, 71–72 Wall function abnormalities, 90
primary mixed, 71–72 Wavelength, 2, 3t
primary restrictive, 72 Wireframe rendering, 439
recent classification, 68 Wraparound, 110

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(c) 2015 Wolters Kluwer. All Rights Reserved.

(c) 2015 Wolters Kluwer. All Rights Reserved.

Scott T. Reeves, MD, MBA, FACC, FASE

(c) 2015 Wolters Kluwer. All Rights Reserved.

Copyright © 2014 by LIPPINCOTT WILLIAMS & WILKINS, a Wolters Kluwer business

Two Commerce Square

Library of Congress Cataloging-in-Publication Data

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(c) 2015 Wolters Kluwer. All Rights Reserved.

Albert T. Cheung, MD Maurice Hogan, MB, BCh, MSc, MBA

Ira S. Cohen, MD Farid Jadbabaie, MD

(c) 2015 Wolters Kluwer. All Rights Reserved.

Wanda C. Miller-Hance, MD Manfred D. Seeberger, MD

Chirojit Mukherjee, MD Roman M. Sniecinski, MD, FASE

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SECTION II: ESSENTIALS OF DOPPLER ECHO

SECTION III: VALVULAR DISEASE

SECTION IV: CLINICAL CHALLENGES

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18. Critical Care Echocardiography .................................................................................................................................... 364

SECTION V: MAN AND MACHINE

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1 Principles and Technology of Two-dimensional

PHYSICAL PROPERTIES OF SOUND WAVES

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Frequency and Wavelength

λ = (1500 m/s)/ f (4)

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TABLE 1.1 Corresponding Frequencies and Wavelengths in Soft Tissue

Frequency (MHz) Wavelength (mm)

WHAT IS SO SPECIAL ABOUT ULTRASOUND?

INTERACTIONS OF SOUND AND TISSUE

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TABLE 1.2 Acoustic Properties of Various Tissues

The Tissue Interface: Acoustic Impedance

Specular and Scattering Reflectors

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TRANSDUCER DESIGN AND BEAM FORMATION

Formation of Ultrasound Waves: The Piezoelectric Crystal

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The Three-dimensional Ultrasound Beam

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sin θ = 1.22λ /D (8)

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Electronic Beam Focusing: The Phased Array

Lateral (Azimuth) Resolution

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Extraneous Sound Beams

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Side Lobe Artifacts

SIGNAL RECEPTION AND PROCESSING

Cycling of Transducer Transmit and Receive Modes

Compression and Display

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Preprocessing and Postprocessing

The Golden Rule: Time is Distance

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TWODIMENSIONAL SCAN SYSTEMS

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