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Oxford Specialist
Handbooks
in Cardiology
Echocardiography
Second edition
Edited by
Paul Leeson
Consultant Cardiologist and BHF Senior Fellow
John Radcliffe Hospital
and University of Oxford, UK
Daniel Augustine
Specialist Trainee in Cardiology &
Cardiovascular Research Fellow
John Radcliffe Hospital
and University of Oxford, UK
Andrew R.J. Mitchell
Consultant Cardiologist
General Hospital, St Helier,
Jersey, Channel Islands, UK
Harald Becher
Professor of Medicine
Mazankowski Alberta Heart Institute,
University of Alberta, Edmonton, Canada
1
1
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v
Preface to the second
edition
Over the last five years echocardiography as a specialty has evolved
dramatically. When the first edition of this book was published, people
were still exploring the potential for clinical uses of 3D echocardiography,
new echocardiography-guided transcatheter interventions were being
evaluated, and routine use of echocardiography in the intensive care and
emergency departments was being considered. All of these developments
are now sufficiently established in day-to-day clinical practice to warrant
inclusion in this essential handbook-guide on how to perform echo-
cardiography.
Importantly, all the basics still form the bulk of the new handbook, so that
even the complete novice can pick up the text and start to learn how to
acquire good quality images and interpret what they see. These sections
have now been enhanced with colour images and video loops as well as
having been reviewed to ensure the information is consistent with numer-
ous new guidelines released by international echocardiography societies.
We are delighted with the success and widespread appeal of this hand-
book. When we wrote the first edition, however, we did not expect to
have to update so much, so soon. This is a reflection of how rapidly
echocardiography as a specialty develops and has allowed us to produce
an even better echocardiography handbook. We hope you enjoy it.
PL
DA
ARJM
HB
2012
vi
Preface to the first edition
Why another book on echocardiography? There are numerous textbooks,
some with excellent descriptions, accompanied by images of normal and
abnormal findings.
This handbook originates from the demands of our trainees and sonogra-
phers for a new approach based on practical guidelines that describe how
to apply current imaging technology to address the common, key issues
in adult echocardiography. The book follows the natural workflow of
echocardiography, detailing what to record, and how to analyse and report
studies. These demands have also been heard by the professional organiza-
tions like the British and American Society of Echocardiography and the
European Association of Echocardiography who have started to provide
guidelines for specific questions. Therefore this handbook combines the
standard acquisition protocols, analysis and reporting for adult transtho-
racic and transoesophageal echocardiography, starting from a minimal
recording dataset, with all the current guidelines relevant to clinical
practice.
The book was designed as a comprehensive compendium of focused
approaches for specific clinical questions. We hope it will be used both
as a means to learn how to perform echocardiography and as a trusted,
easily accessible reference for those who are already proficient.
PL
AM
HB
vii
Contents
Acknowledgements
viii
Contributors
ix
Symbols and abbreviations
xi
References
xiii
1 Ultrasound
1
2 Transthoracic examination
55
3 Transthoracic anatomy and pathology: valves
105
4 Transthoracic anatomy and pathology:
chambers and vessels
191
5 Transoesophageal examination
343
6 Transoesophageal anatomy and pathology:
valves
417
7 Transoesophageal anatomy and pathology:
chambers and vessels
475
8 Intracardiac echocardiography
547
9 Contrast echocardiography
561
10 Stress echocardiography
587
11 Acute echocardiography
627
12 Reporting and normal ranges
649
Index
679
viii
Acknowledgements
We would like to express our sincere thanks to the many individuals who
read the text during its preparation and gave advice on its development.
ix
Contributors
We would like to express our sincere thanks to the contributors to the
original edition and the following people for their expert contributions
and advice that were used as the basis for the following sections in the
new edition (in alphabetical order):
Harald Becher
Jonathan Goldman
Professor of Cardiology,
Consultant Cardiologist, VA
Mazankowski Alberta Heart
Hospital, San Francisco, CA, USA
Institute,
Chapter 4: Left atrial measures
University of Alberta, Edmonton,
Lucy Hudsmith
Canada
Chapters 4 and 7: 3D left
Consultant Cardiologist in Adult
ventricular and right ventricular
Congenital Heart Disease,
function
The Queen Elizabeth Hospital,
Chapter 9: Contrast
Birmingham, UK
echocardiography
Chapters 3, 4, 6, and 7: Tricuspid
valve, Pulmonary valve, and
Will Bradlow
Congenital heart disease
Specialist Trainee in Cardiology,
Xu Yu Jin
John Radcliffe Hospital, Oxford,
UK
Consultant in Surgical Echo-Cardi-
Chapters 4 and 7: 2D right
ology, John Radcliffe Hospital,
ventricular function
Oxford, UK
Chapter 5: Intraoperative
John Chambers
transoesophageal echocardiography
Consultant Cardiologist,
Cardiothoracic Centre, Guy’s and
Theodoros Karamitsos
St. Thomas’ Hospital, London, UK
Honorary Consultant Cardiologist
Chapter 3: Aortic stenosis
and University
Research Lecturer,
Jonathan Choy
John Radcliffe Hospital and
Cardiologist & University of
University of Oxford, UK
Alberta Echo Lab Director,
Chapter 10: Stress
University of Alberta, Edmonton,
echocardiography
Canada
Justin Mandeville
Chapter 4: 3D left ventricular
function
Senior Critical Care Echo Fellow,
John Radcliffe Hospital,
Claire Colebourn
Oxford, UK
Consultant Intensivist, Programme
Chapter 11: Acute echocardiography
Lead Oxford Critical Care Echo
Fellowship, John Radcliffe Hospital,
Oxford, UK
Chapter 11: Acute echocardiography
x
CONTRIBUTORS
Thomas Marwick
Susanna Price
Director, Center for
Consultant Cardiologist and
Cardiovascular Imaging, Heart and
Intensivist, Royal Brompton &
Vascular Institute, Cleveland
Harefield NHS Foundation Trust,
Clinic, Cleveland, OH, USA
London, UK
Chapter 4: Left ventricular function
Andrew R.J. Mitchell
Oliver Rider
Consultant Cardiologist,
Clinical Lecturer Cardiovascular
General Hospital, St. Helier,
Medicine, John Radcliffe Hospital,
Jersey, Channel Islands, UK
Oxford, UK
Chapter 8: Intracardiac
Chapter 1: Ultrasound
echocardiography
Michael Stewart
Saul Myerson
Consultant Cardiologist,
Consultant Cardiologist, John
Cardiothoracic Unit, The James
Radcliffe Hospital, Honorary
Cook University Hospital,
Senior Clinical Lecturer, University
Middlesborough, UK
of Oxford, UK
Chapters 4 and 7: Aorta
Chapters 3 and 6: Aortic
regurgitation
Jon Timperley
Consultant Cardiologist,
Jim Newton
Northampton General Hospital,
Consultant Cardiologist, John
Northampton, UK
Radcliffe Hospital, Oxford, UK
Chapters 3 and 6: Mitral stenosis
Chapters 3 and 6: 3D TOE
and mitral regurgitation
prosthetic valvular assessment and
James Willis
Transcatheter aortic valve
implantation
Research Cardiac Physiologist,
Royal United Hospital, Bath, and
Steffen Petersen
University of Bath, UK
Honorary Consultant Cardiologist,
DVD
Centre Lead for Advanced
Cardiovascular Imaging, Barts and
The London NIHR Biomedical
Research Unit, The London Chest
Hospital, London, UK
Chapter 4: Cardiomyopathies
This new edition was compiled and revised by Paul Leeson and Daniel
Augustine. The text was illustrated by Paul Leeson and Daniel Augustine.
Paul Leeson, Daniel Augustine, Andrew Mitchell, and Harald Becher edited
the final version.
xi
Symbols and abbreviations
b
cross-reference
7
approximately
2D
two-dimensional
3D
three-dimensional
A
A-wave velocity
A4C
apical 4-chamber
Ao
aorta
AR
aortic regurgitation
AS
aortic stenosis
ASD
atrial septal defect
AV
aortic valve
BSA
body surface area
CFM
colour flow mapping
CHD
congenital heart disease
CMR
cardiovascular magnetic resonance
CO
cardiac output
CRT
cardiac resynchronization therapy
CSA
cross-sectional area
CT
computed tomography
CW
continuous wave (Doppler)
d
diastole
DET
deceleration time
E
E-wave velocity
ECG
electrocardiogram
ed
end-diastole
EF
ejection fraction
EROA
effective regurgitant orifice area
HFNEF
heart failure with a normal ejection fraction
Hz
hertz
ICE
intracardiac echocardiography
IVC
inferior vena cava
IVRT
isovolumetric relaxation time
JVP
jugular venous pressure
LA
left atrium
LLPV
left lower pulmonary vein
LUPV
left upper pulmonary vein
xii
SYMBOLS AND ABBREVIATIONS
LV
left ventricle
LVID
left ventricular internal diameter
LVOT
left ventricular outflow tract
LVPW
left ventricular posterior wall
LVS
left ventricular septum
MHz
megahertz
MPR
multiplanar reformatting
MR
mitral regurgitation
MS
mitral stenosis
MV
mitral valve
MVA
mitral valve area
PA
pulmonary artery
PDA
patent ductus arteriosus
PFO
patent foramen ovale
PISA
proximal isovelocity surface area
PLAX
parasternal long axis view
PR
pulmonary regurgitation
PRF
pulse repetition frequency
PS
pulmonary stenosis
PSAX
parasternal short axis view
PV
pulmonary valve
PW
pulse wave (Doppler)
RA
right atrium
RLPV
right lower pulmonary vein
RUPV
right upper pulmonary vein
RV
right ventricle
RVOT
right ventricular outflow tract
s
systole
SAX
short axis
SV
stroke volume
SVC
superior vena cava
TAVI
transcatheter aortic valve implantation
TGC
time-gain compensation
TOE
transoesophageal echocardiography
TR
tricuspid regurgitation
TTE
transthoracic echocardiography
TV
tricuspid valve
V
volt/s
VSD
ventricular septal defect
vti
velocity time integral
xiii
References
Reference Textbooks (alphabetical order)
Feigenbaum H (2004). Echocardiography 6th edition. Philadelphia,
PA: Lippincott, Williams & Wilkins.
Galiuto L, Badano L, Fox K, Sicari R, Zamorano J (2011). The EAE
Textbook of Echocardiography. Oxford: Oxford University Press.
Otto CM (2004). Textbook of Clinical Echocardiography, 3rd edition.
WB Saunders and Co Ltd.
Perrino AC, Reeves ST (2007). A Practical Approach to Transesophageal
Echocardiography 2nd edition. Philadelphia, PA: Lippincott, Williams &
Wilkins.
Rimmington H, Chambers J (2007). Echocardiography: Guidelines for
Reporting—A Practical Handbook, 2nd edition. New York: Informa
Healthcare.
Sidebotham D, Merry A, Legget M, Bashein G (2003). Practical
Perioperative Transoesophageal Echocardiography. Philadelphia,
PA: Butterworth-Heinemann Ltd.
Zamorano J, Bax J, Rademakers F, Knuuti F (2009). The ESC Textbook of
Cadiovascular Imaging. Boston, MA: Springer.
Websites
- American Heart Association M http://www.americanheart.org
- American Society of Echocardiography M http://www.asecho.org
- British Cardiovascular Society M http://www.bcs.com
- British Heart Foundation M http://www.bhf.org.uk
- British Society of Echocardiography M http://www.bsecho.org
- European Association of Echocardiography M http://www.escardio.
org/bodies/associations/EAE
- European Society of Cardiology M http://www.escardio.org
Papers and guidelines
Lancellotti P, Tribouilloy C, Hagendorff A, et al. European Association of
Echocardiography recommendations for the assessment of valvular
regurgitation. Part 1: aortic and pulmonary regurgitation (native valve
disease). European Journal of Echocardiography 2010; 11:223–44.
Rudski L, Lai W, 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. J Am Soc Echocardiogr 2010; 23:685–713.
xiv
REFERENCES
Aune E, Baekkevar M, Rodevand O, et al. Reference values for left
ventricular volumes with real time 3 dimensional echocardiography.
Scandinavian Cardiovascular Journal 2010; 44:24–30.
Horton K, Meece R, Hill J. Assessment of the right ventricle by
echocardiography: a primer for cardiac sonographers. J Am Soc
Echocardiogr 2009; 7:776–92.
Saito K, Okura H, Watanabe N, et al. Comprehensive evaluation of left
ventricular strain using speckle tracking echocardiography in normal
adults: comparison of three dimensional and two dimensional
approaches. J Am Soc Echocardiogr 2009; 22(9):1025–30.
Recommendations for evaluation of the severity of native valvular
regurgitation with two-dimensional and Doppler echocardiography.
A report from the American Society of Echocardiography’s
Nomenclature and Standards Committee and The Task Force on
Valvular Regurgitation, developed in conjunction with the American
College of Cardiology Echocardiography Committee, The Cardiac
Imaging Committee Council on Clinical Cardiology, the American Heart
Association, and the European Society of Cardiology Working Group on
Echocardiography. J Am Soc Echocardiogr 2003; 16:777–802.
Recommendations for chamber quantification: a report of the American
Society of Echocardiography Guidelines and Standards Committee and
the Chamber Quantification Writing Group, developed in conjunction
with the European Association of Echocardiography.
J Am Soc Echocardiogr 2005; 18:1440–63.
Waggoner AD, Ehler D, Adams D, et al. Guidelines for the cardiac
sonographer in the performance of contrast echocardiography:
recommendations of the American Society of Echocardiography.
J Am Soc Echocardiogr 2001; 14:417–20.
Masani N, Chambers J, Hancock J, et al. BSE Echocardiogram Report:
Recommendations for Standard Adult Transthoracic Echocardiography.
From the British Society of Echocardiography Education Committee.
Becher H, Chambers J, Fox K, et al. British Society of Echocardiography
Policy Committee. BSE procedure guidelines for the clinical application
of stress echocardiography, recommendations for performance and
interpretation of stress echocardiography: a report of the British Society
of Echocardiography Policy Committee. Heart 2004; 90(Suppl 6):vi23–30.
1
Chapter 1
Ultrasound
Introduction 2
Sound waves and ultrasound 2
Transthoracic transducers 4
Transoesophageal transducers 6
Other transducers 6
Echocardiography modes 8
Behaviour of ultrasound in tissue 12
Reflection, attenuation, and depth compensation 14
Reverberation artefacts 16
Transmit power 18
Gain 18
Grey scale and compress 18
Image resolution 20
Second harmonic imaging 22
Doppler echocardiography 24
Continuous wave Doppler 26
Pulsed wave Doppler 28
Colour flow mapping 30
Tissue Doppler imaging 32
3D echocardiography 34
3D artefacts 38
Image display 40
3D image rendering 42
Speckle tracking echocardiography 44
Second harmonic mode Doppler for contrast imaging 48
Power mode (amplitude) imaging 48
Basic fluid dynamics
50
Is ultrasound safe?
54
2
CHAPTER 1 Ultrasound
Introduction
Echocardiography is a non-invasive method for imaging the living heart.
It is based on detection of echoes produced by a beam of ultrasound
pulses transmitted into the heart. A working knowledge of the
principles and basic concepts of ultrasound imaging is fundamental to
understanding clinical applications and is necessary for accreditation
examinations.
Understanding the limitations both of fundamental physics and current
technology can ensure image acquisition is performed in a way that
drastically reduces image distortion and artefacts. This will reduce the
chance of misdiagnoses.
An understanding of the concepts behind how images are generated
helps the operator to optimize, interpret, and analyse images.
This chapter is aimed at a basic review of the fundamental principles of
echocardiography that will help the clinician get the most out of, and
understand the limitations of the technique.
Sound waves and ultrasound
Sound waves are often simplified to a description in terms of sinusoi-
dal waves which are characterized by the properties (Fig. 1.1):
The frequency (f, number of cycles per second).
The wavelength (λ, the distance between two identical points on
adjacent cycles).
The velocity (v, the direction and speed of travel).
The relationship between these properties is described by the formula:
V = f λ
In soft body tissues pressure waves travel at about 1500m/s (compared
with 300m/s in air).
Thus, in soft body tissues, at a frequency of 1000Hz (= Hertz, or cycles
per second), the wavelength is 1.5m. Common-sense dictates that this
wavelength is too great to image the heart, which is only about 15cm
across and which contains structures less than 1mm thick. To achieve a
wavelength of 1mm, the frequency has to be 1,500,000 Hz, or 1.5 MHz.
The human ear responds only to frequencies from about 30 Hz to
15,000 Hz, and since the word sound implies a sensation generated
in the brain, the term, ultrasound is used to describe the much higher
frequencies used in echocardiography.
SOUND WAVES AND ULTRASOUND
3
Compression waves
Wave propagation velocity
Wavelength
Pressure waveform
Pressure maximum
Pressure minimum
Frequency = Number of waves per second
Fig. 1.1 Features of a wave.
Velocity of ultrasound in various tissues
Bone: 2-4000m/s
Blood: 1570 m/s
Heart: 1540 m/s
Water: 1520 m/s
Fat: 1450 m/s
Air: 300 m/s.
Calculating wavelength from frequency and velocity
Example: For a 3.5MHz echocardiography transducer:
V = f λ,
1540 = 3,500,000 × λ
λ = 0.44mm
4
CHAPTER 1 Ultrasound
Transthoracic transducers
The transducer (or ‘probe’) held on the patient’s chest transmits
high-frequency ultrasound waves into the thorax and detects echoes
returning from the heart and great vessels (Figs. 1.2 and 1.3).
The transducer contains a layer of piezoelectric crystals which have
several properties:
• They are able to generate and receive ultrasound waves.
• When a current is applied the crystal expands and compresses
which generates the ultrasound wave.
• When an ultrasound wave strikes the piezoelectric crystal an
electric current is generated.
The transducer emits and then switches into receiving mode.
The repetition of this cycle allows the scanner to build an ultrasound
image.
The velocity of these high-frequency sound waves generated by the
transducer depends on the physical properties of the tissues through
which it is travelling.
Transducers for echocardiography typically generate frequencies in the
range 1.5-7MHz.
Denser tissues allow faster propagation. Thus, in softer body tissues
like the heart, the waves travel slower (1540m/s) than in harder tissues
like bone (2000-4000m/s).
Stand-alone probe
The stand-alone continuous wave (CW) Doppler probe comprises a
single transmit element and a single receive element. The probe is con-
sidered to provide more accurate estimation of transaortic velocities
(Fig. 1.4).
3D matrix array transducers
Matrix array transducers (Figs. 1.2 and 1.3) are used to generate 3D
pyramidal volumes in live real time (approximately 30° × 60° in size)
or full volume datasets which are not in real time (approximately
100° × 104° in size).
The transducer uses 3000-4000 elements arrayed in a 2D phase.
Differences between cardiac and vascular transducers?
Vascular ultrasound uses linear array transducers as it is designed
to image linear structures—blood vessels. The elements are aligned
along an axis enabling the beam to be moved, focused, and deflected
along a plane.
As the objects of interest are closer to the probe, higher frequencies
can be used for vascular imaging.
3D imaging using a matrix array probe is possible. Vascular 3D
imaging tends to be based on scanning the artery and creating a 3D
reconstruction from a series of 2D images.
Cardiac transducers tend to have a curved array of elements to
image a volume.
TRANSTHORACIC TRANSDUCERS
5
Fig. 1.2 Left: Toshiba 30BT phased array sector 2D probe. Right: Toshiba 25SX
matrix sector 3D probe. Images courtesy of Toshiba medical systems, Europe.
Fig. 1.3 Left: Phillips 3D X3-1 Probe. Right: Phillips X5-1 probe (2D/3D). Images
courtesy of Phillips Healthcare UK.
Fig. 1.4 Left: Toshiba PC20M stand alone probe. Right: Toshiba Vascular Probes.
Images courtesy of Toshiba Medical Systems, Europe.
6
CHAPTER 1 Ultrasound
Transoesophageal transducers
The probe (Fig. 1.5) is similar in construction to a gastroscope, but
in place of the fibre-optic bundle used for light imaging, a miniature
ultrasound transducer is mounted at its tip.
The plane of the transducer array can be rotated by the operator to
provide image planes that correspond to the orthogonal axes of the
heart despite the fact that these are not naturally aligned with the axis
of the oesophagus.
Precautions have to be taken to prevent accidental harm to the
patient through heating and the potential for it to apply 150V electrical
impulses to the back of the heart requires it to be checked regularly to
ensure integrity of the electrical insulation.
2D imaging from a transducer positioned in the oesophagus has advantages:
There is no attenuation from the chest wall.
It can operate at higher frequencies (up to 7.5MHz), improving image
quality.
3D transoesophageal imaging is increasingly being used, e.g. analysis of
valvular structure and to guide interventional procedures:
The most recent 3D transoesophageal echocardiography (TOE)
probes utilize fully sampled matrix array transducers to allow real-time
3D imaging.
A 2-7MHz transducer incorporates 2500 elements that allow
acquisition of a pyramidal 3D data set.
Other transducers
Intracardiac probes
Intracardiac echocardiography (ICE) allows visualization of cardiac
structures within the heart (see Chapter 8).
ICE probes (Fig. 1.6) have been used for almost 30 years. They provide
improved resolution imaging but due to the high frequency of the
transducers (20-40MHz), penetration of the earlier probes was poor.
The latest ICE probes have improved characteristics:
• Linear phased array and lower multifrequency range (5-10MHz).
• Capability of both pulsed and colour Doppler imaging.
• Improved manipulation with the use of multidirectional steerable
devices.
• A steering lock to maintain catheter angulation.
Intravascular ultrasound probes
High frequency intravascular transducers (30-40MHz) allow imaging
from within the coronary arteries.
The probe positioned in the lumen of the artery emits ultrasound
waves which penetrate into the vascular wall. Reflections are created
at interfaces between tissue components of different acoustic
properties (e.g. plaque, calcification and thrombus).
High-resolution cross-sectional images are produced allowing
measurement of luminal diameter and characterization of the vessel wall.
OTHER TRANSDUCERS
7
Fig. 1.5 Toshiba TEE 512 transoesophageal probe. Image courtesy of Toshiba
Medical Systems, Europe.
Fig. 1.6 AcuNav intracardiac echocardiography catheters. Image courtesy of
Biosense Webster, Inc.
8
CHAPTER 1 Ultrasound
Echocardiography modes (Figs. 1.7, 1.8)
Modern echocardiography machines use arrays of crystals which send
out several ultrasound waves across the sector of view.
Each line of reflected ultrasound waves is then collated to produce an
image of the heart.
Returning echoes strike the piezoelectric crystals, first from structures
closest to the transducer, followed in succession by those from more
distant interfaces.
The minute electrical signals generated are amplified and processed
to form a visual display showing the relative distances of reflecting
structures from the transducer, with the signal intensities providing
some information about the nature of the interfaces.
Repeating this sweep of ultrasound waves across the sector multiple
times per second allows a moving image to be produced. Hence the
spatial resolution of the image is determined by the distance between
scan lines and number of scan lines per sector; the temporal resolution
is determined by the number of sweeps across the sector per second
(frame rate).
ECHOCARDIOGRAPHY MODES
9
Fig. 1.7 Example of M-mode through mitral valve. M-mode images show structures
intersected by a stationary ultrasound beam.
10
CHAPTER 1 Ultrasound
A (amplitude)-mode echocardiography
The oldest type of ultrasound generation was created using A-mode
echocardiography. Here, the amplitude of the reflected ultrasound
wave is plotted against the distance from which the reflection
originates (not in clinical use).
B (brightness)-mode echocardiography
In B-mode imaging the amplitude of the reflected ultrasound wave is
recorded by the brightness (intensity) of a dot (not in clinical use).
M (motion)-mode echocardiography
The reflection of the ultrasound signals are recorded and displayed as
monochromic dots over time (Fig. 1.8).
The direction of the ultrasound beam is fixed, and interrogates
structures along a single axis over time, allowing a very high temporal
resolution when compared to 2D techniques (1000 lines/second
compared to 25 lines/second for a 2D image).
2D echocardiography
Transducer technology allows the ultrasound beam to be scanned
rapidly across the heart to produce 2D tomographic images.
3D echocardiography
The latest transducers are able to instantly acquire the image
contained in a pyramidal volume enabling the generation of a
3D data set.
ECHOCARDIOGRAPHY MODES
11
Fig. 1.8 Types of image: A (amplitude)-mode traces amplitude of a reflection against
distance from probe (of historical interest as one of the first type of ultrasound
image). B (brightness)-mode represents amplitude as intensity or brightness of a dot.
M (motion)-mode traces change in brightness over time. 2D images are generated
from sweeping across the field of interest.
12
CHAPTER 1 Ultrasound
Behaviour of ultrasound in tissue
When ultrasound waves pass through tissue they undergo reflection,
refraction or scattering (Fig. 1.9).
Reflection
As ultrasound waves pass through the chest towards the heart they
encounter several interfaces between different body tissues, e.g.
pericardium and myocardium.
Some of the incident energy is reflected at these interfaces as they act
like a mirror, in the same way as light bounces back off a shiny surface.
Reflected sound waves are termed ‘echoes’, and having undergone
‘specular’ (mirror-like) reflection they are termed ‘specular echoes’.
The reflected ‘echoes’ are transmitted back to the transducer and
vibrate the piezoelectric crystals to form a signal from an electrical
signal, from which a picture of the heart can be built.
The minute electrical signals generated are amplified and processed
to form a visual display showing the relative distances of reflecting
structures from the transducer, with the signal intensities providing
some information about the nature of the interfaces.
Refraction
Refraction is the change in direction of a wave due to a change in
its speed. This is most commonly observed when a wave passes from
one medium to another at any angle other than 90° or 0°.
Refraction of light is the most commonly observed phenomenon,
(e.g. the apparent bending of the angle of a pencil sitting in a glass of
water) but any form of wave, including ultrasound waves are subject to
refraction.
Scattering
Specular echoes used to form images of the heart arise from tissue
interfaces.
When ultrasound encounters much smaller structures, it interacts with
them differently: instead of being reflected along a defined path they
are scattered equally in all directions.
Reflection, scattering, and image quality
Some tissues within the heart allow a lot of specular reflection
(pericardium, epicardium, endocardium, and valves) and have
high signal intensity on echocardiography, others produce a lot of
scattering (i.e. myocardium).
Blood produces very little reflection and as such has very low signal
intensity on echocardiography. This allows the myocardium to be
easily differentiated from the blood.
BEHAVIOUR OF ULTRASOUND IN TISSUE
13
Reflection
Refraction
Scattering
Fig. 1.9 (Top) Reflection: the angle of the transmitted ultrasound influences the
reflection back from the boundary of a medium. (Middle) Refraction: the transmitted
ultrasound wave is transmitted from one medium to another causing a change in
direction. (Bottom) Scattering: echoes are generated from smaller objects and are
less intense and less angle dependent.
14
CHAPTER 1 Ultrasound
Reflection, attenuation, and depth
compensation
Ultrasound waves are quite severely attenuated (Fig. 1.10) as they pass
through ‘spongy’ tissues such as fat and muscle. The degree of attenuation
depends greatly on the ultrasound frequency.
The proportion reflected at a tissue interface depends mainly on the
difference in density of the tissues. Where there is a large difference—
such as an interface with air or bone—most of the incident wave
is reflected, creating an intense echo but leaving little to penetrate
further to deeper structures. It is for this reason that the operator
has to manipulate the transducer to avoid ribs and lungs, and that a
contact gel is used to eliminate any air between the transducer and the
chest wall.
In contrast, there is relatively little difference in the densities of blood,
muscle, and fat, so echoes from interfaces between them are very
small—about 0.1% of the incident amplitude.
Not only is this a very small signal to detect, but the amplification
level required would be vastly greater than that needed for the same
interface closer to the transducer. To overcome this problem, the
machine provides depth compensation or time-gain compensation
(TGC). This automatically increases the amplification during the time
echoes from a particular pulse return, so that the last to arrive are
amplified much more than the first.
Most of this compensation is built into the machine, but the user
can fine-tune it by means of a bank of slider controls that adjust the
amplification at selected depths.
The reflection and attenuation characteristics of various media can be
used to help in their identification. In particular, an interface with air
generates a very strong reflection at the proximal boundary, beyond
which the air strongly attenuates the beam casting a dark shadow.
REFLECTION, ATTENUATION, AND DEPTH COMPENSATION
15
Combined effect of attenuation
and reflection losses
At 5 MHz: 50% of transmitted energy is lost after 2cm
0.1% is reflected at a typical soft tissue interface
50% of the reflected energy is lost during return
2cm
The echo is thus: 1/2 x 1/1000 x 1/2 = 1/4000 of transmitted energy
Wave at interface
Reflected wave
Small change in density
Only part of wave is reflected
Large change in density
All wave is reflected
Fig. 1.10 Attenuation.
16
CHAPTER 1 Ultrasound
Reverberation artefacts
Reverberation artefacts are produced by the presence of structures
with transmission and attenuation characteristics very different from
that of soft tissue (i.e. the heart).
The reflected echoes bounce back and forth between the highly
reflective object and the transducer (Fig. 1.11).
In a reverberation artefact, the ultrasound wave is reflected back into
the chest from the transducer-skin interface and are common sources
of misinterpretation of images creating secondary ‘ghost’ images.
Under normal circumstances this effect is not seen because soft-tissue
reflections are so weak and secondary reflections are too small to
register.
However, if the object is a very strong reflector such as a calcified or
prosthetic valve, then the secondary or higher-order reverberation
echoes are strong enough to be detected.
The clue to their recognition is that they are always exactly twice
as far away from the transducer as a high-intensity echo, and if the
primary structure moves a certain distance, the multiple reflection
echo moves twice as far.
Clues to avoid and recognize reverberation artefacts
Beware of objects that are only seen in one imaging plane.
Beware of objects that do not respect anatomical boundaries,
e.g. a valve lying over a chamber wall or a line lying outside the
heart.
Beware of objects that are twice as far from the transducer as
intense reflectors.
Use the minimum power necessary to obtain an image.
Use adequate ultrasound gel.
Rotating the patient or changing the angle probe to move the
artefact if it is in the required field of view.
Reverberation
Ultrasound image
Time
Two strong
reflectors
Reverberation artefacts
behind object at regular
intervals
Fig. 1.11 Reverberation artefacts.
18
CHAPTER 1 Ultrasound
Transmit power
The amplitude (ultrasound strength) of the transmitted ultrasound
wave is controlled by the transmit power (or mechanical index).
Commercially available echocardiography systems are usually set to a
default transmit power to ensure there are no adverse effects on the
tissue being imaged, e.g. for native imaging MI >1.0.
The adjustment of the transmit power is particularly important during
contrast opacification studies to reduce contrast bubble destruction.
Gain
The brightness of an image depends on the amount of ultrasound
signal received by the probe from the reflected echoes.
The intensity of the reflected signal is dependent on the depth of the
structure being imaged (increased distance reduces signal) and the
inherent reflective properties of the object being imaged.
Objects in the near field appear brighter than those in the far field.
In order to compensate for this depth compensation or time gain
compensation (TGC) is used, which enhances the intensity of signals
returning later (and as such further away from transducer).
TGC automatically increases the amplification during the time echoes
from a particular pulse return, so that the last to arrive are amplified
much more than the first.
Most of this compensation is built into the machine, but the user
can fine-tune it by means of a bank of slider controls that adjust the
amplification at selected depths.
Too high levels of gain result in noise making images appear like
‘a snowstorm’ and difficult to interpret (Fig. 1.12).
Grey scale and compress
The intensity of an echo depends on the nature of the tissue interface.
There are a wide range of echo intensities, with a calcified structure
generating an echo many thousands of times more intense than a
boundary between, say, blood and newly formed thrombus.
The limited dynamic range of the display system can only represent
a fraction of this range (the difference in light intensity between
‘black’ ink printed on ‘white’ paper is only a factor of 30 or so). As a
consequence, ultrasound images show all intense echoes as ‘white’, all
weak echoes as ‘black’, and almost no grey tones.
The number of levels of grey (or the dynamic range) can be altered so
that a range of grey levels in between black and white appear, but at
the expense of boundary definition (Fig. 1.12).
GREY SCALE AND COMPRESS
19
Over gain
Under gain
Reduced dynamic range
Increased dynamic range
Fig. 1.12 Effects of changes in gain and dynamic range (grey scale) on image.
See W Video 1.1, W Video 1.2, W Video 1.3.
20
CHAPTER 1 Ultrasound
Image resolution
Temporal resolution is the overall visualized image quality with respect
to time, a compromise between the frame rate, angle width and
depth. Shallower imaging depths and narrower sector widths will both
increase temporal resolution.
Axial resolution is the minimum separation needed so that two
interfaces located in a direction parallel to the beam (i.e. above
and below each other) can continue to be imaged as two separate
sampling points rather than one. It can be optimized by employing a
higher ultrasound frequency.
Lateral resolution is the resolution side to side, across the 2D image:
the minimum separation of two sampling points aligned perpendicular
to the ultrasound beam so that they continue to be imaged as two
separate interfaces rather than one. It is primarily determined by the
distance from the transducer and, as the echo beam widens with
increased depth the lateral resolution decreases.
Spatial resolution is a measure of how close two reflectors can be to
one another so that they can still be identified as different reflectors.
Focusing
Lateral resolution is the chief factor limiting the quality of all
ultrasound images and is worse than axial resolution by something
like a factor of 10. To improve it, the ultrasound beam must be made
narrower by focusing it.
A plastic lens is fitted on the face of the transducer, in the same way
that a glass lens focuses light, though less effectively. Transducers can
be constructed with short-, medium-, or long-focus lenses.
The pulsing sequence that steers the beam can be electronically
modified to provide additional focusing. This adjustment can be made
by the operator.
Transducer frequency and spatial resolution
The frequencies of various probes differ depending on the application
(see Table 1.1).
The choice of transducer frequency is determined by the depth of
imaging and the resolution required.
Low frequency transducers have good penetration but because of the
longer wavelength, poorer resolution.
High frequency transducers have good resolution but poor
penetration.
Higher frequency transducers with better resolution can be used
where less depth is required, e.g. when imaging children or TOE.
Intravascular ultrasound requires very little penetration but very high
resolution and therefore uses very high frequencies.
IMAGE RESOLUTION
21
Table 1.1 Different ultrasound probes and their specific frequencies
Probe type
Transducer frequency
Transthoracic echocardiography
2-5Mhz
Transoesophageal echocardiography
5-7.5Mhz
Vascular probes
10Mhz
Intravascular probes
30-40Mhz
The effect of transducer frequency on image quality
Axial resolution is dependent on the wave frequency (calculated as
~2 × λ).
When using a 3.5Mhz probe the axial resolution is around 1mm.
Using a high frequency cardiac probe (>3.5MHz) rather than a
standard 2.5MHz probe will increase axial resolution, but will do
so at the expense of tissue penetration, which is lower at lower
wavelengths.
22
CHAPTER 1 Ultrasound
Second harmonic imaging
The frequency of the ultrasound wave sent out is the fundamental
frequency.
The target tissue expands and compresses in response to the wave
which in turn causes distortion of the sound wave. This distortion
generates additional frequencies called harmonics.
This change in wave shape can be shown mathematically to be due
to the addition of a frequency twice that of the original transmitted
frequency (called its ‘second harmonic’) (Fig. 1.13).
Harmonic frequencies are larger than the fundamental frequency.
Both harmonic and fundamental frequencies will return to the
transducer but by filtering out the original fundamental frequency it is
possible to receive the higher harmonic frequencies preferentially.
Advantages
Harmonic imaging combines the penetration power of a transmitted
low fundamental frequency with the improved axial image resolution
of the harmonic frequency which is twice that of the fundamental
frequency.
The harmonic image is derived from deeper structures and thus
reduces artefacts from proximal objects such as ribs.
The harmonic image away from the central beam axis is relatively
weak and thus not so susceptible to off-axis artefacts.
Disadvantages
As the image is now formed from echoes of a single frequency, some
‘texture’ is lost and structures such as valve leaflets may appear
artificially thick.
If the quality of the fundamental frequency image is very good, such
that second harmonic mode offers little benefit, it may be better not
to use it, but in most patients the improvement in image quality greatly
outweighs this minor disadvantage.
SECOND HARMONIC IMAGING
23
Transmitted
wave
Wave distorted
by tissue
Fundamental wave
component
Harmonic wave
component
Fig. 1.13 Harmonic imaging relies on analysing the harmonics of reflected waves to
generate an image.
24
CHAPTER 1 Ultrasound
Doppler echocardiography
Doppler imaging allows the determination of the direction and speed of
blood flow and is used for the detection and assessment of cardiac valvu-
lar insufficiency and stenosis as well as a large number of other abnormal
flow patterns.
The Doppler effect (Fig. 1.14)
First described in 1842, Doppler hypothesized that certain properties
of light emitted from stars depend upon the relative motion of the
observer and the wave source.
Consider a ship setting sail from the shore with an incoming tide with
a wave frequency of one wave per minute. As the ship is moving out
to sea would it meet the waves with more frequency than one per
minute? The converse is also true that if the same ship turned around
to set sail to shore, it would meet less than one wave per minute.
Although initially described for light, the Doppler effect applies to all
waveforms including ultrasound. As blood is moving, the frequency of
the backscattered echoes is modified by the Doppler effect, termed
‘the Doppler shift’.
The change in frequency of reflected echo waves will be either
increased if blood is travelling towards the probe or decreased if
travelling away from the probe, with the size of the Doppler shift
determines the speed of the blood.
The Doppler equation describes the change in frequency that occurs:
2f V cosθ
Δ =
C
ZF is the Doppler shift in frequency.
fo is the ultrasound frequency of the transducer.
V is the velocity of the blood.
θ is the angle between the flow and the ultrasound beam.
C is the velocity of ultrasound in tissue (1540 m/s).
The returning ultrasound signal is demodulated to extract the Doppler
shift and the velocity is then determined.
Doppler shifts are usually in the audible range (20Hz-20KHz) and heard
during the Doppler examination, the higher the pitch of the sound the
higher the Doppler shift and blood velocity.
DOPPLER ECHOCARDIOGRAPHY
25
Transmitted wave
Reflected wave
stationary object
Received
wavelength
increases
Reflected wave—
object moving away from probe
Received
wavelength
decreases
Reflected wave—
object moving towards probe
Fig. 1.14 The Doppler effect.
26
CHAPTER 1 Ultrasound
Continuous wave Doppler
Continuous wave (CW) Doppler requires transmission of a
continuous train of ultrasound waves, with simultaneous reception of
the returning backscattered echoes (Fig. 1.15).
The frequency of backscattered echoes from moving blood is different
to that from the transmitted frequency. This difference is known as the
Doppler shift or Doppler frequency.
As blood in an artery does not flow at a constant rate, the ultrasound
beam generates a large number of different Doppler frequencies, all
of which are used by the machine to generate the spectral Doppler
display.
This all requires two piezoelectric crystals (one for transmission one for
reception) rather than the one used in pulsed wave Doppler (Fig. 1.16).
Different probes have different arrangements of crystals with stand
alone ‘pencil’ probes having separate transmit and receive crystals and
normal probes assigning crystal groups to either a transmit or receive.
As transmission and reception of ultrasound is continuous it can’t
provide depth discrimination, and a particular Doppler shift may have
arisen from anywhere along the beam axis.
Although this would appear to be a problem, it usually is not the case
in clinical practice, since identification of the source of a high-velocity
jet is usually apparent from the 2D image and from the flow velocity
profile.
The density of the spectral trace is proportional to the amplitude of
the signal at each Doppler frequency and thus a representation of the
blood flow at that velocity.
Limitations of CW Doppler for measuring pressure
gradients
For successful application of CW Doppler the ultrasound beam
needs to be aligned accurately with the direction of blood flow
(within 15° of the flow, for which the cosine is 0.97 and error in the
value of [velocity]2 is <7%).
A colour-flow image can be used to guide beam alignment and in the
case of aortic stenosis the measurements should be checked by using
two different views (e.g. apical and upper right parasternal).
It is also necessary to align the beam with the centre of the jet
passing through the restriction.
The ‘pencil probe’, which is optimized for CW Doppler, is strongly
recommended for recording high-velocity valve jets.
CONTINUOUS WAVE DOPPLER
27
Fig. 1.15 Example of continuous wave Doppler.
With continuous transmission individual echoes cannot be identified
A brief pulse generates one echo, allowing echo delay to be measured
d
Distance (d) = ½ x Propagation Velocity x Echo Delay
Fig. 1.16 Continuous wave and pulsed wave.
28
CHAPTER 1 Ultrasound
Pulsed wave Doppler
This is a single piezoelectric crystal technique which uses alternating
transmission and reception of ultrasound waves (Fig. 1.17).
The depth of the region of interest (‘sample volume’) determines this
interval between transmission and reception of the ultrasound waves.
The cycle of alternating transmission and reception of pulses is termed
the pulse repetition frequency (PRF).
Information is gathered over a small sample, which can be moved to
any region of interest.
The main advantage of pulsed Doppler is the high spatial resolution
that can be obtained (typically a 1-5mm sample size can be
interrogated), and is useful for investigating velocities in specific areas,
i.e. the left ventricular outflow tract.
Pulse repetition frequency
With pulsed wave (PW) Doppler the time interval between sequential
pulses must be sufficient so that the initial pulse has enough time to
reach the target and return to the probe.
If this interval between pulses is too short so that the second pulse is
sent before the first is received back, then it is difficult to differentiate
between reflected signals from the sample volume.
The closer the region of interest to the probe, the higher the PRF.
Lower PRFs are usually used to evaluate low velocities as the
increased time between pulsed transmission-reception cycles allows
better chance for the scanner to identify slower flow (e.g. venous).
Aliasing
With pulsed Doppler, transmitted waves must be sampled at least
twice in each cycle to allow determination of wavelength (this is an
example of Nyquist’s theorem).
The maximum velocity (Doppler shift) that can be measured
accurately is equal to half of the PRF (this value is the Nyquist limit).
If pulsed Doppler waves travel to greater depths then the time interval
to receive the reflected signal is increased and thus the PRF is lower.
The Nyquist limit (aliasing level) is therefore lower at greater sampling
depths.
Practical considerations of PW Doppler
The practical effect of aliasing is that the ‘tops’ of the positive
velocities that exceed the Nyquist limit are cut off and displayed as
negative velocities (Fig. 1.18).
Provided that the flow is predominantly towards or away from the
transducer, and not bi-directional, the zero velocity baseline can be
shifted to favour one direction at the expense of the other, and it is
thus possible to increase the aliasing velocity by a factor of up to 2,
but beyond this nothing can be done.
When looking at the display of a pulsed wave trace if the flow being
measured is laminar then the trace has a defined outline, if the flow
is turbulent then flow fills in to form a more solid flow trace.
PULSED WAVE DOPPLER
29
Fig. 1.17 Example of normal pulsed wave Doppler placed in aortic arch.
Fig. 1.18 Example of pulsed wave Doppler with aliasing.
High pulse repetition frequency PW Doppler
This is the deliberate use of high PRFs to increase the aliasing
velocity and thus increase the maximum velocity that can be
measured with PW Doppler.
Sequential pulses are transmitted without waiting for the original one
to be received. This increases the PRF and allows a spectral trace
which is not aliased.
The trade off with using high PRFs to sample increased velocities is
that some of the ultrasound waves will penetrate beyond the depth
of interest and so signals from different sampling depths may be
recorded.
In practice this is overcome by judicious placement of the beam to
ensure that the additional sample volumes do not arise from high-
velocity areas that are not of interest.
30
CHAPTER 1 Ultrasound
Colour flow mapping
The PW Doppler principle can be extended to display a pictorial
representation of PW Doppler readings over a designated region of
interest (determined on the 2D image).
Pulses are rapidly emitted from the probe so that sequential pulses
hit the same moving scatterer. Thus, a representation of how far the
scatterer has moved either towards or away from the probe can be
determined.
Standard designation of colours occurs according to direction as Blue
Away and Red Towards (BART) the probe (Fig. 1.19). On CW or PW
Doppler, blood flowing towards the transducer would appear as a
spectral trace above the time line, whereas blood flowing away from
the transducer would appear as a spectral trace below the time line.
Limitations of colour flow mapping
Aliasing
Simultaneous imaging and Doppler lower the effective PRF and aliasing
in a colour flow image typically occurs at velocities above 0.5m/s.
Aliasing manifests on a colour display as colour inversion: red turning
to blue, and vice versa. For steady flow towards the transducer, a
velocity of 0.4m/s is represented by pale red but as it increases to
0.6m/s it becomes pale blue (Fig. 1.20). At 1.0m/s (twice the aliasing
velocity) the colour display again shows black, and with further
increase in velocity red, then blue, and so on.
Turbulent flow (variance mapping)
When flow is turbulent, there is a wide spectrum of local velocities:
high and low, forward and reverse. This is indicated on a CW display
as broadening of the spectral band, but cannot be indicated by colour
Doppler, since it can only display flow velocity at one point and at one
time by a single colour.
A solution is provided by analysing the time-variance of local velocity,
so that when the same pixel detects greatly different velocities in
successive images, the display is modified, for example by showing
those pixels in green.
This is called variance mapping, but it places further strain on frame
rates and aliasing velocity.
COLOUR FLOW MAPPING
31
Fig. 1.19 Example of BART principle. On colour Doppler mapping flow away from
the transducer is blue and a continuous or pulsed Doppler trace (blue spectra in
figure) would appear as a spectral trace below the time line. Flow towards the
transducer is red and a continuous or pulsed Doppler trace (red spectra in figure)
would appear as a spectral trace above the time line.
Differences in colour
Region of interest
and intensity describe
velocity and direction
Fig. 1.20 Example of colour flow mapping. The homogenous blue colour in the
left ventricle indicates blood flow away from the transducer. The flow becomes
turbulent when the blood is pushed through the leaky mitral valve, which can be
seen as a mosaic pattern of different velocities.
32
CHAPTER 1 Ultrasound
Tissue Doppler imaging
Tissue Doppler imaging (TDI) allows the velocities of myocardial
segments and other cardiac structures to be measured (Fig. 1.21).
Whereas conventional Doppler techniques assess the velocity of
blood flow by measuring high-frequency, low-amplitude signals from
small, fast-moving blood cells, TDI uses the same Doppler principles
to quantify the higher amplitude, lower-velocity signals of myocardial
tissue motion (Figs. 1.21 and 1.22).
TDI allows the measurement of myocardial motion relative to the
adjacent myocardium rather than the transducer which is susceptible
to tethering of adjacent tissue.
High-velocity signals from blood are filtered out and amplification
scales suitably adjusted so that Doppler signals from tissue motion can
be recorded.
Practical considerations for tissue Doppler imaging
The accuracy of TDI is angle dependent and only measures the vector
of motion that is parallel to the direction of the ultrasound beam.
High frame rates (100-150 frames per second) should be used in order
to maximize the information gathered in the spectral trace.
The sample volume should remain within the tissue of interest during
the cardiac cycle.
Respiratory motion can cause drifting of the strain curve as the sample
volume moves out of the desired region of interest and therefore
images should be acquired at end expiration.
Tissues close to the body surface can cause false echoes from their
reflections (‘reverberation artefacts’). In PW TDI these can be seen as
an increased intensity at zero velocity.
The lowest readable gain setting should be used to acquire and analyse
the spectral trace. Too much gain increases the width of the spectrum
and increasing the gain intensity increases the peak TDI value.
Strain rate imaging by tissue Doppler
Strain is a measure of the change in shape (‘deformation’) of a region
of interest. The relative amount of this deformation over time is
termed the strain rate.
The peak systolic strain is the maximum deformation seen during
systole.
Peak systolic strain rate is the maximum rate of deformation during
systole.
Strain rate by tissue Doppler measures the velocity gradient between
two points within a segment at a fixed distance apart.
TISSUE DOPPLER IMAGING
33
Fig. 1.21 Example of pulsed wave tissue Doppler imaging placed at basal left
ventricular septum.
IVCT
IVRT
S
A’
E’
Fig. 1.22 Schematic of pulsed wave tissue Doppler trace showing the isovolumic
contraction time (IVCT), the peak systolic myocardial velocity (S), the isovolumic
relaxation time (IVRT), the early diastolic myocardial velocity (E’) and the late
diastolic myocardial velocity (A’).
34
CHAPTER 1 Ultrasound
3D echocardiography
Introduction
3D image acquisition has the advantage of taking into account variation
in ventricular shape in all directions rather than just the two of biplane
measurements. It is dependent on capturing the whole left ventricle
within the 3D-probe sector and requires images to have good
endocardial border definition.
3D echocardiography is well suited for the evaluation of valvular
disease and has the advantage of offering depth as an additional
dimension over 2D echocardiography and the ability to view the valve
from multiple different angles.
3D image acquisitions are either true ‘live’ images or near real-time
(full volume) images. Live images offer instant feedback although are
limited by a narrow display sector. Near real-time images occur when
the electrocardiogram (ECG) recording is used to acquire individual
subvolumes over sequential cardiac cycles (Fig. 1.23).
3D acquisition modes
Full volume 3D data sets
This mode allows the generation of a 3D data set with the final
image of the heart created by acquiring several subvolumes (usually
1-7 depending on the vendor) over the corresponding number of
sequential cardiac cycles.
A regular cardiac rhythm and adequate breath-holding capabilities of
the patient are needed to reduce the incidence of artefact when the
subvolumes are merged together.
The greater the number of subvolumes used, the higher the frame rate
and temporal resolution (Fig. 1.24).
Once all of the subvolumes have been acquired a final image is formed.
This image is therefore not ‘live’.
3D ECHOCARDIOGRAPHY
35
Fig. 1.23 Diagrammatic representation of subvolume acquisition. The first subvolume
(red) is taken during the first cardiac cycle (red), the second subvolume (orange)
is taken during the second cardiac cycle (orange) and so on. All subvolumes are
merged together to create the final dataset.
Fig. 1.24 2-beat 3D left ventricle (LV) full volume acquisition (left) is composed of
2 subvolumes acquired over 2 consecutive cardiac cycles and has a lower volume
rate and temporal resolution than a 7-beat 3D LV full volume acquisition (right).
See W Video 1.4 and W Video 1.5.
36
CHAPTER 1 Ultrasound
Live 3D
Live volume images generate real-time 3D acquisitions of the heart.
This mode allows the generation of a 3D data set which is usually
smaller than the full volume acquisition to achieve adequate frame
rates.
It is well suited to imaging during percutaneous interventions or closer
inspection of valvular pathology, where a smaller volume of interest is
being examined or during irregular cardiac rhythms (Fig. 1.25).
3D colour Doppler
This combines grey scale volumetric data with colour Doppler and is
useful for examination of regurgitant lesions or shunts (Fig. 1.26).
Applications and limitations of 3D echocardiography
Applications
3D echocardiography has been shown to be accurate for the
assessment of left and right ventricular function and volumes.
There has been research into whether 3D datasets provide novel
indices for left ventricular dyssynchrony assessment.
3D echocardiography also allows for quantification of valvular
abnormalities and also to guide cardiac interventions (e.g. PFO/ASD
closure, TAVI and mitral clip implant).
Limitations
Misalignment can occur when the subvolumes are merged
together—called stitching artefacts, see Fig. 1.27.
3D image quality greatly depends on the quality of the 2D image.
3D ECHOCARDIOGRAPHY
37
Fig. 1.25 Left: parasternal left ventricle (LV) 3D full volume acquisition. Right:
live 3D parasternal acquisition of mitral valve (MV). RV = right ventricle.
See W Video 1.6 and W Video 1.7.
Colour Doppler
MV
Fig. 1.26 3D full volume colour Doppler acquisition of mitral valve (MV) and aortic
valve (AV). See W Video 1.8.
38
CHAPTER 1 Ultrasound
3D artefacts
Stitch artefacts
These occur during the acquisition of 3D full volume images where
subvolumes are recorded and triggered by the cardiac cycle.
Stitch artefacts are seen when subvolumes do not neatly merge
together and instead the boundary between individual subvolumes can
be identified (Fig. 1.27).
Causes of stitch artefacts include an irregular cardiac rhythm, probe
motion during acquisition or patient movement during acquisition
(e.g. respiration).
Drop out artefacts
These can occur when the volume of interest is acquired and a
suboptimal gain setting used.
For instance, when imaging the mitral valve, as the leaflets may be
quite thin then if the gain setting is too low, a drop out may occur.
Conversely if too high a gain setting is used this may lead to other
imaging artefacts.
Attenuation artefacts
As with 2D echocardiography, attenuation artefacts can occur. This is
the process of a gradual deterioration of the signal intensity distal to
the volume target due to reduced backscatter and absorption.
3D ARTEFACTS
39
Stitch artifact
Fig. 1.27 2D short axis slice from a 3D full volume left ventricle acquisition.
Cropping the ventricle in a short axis plane has revealed a stitch artefact.
40
CHAPTER 1 Ultrasound
Image display
Following the acquisition of the 3D data sets, the advantages of 3D
echocardiography become appreciated as all commercially available 3D
echocardiography machines allow post processing.
Post processing can be performed either directly on the same unit
as that used for acquisition or indirectly via a stand alone software
package.
The use of post processing allows visualization of cardiac landmarks
that would not have been possible with 2D echocardiography alone
(e.g. surgical ‘en face’ view of the mitral valve).
Commercially available 3D software packages are able to perform post
processing techniques (although the individual names of the techniques
vary from vender to vender):
Cropping
This allows the operator to remove unwanted information from the
initial data set to focus solely on the target anatomy, e.g. cropping the
ventricle to view the mitral valve looking from the apical position.
Most commercially available 3D operating systems allow cropping
(Fig. 1.28) to be performed either by rotating and removing unwanted
data in a single plane through the image or using a 3-plane technique.
Following image cropping and rendering, the
3D acquisition can be
displayed.
There are several modes such as a volume rendered image, wire frame
display, or multiplanar reformatting (MPR) slice display where three
simultaneous orthogonal 2D-like slices can be presented.
Slice modes
Most commercial 3D echocardiography systems offer a ‘slice’ format
through which the data can be presented (e.g. Phillips iSlice; Fig. 1.29).
Here, the 3D image volume can initially be optimized to avoid any
foreshortening and then volume can be viewed as a number of
uniformly spaced slices in the horizontal plane.
IMAGE DISPLAY
41
Fig. 1.28 Top 2 panels: full volume 3D acquisition of left ventricle (LV) from the
apical view (left image) which has been rotated and cropped to show a short axis
view of the left ventricle at papillary level (right image). AL = anterolateral papillary
muscle; PM = posteromedial papillary muscle; RV = right ventricle.
Fig. 1.29 3D full volume data sets of the left ventricle processed on Philips QLAB
7.1. Multiplanar reformatting (left) showing three orthogonal slices. Philips iSlice
(right) allows the LV to be cut into 9 short axis slices.
42
CHAPTER 1 Ultrasound
3D image rendering
Image rendering is vital to fully appreciate the target volume in detail.
As with 2D echocardiography, it is a process which should begin prior
to volume acquisition to ensure that the optimal image is acquired
and can be completed post image acquisition to optimize the acquired
image for visual presentation.
Most commercial 3D echocardiography packages offer different image
rendering capabilities, the main ones being:
Smoothness: this allows adjustment of image so that the finer detail
at closer inspection is free from minor ‘roughness’,
Gain adjustment: it is particularly important during 3D image
optimization to carefully adjust the overall gain of the image. High
gain levels make the image appear more 2D like whereas lower
gain reveals deeper tissue structure so that deeper tissues are more
appreciated in the overall volume; see Fig. 1.30.
Opacification/compression: this determines how solid or transparent
the final image is. Lowering the compression increases the image
transparency and vice versa.
Brightness.
3D vision/colour maps: all 3D post processing systems offer a
variety of colour maps or different ‘3D vision’ which the operator
can select from, each separate selection offering a combination of
different colours to alter depth perception.
Magnification: allows the acquired image to be enlarged to
appreciate finer structures in more detail.
Fig. 1.30 3D full volume data sets of the left ventricle processed on Philips QLAB 7.1 demonstrating image rendering. 3D LV full volume data set with
increased gain (left) and subsequently reduced gain (right) to allow deeper tissue structures to be appreciated. See W Video 1.9 and W Video 1.10.
44
CHAPTER 1 Ultrasound
Speckle tracking echocardiography
When imaging myocardial tissue, the ultrasound image of backscatter gen-
erated by the reflected ultrasound beam appears as a pattern of grey
values. This is termed the ‘speckle pattern’. The myocardial fibre orienta-
tion of the LV is complex. In healthy individuals myocardial fibres move in
several different planes which can be detected by speckle tracking.
The speckle pattern is unique for each myocardial region. Speckle track-
ing software allows individual speckles within a region of interest to be
tracked throughout the cardiac cycle, frame by frame. The scanner speckle
tracking algorithm allows the displacement, velocity, strain, and strain rate
for a myocardial region to be calculated.
Speckle tracking strain measurements
Peak strain values during systole are represented as a percentage of the final
position of the speckles in relation to their original position. Longitudinal
strain is measured from the LV apical views whereas radial and circumfer-
ential strains can also be obtained from LV short axis views (Fig. 1.31).
Longitudinal strain: the motion from base to apex. During systole the
contraction in this plane leads to fibre shortening, represented as
a negative percentage value (i.e. the more negative the value—the
greater the deformation which has occurred).
Radial strain: the amount of thickening of the myocardium which
occurs. During systole myocardial contraction leads to fibre thickening
in the radial plane. This is represented as a positive percentage value
(i.e. the more positive the value—the greater the deformation which
has occurred).
Circumferential strain: the change in radius in the short axis. During
systole, myocardial contraction leads to fibre shortening. This is
represented as a negative percentage value (i.e. the more negative the
value, the greater the deformation which has occurred).
Cardiac twisting
During the cardiac cycle the left ventricle also undergoes a twisting mo-
tion. During systole the apex rotates counterclockwise whilst the base
rotates in a clockwise fashion. These movements can also be estimated
by speckle tracking:
Rotation (degrees): the angular displacement of a myocardial
segment in the short axis view.
Twist or torsion (degrees): the net difference between apical short
axis and basal short axis rotation.
SPECKLE TRACKING ECHOCARDIOGRAPHY
45
Initial longitudinal distance
pre systole (L0)
Longitudinal distance post
systole (L1)
Initial radial length
Radial length post
pre systole (R0)
systole (R1)
Initial circumferential
Circumferential
length pre systole
length post systole
(C0)
(C1)
L1 − L0 × 100
Longitudinal strain =
L0
C1 − C0 × 100
Circumferential strain =
C0
R1 − R0 × 100
Radial strain =
R0
Fig. 1.31 Representation of longitudinal, circumferential, and radial strain.
46
CHAPTER 1 Ultrasound
2D vs. 3D speckle tracking (Fig. 1.32)
All of the described strain parameters can be measured in 2D. In
reality, speckles move through 3D space rather than remaining
within the 2D sector (Fig. 1.32).
Newer technology is now available allowing the measurement of 3D
speckle tracking strain (Fig. 1.33). This has the advantage of tracking the
motion of speckles within the scan volume, irrelevant of its direction.
Practical considerations for speckle tracking
Unlike TDI, speckle tracking is an angle-independent technique and so
the transducer can be placed off axis to obtain the optimal image.
Clear delineation of the endocardial border is necessary for reliable
tracking.
To reduce through plane motion acquisitions should be made during
breath hold.
Drop out or reverberations if present are sometimes tracked, resulting
in incorrect calculation of strain.
The optimal frame rate for acquisition of images is around 50-90
frames per second (FPS), much lower than frame rates needed for TDI
(>120 FPS). In patients with tachycardia or during rapid events in the
cardiac cycle, these lower frame rates mean that there may be under
sampling, with peak strain and strain rate values being lower than the
true value.
Higher frame rates will reduce the problem of under sampling but at
the expense of spatial resolution. Lower frame rates are thus used to
ensure optimal spatial resolution but care must be taken not to lower
the frame rate too much otherwise the speckle will not be able to be
tracked from frame to frame.
A good balance between temporal and spatial resolution can be
achieved by adjusting the sector width so that it is just wider than the
myocardial wall.
Whilst optimizing the image quality is important, it is also necessary to
remember that speckle tracking is also dependent on the implemented
vendor algorithm. Different vendor algorithms may produce different
results.
Langranian and natural strain
There are two types of strain, Lagranian and natural strain. Lagrangian strain
is defined on the basis of deformation from an original length. Whereas,
natural strain is defined relative to deformation from a length at a previ-
ous time, which may not necessarily be the original length. Natural strain
is more relevant to cardiac imaging as you may want to know how strain
changes during the cardiac cycle rather than just relative to the start.
SPECKLE TRACKING ECHOCARDIOGRAPHY
47
2D speckle
3D speckle
Fig. 1.32 Representation of 2D versus 3D speckle tracking. Individual speckles
move in and out of the scan plane between the two blue dots. With 2D speckle
tracking (left image) a narrow sector of speckles will be tracked (red dots). 3D
speckle tracking (right image) tracks the motion of the speckles within the entire
volume. Image courtesy of Toshiba Medical Systems, Europe.
Fig. 1.33 Post processing (using TomTec, Germany) of a 3D LV full volume data set
to show global 3D strain by speckle tracking. Strain curves during the cardiac cycle,
colour coded for each of the LV myocardial segments, are displayed.
48
CHAPTER 1 Ultrasound
Second harmonic mode Doppler for
contrast imaging
Second harmonic imaging was originally developed in order to enhance
signals from encapsulated contrast media (see Chapter 9).
These are proprietary products and comprise very small (1-3μm)
microspheres of gas contained within a hard outer shell.
At very low ultrasound power levels, the microspheres act as
conventional scatterers, but with slightly greater power (though still
lower than normally used for imaging) the pressure waves distort them
and they vibrate, emitting energy at the second harmonic frequency.
A display derived from the second harmonic Doppler frequency thus
selectively comes from the microspheres and not from surrounding
tissue or blood.
The addition of contrast greatly enhances the quality of both images
of blood-filled cavities and of Doppler signals, giving a clear velocity
profile for even very small jets.
At higher ultrasound power levels, the microspheres shatter, releasing
the contained gas, and generating a brief, but very intense, echo.
Power mode (amplitude) imaging
As stated previously, the Doppler shift is determined by velocity, but
the intensity of the Doppler signal relates to the number of scatterers
within the ultrasound beam.
If there are a lot of scatterers moving in random directions, the net
velocity will be zero, but the amplitude of the Doppler signal quite
high.
A display showing the amplitude or power of the Doppler signal shows
the density of scatterers, regardless of the velocities. This type of
display is used, often in conjunction with harmonic mode, in contrast
studies.
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50
CHAPTER 1 Ultrasound
Basic fluid dynamics
Volumetric flow
For steady-state flow (i.e. when velocity is constant) the volume of
liquid flowing through a pipe for a given time period (T) is the product
of the cross-sectional area of the pipe (A) and the mean velocity (V).
Volume = A x V x T
If flow is pulsatile (e.g. blood flow in the circulation) then velocity
increases and decreases over time. The product of velocity and time is
replaced by use of the velocity time integral (VTI).
VTI = (V x dT)
Continuity equation (Fig. 1.34)
If a fluid, which is not compressible, flows along a rigid-walled pipe, the
amount entering one end of the pipe must be the same as that leaving
the other end.
If the diameter of the pipe is greater at the end than the start (i.e.
cone-shaped) this still holds true.
In order to maintain flow across a reduced cross-sectional area an
increase in mean velocity of flow must occur.
This is the explanation for the increased flow speed when squeezing
the end of a hose pipe. This basic principle is described by the
continuity equation:
A1 x V1 = A2 x V2
Where:
A1 is the cross sectional of area of the entrance to the tube.
V1 is the velocity of flow at position A1.
A2 is cross sectional of area of the exit of the pipe.
V2 the velocity at position A2.
Providing that three of the terms in the equation are known, the
fourth can be derived.
The equation is used, for example, to determine the valve area in
aortic stenosis:
• Area of the left ventricular outflow tract (ALVOT) is taken as the
entrance to the tube (assumed to be circular and calculated from
diameter as π rLVOT2)
Entrance flow being pulsatile is replaced with velocity time integral
measured with pulsed wave Doppler in the left ventricular outflow
tract (VTILVOT).
Exit flow is measured as the velocity time integral across the aortic
valve (VTIAV) with continuous wave Doppler, i.e.:
ALVOT x VTILVOT = AAV x VTIAV
BASIC FLUID DYNAMICS
51
Cross-sectional area
e.g. = 2 cm2
Velocity
e.g. = 1cm/s
Volume = cross-sectional area × velocity × time
e.g. 2 × 1 × 1 = 2cm3
2 × 1 × 2 = 4cm3
After 1 second
After 2 seconds
Velocity
Actual velocity profile
4
5
6
3
2
7
1
8
Time
Volume during time period 1 =
Mean velocity during 1 × Time period 1 × Cross-sectional area
Total volume = Volume during 1 + 2 + 3 + 4 + 5 + 6 + 7 + 8
Velocity
Actual velocity profile
Area under the curve
= velocity time integral
Time
Total volume =
Velocity time integral × Cross sectional area
Volume of blood that passes through pipe 1 in fixed time period
must equal volume that passes through pipe 2 in same time period
Area 1 × Velocity 1 = Area 2 × Velocity 2
Area 1
Velocity 1
Area 2
Velocity 2
Pipe 1
Pipe 2
Fig. 1.34 Continuity equation.
52
CHAPTER 1 Ultrasound
Bernoulli equation (Fig. 1.35)
The Bernoulli equation describes the relationship between pressure
and velocity of a flow within a tube of fixed diameter.
Liquid only flows along a pipe if there is a pressure difference between
its ends.
For a fixed pipe diameter, and steady-state flow, only a small pressure
difference is required to overcome frictional losses.
If the pipe becomes narrower in order to increase flow velocity
(necessary to maintain flow) a higher pressure difference is required
across the pipe. Again this is observed when putting your thumb on
the end of a hose pipe, the pressure against your thumb increases as
the velocity of water coming out of the narrowed end increases to
maintain a steady state of flow through the pipe.
Neglecting the frictional losses, the relationship between pressure and
velocity is:
- V12)
Where:
V1 is the velocity upstream to the narrowing.
P1 is the pressure at that point upstream to the narrowing.
V2 is the velocity after the narrowing.
P2 is the pressure after the narrowing.
ρ is the density of the liquid.
In most clinical cases of obstructed blood flow (e.g. aortic stenosis)
the velocity before the narrowing (V1) is small compared to that after
the narrowing (V2), for example 1m/s in the left ventricular outflow
tract versus 4m/s across the aortic valve, and the difference is further
magnified when the values are squared (i.e. V1 = 1 and V2 = 16) The
equation simplifies by removing V1 with little change in the pressure
results and becomes:
In echocardiography the pressure difference relates to blood (for
which ρ is constant), the pressure is measured in mmHg and velocity
in m/s. The equation can then be simplified further to:
If the upstream velocity is not small compared to the downstream for
example in combined hypertrophic cardiomyopathy and aortic stenosis
where a muscular subvalvular restriction can be combined with a valve
stenosis then is not possible to omit V1 from the Bernoulli equation.
It is always worth remembering that a velocity of 2m/s across an aortic
valve does not represent a pressure gradient of 16mmHg across the
valve if the velocity in the outflow tract is 1.5m/s. In these cases (and
for BSE exams) the full equation is:
- V12)
FLUID
FLUID
High velocity
Low velocity
Small pressure
Large pressure
difference
difference
Pressure difference can be calculated by the Bernoulli equation if change in velocity is known
Fig. 1.35 Bernoulli equation.
54
CHAPTER 1 Ultrasound
Is ultrasound safe?
No case of harm to a patient from diagnostic ultrasound has ever
been documented in adult echocardiography. By any standards, the
risk:benefit ratio of echocardiography is negligibly low, but there is
no such thing as zero risk and to minimize it the user should always
employ the ‘ALARA’ principle (As Low As Reasonably Achievable) for
machine power levels and patient exposure times.
Ultrasound at high power levels can be used to coagulate tissues,
heat deep muscles, or clean dirty surgical instruments; however,
commercially available ultrasound machines do not allow the
transmission of power which may have potentially adverse bio-
effects. Potential harmful effects are related to the beam intensity and
ultrasound frequency.
Thermal index
The energy lost through attenuation as the beam passes through
tissues is largely converted to heat. The peak intensity as the
ultrasound pulse passes may be quite high, but there are large gaps
between pulses (pulse duration 2μs, interval between pulses 200μs) so
the average heating is quite low.
The term used to express this is thermal index and is the ratio of the
actual beam power to that required to raise the temperature of a
specific tissue by 1ºC.
Temperature and transoesophageal echocardiography
A particular issue arises with transoesophageal scanning, where the
transducer face is in contact with the oesophagus and local heating
could, in the event of a fault within the transducer, cause tissue necrosis.
For this reason, the probe tip temperature is monitored and there is an
automatic thermal cut-out if it becomes too high.
Mechanical index
Increasing transmitted power causes higher pressure fluctuations as
the ultrasound waves travel through tissues.
The potential for harm is quantified by the mechanical index (MI), a
parameter derived by dividing the peak negative wave pressure by the
square root of the ultrasound frequency. Most commercial cardiac
scanners limit the maximum power to MI 1.1.
Contrast echocardiography
In contrast, echocardiography safety issues relate to the contrast itself and
how it is broken down. Tissue bio-effects are negligible at the diagnosti-
cally recommended scanner settings. However, allergic or pseudo allergic
reactions are possible but very rare (see b p.570).
55
Chapter 2
Transthoracic
examination
Patient information 56
Patient preparation
56
Preparing machine and probe 58
Probe handling and image quality 58
2D image acquisition 60
3D image acquisition 62
Multiplane image acquisition 64
Data acquisition
66
Parasternal long axis view
68
Parasternal right ventricle inflow view
70
Parasternal right ventricle outflow view
70
Parasternal short axis (aortic) view
72
Parasternal short axis (mitral) view
74
Parasternal short axis (ventricle) views
74
Parasternal 3D views 76
Apical four chamber view 78
Apical five chamber view 80
Apical two chamber view 82
Apical three chamber view 84
Apical 3D views 86
Subcostal views 88
Inferior vena cava view 90
Abdominal aorta view 90
Suprasternal view 92
Right parasternal view 94
Standard examination 96
56
CHAPTER 2 Transthoracic examination
Patient information
Transthoracic echocardiography is a simple, non-invasive investigation.
The patient can be given simple information on what is intended and
how the pictures are created with sound waves.
They should be aware that they will need to undress to the waist and
lie on a bed on their side for around half an hour. If there is a sex
discrepancy between echocardiographer and patient there should be
the option of a chaperone.
The operator should be alert to the fact that the patient may find lying
in a fixed position on one side for a period of time uncomfortable
(e.g. hip or knee problems) and give opportunities for the patient to
move or consider alternative imaging positions. Furthermore the patient
may find having the probe pressed against the chest uncomfortable.
The operator should be aware of any complicating medical problems
such as increased body mass index, chest deformities, lung disease,
breast disease, or heart failure that may make imaging difficulty.
Patient preparation
Ask the patient to undress to the waist and explain that this is ‘so you
can image the whole of the heart’. A woman may appreciate a sheet or
gown to cover them while preparations are in progress.
Ask them to sit on the couch. The ideal position is with the patient
sitting up at 45º supported by the raised head of the couch but rolled
over onto their left side. Patients can find the concept of lying on their
left side while sitting up confusing. They tend to slide down the bed
on rolling over and end up lying down. Demonstrate the position if
necessary and explain that they need to lie on their left side to ‘bring
the heart close to the chest wall’. If the patient is more comfortable lying
flat this is an acceptable alternative position.
Ask them to raise their left arm and place their hand behind their head
(some couches have a handle to hold onto). Explain that this is to
‘make it easier to get to the heart’.
Make sure the patient is comfortable as they will need to stay in
position for sometime.
Attach ECG electrodes between patient and ultrasound machine
and check there is a clear trace on the screen both to time images
and trigger loop capture. Aim to have a large QRS complex without
artefact. Usually the red electrode is placed by the right shoulder,
yellow by left shoulder, and green on the lower chest (usually away
from the apex to avoid the imaging window). Alternative positions are
with the yellow electrode on the back and/or red in the centre of the
chest. Consider more careful skin preparation or changing electrode
stickers if the trace is not clear. Some machines allow you to rotate
through lead combinations (e.g. I, II, III) to find the best trace. ECG
gain can be changed to increase the size of the QRS complexes.
Enter patient demographic details (and, ideally, details of body size)
onto the machine.
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58
CHAPTER 2 Transthoracic examination
Preparing machine and probe
Set up an ergonomic orientation of machine, patient, and operator.
This will depend on your preferred operator position. A standard way
is to have the operator sitting behind the patient on the edge of the
couch with their right arm holding the probe and wrapped over the
patient. The machine is then operated with the left hand. Another
standard method is to sit facing the patient holding the probe against
the chest wall with the left hand (arm rested on the couch) and with
machine operated by the right hand.
Check transthoracic image settings on machine, with harmonic imaging
(if available) and your preferred image post-processing options
selected. Set overall gain, compress and transverse or lateral gain
controls to standard positions.
Make sure there is an ECG tracing on the echo machine and patient
details are entered.
Make sure image storage is possible (to magneto-optical disc,
download to image server or videotape).
Take the appropriate transthoracic probe, apply gel to transducer and
start imaging.
Probe handling and image quality
The probe should be held in one hand and pressed firmly against
the chest wall. Varying the pressure will alter image quality. Ensure
sufficient pressure to optimize the image but not too much to make it
uncomfortable for the patient. The usual problem while learning is not
to apply enough pressure to get good image quality.
A layer of gel ensures good contact between probe and chest wall.
It excludes any air (that would degrade image quality). However, too
much gel makes it difficult to keep a stable position so, once a layer
is established, try not to apply more gel as image quality will not
improve.
The probe has a dot on one side to orientate the probe in your hand
with the image on the screen.
The probe can be moved in multiple directions but the four key
movements are (1) rotation around a point, (2) rocking back and
forwards, (3) rocking side to side, and (4) sliding across the chest.
Movements needed to improve image quality are usually quite small
and with experience hand movements are almost subconscious.
Remember that image quality may be improved by different patient or
heart positions. These can be altered by physically rolling the patient,
a little, one way or the other, readjusting the patient to ensure they
are sitting up, or asking the patient to breathe in or out to move the
diaphragm (and heart) up or down.
Imaging well is hard work and requires concentration. If it is proving
difficult to find, keep, or return to an image during a study remember
a short break can help. Remove the probe from the chest, re-apply gel
and start again.
PROBE HANDLING AND IMAGE QUALITY
59
2D image optimization
There are four things that can be altered to improve image quality.
Check each when you change a view to ensure you have the optimal
image. In certain situations a completely different approach is needed,
e.g. contrast imaging.
Contact between probe and chest—this minimizes acoustic loss
between probe and heart. Ensure there is a sufficient layer of gel and
that you are applying enough pressure on the probe (more pressure
might be needed if there is significant fat or tissue under probe).
Patient position—this can move the heart closer to the probe.
Ensure the patient has not slipped out of position. See if rolling the
patient slightly, one way or the other, improves the image.
Cardiac and lung position—these two factors are altered by asking
the patient to breath in or out. The heart moves up and down with
the diaphragm and any lung tissue between the probe and heart
(which contains air and therefore degrades the image) may also
move out of the way. Ask the patient to breath in and out slowly.
Watch the image. The best image may be at end inspiration or end
expiration, or somewhere in between! Ask the patient to hold their
breath when the image is at its best.
Machine settings.
Machines usually have tissue harmonic imaging, which should routinely
be selected.
Overall, as well as, transverse and lateral gains should be adjusted
along with contrast controls (e.g. compress) to optimize contrast
between blood and myocardium. Newer machines perform all these
image optimization procedures automatically just by pressing an
optimization button.
Maximize the frame rate (which determines resolution) while filling the
screen with all required information. This can be done by adjusting depth
to just behind the heart (or area of interest) and reducing sector width to
the area being studied (particularly important for colour flow mapping
and tissue Doppler, which reduce frame rate when switched on but,
perversely, require relatively high frame rates to be useful.)
60
CHAPTER 2 Transthoracic examination
2D image acquisition
Standard acquisition
Images are acquired in a standard way—with a set sequence of views.
The standard views should always be collected to ensure comprehensive
data collection, with additional views when necessary. Even when there
is a specific question a full dataset should be acquired to ensure nothing
is missed.
Windows
There are 3 key areas or ‘windows’ on the chest and abdomen to collect
standard images (with additional windows available if needed) (Fig. 2.1). It
is normal to image through each window in turn starting with parasternal
windows. However, it may be necessary to go back to windows as pathol-
ogy is found that needs more detailed study.
1. Parasternal window
This window is usually just to the left of the sternum around the 3rd or 4th
intercostal space. However, the best position for parasternal views varies
with each patient. To find the best window move the probe up or down
an intercostal space, and away from or towards the sternum.
2. Apical window
As the name suggests this is at the cardiac apex so normally will be at the
bottom, left, lateral point of the chest. The apex beat may be felt under
the probe. The window should, ideally, be from the true apex to avoid
foreshortening. To optimize, ensure probe is lateral enough and move up
or down an intercostal space.
3. Subcostal window
This lies below the xiphisternum in the epigastrium. Lie the patient on
their back with stomach relaxed (may be easier if the patient bends their
legs). Place probe on the abdomen, press it in and point it back up into the
chest so that the image plane tucks under the ribs.
Additional windows
Suprasternal window
This is the suprasternal notch. Lie the patient on their back and raise the
chin. Rest the probe in the notch and point it down into the chest.
Right parasternal window
This is often used to look at flow in the ascending aorta. A normal or a
stand alone probe can be used. The patient should roll all the way over to
lie on their right side. The window is on the right of the sternum usually
slightly higher than the equivalent left parasternal window.
Supraclavicular window
This is rarely needed but can be used to look at vascular structures and
the aorta. It lies above the clavicles.
2D IMAGE ACQUISITION
61
Suprasternal
Parasternal
Right
parasternal
Apical
Subcostal
Fig. 2.1 Standard windows for transthoracic echocardiography.
Standard sequence of views
Parasternal windows
Parasternal long axis view
(Optional—parasternal right ventricle inflow)
(Optional—parasternal right ventricle outflow)
Parasternal short axis view (apex)
Parasternal short axis view (papillary level)
Parasternal short axis view (aortic level)
(Optional—right parasternal window).
Apical window
Apical four chamber
Apical five chamber
Apical two chamber
Apical three chamber.
Subcostal window
Subcostal long and short axis
Inferior vena cava
(Optional—aorta view).
Suprasternal window
(Optional—aorta view).
62
CHAPTER 2 Transthoracic examination
3D image acquisition
3D acquisition differs in that it is used to supplement data collection to
answer questions raised by 2D imaging. The windows selected are chosen
to optimize data collection for a particular area of the heart. The probe is
placed in the same positions on the chest as for 2D acquisition.
Windows
Apical window
The apical window is the main window used for 3D left and right ventricu-
lar acquisition. The setup of the image is nearly always the same as for 2D
imaging with a need to identify the true apex. The probe can be altered to
focus either on the right or left ventricle.
The apical window can also be used to evaluate the aortic, mitral, and
tricuspid valves (Fig. 2.2).
Parasternal window
This is used in 3D echocardiography to acquire 3D datasets of the left ven-
tricle, mitral, aortic, and tricuspid valves (Fig. 2.3). The window is found the
same way as for 2D imaging as the 3D dataset is set up based on biplane
2D imaging. However, often modified parasternal windows are required in
order to focus on a particular area of the heart, e.g. the tricuspid valve.
3D image optimization
When acquiring real-time 3D full volume datasets the following steps
will help to optimize the final image:
A good ECG signal with clear R wave is necessary to allow 3D full
volume triggering.
Adjust the scanner settings (as you would do for 2D imaging) to get
the best 3D resolution:
• Adjust gain setting.
• Ensure the region of interest is within the 3D volume sector.
• Minimize the sector (angle and depth) to focus on region of
interest.
• Maximize the number of subvolumes according to patient breath
holding capability.
• Select appropriate line density—the higher densities allow better
resolution although at the expense of a narrower angle sector.
• Optimize the volume size. All commercial scanners allow the final
volume size to be adjusted slightly which may be beneficial in
certain circumstances (e.g. dilated cardiomyopathy).
• Acquire images with the probe maintained in a steady position
and at end expiration.
Following acquisition, review image to look for any stitch artefacts.
When happy with the image then accept the acquisition.
3D IMAGE ACQUISITION
63
PV
AV
TV
MV
Fig. 2.2
3D full volume acquisition from the apical window. Subsequent rotation
and cropping allows visualization of all 4 cardiac valves. AV = aortic valve;
MV = mitral valve; PV = pulmonary valve; TV = tricuspid valve. See W Video 2.1.
TV
RV
AV
LV
MV
LA
Fig. 2.3 Full volume 3D acquisition of the left ventricle (LV) imaged from the
parasternal window. Rotation and cropping of the image shows the aortic valve
(AV); left atrium (LA); mitral valve (MV); right ventricle (RV). With tilting the
tricuspid valve (TV) is also seen. See W Video 2.2.
64
CHAPTER 2 Transthoracic examination
Multiplane image acquisition
Biplane imaging
Commercial scanners allow the ability to view the image which is being
acquired in two planes. Classically this has been used to assess left
ventricular volumes and ejection fraction.
Initially an optimal 4 chamber view of the left ventricle is acquired.
When in biplane mode the orthogonal view (i.e. 2 chamber is shown in
a split screen).
Biplane has the advantage of maintaining the same probe position
for the acquisition of both the 4 chamber and 2 chamber views thus
reducing errors which may occur due to the use of different probe
positions.
Biplane echocardiography also has the advantage of viewing the target
from 2 planes and so ensuring that foreshortening can be minimized.
Triplane imaging
Recently, triplane imaging has allowed the target volume to be
acquired and simultaneously viewed from 3 different orthogonal
planes.
When acquiring a 4 chamber view of the LV in triplane mode, the LV
2 chamber and 3 chamber views are simultaneously displayed (Fig. 2.4).
xPlane and iRotate
These modes available on Phillips echocardiography systems allow differ-
ent planes selected by the operator to be imaged simultaneously from one
acoustic window with a fixed probe position.
X-plane: This has the advantage of being able to compare directly two
individual planes side-by-side with the primary image displayed on
the left and the secondary image selected by the operator (Fig. 2.5)
displayed next to it.
iRotate: In this technique the operator can alter the angle of the plane
being viewed without moving the probe, using the controls on the
machine, similar to changing the plane in TOE imaging.
MULTIPLANE IMAGE ACQUISITION
65
Fig. 2.4 Triplane acquisition of left ventricle: acquired 4 chamber apical view (top
left); 2 chamber view (top right); 3 chamber view (bottom left) and representation
of the acquired image planes (bottom right).
Fig. 2.5 xPlane mode (Phillips). The primary image (left) of parasternal LV view
is acquired and a secondary imaging plane is selected (red dashed line) and
secondary image of LV short axis is displayed on the right of the split screen.
See W Video 2.3.
66
CHAPTER 2 Transthoracic examination
Data acquisition
Techniques for each view
In each view, start the study with 2D imaging and then consider whether
further echocardiography techniques are required to document the find-
ings. Although a standard minimal dataset acquisition (b p.96) is vital, it is
equally important that you analyse and interpret the images as you do the
study. It is easy to save a standard set of images for later analysis but if you
only notice pathology after the study you will not have acquired the right
images. The preliminary analysis needed to search and identify pathology
should be done during the study with detailed confirmation during later
reporting. Consider in each view:
Colour flow mapping
M-mode
CW Doppler
PW Doppler
Tissue Doppler imaging
Speckle tracking imaging
3D imaging
Contrast imaging.
In all views 2D and colour flow mapping are used. Most views also use
CW and PW Doppler as well as occasional M-mode. In some views 3D,
contrast and tissue Doppler imaging may be needed.
Image storage
All images and data must be stored for future reference. With
the current ease of storage it is no longer acceptable to perform
an echocardiogram and only keep handwritten notes, even in
emergencies.
Images are usually stored and commonly then transferred directly to a
main server. Digital storage is usually based on storing a single cardiac
cycle loop, triggered off the ECG trace. If the patient has an arrhythmia
with variable cardiac cycle length then it may be better to store 3-5
beats.
It is desirable to have a digital laboratory to store all acquired views.
Storage on digital media enables better post-processing and follow-up
comparisons.
Formats
The current preferred means of storage of studies is Digital Imaging
and Communications in Medicine (DICOM). DICOM defines the way
in which patient data is stored, transported, and retrieved.
For movie storage image acquisitions can be stored commonly as AVI
or MPEG formats.
Widely used formats for still screen/non-movie storage for use in
presentations include BMP, TIF, and JPEG.
DATA ACQUISITION
67
Image compression
In order to reduce overall storage requirements, image compression
can be used.
Image compression can either be lossless or lossy. Lossless image
compression reduces the final file size by 2-5 times but allows an
identical version of the original to be created if the compression is
reversed. Lossy image compression reduces the final file size by a
greater amount (up to 20 times) but this is at the potential expense
of image degradation.
68
CHAPTER 2 Transthoracic examination
Parasternal long axis view
The first view. Gives an immediate over all impression of the major valves,
left and right ventricle, aorta, and pericardium (Fig. 2.6).
Finding the view
In the parasternal window hold the probe with the dot pointing to the
right shoulder. Adjust probe with slight rotation and rocking.
The optimal image cuts through the middle of mitral and aortic valves
to display left ventricular inflow and outflow. Left ventricular walls lie
parallel and straight across screen (anterior border of septum should
be same distance from transducer as anterior wall of ascending aorta).
Ascending aorta should be a tube with parallel walls.
Sometimes not all structures can be aligned in a single view, in this
situation record several views focused on each detail.
What to record?
2D images.
Colour flow: aortic valve, left ventricle outflow tract, mitral valve.
M-mode: aortic valve/left atrium, mitral valve, left ventricle.
What do you see?
Left ventricle: septum (anteroseptal portion), inferolateral (also some-
times called posterior) wall and cavity are seen. Use 2D (and M-mode)
to assess left ventricle size, function, and hypertrophy. Also excellent for
LV outflow tract size measurements and evidence of flow acceleration on
colour flow. Septal defects may be seen with colour flow.
Aortic valve: right coronary cusp is at top and non-coronary cusp at bot-
tom. 2D and M-mode can assess movement. Colour flow demonstrates
regurgitation.
Aortic root: entire aortic root, including sinuses, sinotubular junction, and
ascending aorta should be visible for measurement with 2D or M-mode.
Ascending aorta: slight adjustment by rocking the probe to one side can
bring the proximal portion of the ascending aorta into view.
Descending aorta: seen in cross-section as a circle behind mitral valve. Use
as landmark for studying pericardial and pleural fluid.
Mitral valve: A2 and P2 segments usually seen. 2D will pick up move-
ment (prolapse, stenosis, etc.) and tip movement can be documented with
M-mode. Use colour flow to identify regurgitation. Vena contracta or flow
convergence may be evident.
Left atrium: left atrial size can be judged and measured with M-mode.
Right ventricle: the right ventricle lies near the probe and can be measured.
Pericardium: seen anteriorly in front of right heart and posteriorly behind
heart. Good view to identify an effusion and measure size.
PARASTERNAL LONG AXIS VIEW
69
Septum
RV
Ascending
aorta
LV
AV
right coronary cusp
Inferolateral wall
non coronary cusp
LA
MV
Descending
anterior leaflet
aorta
posterior leaflet
Fig. 2.6 Parasternal long axis view. See W Video 2.4.
70
CHAPTER 2 Transthoracic examination
Parasternal right ventricular inflow view
A useful extra view to look at tricuspid valve and right ventricular inflow
(Fig. 2.7).
Finding the view
From parasternal long axis view, rock probe slowly to point
downwards. The tricuspid valve should come in to view. There usually
needs to be some slight rotation to optimize the image.
Optimal images demonstrate the tricuspid valve with right atrium
behind and sometimes vena caval inflow.
What to record?
2D image.
Colour flow across the tricuspid valve.
CW and PW Doppler across the tricuspid valve.
What do you see?
Tricuspid valve: main feature. Two leaflets seen in centre of screen. Use
colour flow to document regurgitation. Jet may be aligned for Doppler
measures of inflow and right ventricular systolic pressure.
Right atrium: lies behind tricuspid valve and slight rotation may
demonstrate right atrial appendage, Eustachian valve and inflow from
vena cavae.
Right ventricle: portion of right ventricle close to tricuspid valve seen.
Parasternal right ventricular outflow view
A useful extra view to look at pulmonary valve and artery (Fig. 2.7).
Finding the view
From parasternal long axis view, rock probe slowly to point upwards.
Pulmonary valve should come into view. Slight rotation will optimize
image to include pulmonary artery.
Optimal image demonstrates the pulmonary valve with pulmonary
arterial trunk to bifurcation.
What to record?
2D image.
Colour flow pulmonary valve.
Continuous and pulsed wave Doppler across pulmonary valve.
What do you see?
Pulmonary valve: main feature. Two leaflets seen in centre of screen.
Use colour flow to document regurgitation. Jet normally aligned for
Doppler measures of outflow and regurgitation.
Pulmonary artery: in the far field. With slight adjustments can usually be
followed to bifurcation. Can measure size and look for abnormal jets
(patent ductus) or thrombus (pulmonary embolus).
PARASTERNAL RIGHT VENTRICULAR OUTFLOW VIEW
71
RV
RV
TV
PA
RA
PV
Fig. 2.7 Right ventricular inflow and outflow views. See W Video 2.5 and W Video 2.6.
72
CHAPTER 2 Transthoracic examination
Parasternal short axis (aortic) view
A series of parasternal short axis views are gathered in order to scan
through the heart in cross-section. Together they give an impression
of left ventricular function, aortic and mitral structure, and the right heart
(Fig. 2.8).
Finding the view
From the parasternal long axis view, rotate the probe around 90º so
that the dot points to the left shoulder. Try and rotate from a long axis
view with the aortic valve in the centre. Focus on keeping the valve
in the centre and you should end up with the classic cross-section
through the aortic valve.
It can be difficult to get a true on-axis cut. To optimize the image try
slight rotation around the point until the aortic valve appears circular
with the right ventricle wrapped around the valve. Then rock the
probe back and forward until the cut is straight.
Optimal image should have a round aortic valve with 3 cusps evident.
The tricuspid valve should be visible on the left and pulmonary valve
on the right.
If all structures are not seen remember to record several views
focused on each detail.
What to record?
2D images.
Colour flow: aortic, tricuspid, and pulmonary valve (also sometimes
atrial septum).
Doppler: pulmonary and tricuspid valve.
What do you see?
Aortic valve: lies in centre with classic Y-shape: left coronary cusp on
right, right towards the top, and non-coronary on the left. Use colour
flow to identify regurgitation. Left main stem sometimes seen by left
cusp.
Right ventricle: basal right ventricle lies near the probe wrapped around
aortic valve. Ventricle can be measured.
Tricuspid valve: seen to left of aortic valve. Use colour flow to check
for regurgitation. May be aligned for CW Doppler.
Pulmonary valve: to right of aortic valve. Colour flow demonstrates
regurgitation. CW and PW Doppler will document velocities.
Left atrium: lies behind aortic valve.
Interatrial septum: septum lies at 7 o’clock and view may be useful to
identify septal defects with colour flow.
Pericardium: seen anteriorly, in front of right heart.
PARASTERNAL SHORT AXIS (AORTIC) VIEW
73
LA
RA
LV
TV
PV
RV
RCC
LCC
NCC
PA
RA
Atrial septum
LA
AV
Fig. 2.8 Parasternal short axis (aortic) view. See W Video 2.7.
74
CHAPTER 2 Transthoracic examination
Parasternal short axis (mitral) view
The classic en face or ‘fish-mouth’ view of the mitral valve (Fig. 2.9).
Finding the view
From the parasternal short axis aortic view, rock the probe slightly
towards the cardiac apex. By starting the parasternal cuts from the
aortic valve the views tend to stay ‘on-axis’.
Optimal image should have a left ventricle with the ‘fish mouth’ mitral
valve clearly seen.
What to record?
2D images. Consider 2D planimetry if stenosis.
Consider colour flow across mitral valve, if regurgitation.
What do you see?
Mitral valve: a classic en face view of the mitral valve to look at valve
morphology (including the separate scallops) and movement. Consider
colour flow or 3D imaging if abnormalities. Can also be used to
measure valve opening with planimetry.
Parasternal short axis (ventricle) views
The classic short axis views of the left ventricle (Fig. 2.9).
Finding the view
From the parasternal short axis mitral view, rock probe slightly more
towards apex until left ventricle is in cross-section. The papillary level
has the bodies of both papillary muscles evident.
Further rocking towards apex creates an apical view distal to papillary
muscles.
Usually important to avoid off-axis images so that true assessment of
left ventricle function is possible. Slight rotation helps bring out the
circular ventricular shape. If it is proving very difficult to get a clear
image consider moving the probe position slightly within the window.
Optimal images should have a cross-section of the left ventricle.
What to record?
2D images at papillary level for measures: left ventricle size and mass.
Consider a view recorded at apical level.
Consider M-mode measures: left ventricle.
Tissue Doppler imaging sometimes used in short axis.
Speckle tracking imaging.
What do you see?
Left ventricle: the short axis demonstrates septum, anterior, lateral, and
inferior walls (in order clockwise). Use for measures of left ventricle size
and thickness and to assess regional function of mid segments of walls.
Right ventricle: right ventricle is seen as a crescent around the
left ventricle. Use to judge right ventricle size, function, and
haemodynamics.
PARASTERNAL SHORT AXIS (VENTRICLE) VIEWS
75
LA
RA
LV
RV
Anterior
RV
leaflet
LV
MV
Posterior leaflet
Posteromedial
Anterolateral
Papillary muscles
Fig. 2.9 Parasternal short axis (mitral and ventricle) views. See W Video 2.8
and W Video 2.9.
76
CHAPTER 2 Transthoracic examination
Parasternal 3D views
Finding the view
The initial window is located in a similar fashion as for 2D acquisition
with the probe marker pointing towards the right shoulder and the
probe positioned in the 3rd or 4th intercostal space.
Slight probe adjustment either laterally or medially to the sternum
or manoeuvring the probe to an adjacent intercostal space will help
identify the optimal position for acquisition.
What to record?
Left ventricle full volume acquisition.
Mitral valve full volume or live 3D acquisition.
Mitral valve colour Doppler acquisition.
Aortic valve full volume and/or live 3D acquisition.
Aortic valve colour Doppler acquisition.
What do you see?
Similar anatomical landmarks can be appreciated as in the
2D view
(Figs. 2.10 and 2.11). The advantage of 3D acquisition is appreciated fol-
lowing data collection when the dataset can be rotated to see anatomy
(Fig. 2.12) and the spatial associations of different pathologies, e.g. mitral
valve prolapse and the insertion of chordae.
Fig. 2.10
3D live zoom acquisition of the aortic valve (AV) taken from the
parasternal view. The anterior mitral valve leaflet is also seen (AMVL).
See W Video 2.10.
PARASTERNAL 3D VIEWS
77
Fig. 2.11
3D live zoom acquisition of the mitral valve (MV) taken from the
parasternal view. AMVL = anterior mitral valve leaflet; LA = left atrium; LV = left
ventricle; PMVL = posterior mitral valve leaflet. See W Video 2.11.
Fig. 2.12 Full volume 3D acquisition of left ventricle (LV) taken from the
parasternal view. The image has been rotated and cropped to view from towards
the left atrium. Image stopped in systole. The anterior mitral valve leaflet (AMVL)
and posterior mitral valve leaflet (PMVL) and aortic valve (AV) position can be seen.
See W Video 2.12.
78
CHAPTER 2 Transthoracic examination
Apical four chamber view
Finding the view
In the apical window, hold the probe with the dot pointing towards
the couch.
Probe needs to be as close to the left ventricular apex as possible
so alter the image, focusing on obtaining the optimal Ieft ventricular
size and shape. The identifying characteristics of the apex are that it
moves less than the other walls and is thinner. In a true apical view
the left ventricle will be at its longest. Once you have identified the
apex optimize the view with rotation and rocking to bring in the right
ventricle, left and right atrium, as well as, mitral and tricuspid valves.
Exclude the left ventricular outflow and aortic valve by tilting the probe.
Optimal image should be at apex with both ventricles, both atria and
both mitral and tricuspid valves visible. Septa should be straight down
the centre of the image.
What to record?
2D images.
Colour flow mapping: mitral and tricuspid valves.
CW and PW Doppler: mitral and tricuspid valve.
Consider Doppler of right upper pulmonary vein.
Consider tissue Doppler imaging of right and left ventricle.
Speckle tracking.
3D datasets.
When appropriate use contrast.
What do you see ? (Fig. 2.13)
Mitral valve: A2 and P2 segments of mitral valve are seen. 2D for
movement. Colour flow mapping will show regurgitation (vena
contracta, flow convergence, etc.) Doppler well aligned for stenosis
and valve inflow. Tissue Doppler of lateral and septal sides of mitral
ring may be possible.
Tricuspid valve: lateral and septal leaflets displayed. As for mitral valve,
colour flow, Doppler and tissue Doppler are possible.
Left and right atrium: both atria and the interatrial septum can be
seen. Pulmonary veins as well as vena cavae may be seen in far field.
Use to measure atrial volumes.
Left ventricle: key view to study global and regional left ventricle
function. Septum, apex, and lateral wall are displayed. Good for
2D volume measures if endocardial border is clear. If assessing
left ventricle function consider contrast and/or 3D to improve left
ventricle data collection. Tissue Doppler of different wall segments is
also possible.
Right ventricle: a key view to look at right ventricle size and function.
Usually compared relative to left but also tissue Doppler or M-mode
of tricuspid free wall annulus can be considered.
Pericardium: important view to see size and location of pericardial
fluid. May also be used for ultrasound-guided pericardiocentesis.
APICAL FOUR CHAMBER VIEW
79
LA
AO
LV
RA
RV
Ventricular septum
Lateral wall
(papillary muscle
usually not seen)
LV
RV
MV
posterior leaflet
RA
Anterior leaflet
TV
Lateral leaflet
LA
Septal leaflet
Interatrial septum
RUPV
Fig. 2.13 Apical four chamber view. See W Video 2.13.
80
CHAPTER 2 Transthoracic examination
Apical five chamber view
Used to look at left ventricular outflow and aortic valve (Fig. 2.14).
Finding the view
From the apical four chamber view tilt the probe to bring the aortic
valve and outflow tract into view.
Sometimes a better alignment through aortic valve and ascending aorta
is obtained by moving probe laterally on chest wall (more into axilla).
This foreshortens left ventricle and alters alignment for other valves so
use only to study the aortic valve.
Optimal image looks similar to apical four chamber but with the aortic
valve evident and ascending aorta in far field.
What to record?
2D images.
Colour flow mapping: aortic valve.
CW and PW Doppler: aortic valve and left ventricle outflow tract.
What do you see?
Aortic valve: right and non-coronary cusps (although may not be easy
to see). Colour flow demonstrates regurgitation. CW for stenosis and
regurgitation.
Left ventricular outflow tract: use colour flow mapping for aortic
regurgitation or flow turbulence due to obstruction. Best view to place
PW Doppler to assess outflow and obstruction.
APICAL FIVE CHAMBER VIEW
81
AO
LV
LA
RA
RV
LV
RV
LVOT
MV
RA
LA
TV
AV
Fig. 2.14 Apical five chamber view. See W Video 2.14.
82
CHAPTER 2 Transthoracic examination
Apical two chamber view
An important view for global and regional left ventricular assessment
(Fig. 2.15).
Finding the view
From the apical four chamber view, rotate the probe around 90º
anticlockwise. Watch the picture and try and keep the mitral valve in
place. If the apex of the ventricle changes you were probably not at
the apex and are foreshortening.
Keep rotating until right ventricle disappears completely but before left
ventricular outflow tract comes into view.
Optimal image contains left ventricle (no right ventricle) from apex,
centred in the image. Mitral valve is cut through the commissure. Left
atrium is in far field and left atrial appendage may be visible.
What to record?
2D images.
Consider Colour flow and Doppler measures across mitral valve.
Consider tissue Doppler imaging of ventricle.
What do you see?
Left ventricle: inferior wall on left, and anterior wall on right. Good
for regional assessment. Use plane for ventricle volume measures and
tissue Doppler of wall segments.
Mitral valve: ideal image is of a commissural view with P3, A2, and P1
segments visible from left to right. Colour flow and Doppler measures
are possible as well as assessment of the long axis of the mitral valve
ring.
Left atrial appendage: sometimes visible as a curved finger pointing
towards probe around right side of mitral valve.
Coronary sinus: the coronary sinus is usually seen in cross-section on
the left of the mitral valve.
Adaptation of view
Right ventricle: slight tilting of probe to point forwards can scan into a
two chamber view of right ventricle (not a standard view).
APICAL TWO CHAMBER VIEW
83
LV
LA
Anterior wall
Inferior wall
LV
MV
Left atrial
appendage
LA
Coronary sinus
Fig. 2.15 Apical two chamber view. See W Video 2.15.
84
CHAPTER 2 Transthoracic examination
Apical three chamber view
Similar to the parasternal long axis view but includes left ventricular apex
(Fig. 2.16).
Finding the view
From the apical two chamber view continue rotating the probe
anticlockwise to around 135º from the four chamber view.
Watch the picture and keep the mitral valve in place, rotating until
the left ventricle outflow and aortic valve come into view. As for the
translation from four to two chamber.
Optimal image contains left ventricle from apex straight down the
screen with mitral valve, left atrium, left ventricle outflow, and aortic
valve in far field.
What to record?
2D images.
Consider tissue Doppler and speckle tracking imaging of ventricle.
Consider colour flow and Doppler measurements across aortic valve
as may be well aligned.
Consider colour flow and Doppler measures across mitral valve.
What do you see?
Left ventricle: good view to assess septum on right of image, apex and
inferolateral (posterior) wall on left of image.
Aortic valve: right coronary cusp is on right and non-coronary cusp on
left. Colour flow will demonstrate regurgitation and valve is usually
aligned for Doppler measurements.
Mitral valve: A2 and P2 segments of valve seen and can consider
colour flow and other Doppler measures if not enough detail from
other views.
Left atrium: atrium lies behind mitral valve.
APICAL THREE CHAMBER VIEW
85
AO
LV
LA
LV
Septum
MV
LVOT
AV
Inferolateral wall
LA
Ascending
aorta
Descending
aorta
Fig. 2.16 Apical three chamber view. See W Video 2.16.
86
CHAPTER 2 Transthoracic examination
Apical 3D views
Finding the view
The initial window is located in a similar fashion as for 2D acquisition
of the apical four chamber view (see b p. 78).
What to record?
Left ventricle full volume acquisition.
Right ventricle full volume acquisition.
Mitral valve full volume and live 3D acquisition.
Mitral valve colour Doppler acquisition.
Aortic valve full volume and live 3D acquisition.
Aortic valve colour Doppler acquisition.
Tricuspid valve full volume and live 3D acquisition.
Tricuspid valve colour Doppler acquisition.
What do you see?
Similar anatomical landmarks can be appreciated as in the
2D view
(Fig. 2.17). Following data acquisition, the 3D image can be rotated to
make it easier to understand how any pathology relates to the different
parts of the heart.
APICAL 3D VIEWS
87
LV
RV
LA
RA
Fig. 2.17 Full volume 3D acquisition of the right ventricle (RV) imaged from the
apical window. LA = left atrium; LV = left ventricle; RA = right atrium.
See W Video 2.17.
88
CHAPTER 2 Transthoracic examination
Subcostal views
Very useful views to study pericardial effusions, assess right ventricular
inflow, and screen for septal defects (Fig. 2.18). Also, alternative window
for equivalent of parasternal views if parasternal window not possible.
Finding the view
In the subcostal window have the probe flat and pressed into the
stomach so that the imaging plane is directed upwards under the ribs.
With slight rotation and tilting back and forward you will find the
heart. You will need to increase the depth. If it is difficult to get an
image, ask the patient to take a breath in. This drops the diaphragm
and often brings the heart into view. Once you have found the heart
optimize the image with gentle movements of the probe.
Optimal image will look like a four chamber view but from the side.
Both ventricles and both atria should be seen with the atrial and
ventricular septa aligned horizontally across the screen. Both mitral
and aortic valves should be evident.
The probe can also be rotated 90º in this view to create a short axis
subcostal view. By tilting back and forward this can be used to look at
left and right ventricle and pulmonary valve.
What to record?
2D images.
Colour flow mapping: tricuspid valve and septa (atrial and ventricular).
What do you see?
Right ventricle: close to probe and both free wall and septum are seen.
Wall thickness can be measured. The septum is flat across the screen
so good alignment for colour flow mapping of septal defects.
Right atrium: good view to look at right ventricle inflow as close
to probe. May see Eustachian valve and entry of inferior vena cava.
Because of horizontal alignment of interatrial septum an ideal view for
colour flow mapping of atrial septal defects and Doppler alignment to
quantify flow across defects.
Tricuspid valve: close to probe and can be used for colour flow
mapping of regurgitation.
Pericardium: excellent view to assess size and depth of effusion when
planning pericardiocentesis as probe in position of a subxiphisternum
approach.
Left ventricle: in far field. Septum and lateral wall are seen.
Mitral valve: in far field and little extra information provided.
Left atrium: little extra information provided about left atrium.
SUBCOSTAL VIEWS
89
RA
IVC inflow
RV
RA
LV
LA
Fig. 2.18 Subcostal view. See W Video 2.18.
90
CHAPTER 2 Transthoracic examination
Inferior vena cava view
Essential to assess right atrial pressure (Fig. 2.19).
Finding the view
From the subcostal view rotate the probe anti-clockwise.
Keep the right atrium in the centre of the image and focus on the
atrium as you rotate the probe. The opening of the inferior vena cava
should become more obvious. As you rotate the probe the vena cava
should open out into a long tubular structure horizontally across the
screen. If you are worried it may be the aorta, not the vena cava, use
pulsed wave Doppler to demonstrate continuous, low velocity venous
flow rather than pulsatile, high velocity aortic flow.
Optimal image is of the vena cava like a railway track across the screen
perhaps seen opening into right atrium. Hepatic veins emptying into
vena cava may also be seen.
What to record?
2D images with inspiration and expiration (a 5-beat loop may be
required).
M-mode measures with respiration.
Consider pulsed wave Doppler in aligned hepatic veins.
What do you see?
Inferior vena cava: use to measure diameter and whether it reduces in
size with inspiration (normally should do).
Liver and hepatic veins: these can be seen draining into the vena cava
and may be aligned for Doppler measures. If right atrial pressures are
high they may be dilated.
Abdominal aorta view
Not an essential view but interesting (Fig. 2.19)! A simple screening test
for aortic aneurysm.
Finding the view
From the subcostal inferior vena cava view tilt the probe out of the
plane of the inferior vena cava. The aorta should come into view and
look very similar to the vena cava. It usually lies to the left of the vena
cava and slightly deeper. Confirm it is aorta with PW Doppler to
demonstrate arterial flow.
Optimal image is of the aorta like a ‘railway track’ across the screen.
What to record?
2D images.
What do you see?
Aorta: may see wall thickening, aneurysm or even gross mobile
thrombus and plaque.
ABDOMINAL AORTA VIEW
91
RA
RV
IVC
AORTA
Aortic view
Inferior vena cava view
Hepatic
veins
Aorta
RA
IVC
Fig. 2.19 Subcostal abdominal aorta view (left) and inferior vena cava view (right).
See W Video 2.19.
92
CHAPTER 2 Transthoracic examination
Suprasternal view
A view to look at size of aorta and aortic flow for coarctation or aortic
regurgitation (Fig. 2.20).
Finding the view
In the suprasternal window have the probe pointing, slightly rotated,
into the chest behind the sternum. The dot on the probe should
be towards the left shoulder. Use light pressure (with extra gel to
maintain contact between probe and skin if necessary) as it can be
uncomfortable.
Tilt probe back and forward until the arch comes into view then rotate
to maximize the curve of the arch. Colour flow may help identify flow
in the aorta.
Optimal image has distal ascending aorta, arch, and proximal
descending aorta with origin of the left subclavian on the right, and
potentially origin of left carotid and brachiocephalic.
What to record?
2D images.
Doppler of flow in ascending and descending aorta.
Consider colour flow mapping around arch and subclavian artery
(looking for jets associated with patent ductus arteriosus, coarctation
or obstruction).
What do you see?
Aortic arch: curves through picture and can be measured.
Ascending aorta: can be difficult to see clearly but can provide
alignment for CW Doppler measures in aortic stenosis.
Descending aorta: usually better seen than ascending aorta. Size can
be measured and is aligned for Doppler studies of aortic flow to grade
aortic regurgitation or coarctations.
Left subclavian artery: easiest branch to see and important landmark
for isthmus (common site of dissection and coarctation).
SUPRASTERNAL VIEW
93
RA
Brachiocephalic
Left carotid
Ascending aorta
Left subclavian
Descending aorta
Pulmonary
artery
Fig. 2.20 Suprasternal view. See W Video 2.20.
94
CHAPTER 2 Transthoracic examination
Right parasternal view
An extra view to look at ascending aorta and judge severity of aortic
stenosis but can be difficult to find (Fig. 2.21).
Finding the view
Roll patient over onto right side. Place probe on right side of sternum
pointing down and under sternum (both stand alone and 2D probes
can be used).
Adjust probe in all directions looking for Doppler across aortic valve
and up ascending aorta. If using stand alone Doppler probe look for
the aortic spectral pattern and if using a 2D probe use colour flow
mapping to identify ascending aorta. Once a signal has been found
keep adjusting probe position until maximal Doppler signal.
Optimal image has ascending aortic flow aligned with probe.
What to record?
2D images with colour flow to demonstrate aorta.
CW Doppler of flow through aortic valve.
What do you see?
Ascending aorta: often little to see but can be very useful for a second
measure of an aortic gradient if there is concern that it is being
underestimated. The alignment of flow through the aortic valve for
Doppler measures is often better in the right parasternal view than the
apical or suprasternal views.
RIGHT PARASTERNAL VIEW
95
ECG
Colour flow in
ascending aorta
Continuous wave Doppler
Continuous wave
Doppler of flow
across aortic valve
Fig. 2.21 Right parasternal view. Used to measure flow across aortic valve and in
ascending aorta.
96
CHAPTER 2 Transthoracic examination
Standard examination
The minimal sequence of views and measurements needed to perform
a study can be standardized to ensure collection of a minimal dataset.
Minimal datasets are published by bodies of experts as a guide to what
information should be collected.
A graphic description of a standard examination in the order of data col-
lection is given in Figs. 2.22–2.29.
Quality of echocardiographic recordings
The quality of echocardiographic recordings is based on:
Is the dataset complete i.e. a full standard examination and minimal
dataset?
Are all the recordings obtained from the appropriate imaging points,
i.e. correct apical position etc.?
Is image quality good, i.e. are the views appropriately recorded,
correct gain and depth, etc.?
Image quality
2D/3D imaging is best judged on endocardial border definition. Look at
the proportion of the border that is clearly seen in the 3 apical views.
Judge image quality as:
Good if >80% of the border is seen in the 3 apical views.
Poor if the endocardium is not visible.
Image quality is moderate if endocardial border is visible but <80%.
For stress echocardiography good image quality is required and
there should be a maximum of 2 segments not seen in any view.
Spectral Doppler should be judged as:
Good if the cursor position is displayed, there is good alignment
(with the angle between flow and beam <30º) and the spectrum has
a clear envelope.
Poor if the angle between flow and beam is >30º or the spectrum is
incomplete.
Only good spectral Doppler tracing should be used for quantitative
analysis.
Colour flow mapping should be judged as:
Good if the flow of interest is aligned with the probe and gain
settings are correct (just below the level that produces background
noise). If for flow convergence, the baseline has been shifted.
Poor if the flow is not aligned or gain settings are incorrect.
For assessment of regurgitation colour flow mapping must be good.
When used to align spectral Doppler then suboptimal settings may be
sufficient.
STANDARD EXAMINATION
97
Parasternal long axis view
2D IMAGE
Can be used for measurements
Acquire right ventricle
inflow and outflow views if required
RV
LV
LA
COLOUR FLOW
1. Aortic valve
2. Mitral valve
RV
LV
M-MODE
1. Aortic root and left atrium
2. Mitral valve movement (trace not shown)
3. Left ventricle size
Measurements are edge to edge
RV
LV
LA
1
3
2
End-systolic
Sinus of valsalva (aortic root) at end diastole
diameter
RV
IVS
aortic
LV
root
PW
LA
End-diastolic
diameter
Left atrial diameter at end systole
Fig. 2.22 Summary of parasternal long axis view.
98
CHAPTER 2 Transthoracic examination
Parasternal short axis view—ventricle and mitral valve
2D IMAGE
Assess LV function and regional abnormalities
Assess RV
Can be used for M-mode or 2D measures of LV size and function
Anterior
Septum
LV
Lateral
Inferior
2D IMAGE
Assess mitral valve morphology
Consider colour flow across mitral valve and planimetry
A3
A2
A1
P3
P2
P1
Fig. 2.23 Summary of parasternal short axis view.
STANDARD EXAMINATION
99
Parasternal short axis view—aortic valve level
2D IMAGE
Assess tricuspid, aortic, and pulmonary valve morphology
Can measure right ventricle size
RV
RA
LA
Pulmonary
artery
COLOUR FLOW
Assess tricuspid, aortic, and pulmonary valve
Can assess atrial septum
RV
Pulmonary
artery
DOPPLER
Use continuous wave to assess pulmonary regurgitation and stenosis
Pulsed wave Doppler can measure right ventricle outflow
Continuous wave can be used at tricuspid valve to assess regurgitation
RV
RA
LA
Pulmonary
regurgitation
Pulmonary valve
velocity
Fig. 2.24 Summary of short axis view—aortic valve level.
100
CHAPTER 2 Transthoracic examination
Apical views—four chamber
2D IMAGE
Assess LV size, thickness, function, and regional wall motion
Assess RV size and function
Look at mitral and tricuspid morphology
LV
RV
RA
LA
COLOUR FLOW
Assess mitral and tricuspid valves
LV
RV
RA
LA
Fig. 2.25 Summary of apical four chamber view.
STANDARD EXAMINATION
101
Apical views—four chamber: Doppler
DOPPLER-MITRAL VALVE
Use PW at mitral valve tips to assess left ventricle inflow
Use CW across valve to assess mitral regurgitation
LV
LV
RV
RV
RA
LA
RA
LA
E and A waves of inflow
Mitral
regurgitation
DOPPLER-TRICUSPID VALVE
Assess tricuspid regurgitation with CW across valve to
estimate right ventricle pressure
LV
RV
RA
LA
Tricuspid regurgitation
velocity
Fig. 2.26 Summary of apical four chamber view—Doppler.
102
CHAPTER 2 Transthoracic examination
Apical views—five chamber
2D IMAGE
Identify left ventricle outflow
RV
LV
RA
LA
COLOUR FLOW
Assess aortic regurgitation
LV
RV
RA
LA
DOPPLER—AORTIC VALVE
Use PW to measure LVOT velocity
Use CW to measure velocity across valve and assess regurgitation
LV
LV
RV
RV
RA
RA
LA
LA
Aortic
regurgitation
LVOT velocity
Aortic
velocity
Fig. 2.27 Summary of apical five chamber view.
STANDARD EXAMINATION
103
Apical views—two and three chamber
2D IMAGE
Assess LV function and regional abnormalities
Assess mitral valve morphology
LV
LA
Left atrial
appendage
2D IMAGE
Assess LV function and regional abnormalities
Assess mitral and aortic valve morphology
Can use Doppler at aortic and mitral valves
LV
RV
LA
Fig. 2.28 Summary of apical two chamber view.
104
CHAPTER 2 Transthoracic examination
Subcostal and suprasternal views
2D IMAGE
Assess right heart and look for pericardial effusion
RA
RV
LA
LV
COLOUR FLOW
2D and M-MODE -INFERIOR VENA CAVA
Assess atrial and ventricular
Assess right atrial pressure from IVC series with
septum
respiration
RV
IVC
RA
LV
M-mode cursor
2D IMAGE and DOPPLER
Assess aorta
Use Doppler in descending aorta to
assess aortic regurgitation
AORTIC ARCH
ASCENDING
AORTA
DESCENDING
AORTA
Fig. 2.29 Summary of subcostal and suprasternal views.
105
Chapter 3
Transthoracic anatomy
and pathology: valves
Mitral valve
106
Mitral stenosis
110
Mitral regurgitation
116
PISA (proximal isovelocity surface area) 126
Mitral valve prolapse
128
Aortic valve
132
Aortic stenosis
134
Aortic regurgitation
142
Bicuspid and quadricuspid valves 152
Lambl’s excresences 152
Tricuspid valve
154
Tricuspid regurgitation
156
Right heart haemodynamics 162
Tricuspid stenosis
164
Tricuspid valve surgery
166
Carcinoid syndrome 166
Infective endocarditis
166
Ebstein anomaly 166
Pulmonary valve 168
Pulmonary regurgitation 170
Pulmonary stenosis 174
Mechanical prosthetic valves 176
Bioprosthetic valves
180
Prosthetic valve abnormalities
182
Prosthestic valve stenosis
184
Prosthetic valve regurgitation
186
Endocarditis 188
106
CHAPTER 3 Transthoracic valves
Mitral valve
Normal anatomy
The mitral valve has two leaflets (anterior and posterior). The posterior
is long and thin, and forms a crescent around the wider anterior leaflet.
The surface area of both leaflets is approximately equal but the distance
between mitral ring and coaption line is shorter on the posterior leaflet.
Each leaflet has 3 scallops which meet each other along the coaption line.
They are named: A1, A2, A3 (anterior) and P1, P2, P3 (posterior). P1 and
A1 are adjacent to the anterolateral commissure and A3 and P3 nearest
the right heart. Below the valve are two papillary muscles: a larger ante-
rolateral (usually a single trunk) and a smaller posteromedial (often 2-3
distinct trunks). These support chordae tendinae: 1st order attached to
leaflet tips, 2nd order to undersurface of leaflets, and 3rd order run directly
from ventricular wall to leaflet undersurface. Chordae from both papillary
muscle attach to both leaflets. The valve leaflets are supported by the
mitral valve annulus, which divides the left atrium and ventricle, and is a
fibrous elliptical structure.
Normal findings
2D views
The mitral valve can be seen in most views (Fig. 3.1). Parasternal long
axis and parasternal short axis (mitral valve level) are particularly
useful to look at valve motion and structure.
The 3 apical views offer the ability to scan through the mitral valve in
multiple planes and do Doppler measurements.
2D findings
Parasternal long axis: segments of the anterior leaflet (A2—nearest
the left ventricular outflow tract) and posterior leaflet (P2) are seen
as thin structures uniform in echogenicity. The posteromedial papillary
muscle may be seen attached to the posterior wall.
Parasternal short axis: at the mitral valve level, all three segments of
each leaflet are seen and the 2 commissures. This creates the classic
‘fish mouth’ appearance. At the mid level of the left ventricle the
bodies of the two papillary muscles can be seen.
Apical 4-chamber view: the A2 and A1 segments of the anterior leaflet
are shown on the left and the P1 segment of the posterior leaflet on
the right. The mitral valve annulus is usually slightly out of line with the
tricuspid valve annulus (the tricuspid annulus is normally up to 1cm
closer to the right ventricular apex).
Apical 2-chamber view: the P1 and P3 segments are seen either side of
the A2 segment of the anterior mitral valve leaflet.
Apical 3-chamber view: the A2 and P2 segments are visualized similar
to the parasternal long axis view.
MITRAL VALVE
107
Anterolateral
papillary muscle
RV
LV
A2
LV
P2
Posteromedial
papillary muscle
Parasternal long axis
Parasternal short axis
Anterolateral
commissure
RV
LV
RV
Posteromedial
A2 A1 P1
commissure
RA
LA
Parasternal short axis
Apical 4 chamber
LV
LV
RV
P1
A2
P3
P2
A2
Apical 2 chamber
Apical 3 chamber
Fig. 3.1 Standard echocardiography views of mitral valve.
108
CHAPTER 3 Transthoracic valves
3D views
Real-time 3D transthoracic imaging is now available and is an excellent
tool in assessment of the mitral valve. Biplane 2D live images are
optimized to ensure accurate probe position to assess the lesion in
question before full volume acquisition.
The parasternal long axis, parasternal short axis basal ventricular level
and apical 4-chamber views are the most suitable for imaging the mitral
valve in 3D.
All the 3D acquisitions modes (b p.34) can be used: full volume
datasets/live 3D imaging (Fig. 3.2)/live 3D zoom and 3D colour
Doppler imaging.
3D echocardiography findings are enhanced by rotation and cropping
of the 3D volume either after acquisition or during live monitoring.
This rotation allows the mitral valve to be viewed from multiple
angles and allows for the generation of specialized views such as the
‘surgeons view’. i.e. a view of the mitral valve from the left atrium with
the left atrial appendage on the left and the aorta at the top of the
image.
3D findings
Use the surgeon’s view to assess all 3 scallops of the anterior and
posterior leaflets.
3D mitral valve reconstruction and post-processing also allows the
unique shaped curvature of the mitral valve to be modelled for precise
measures of annulus size, extent of prolapse, etc.
MITRAL VALVE
109
AO
AMVL
PMVL
Fig. 3.2 Live 3D acquisition of mitral valve. Subsequent rotation and cropping to allow
visualization of the valve from the LV apex. AMVL = anterior mitral valve leaflet;
PMVL = posterior mitral valve leaflet and aorta (AO). See W Video 3.1.
110
CHAPTER 3 Transthoracic valves
Mitral stenosis
General
The commonest cause of mitral stenosis is still rheumatic disease. Systemic
lupus erythematosus is a rare cause and congenital mitral stenosis is very
rare. Clinically, atrial myxoma and cor triatriatum may mimic mitral ste-
nosis. Mitral annular calcification is common in the elderly and can involve
the entire posterior part of the annulus. Occasionally annular calcification
can extend to the base of the leaflets leading to stenosis but more com-
monly leads to regurgitation.
Assessment
Echocardiography should be used to diagnose stenosis and describe
probable aetiology based on appearance.
Severity should be graded according to: valve area; pressure gradient
across the valve; changes to left atrium, left ventricle, and right heart.
The examination should also be used to look for associated valvular
lesions (in particular rheumatic aortic disease) and complications such
as endocarditis.
Appearance
Comment on the valve:
Mobility of base of leaflet compared to tips. In rheumatic disease the
tips tend to be restricted so the valve appears to ‘dome’. This may also
be referred to as a ‘hockey stick’ or’elbowing’ appearance (Fig. 3.3).
Thickening or calcification of leaflets, annulus and subvalvular apparatus.
Evidence of fusion of the commissures. Use a short axis view.
Chordae—thickening, shortening, calcification.
Comment on associated features:
Associated valvular lesions (aortic rheumatic disease).
Left atrium:
• Usually grossly enlarged. Give measurement.
• Spontaneous left atrial contrast (associated with significant stenosis
and suggests very slow atrial blood flow or stasis).
Right heart:
• Tricuspid regurgitation and right ventricular pressure.
• Right ventricle and atrial size.
Left ventricular function.
Differentiation of rheumatic mitral stenosis from
calcification
In rheumatic disease (in contrast to degenerative mitral valve disease):
Thickening comes first with calcification later.
Leaflet thickening affects the commissures and leaflet edges whereas
mitral annular calcification tends to spare the leaflet tips.
There is subvalvular involvement with shortening of chordae.
Combination of loss of leaflet mobility due to commissural fusion
and chordal shortening and tethering leads to ‘doming’ or ’hockey-
stick’ appearance of, in particular, the anterior leaflet.
MITRAL STENOSIS
111
Calcified, elbowing mitral leaflets
LV
RV
RA
LA
Enlarged right heart
Grossly dilated left atrium
Fig. 3.3 Apical 4-chamber view demonstrating rheumatic mitral stenosis with
doming, calcified valve. The left atrium is grossly dilated. See W Video 3.2.
112
CHAPTER 3 Transthoracic valves
Grading of mitral stenosis
Grade stenosis as mild, moderate, or severe based on valve area
(Table 3.1). Use planimetered measurements and pressure half-time
across the valve. Also, report the actual measures.
Back this up with assessment of pressure gradient across the valve.
Comment on associated changes that support your assessment.
Include changes to the left atrium and right-sided pressures.
Planimetry: 2D
In parasternal short axis view, angle the probe to the mitral valve level.
Move the probe back and forth until you are sure you are at the
level of the leaflet tips. If the plane is too basal, stenosis will be
underestimated.
Record a loop and scroll through to find the maximum opening in
diastole (Fig. 3.4).
Trace along the inner edge of the leaflets. This may be difficult in
heavily calcified valves so comment if there is a lot of calcification.
Report the surface area of the orifice.
3D in assessment of mitral stenosis
3D transthoracic echocardiography (Fig. 3.5) is more accurate, quicker
and reproducible than 2D for planimetered measures because it is easier
to be confident you have the smallest area. To planimeter mitral valve
area in 3D:
Optimize a 3D view from the parasternal short axis mitral valve
level. Using this view reduces distance between probe and valve, so
will improve resolution.
Ensure the volume includes the ‘mouth’ of the mitral valve to ensure
planimetry of the stenosis is possible.
Acquire a volume dataset and then use postprocessing software
such as QLAB (Philips) to identify the 2D plane that cuts through the
mitral leaflet tips. Then trace around the inner edge of the leaflets as
for 2D imaging.
Report the surface area of the orifice.
Problems with planimetry
Planimetered mitral area methods are useful as they are not affected
by haemodynamic changes but can overestimate size if the tips of the
leaflets are not identified.
It is important when estimating the planimetered area that the
optimal plane is used to ensure that the smallest area from the
leaflets free edge is traced.
MITRAL STENOSIS
113
Planimetered orifice
Fig. 3.4 2D planimetered mitral valve orifice in parasternal short axis.
Fig. 3.5 Full volume acquisition of mitral valve taken from apical 4-chamber view.
Subsequent rotation and cropping to view this valve of a patient with mitral stenosis
from the atrial side. Image shown at end diastole. See W Video 3.3.
114
CHAPTER 3 Transthoracic valves
Pressure half-time
In the apical 4-chamber view get a good view of the mitral valve.
Align continuous wave Doppler with the inflow jet through the
stenosis. Try and minimize any angle between the beam and the jet.
Record a spectral trace and measure the slope of the diastolic flow
across the valve (Fig. 3.6).
Use the E-wave if both E-wave (diastolic filling) and A-wave
(atrial systole) are present (often there is no A-wave because the
patient is in atrial fibrillation). If the trace is slightly curved with a
steep start (a ’ski-slope’). Ignore the start and use the flatter portion.
The machine automatically reports pressure half-time and mitral valve
area. The relation between these measures is simple:
2
Mitral valve area in cm
220/pressure half-time
in ms
Mean transmitral valve diastolic pressure gradient
Use the same technique/recording as used for pressure half-time.
Trace the Doppler profile of the transmitral diastolic flow. The
machine automatically reports the mean pressure gradient.
Pressure gradient varies significantly with the filling time. If the patient
is in atrial fibrillation this will vary so report the mean of 2-3 beats.
Problems with pressure half-time and pressure gradient
Quantification based on pressure half-time assumes normal left
ventricle pathophysiology. Significant changes in left ventricular
compliance (e.g. left ventricular hypertrophy) or pathology that
increases left ventricular pressure during diastole (e.g. aortic
regurgitation) shorten the pressure half time. Valve area is
overestimated.
Normal atrial pathophysiology is also assumed. An atrial septal
defect with left-to-right shunt shortens the pressure half time
(as blood also leaves from left to right atrium) and valve area is
overestimated. Conversely a right-to-left shunt will lengthen the
pressure half time.
MITRAL STENOSIS
115
E
A
P1/2 time—Measure slope
Mean pressure gradient : Trace
of E wave, ignore A wave
Doppler of mitral inflow
Fig. 3.6 Pressure half-time and mean pressure gradient.
Table 3.1 Parameters to determine severity of mitral stenosis
Mild
Moderate Severe
MV area (cm2)
2.2-1.5
1.5-1.0
<1.0
MV pressure half-time (ms)
100-150
150-220
>220
Mean pressure gradient (mmHg)
<5
Variable
>10
Tricuspid regurgitant velocity (m/s)
<2.7
Variable
>3
Pulmonary artery pressure (mmHg)
<30
Variable
>50
116
CHAPTER 3 Transthoracic valves
Mitral regurgitation
General
Mitral regurgitation is common. A trace of ‘physiological’ mitral regur-
gitation is seen in up to 50% of people with normal cardiac anatomy.
Pathological mitral regurgitation can be caused by changes in the leaflets
(e.g. endocarditis, myxomatous change), subvalvular apparatus (e.g. papil-
lary muscle rupture) or mitral annulus (e.g. left ventricular dilatation).
Assessment
Mitral regurgitation is easily identified with colour flow placed over the
mitral valve and left atrium in parasternal long axis and apical views.
Once identified a wider study of the appearance of the valve,
subvalvular apparatus, and left ventricle should be used to determine
aetiology and impact on cardiac function.
Severity should be judged by combining measurements from all main
Doppler modalities (colour flow, continuous and pulsed wave) and 2D
echocardiography.
Appearance
Map the regurgitant jet with colour flow in parasternal and apical views
(Fig. 3.7). Establish the shape and pattern. Comment on:
• Where the regurgitation passes through the valve, e.g. central, by a
commissure, or through a perforation.
• The direction of eccentric jets (anterior or posterior). Anteriorly-
directed suggests a posterior leaflet problem and posteriorly-
directed suggests an anterior leaflet problem. Note which left atrial
wall the jet entrains against and how far back it goes.
• If there are several jets, comment on each one.
• Spectral Doppler and colour M-mode can define the timing of
regurgitation e.g. confined to a short period after valve closure
(closing volume) or to late systole (often found in mitral valve
prolapse).
In parasternal and apical views use M-mode and 2D to look at both
valve leaflets. Comment on:
• Movement, evidence of prolapse, calcification, masses, vegetations.
Look at subvalvular apparatus. Comment on:
• Papillary muscle and chordae with reference to shortening, rupture.
Report associated features:
• Left atrial size, left ventricular size and function—important when
considering surgery, any changes to right heart and right ventricular
systolic pressure.
MITRAL REGURGITATION
117
Physiological, mild, or trace (trivial) regurgitation
It is reasonable to decide mitral regurgitation is mild if:
Jet is small (jet area <4 cm2 or <20% left atrial area) and central.
No flow convergence zone is displayed.
Trace regurgitation is a qualitative description that implies ‘not as
severe as mild.’
To call mitral regurgitation physiological make sure:
Valve morphology is normal.
The regurgitation has a short duration (typically post valve closure).
It is mild or trivial.
LV
RV
RA
LA
APICAL FOUR CHAMBER
Anteriorly directed mild
mitral regurgitation
LV
RV
LA
RA
APICAL FOUR CHAMBER
Posteriorly directed moderate
mitral regurgitation
RV
LV
LA
Severe central mitral regurgitation
PARASTERNAL LONG AXIS
Fig. 3.7 Colour flow mapping of mitral regurgitation with eccentric and central jets.
See W Video 3.4, W Video 3.5, W Video 3.6.
118
CHAPTER 3 Transthoracic valves
Grading severity
Gauge severity as mild, moderate or severe based on the combination
of jet area, vena contracta, flow convergence (PISA) and changes in
systolic pulmonary vein flow (if technically possible) (Table 3.2).
Gross pathology, e.g. a flail leaflet, points to severe regurgitation.
Once you have an impression of severity use CW Doppler waveform
density, changes in left ventricular mitral inflow, and left ventricular
function to support your assessment.
You can provide further quantification of regurgitation with
measurement of effective regurgitant orifice area (EROA), regurgitant
volume, and regurgitant fraction.
Colour Doppler jet area
Establish an apical image that includes the whole left atrium.
Using colour flow mapping, optimize the image to include the whole
regurgitant jet. Set Nyquist limit at 50-60cm/s.
Record a loop and scroll through to reach the frame with the
maximum jet size.
Trace the regurgitant jet. Trace the border of the left atrium (Fig. 3.8).
If there are multiple jets add the separate jet areas together.
Report the absolute size of the jet and the size relative to the size of
the left atrium (percentage).
Grade the severity but bear in mind:
• If the jet area relative to left atrium suggests the regurgitation is
mild or moderate but the left atrium is very large (>70mm2) then
grade it as moderate or severe respectively.
• If the jet area suggests the regurgitation is severe but the
regurgitation is not pansystolic then overall regurgitation may be
moderate.
Problems with jet area to gauge severity
Correlation between jet area and severity of mitral regurgitation is poor
and the measurement should be used only in combination with the
other methods. This is because:
The regurgitant jet area includes turbulent (aliased) flow signals
as well as laminar velocities in the same direction as the mitral
regurgitation jet. Movement of blood already in the left atrium that
moves with the regurgitant jet (entrainment) is therefore included.
Jet area can be artificially changed. Reducing the scale increases
the area because the lower filter setting means lower velocities
are displayed. Try and use average scale settings (50-60 cm/s) and
ensure the same setting on follow up scans.
Eccentric jets are underestimated as they flatten out against walls
and go out of plane.
MITRAL REGURGITATION
119
Table 3.2 Assessment of severity of mitral regurgitation
Specific signs of severity
Mild
Severe
Jet
<4cm2 or <20% left
40% or 10cm2
(Nyquist 50-60cm/s)
atrium; small & central large & central or wall
impinging and swirling
Vena contracta
<0.3cm
>0.7cm
PISA r (Nyquist
None/minimal
Large (>1cm)
40cm/s)
(<0.4cm)
Pulmonary vein flow
-
Systolic reversal
Valve structure
-
Flail or rupture
Supportive signs of severity
Mild
Severe
Pulmonary vein flow
Systolic dominant
Mitral inflow
A-wave dominant
E-wave dominant (>1.2 m/s)
CW trace
Soft & parabolic
Dense & triangular
LV and LA
Normal size LV if
Enlarged LV & LA if no
chronic MR
other cause
Report as moderate if signs of regurgitation are greater than mild but there are no features
of severe regurgitation.
Jet area
Left atrium area
Fig. 3.8 Colour jet area and area of left atrium as marker of severity.
120
CHAPTER 3 Transthoracic valves
Vena contracta
Obtain a clear view of the colour flow through the mitral valve in
parasternal long axis or apical 4-chamber views.
If necessary, scan along the commissural line to ensure you have the
point of regurgitation through the valve.
Zoom in on the colour flow through the mitral valve.
Record a loop and scroll through to identify the image with maximal
flow through the valve.
The vena contracta is the narrowest region of the regurgitant jet
(usually just below the valve in the left atrium).
Report the diameter. >0.7cm suggests severe regurgitation.
A parasternal short axis view just below the mitral valve level can be
used and cross-sectional area of the regurgitant jet recorded. The
cross sectional area is one way of measuring the EROA.
Problems with vena contracta as marker of severity
This method is simple and thought to be independent of haemodynam-
ics, driving pressure, and flow rate. However, low colour gain, poor
acoustic windows, or failure to assess multiple jets can underestimate
the vena contracta. A high colour gain, irregular shape of jet, or atrial
fibrillation can lead to overestimation.
Flow convergence (PISA—proximal isovelocity surface area) (see b p.126)
Pulmonary venous flow
Normally blood flows from the pulmonary veins throughout the cardiac
cycle. As mitral regurgitation becomes more severe left atrial pressure
increases more rapidly during systole and reduces the amount of blood
that can flow from the pulmonary vein (blunted systolic pulmonary vein
flow). With severe regurgitation atrial pressures are high and blood starts
to be forced back into the veins (reversed systolic pulmonary flow).
Obtain an apical 4-chamber view with enough depth to see the back of
the left atrium.
Try to identify the pulmonary vein orifices on the back of the left
atrium. With transthoracic echocardiography, often only the right
upper pulmonary vein (by the atrial septum) is seen and can be aligned.
Place the PW sample volume 71cm into the ostium of the vein
(Fig. 3.9).
A good spectral tracing confirms you are in the right place.
Look at the systolic and diastolic components.
• If they are in opposite directions with the systolic component going
away from the probe report reversed systolic flow.
• If in the same direction, measure the height of the two waves and
comment if the systolic wave is blunted relative to diastolic or the
relation is normal (systolic slightly larger—systolic dominant).
MITRAL REGURGITATION
121
Problems with pulmonary venous flow
Any pathology that increases left atrial pressure can blunt pulmonary
vein flow. If systolic flow reversal is present then this is very specific but
not very sensitive for severe regurgitation.
RV
LV
LA
Vena contracta
S
D
A
Normal
D
S
A
APICAL FOUR CHAMBER
Systolic flow reversal
LV
PW placed in pulmonary
RA
vein close to atrial septum
LA
Fig. 3.9 Measuring pulmonary vein flow.
122
CHAPTER 3 Transthoracic valves
Supportive measures
Mitral inflow
As regurgitation becomes more severe the amount of blood forced into
the left atrium during systole increases. This increased volume of blood
increases left atrial pressure. Therefore, blood leaves the atrium more
quickly at the start of diastole i.e. peak early diastolic velocity increases.
In an apical 4-chamber view place the PW Doppler cursor at the mitral
valve tips.
E wave >1.2m/s is indicative of severe mitral regurgitation (Fig. 3.10).
However, a hyperdynamic circulation or even minor degrees of mitral
stenosis can also increase E wave amplitude. If the A wave is dominant,
severe mitral regurgitation is virtually ruled out.
Continuous wave Doppler intensity/shape
In an apical 4-chamber view place the CW Doppler through the mitral
valve orifice and record a spectral trace (Fig. 3.11).
Make a qualitative judgement about the density of the systolic regurgitant
waveform relative to the mitral inflow density. If they are the same this
suggests there is as much blood flow into the atrium during systole as
back into the ventricle during diastole and regurgitation is severe. (Peak
velocity allows calculation of regurgitant orifice area (b p.126).)
Regurgitant volume/regurgitant fraction
The principle behind the regurgitant volume is that the amount of blood
that flows through the mitral valve into the left ventricle during diastole
(assuming there is no aortic regurgitation to fill the ventricle as well)
should equal the amount of blood that leaves the left ventricle during sys-
tole. The amount of blood leaving through the aortic valve in systole can
be calculated and subtracted from the amount flowing across the mitral
valve in diastole. The difference is the volume flowing back through the
incompetent mitral valve. Regurgitant volume is not usually calculated as
accuracy depends on accurate measures of the outflow tract and mitral
valve area. The mitral ring is difficult to assess because it is not circular and
changes throughout the cardiac cycle. To measure:
In apical 4-chamber view record PW at the mitral valve (it is controversial
whether the sample volume should be at annulus or valve tip level). Trace
the vti. Estimate mitral valve cross-sectional area (CSA). Use annulus
width and assume a circular orifice (alternatively measure the annulus in
two perpendicular planes and calculate area as an oval).
Mitral inflow volume = vti CSA mitral valve
In apical 5-chamber view record PW in left ventricular outflow and
measure vti. Measure outflow tract diameter in parasternal long axis
and estimate CSA (assuming it is circular).
Left ventrication outflow = vti CSA left ventricular outflow
Mitral regurgitant volume is:
Mitral inflow volume left ventricular outflow volume
Regurgitant fraction is: (<20% mild, >50% severe regurgitation)
Mitral regurgitant volume mitral inflow volume
MITRAL REGURGITATION
123
Maximum E-wave
velocity
E
A
Fig. 3.10 Pulsed wave Doppler trace of a patient with severe mitral regurgita-
tion. Maximum E-wave velocity >1.2 m/s indicating severe regurgitation. E = early
diastolic filling velocity; A = velocity during atrial contraction.
Compare density of
regurgitation to
forward flow
Fig. 3.11 Severe regurgitation is suggested if density of regurgitation is similar to
forward flow. Peak velocity can be used with PISA to calculate effective regurgitant
orifice area (b p.126).
124
CHAPTER 3 Transthoracic valves
3D in assessment of mitral regurgitation?
3D colour flow imaging may be useful for:
Qualitative assessment of regurgitant jet
3D colour flow mapping of mitral regurgitation allows the mitral
regurgitation to be assessed in all planes, proving useful in the
analysis of eccentric mitral regurgitation or visualization of multiple
jets (Fig. 3.12).
Quantitative assessment of regurgitant jet
3D can also be used to measure the same parameters that have been
measured by 2D. There is no unique, additional 3D parameter but 3D
can be particularly useful to ensure accuracy of measures. For example:
Estimation of the PISA value by the operator assumes that flow
acceleration is symmetrical towards the regurgitant orifice. This
geometric assumption is not always true and can be evaluated in 3D
as the entire flow convergence area can be displayed and viewed
from the left atrium. Thus 3D allows for a better judgement of the
likely accuracy of 2D PISA values. Theoretically, it would be possible
to measure the area in 3 dimensions to obtain a very accurate PISA.
3D echocardiography also allows the anatomic regurgitant orifice
area to be measured directly using planimetry of the regurgitant
orifice or regurgitant jet where it passes through the valve. This
has been shown to correlate well with the EROA calculated by the
proximal convergence method.
Remember that acquisition of 3D colour flow often requires more cycles
to be captured than for anatomical images. Therefore reconstruction
can be difficult as there may be problems with artefacts, especially with
atrial fibrillation. However, advancing technology is heading towards
clinically useful real-time 3D colour flow mapping.
Fig. 3.12 3D full volume colour Doppler acquisition of a patient with mitral regurgitation (MR). Images were initially acquired from the apical window. Left:
cropping towards the mitral valve (MV) leaflet tips to find the level of the vena contracta. Right: the vena contracta is then tilted to give an ‘en face’ view
allowing its measurement. LA = left atrium. See W Video 3.7 and W Video 3.8.
126
CHAPTER 3 Transthoracic valves
PISA (proximal isovelocity surface area)
PISA or flow convergence zone is a measurement of how much blood trav-
els through a valve. It has been applied in several situations (e.g. aortic
regurgitation, mitral stenosis) but is validated for assessment of mitral
regurgitation. If regurgitation is mild, only blood near the valve moves
towards the atrium. With severe regurgitation blood further away in the
ventricle moves backwards. An impression of how far this flow convergence
zone extends into the ventricle is obtained by looking at the velocity of
blood flow in the ventricle with colour flow mapping. To quantify the
distance you use the principle that at a certain velocity the colour flow
will alias (change colour). The further away this change in colour, the more
blood is being funnelled back through the mitral valve, and the more se-
vere the regurgitation. In 3D the aliasing layer is a coloured hemisphere
sitting on the mitral valve. The PISA refers to the surface area of the hemi-
sphere (Fig. 3.11) and correlates to the regurgitant flow.
Assessment
Get a good image of the mitral valve (usually the apical 4-chamber
view is best) and ensure you are in the plane of the regurgitant jet.
You
can use this velocity if the flow convergence is obvious but to optimize
the colour contrast at the boundary layer it is normal to shift the zero
of the baseline so that the aliasing velocity is 40cm/s.
Acquire a loop of the cardiac cycle and scroll through to identify the
mid-systolic hemisphere shell. (Fig. 3.13).
Measure the radius (r) from valve orifice to point of colour change.
If the colour flow is obscuring the valve orifice on your loop, place a
caliper at the aliasing zone then suppress the colour flow and position
the second cursor on the valve.
Report severity based on the parameters listed in b ‘Grading
severity’, p. 126.
Grading severity
Radius (r):
A simple approach is just to record r with the aliasing velocity set at 40cm/s.
Severe mitral regurgitation is present if r >1cm and mild if <0.4cm.
Regurgitant flow:
and has been validated
against angiographic grades of regurgitation. Clinically it is normally used
with the continuous wave Doppler velocity to measure orifice area.
Effective regurgitant orifice area:
Regurgitant flow can be combined with the peak continuous wave velocity
(b p.122) to calculate effective regurgitant orifice area (EROA).
regurgitant flow
EROA
peak velocity on CW
0-20 mm2: mild; 20-40 mm2: moderate; >40 mm2: severe.
PISA
127
Aliasing velocity
r
r
Regurgitant flow = 2
r2
aliasing velocity
Fig. 3.13 Calculation of regurgitant flow in mitral regurgitation using the principle
of proximal isovelocity surface area. Note the zero baseline shift to get an aliasing
velocity of 40cm/s and measurement of radius from valve orifice to edge of aliasing
boundary.
128
CHAPTER 3 Transthoracic valves
Mitral valve prolapse
Early studies suggested a high prevalence of up to 20% for mitral valve
prolapse but revised criteria for diagnosis have lead to more conservative
estimates of around 2%. The key to the change is the differentiation of an
anatomically normal valve that bows more than normal from a thickened
valve, classically with myxomatous degeneration, that truly prolapses. This
is important because it is only the latter patients who have clinical com-
plications. Prolapse can be seen with M-mode but 2D is usually preferred
to identify the condition. 3D echocardiography allows detailed anatomical
assessment of all mitral valve scallops, the geometry of the mitral valve
annulus, and the anatomy of the subvalvular apparatus. Studies have shown
that when image quality is adequate, 3D transthoracic echocardiography
has a similar accuracy for identifying segmental prolapse as transoesopha-
geal 2D echocardiography.
Assessment
Study the valve in the parasternal long axis view.
Comment on leaflet thickening or abnormal appearance.
Report mitral valve prolapse if one or both leaflets entirely crosses
the plane of the mitral valve annulus back into the left atrium during
systole and the tip is >2mm into the left atrium. If the tip is within the
plane of the annulus and there is no more than trivial regurgitation
then this can be reported as bowing, without prolapse (Fig. 3.14).
The leaflet position relative to the valve plane is determined precisely
by drawing a line between each side of the annulus.
Comment on which leaflets (and scallops if possible) prolapse and
check if any part of the prolapsing leaflet is flail (see b p. 130).
Report any associated changes in the subvalvular apparatus (papillary
muscle or chordae rupture).
Report degree of regurgitation (remember anterior leaflet prolapse
will be related with posteriorly-directed regurgitation and vice versa).
3D in assessment of mitral prolapse?
3D echocardiography allows the mitral valve anatomy to be viewed from
multiple planes from different directions, thus increasing the operator’s
understanding of the mechanism of the mitral valve prolapse.
Obtain a 3D view from the parasternal rather than apical windows as
this improves imaging with the probe closer to the valve.
Rotate the image to obtain an en face or ‘surgeon’s view’ looking
from the left atrium.
Report prolapsed position and extent.
Use the reconstructed full volume dataset to demonstrate and
measure the maximal position of prolapse (Fig. 3.15).
Use 3D colour flow to confirm the direction, number and extent of
eccentric jets.
MITRAL VALVE PROLAPSE
129
LA
LV
NORMAL
Tip pointing
towards left
ventricle
BOWING
PROLAPSE
(tip >2mm behind line of
annulus)
Tip pointing
towards left
atrium
FLAIL
Fig. 3.14 Definitions of normal, prolapsing and flail.
Fig. 3.15 Left: 3D full volume dataset of mitral valve taken from the apical
window. Subsequent cropping and rotation to show an en face view of the valve
demonstrating P2 mitral valve leaflet prolapse. Right: 3D full volume colour
Doppler acquisition of mitral valve from the apical view. LA = left atrium; LV = left
ventricle; MR = mitral regurgitation. See W Video 3.9 and W Video 3.10.
130
CHAPTER 3 Transthoracic valves
Flail leaflets
Flail leaflets (Fig. 3.16) usually occur due to damage to the subvalvular appa-
ratus. This can be secondary to degeneration, destruction by endocarditis,
or ischaemia associated with myocardial infarction. The extent of the flail
can vary from just the leaflet tip (due to chordae failure) through to the
whole valve (usually papillary muscle rupture). The degree of flail associates
with the severity of the associated regurgitation. This can vary from mild to
severe and clinically from asymptomatic to haemodynamically unstable.
Report a flail leaflet/leaflet scallop/leaflet tip if part of the leaflet points
back into the left atrium in systole rather than towards the ventricle.
Comment on which leaflet is affected. If you can see, mention how
extensive and which scallop.
There will be regurgitation so report severity.
Assess both papillary muscles and the chordae to look for ruptures.
To look at the subvalvular apparatus use a combination of views—
parasternal long and short axis, all the apical views (2-chamber view
can be good to see both papillary muscles) and subcostal views.
Report related findings according to suspected clinical aetiology,
e.g. regional wall motion abnormalities and left ventricle function in
myocardial infarction, vegetations in endocarditis.
Transthoracic assessment for mitral valve repair
When assessing the echocardiographic suitability for mitral valve repair,
note:
Leaflet motion and structure
Record whether the leaflet motion appears normal, excessive due to
prolapse, or restricted.
The anatomy of each leaflet and its integrity should be noted.
Normal leaflet thickness is <5mm.
Annulus size
Accurate annulus size measurement should be performed and
documented.
Calcification
The presence and degree of calcification should be accurately
documented at the annulus, leaflets, and subvalvar apparatus.
Mitral regurgitation severity and mechanism
The MR jet direction, severity and mechanism should be reported.
If there is a question over the MR severity/mechanism or the quality of
transthoracic images obtained then TOE is indicated.
MITRAL VALVE PROLAPSE
131
Posterior leaflet prolapse behind line of annulus
LV
LA
Flail leaflet would point back into atrium
Fig. 3.16 Example of a prolapsing posterior mitral leaflet seen in a parasternal long
axis view with superimposed figure of a flail element. See W Video 3.11.
132
CHAPTER 3 Transthoracic valves
Aortic valve
Normal anatomy
The aortic valve has 3 cusps of similar size, which close to form a Y shape.
Each cusp tip has a small thickened nodule (nodule of Arantius). The cusp
edges usually overlap by 2-3mm and the lines where they meet are called
commissures. Closure of the cusps is referred to as coaption and opening
as excursion. Around each cusp are outpouchings of the aortic root called
the sinuses of Valsalva. The sinuses create a pool of blood above the valve
in diastole that improves blood flow down the coronaries and ensures a
tight seal. Cusps and associated sinuses are named according to the coro-
nary artery that originates from the sinus (right, left, and non). Above the
valves the bulging sinuses merge into the tubular ascending aorta at the
sinotubular junction. Below the valve is the left ventricular outflow tract made
up of the membranous interventricular septum, anterior mitral valve leaflet,
and anterior left ventricular wall.
Normal findings (Fig. 3.17)
2D views
The minimal views are: parasternal long axis, parasternal short axis
(aortic valve level), and apical 5-chamber.
Aortic valve velocities are also obtained from the right parasternal
view, which can be used for detailed assessment of aortic stenosis.
Apical 3-chamber and subcostal views can also be used.
Suprasternal view allows measurement of flow in the aorta for
assessment of aortic regurgitation.
2D findings
Aortic valve
Parasternal long axis: 2 cusps are seen (usually right coronary by
septum and non-coronary by mitral valve). The leaflets open to lie
parallel to the aorta and close to form 2 curved lines.
Parasternal short axis (aortic valve level): all 3 cusps are seen (left
cusp on the right, right cusp at the top, and non-coronary cusp on the
right). This is the classic Y-shape view. The left main coronary artery
may be seen and helps identify the left coronary cusp.
Apical 5- and 3-chamber: the valve is aligned for Doppler measures
and 2 cusps are seen (usually non-coronary cusp next to atrium and
right coronary cusp next to septum).
Sinuses of Valsalva and sinotubular junction
Parasternal long axis: the sinuses bulge to the right of the valve and the
sinotubular junction is the point where the ascending aorta starts.
Parasternal short axis (aortic valve level): sinuses surround each cusp.
Left ventricular outflow tract
Best seen in parasternal long axis. Formed by septum and anterior
mitral valve leaflet. Usually around 2cm wide and roughly circular.
AORTIC VALVE
133
Right coronary
cusp
RV
RV
LV
LA
RA
LA
Non-coronary
cusp
Left coronary
cusp
Parasternal long axis
Parasternal short axis
LV
RV
LV
RV
RA
LA
LA
Apical 5 chamber
Apical 3 chamber
Fig. 3.17 Key views to study the aortic valve.
3D views and findings
3D datasets are best obtained from the parasternal window and can
be used to assess valve pathology. Detailed evaluation can be limited
by image quality but can be very useful to perform measures of size.
134
CHAPTER 3 Transthoracic valves
Aortic stenosis
General
Aortic stenosis is common. Aortic valve thickening occurs in 25% of peo-
ple aged >65 and severe stenosis occurs in 3% aged >75. In the West, the
predominant cause is calcific degenerative disease. A bicuspid valve occurs
in 2% of the population. Rheumatic disease is now uncommon.
Assessment
The echocardiographic study is aimed at determining the appearance of
the valve, the grade of stenosis, the effect on the left ventricle, and the
presence of associated disease.
Appearance
Comment on:
Degree and distribution of thickening. The term aortic sclerosis
describes valve leaflet thickening (>2mm) without significant stenosis
(Vmax < 2.5m/s).
How many functional cusps (2 in a bicuspid valve, 3 in rheumatic or
calcific degenerative disease)? (Fig. 3.18)
Is the closure line central (calcific degenerative or rheumatic disease)
or eccentric (bicuspid valve)?
Motion: normal or reduced? Systolic bowing (bicuspid or rheumatic)?
Commissural fusion (rheumatic disease).
Associated rheumatic mitral stenosis suggests a rheumatic aetiology.
Grading severity
Grade stenosis from peak velocity across the valve, mean pressure gradient,
and effective orifice area (calculated from the continuity equation) (Table 3.3).
Sometimes further supportive measures can be used such as direct
planimetry of the aortic valve area using 2D or 3D.
Aortic peak velocity
In apical 5-chamber view (or 3-chamber) align the continuous wave
Doppler, from the apex, through the aortic valve into the aorta. Spend
some time looking for the maximum velocity. Always repeat this
measurement with the stand alone CW probe from the apex.
Record several beats and measure the peak velocity on the spectral
trace with the greatest velocity. This can be affected by the filling time
so ignore ectopic or post-ectopic beats and in atrial fibrillation average
2 or 3 beats. (Fig. 3.19).
Repeat the measurement in at least one other approach
(e.g. suprasternal or right parasternal) and report the maximum
velocity found from all measures.
AORTIC STENOSIS
135
Table 3.3 Parameters to assess severity of aortic stenosis
Mild
Moderate
Severe
Peak velocity (m/s)
2.5-2.9
3.0-4.0
>4.0
Peak gradient (mmHg)
<35
35-65
>65
Mean gradient (mmHg)
<20
20-40
>40
Valve area (cm2)
>1.5
1.0-1.5
<1.0
Thickened calcified
Left ventricular
aortic cusps
hypertrophy
RV
Aortic dilatation
LV
LA
Fig. 3.18 Parasternal long axis demonstrating calcified aortic valve.
See W Video 3.12.
136
CHAPTER 3 Transthoracic valves
Peak pressure gradient
The peak gradient is usually automatically calculated by the machine from
the peak velocity. The relation between the two is very simple (the simpli-
fied Bernouli equation).
2
gradient =
× peak velocity
The equation is less accurate if the peak velocity is <3.0m/s and the long
form of the Bernoulli equation can be used:
Peak gradient =
× (V V )
where v2 = peak aortic velocity and v1 = peak left ventricular outflow
tract velocity.
Mean pressure gradient
To obtain the mean pressure gradient trace the continuous wave spectral
trace of flow through the aortic valve (Fig. 3.19) and the machine will
automatically calculate the vti (velocity time integral) and mean pressure
gradient (mean pressure across the valve during systole).
Effective orifice area/valve area
The continuity equation is based on the principle that the volume of blood
that flows through the left ventricle outflow tract during 1sec must equal
the blood through the aortic valve during 1sec.
Obtain the continuous wave Doppler trace through the aortic valve
(Fig. 3.19) and record the peak velocity and vti(VALVE).
In an apical view, record PW Doppler in the left ventricle outflow
tract (LVOT). Trace the waveform and record peak velocity and
vti(LVOT). (Fig. 3.20).
In the parasternal long axis view zoom in on the LVOT and measure
the diameter. Record the maximum edge-to-edge diameter just below
the insertion of the aortic valve leaflets.
Calculate the CSA of the LVOT:
2
Area LVOT =
×(LVOT diameter
)
Put the figures into the rearranged continuity equation:
Valve area = Area LVOT × vti
vti
(LVOT
)
(VALVE)
The equation can be calculated with peak velocity substituted for vti.
137
Trace spectral for
mean pressure
gradient and vti
Fig. 3.19 Continuous wave in an apical view to measure velocities.
LVOT diameter
Aortic CW peak
or vti
LVOT PW peak
or vti
Area of LVOT = π x (LVOT diameter/2)2
Effective orifice area = area of LVOT x LVOT vti
aortic valve vti
(peak velocity can be substituted for vti)
Fig. 3.20 Two views and three measures are needed for continuity equation. Use
a parasternal long axis view to measure left ventricular outflow tract diameter
using zoom (top). In an apical 5-chamber view measure continuous wave Doppler
across the aortic valve (middle) and PW Doppler in the left ventricle outflow tract
(bottom).
138
CHAPTER 3 Transthoracic valves
3D in assessment of aortic stenosis?
Planimetry of the aortic valve area can be undertaken on 2D images
although this can be inaccurate. As with 3D transthoracic imaging of
mitral stenosis, a combination of live 3D and full volume acquisitions
has been employed to estimate aortic valve area by planimetry using
3D. Recent papers suggest assessment of aortic stenosis by planimetry
of transthoracic 3D images has good agreement with standard 2D tran-
soesophageal imaging. However, planimetry is limited due to limited
spatial resolution and to be accurate requires excellent image quality.
Valvular calcification related to the aortic stenosis can be problematic
as it causes drop-out artefacts distal to the probe. Sometimes, apical
windows (Fig. 3.21) may provide a more effective window as drop-out
from the calcification extends into the aorta rather than across the
posterior part of the valve. However, resolution may be reduced
because of the increased distance between probe and valve. If you want
to use 3D to support suspicions of severity gathered by 2D imaging then
do the following:
Obtain a 3D volume of the aortic valve, ideally from a parasternal
window as this is closest to the valve.
Use post-processing analysis software to align a 2D plane accurately
through the tips of the aortic valve.
Trace around the inner edge of the valve and calcifications and
report planimetered valve area.
Effect of other diseases on diagnosing and grading stenosis
Moderate or severe aortic regurgitation will increase transaortic
flow and may lead to overestimation of the grade of stenosis if using
gradient alone. The continuity equation remains valid and should be
used.
Left ventricular dysfunction can be associated with lower transaortic
and LVOT velocities and therefore underestimation of gradient. The
continuity equation remains valid and should be used.
A subaortic membrane or septal hypertrophy may occasionally be
mistaken for valvular stenosis. Use PW Doppler in different positions
in the LVOT to identify whether the blood starts to accelerate
below or at the level of the valve.
Examine the aorta for dilatation of the ascending aorta (commonly
associated with bicuspid aortic valve, but also with calcific
degenerative disease). If a bicuspid valve is suspected, use the
suprasternal window to look for associated aortic coarctation.
Pulmonary hypertension is common in severe aortic stenosis and
is associated with a high operative risk. Estimate pulmonary artery
pressure and assess the right ventricle.
AORTIC STENOSIS
139
Fig. 3.21 3D full volume apical 3D dataset obtained from an apical window.
Subsequent cropping and rotation reveals the aortic valve (AV) orifice and the right
(RCC), left (LCC), and non-coronary cusps of the aortic valve. Image seen at peak
systole. AMVL = anterior mitral valve leaflet; PMVL = posterior mitral valve leaflet.
See W Video 3.13.
140
CHAPTER 3 Transthoracic valves
Effect on the left ventricle
Left ventricular hypertrophy or concentric remodelling (relative wall thick-
ness >0.45 without hypertrophy (see b p.218) are usual in compensated
severe aortic stenosis. The left ventricle can also dilate if there is high wall
stress as a result of severe pressure load, excessive fibrosis, or another
cause of left ventricle dysfunction (e.g. myocardial infarction).
During assessment of aortic stenosis also report a full evaluation of the
left ventricle (for function, see b p.226 and for hypertrophy, see b
p.218).
A common dilemma in the relation between the left ventricle and aortic
stenosis is whether any left ventricular dysfunction is secondary to the
stenosis or another pathology (e.g. ischaemia). Also, an apparently small
gradient or a decline in gradient may be secondary to impaired left ventri-
cle function. The continuity equation remains accurate and should be used
to assess valve area.
If the mean gradient is <30mmHg (suggesting mild to moderate
stenosis) but the valve area calculated by the continuity equation
is <1.0cm2 (suggesting severe stenosis) then a dobutamine stress
echocardiogram can be considered to differentiate:
• End-stage severe aortic stenosis.
• Moderate aortic stenosis associated with left ventricle dysfunction
from another cause (e.g. myocardial infarction or myocarditis).
Dobutamine stress echocardiography
Give low-dose dobutamine intravenously (5 then 10, if necessary 20 mi-
crograms/kg/min in 5-min stages). Aim for a 10% increase in heart rate or
20% increase in LVOT or aortic valve vti (Fig. 3.22). If the patient also has
coronary artery disease, ischaemia may occur at very low levels of stress
in the presence of aortic stenosis.Therefore carefully monitor wall motion
and left ventricle size to look for evidence of ischaemia during the study
(see Chapter 10).
There are two things to look for during the study. The first is to deter-
mine whether severe aortic stenosis is present or not. The second is to
determine whether the impaired left ventricle is able to increase output
(ventricular reserve is present). This is important because the risk of
mortality following aortic valve replacement for severe aortic stenosis is
approximately 5% if contractile reserve is present and 35% if absent.
Severe aortic stenosis is defined by:
• Mean gradient >30 mmHg at any time during dobutamine stress.
• Valve area <1.2 cm2 throughout the infusion.
Ventricular reserve is present if there is:
• A rise in LVOT vti by >20% during the study.
AORTIC STENOSIS
141
REST
STRESS
Aortic velocity
increase on stress
Fig. 3.22 Stress echocardiography in a patient with aortic stenosis and impaired left
ventricle function. Velocities during stress are consistent with a mean gradient of
>30mmHg (severe aortic stenosis) and the increase in vti is >20%, suggesting
preserved ventricular contractile reserve.
142
CHAPTER 3 Transthoracic valves
Aortic regurgitation
General
Aortic regurgitation (AR) is usually seen easily with colour flow Doppler
imaging over the aortic valve, which has 95% sensitivity and 100% spe-
cificity. Traces of central regurgitation are seen more frequently with
increasing age (<1% below 40 years; 10-20% at 60 years; and in the major-
ity >80 years), but are not clinically significant.
Causes of AR are listed in Box 3.1; changes in either the aortic root or the
valve itself can be the underlying pathology.
Assessment
Use colour flow mapping to identify and describe any AR (Fig. 3.23). The
study should then look for probable aetiology, grade severity, and check
for associated problems.
Appearance
Map the regurgitation with colour flow. Use colour flow mapping to
identify and describe any AR. The study should then look for probable
aetiology, grade severity, and check for associated problems.
• Visualize the regurgitation with colour flow.
• Look at the jet in all views and establish the shape and pattern of
the regurgitation.
• Comment on whether it is central, eccentric, along a commissure,
or even through a perforation (often easiest to see in parasternal
short axis views).
Use a systematic approach to establish cause based on the clinical
situation:
• Aortic root: in the parasternal long axis, measure aortic root
dimension, look for a dissection flap. In parasternal short axis look
at the aortic root for evidence of thickening or abscess.
• Aortic valve: parasternal long axis—abnormal valve motion/
prolapse, vegetations, calcification/rheumatic changes. Parasternal
short axis—number of cusps.
• Look at the rest of heart: Evidence of congenital abnormalities that
may relate to AR, e.g. ventricular septal defect?
For prosthetic valve regurgitation, comment on whether the
regurgitation is through the valve (valvular) or around the side
(paravalvular), and document any degree of valve motion relative to
the annulus (‘rocking’).
AORTIC REGURGITATION
143
Box 3.1 Causes of aortic regurgitation
Aortic valve
Degeneration: calcific
Infectious: endocarditis, post rheumatic fever
Congenital:
Bicuspid valve
Associated with other congenital abnormalities.
Aortic root dilatation
Hypertension
Dissection/aneurysm
Trauma
Congenital (e.g. Marfan’s, Ehlers-Danlos)
Osteogenesis imperfecta
Inflammatory:
Rheumatoid arthritis
Systemic lupus erythematosus
Syphilis, Reiter’s syndrome
Giant cell arteritis, ankylosing spondylitis.
Aortic regurgitation
RV
LV
LA
Fig. 3.23 Examples of colour flow Doppler of aortic regurgitation. Top: apical
5-chamber view demonstrating severe regurgitation with a long, broad jet. Bottom:
parasternal long axis view showing mild regurgitation. See W Video 3.14.
144
CHAPTER 3 Transthoracic valves
Grading severity
Assess the severity of AR using jet width, vena contracta and descending
aortic flow (Table 3.4). Once you have an impression of the severity use
pressure half-time and LV function to further your assessment.
Vena contracta
The vena contracta is the narrowest part of the colour Doppler jet,
where flow convergence occurs. Best seen in parasternal long axis
view.
Measure the vena contracta width perpendicular to the jet direction
with calipers and report the absolute measurement. Severe
regurgitation is associated with width >0.6cm (Fig. 3.24).
The same measurement can be done in cross-section in the
parasternal short axis view, though it is difficult to be sure you are at
the correct level (at the narrowest point).
Jet width as proportion of outflow tract
Measure the vena contracta (jet width).
Suppress the colour and measure the width of the LVOT at the same
point.
Report the jet width as a percentage of LVOT. Severe regurgitation is
suggested by a jet that is >65% of outflow tract.
Jet size assessed in parasternal short axis can also be used (although
technically more difficult and does not supply more information).
Report area relative to left ventricle outflow tract area in the same
view.
Problems using jet width to assess AR
Eccentric jets tend to ‘flatten out’ along the outflow tract wall and
are no longer circular in cross-section, so will have different widths
depending on the orientation of the image plane.
Changes in gain and colour scale will affect jet width, so control
settings should be kept constant (50-60cm/s), especially for F/U.
Descending aorta flow
In the suprasternal view, obtain a view of the aortic arch and
descending aorta (Fig. 3.25).
Place the PW Doppler cursor in the centre of the descending aorta
and look at the spectral trace.
Flow down the descending aorta is normally away from the probe
(below the line) for virtually all of the cardiac cycle.
Examine diastolic flow—a small amount of flow reversal (above
the line) may be seen at the start of diastole. However, in severe
regurgitation, all flow during diastole is reversed (back towards the
heart) as a large volume of blood flows back into the ventricle. If this is
seen, report holodiastolic aortic flow reversal (Fig. 3.25).
AORTIC REGURGITATION
145
Table 3.4 Parameters to determine severity of aortic regurgitation
Mild
Severe
Specific signs of severity
Vena contracta
<0.3cm
>0.6cm
Jet (Nyquist
central, <25% of LVOT central, >65% of LVOT
50-60cm/s)
Descending aorta
No or brief early-
Holodiastolic flow reversal
diastolic flow reversal
Supportive signs of severity
Pressure half time
>500ms
<200ms
Left ventricle (only for
Normal LV size
Moderate or greater LV
chronic lesions)
enlargement (no other cause)
Report as moderate if signs of regurgitation are greater than mild but there are no features
of severe regurgitation.
LVOT
Vena contracta
Jet width as
proportion of LVOT
Fig. 3.24 Parasternal long axis with vena contracta and left ventricular outflow tract
diameter marked. See W Video 3.15.
146
CHAPTER 3 Transthoracic valves
Supportive signs
Pressure half time
Obtaining the spectral Doppler trace
In the apical 5-chamber (or 3-chamber) view, align the CW Doppler
through the AR jet (identified with colour flow mapping). Try and
ensure the Doppler passes through the regurgitant orifice of the valve
and is in line with the jet direction (for eccentric jets the view may
need to be adjusted).
On the spectral trace, the regurgitant jet will be seen as a broad trace
with a flat, sloped top, above the baseline that coincides with diastole
on the ECG (Fig. 3.26).
Measure the slope of the flat part of the curve. The deceleration slope
(the slope of the curve) and pressure half-time (time for pressure to fall
by a half) are usually calculated automatically. The two measures are
generally correlated.
Parameters to assess
Density of the waveform compared to the systolic waveform. Similar
density suggests severe regurgitation.
Peak diastolic velocity (usually 4-6m/s).
The pressure half-time: <200ms indicates the pressure between the
aorta and left ventricle equalizes very quickly in diastole (usually due to
a large regurgitant volume) and suggests severe regurgitation. See also
b p.150.
The deceleration slope: >400cm/s2 indicates severe AR (the larger the
number, the steeper the slope).
Left ventricle
Serial studies of changes in left ventricular size are useful in monitoring
progression of AR and help decide the timing for intervention.
Assessment can be based on standard measures of LV size (b p.196).
A LV end-diastolic dimension of >7cm and/or LV end-systolic
dimension of >4.5 cm are markers of severe LV dilation ± dysfunction
2° to chronic AR.
AORTIC REGURGITATION
147
Descending aorta
PW
Abnormal - holodiastolic
reversed flow
Normal - forward
diastolic flow
Fig. 3.25 A suprasternal view with pulsed wave Doppler placed in the descending
aorta. The spectral trace shows reversed holodiastolic flow.
Doppler slope for
pressure half time
SEVERE
MILD
Fig. 3.26 Continuous wave traces from an apical 5-chamber view to measure
pressure half-time.
148
CHAPTER 3 Transthoracic valves
Other possible measures of AR severity
Length of the jet
A rough estimation of the severity of AR can be made on the length of the
jet: if the jet reaches the end of the anterior mitral valve leaflet (moder-
ate) or extends into the body of the LV (severe); Fig. 3.27. Originally this
was performed using PW Doppler to identify the jet, but this has been
extrapolated to colour flow jets which are highly dependent on control
settings due to the low velocities at the boundary layers.
Jet area
Judging the severity of AR by the size (area) of the regurgitant jet is
inaccurate—it is susceptible to loading conditions, angles of the jet and
image plane, and colour flow settings, and should not be relied upon. In
addition, eccentric jets may be long and thin as they track along structures
and the severity is easily underestimated.
Colour M-mode
If the M-mode cursor is placed below the valve in a parasternal long axis
view with colour flow (Fig. 3.27), the position of the regurgitation within
the outflow tract and timing during diastole can be studied (e.g. late dias-
tole due to aortic leaflet prolapse or mild regurgitation in early diastole).
Measurements of jet width and left ventricular outflow tract can also theo-
retically be done with the same tracing.
3D assessment of aortic regurgitation?
3D echocardiography modes (full volume datasets, live 3D or colour
Doppler imaging) can be used to aid quantification of the severity of aor-
tic regurgitation. The same parameters as developed in 2D are used but
the 3D datasets allow better alignment for assessment. This is because
the pyramidal datasets can be cropped in any plane so even eccentric
jets can have accurate plane alignment. Studies have demonstrated that
the measurement of vena contracta width and vena contracta area show
good correlation with the angiographic grading of the aortic regurgita-
tion severity.
To measure vena contracta use the parasternal window to obtain a
3D dataset.
To measure vena contracta area use postprocessing to create an en
face 2D view of the regurgitation jet as it passes through the aortic
valve and LVOT. Then scan up and down the jet to identify the
narrowest past and trace around the vena contracta. Report the area
relative to the outflow tract area at that level.
For the vena contracta width postprocess the 3D dataset as for
area but this time create an imaging plane that lies parallel to the
regurgitant jet. Then scan through the jet to identify the plane that
cuts through the narrowest point. Measure the jet width and report
the value relative to the outflow tract width.
AORTIC REGURGITATION
149
Severe
Moderate
Mild
RV
LA
RA
Colour flow in diastole
Valve opening
Fig. 3.27 Additional measures to assess aortic regurgitation: length of jet extending
into the ventricle based on an apical 4-chamber view (top figure) and colour
M-mode in a parasternal long axis view to demonstrate the regurgitant flow in the
outflow tract during diastole (bottom figure).
150
CHAPTER 3 Transthoracic valves
Quantifying regurgitant volume
This can be calculated because blood flow across the aortic valve in sys-
tole should be the same as the blood flow into the LV during diastole.
The diastolic component comprises blood flow across the mitral valve
plus any AR. Both flow across the aortic valve in systole and mitral inflow
can be calculated and the aortic regurgitant flow will be the difference
between the two:
gurgitant volume
mitral valve inflow
The principle is the same as that used for determining regurgitant volume
in mitral regurgitation, and the same measures (mitral valve inflow and LV
outflow tract flow) are used (see b p.122 for how to measure these).
Interestingly, the stroke volume should be the same at any valve in the heart
if it is competent and there is no shunt, so if measurements are difficult at
the mitral valve, the pulmonary or tricuspid could be used. Theoretically,
the proximal isovelocity surface area (PISA) method (b p.126) can be used
at any regurgitant valve, although it is usually only practical and validated
for the mitral valve.
However, the calculation has several potential areas of inaccuracy:
Measuring LVOT flow and mitral inflow involves significant
assumptions and calculations, and these may be inaccurate. Calculating
a third measurement from these 2 derived parameters carries a high
risk of further inaccuracy.
Significant mitral regurgitation reduces systole aortic flow and distorts the
measurement.
Acute or chronic regurgitation?
In acute severe AR, the LV is usually of normal dimension and
thickness, with vigorous function. In chronic severe AR there has
been time for dilatation and possibly eccentric hypertrophy.
Acute severe AR is usually poorly tolerated by patients, due to the
lack of time for LV compensation, and they are very symptomatic,
often in heart failure.
Cause: dissection and endocarditis are likely causes of acute AR.
Pressure half-time is particularly useful as a marker of severity in
acute regurgitation. With chronic regurgitation left ventricular
function and aortic compliance change to accommodate larger
regurgitant volumes. This slows down the equalization in pressure
and leads to a longer pressure half-time.
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152
CHAPTER 3 Transthoracic valves
Bicuspid and quadricuspid valves
The aortic valve can occur with fewer or more than 3 cusps. Bicuspid
valves are seen in 2% of the population and quadricuspid valves in 0.04% of
the population (Fig. 3.28). 5 cusps have also been reported although this
may often be secondary to endocarditis. Sometimes valves have 3 cusps
but are functionally bicuspid because of fusion of 2 cusps along a commis-
sure. Bicuspid valves are often associated with aortic stenosis and multiple
cusps with aortic regurgitation.
It is very easy to make a tricuspid valve appear bicuspid in a parasternal
short axis view if the plane is slightly off axis. If you suspect a bicuspid valve
make sure this is consistent in several views. Clues to a valve being truly
bicuspid include:
Leaflets of unequal size. True congenital bicuspid valves occur because
of failure of separation of the right and non-coronary cusp or failure of
separation of the right and left coronary cusps.
An atypical orientation of the commissure in the parasternal short axis.
This will either lie roughly horizontal (between 10 and 4 o’clock) or
roughly vertical.
Abnormal valve motion (best seen in a parasternal long axis view). The
valve typically domes with the valve opening off centre.
When assessing a bicuspid valve report the suspected cause, e.g. true
congenital or due to valve fusion, degree of calcification (they are more
prone to degeneration), associated functional problems (regurgitation and
stenosis), associated congenital problems (they are linked with coarcta-
tion of the aorta), and associated changes to the aorta (e.g. dilatation or
dissection).
Lambl’s excresences
These are thin strands attached to the aortic cusps several millimetres
long. They are also seen on the mitral valve. They are not clinically signifi-
cant although their relevance will depend on the clinical situation as it is
important not to miss endocarditis vegetations.
LAMBL’S EXCRESENCES
153
Bicuspid valve
Quadricuspid valve
Fig. 3.28 Examples of bicuspid and quadricuspid aortic valves. See W Video 3.16,
W Video 3.17, W Video 3.18, W Video 3.19, W Video 3.20.
154
CHAPTER 3 Transthoracic valves
Tricuspid valve
Normal anatomy
The tricuspid valve has 3 cusps of unequal size: anterior (largest) extends
from infundibulum anteriorly to the inferolateral wall posteriorly. The pos-
terior leaflet arises along the posterior margin of the annulus from the
septum to the inferolateral wall and the septal (smallest) leaflet extends
from the interventricular septum to the posterior ventricular border
(Fig. 3.29). Their anatomy is very variable. The free margins of the cusps
are attached to chordae tendinae which are, in turn, attached in groups to
three papillary muscles (anterior, posterior, and septal) that project from
the septum and right ventricular free wall. Chordae from each papillary
muscle attach to all leaflets. The valve has an annulus and valve ring with a
normal area of 5-8cm2. The valve allows free flow of blood from the right
atrium during diastole but closes as systole increases the intraventricular
pressure. Abnormalities of the tricuspid valve must not be overlooked,
especially in mitral valve disease.
Normal findings
2D views
The best views are: parasternal short-axis (aortic valve level), right
ventricular inflow, apical 4-chamber, and subcostal views.
2D findings
Parasternal short axis (aortic valve level): the tricuspid valve lies to
the right of the aorta. The anterior leaflet is seen on the left and
septal is closest to the atrial septum. In all views the tricuspid leaflets
demonstrate wide diastolic opening and a normal coaptation in systole.
Right ventricular inflow: this gives a very good view of the posterior
(on the left) and anterior (on the right) leaflets as well as the right
atrium, right ventricle and, sometimes, the inferior vena cava, coronary
sinus and Eustachian valve.
Apical 4-chamber: the anterior and septal leaflets are seen (septal
nearest the septum). In this view the tricuspid annulus (normal adult
28 ± 5mm) should lie closer to the apex (up to 1cm) than the mitral
annulus. This plane also provides a good view of the right heart.
Subcostal 4-chamber: this view allows good access to images of the
right atrium, atrial septum and inferior vena cava. The tricuspid valve
(anterior and septal leaflets) is usually clearly seen similar to the apical
4-chamber view.
3D views and findings
3D datasets are best obtained from the apical position. However, it is
possible to use a modified position within the parasternal window that
lies close to the tricuspid valve, or sometimes a subcostal window.
The tricuspid valve and apparatus has a complex geometrical shape
and 3D views can be used for a more detailed quantitative assessment
of the anatomy prior to surgical intervention.
TRICUSPID VALVE
155
Anterior leaflet
RV
RV
RA
RA
LA
Posterior leaflet
Septal leaflet
Right Ventricle Inflow
Parasternal Short Axis
Anterior leaflet
LV
RV
LA
RA
Septal leaflet
Apical 4 Chamber
Subcostal
Fig. 3.29 Key views to study the tricuspid valve.
156
CHAPTER 3 Transthoracic valves
Tricuspid regurgitation
General
Tricuspid regurgitation is common. Because the leaflets are irregular a
small amount of central, physiological regurgitation is seen in up to 70%
of normal individuals. Physiological regurgitation is associated with normal
valvular anatomy and no dilatation of the RV. Pathological regurgitation
is usually secondary to right ventricular and tricuspid annular dilatation.
Primary causes of tricuspid regurgitation are due to changes to the valve
or subvalvular apparatus (Box 3.2).
Tricuspid regurgitation is usually seen in patients with multiple valve
lesions, including aortic and mitral.
Assessment
‘Physiological’ regurgitation should be commented upon (<1cm adjacent
to valve closure). Transthoracic echocardiography should aim to establish
the aetiology of pathological tricuspid regurgitation and provide a quanti-
tative estimate of severity. The assessment must also include evaluation of
the right-sided chambers (Table 3.5).
Appearance
Anatomy: assess for prolapsing (usually septal and anterior), flail,
or billowing valve. An apical 3D full-volume set enables detailed
assessment of tricuspid valve apparatus from multiple views and
commissural fusion/leaflet coaptation can be assessed using the
en face’ view.
Look at the regurgitant jet with colour flow Doppler in several views
and comment on the direction and size of the jet.
Report abnormal valve appearance (restricted motion and thickening
of carcinoid, vegetations of endocarditis or valve rupture).
Report tricuspid valve annulus size.
Report right heart size and function (b p.264) and assess right
ventricular systolic pressure (b p.162).
Pacemakers and tricuspid regurgitation
Tricuspid regurgitation is more common with a pacemaker lead (both
temporary and permanent) because it disrupts leaflet coaption. Tricuspid
valve velocity however will not be affected as this is determined by right
ventricular systolic pressure.
TRICUSPID REGURGITATION
157
Box 3.2 Causes of tricuspid regurgitation
Valve and apparatus
Infection
Endocarditis
Rheumatic heart disease
Congenital: Ebstein’s anomoly
Metabolic: carcinoid
Connective tissue disease
Subvalvular
Chordal rupture
Papillary muscle dysfunction
Infiltration
Malignancy
Non-penetrating trauma.
Right heart
Pulmonary hypertension
Right heart failure with lung pathology
Ischaemic heart disease
Pulmonary valve disease
Cardiomyopathy
Volume overload
Pacing lead
Table 3.5 Parameters to assess severity of tricuspid regurgitation
Mild
Severe
Qualitative
Valve structure
Normal
Abnormal
Jet (Nyquist 50-60cm/s)
<5cm2
>10cm2
CW trace
Soft & parabolic Dense & triangular
Semi-quantitative
Vena contracta
-
>0.7cm
PISA r (Nyquist 40cm/s)
<0.5cm
>0.9cm
Tricuspid inflow
Normal
E wave dominant >1m/s
Hepatic vein flow
Normal
Systolic reversal
Quantitative
EROA
Not defined
40mm2
R vol
Not defined
>45mL
RV/RA/IVC
Normal size
Usually dilated
Report as moderate if signs of regurgitation are greater than mild but there are few
features of severe regurgitation.
158
CHAPTER 3 Transthoracic valves
Grading severity
The methods to grade severity are borrowed directly from those used
for mitral regurgitation. Assessment of tricuspid regurgitation tends to
be more subjective with less clinical need for accuracy. Colour flow
imaging should be used to diagnose TR. Quantitative assessment is
performed using vena contracta, flow convergence (PISA), continuous
wave density, and contour. There are also changes in hepatic vein flow
which are equivalent to changes in pulmonary vein flow seen in mitral
regurgitation (see Table 3.5). It is essential to use multiple views to
assess severity.
Vena contracta
In the apical 4-chamber view place colour flow over the tricuspid valve
and obtain a plane that demonstrates the regurgitant orifice.
Zoom in on the valve and measure the vena contracta (narrowest
diameter of the colour flow jet as it passes through the valve)—>7mm
suggests severe regurgitation, see Fig. 3.30.
Continuous wave Doppler waveform
In the apical 4-chamber, parasternal short axis or right ventricular
inflow views drop the continuous wave through the tricuspid valve
aligned with the regurgitant jet.
Report the signal intensity relative to the antegrade flow and comment
on the waveform (parabolic or triangular). Triangular and dense
suggests severe regurgitation, see Fig. 3.31.
Use TR jet to determine RV or pulmonary artery systolic pressure
(b p.162)
Jet area
In the apical 4-chamber view obtain an image that includes the entire
right atrium and the main plane of the regurgitant jet.
Record a loop and scroll through to a frame with the largest jet.
Trace around the jet and report the area. >10cm2 suggests severe
regurgitation.
Right ventricular inflow
Flow of blood into the right ventricle can be used as a guide to
severity (equivalent to measurement of E wave velocity in mitral
regurgitation). Peak E velocity at the tricuspid valve of 1m/s
suggests severe tricuspid regurgitation.
Hepatic vein flow
In a subcostal view place the PW Doppler cursor in a hepatic vein that
aligns with the probe and record a spectral tracing of flow. Normally
flow through both systole and diastole is towards the right atrium. In
severe tricuspid regurgitation the rise in right atrial pressure leads to
flow away from the right heart during systole. Report systolic flow
reversal if seen.
TRICUSPID REGURGITATION
159
Trace jet area
Vena contracta
Fig. 3.30 Measurement of jet area (top) and quantify your assessment with a vena
contracta (bottom) or PISA measurement.
SEVERE
triangular
dense
waveform
MILD
parabolic
dense
waveform
Fig. 3.31 Density and shape of Doppler can give clues to severity.
160
CHAPTER 3 Transthoracic valves
3D for assessment of tricuspid regurgitation?
3D echocardiography can be used to help quantify tricuspid regurgitation
severity and also the mechanism, in particular the annulus size (Fig. 3.33).
Colour flow mapping
As with 3D the assessment of mitral regurgitation, full volume
colour Doppler imaging permits the regurgitant jet to be rotated and
cropped to ensure that the vena contracta is being measured in a
plane that is parallel to the jet and also at the narrowest point during
maximal flow (Fig. 3.32).
3D echocardiography allows the valve to be assessed from the ‘en
face’ view to help identify prolapsing valve segments accurately.
Tricuspid annulus
Real-time 3D transthoracic echocardiography is routinely available
and allows simultaneous assessment of the morphology, movement
of the three leaflets and attachment to the tricuspid annulus.
It has been shown that 3D echocardiography allows visualization
and measurement of the entire oval-shaped annulus in patients
with dilated or normal sized annuluss, something which was
underestimated by 2D echocardiography.
Mild and severe tricuspid regurgitation
Fig. 3.32 Colour flow mapping of tricuspid regurgitation in apical 4-chamber views
with examples of mild (top) and severe (bottom) regurgitation. See W Video 3.21.
TRICUSPID REGURGITATION
161
Fig. 3.33 3D full volume acquisition of the tricuspid valve. The initial image was
taken from apical 4-chamber view. Top: subsequent rotation and cropping to reveal
the TV from the ventricular side and show the anterior leaflet (A), septal leaflet
(S), and posterior leaflet (P). Anterior (AMVL) and posterior (PMVL) mitral valve
leaflets also seen. Bottom: TV rotated and leaflets seen from the right atrial view.
Full volume 3D acquisition of the tricuspid valve. The oval shape of the annulus is
appreciated. See W Video 3.22.
162
CHAPTER 3 Transthoracic valves
Right heart haemodynamics
The most widely reported haemodynamic measure in echocardiography is
right ventricular systolic pressure. This is partly because it has a broad clini-
cal relevance and partly because it is easy to measure as it uses tricuspid
regurgitation—found in 70% of individuals.
Measurement is based on velocity of regurgitation across the tricuspid valve.
This is used to calculate pressure across the valve—the higher the pressure
in the right ventricle relative to the right atrium, the higher the velocity
of regurgitant blood. To calculate right ventricular systolic pressure right
atrial pressure must be added to this pressure. Fortunately, there are clinical
(jugular venous pressure [JVP]) and echocardiographic methods (inferior
vena cava [IVC] and right atrial size) to estimate right atrial pressure.
Right atrial pressure
JVP can be used but requires accurate clinical assessment with the
patient lying at 45°. The measure lacks accuracy if very low or very high
and is directly affected by moderate to severe tricuspid regurgitation.
A floating constant of 5, 10, or 15 mmHg can be used based on the
pattern of changes in right atrial size, inferior vena cava, and tricuspid
regurgitation severity (Table 3.6).
• Assess right atrial size from an apical four chamber view (b p.284).
Report as normal, dilated, or very dilated. Measure IVC diameter
from a subcostal view (<1.7 cm is normal, except in athletes when
diameter can be 2-3cm) and check for respiratory variation (ask the
patient to sniff). IVC should reduce in size by around 50% (Fig. 3.34).
Tricuspid regurgitation severity is assessed routinely (b p.158).
If accurate assessment of right atrial pressure is not possible then
a constant of 10mmHg (or 14mmHg) can be used but this will
systematically overestimate right systolic ventricular pressures (RSVP) at
low levels and underestimate it at high levels.
Recently, an alternative approach has been suggested based on IVC
diameter and response to sniff. If IVC <2.1cm and collapses >50% then
RA pressure is 3mmHg. If IVC >2.1cm and collapses <50% then RA
pressure is 15mmHg. Otherwise assume pressure is 8mmHg.
Tricuspid velocity and right ventricular systolic pressure
In apical four chamber, parasternal short axis or right ventricular inflow
view, align continuous wave through the tricuspid valve regurgitation.
Record a spectral trace and measure the peak velocity (Fig. 3.35).
Based on the simplified Bernoulli equation:
Pressure gradient
u peak velocity2
Report right ventricular systolic pressure as the tricuspid pressure
gradient plus the estimate of right atrial pressure.
Pulmonary artery systolic pressure
By subtracting the pressure gradient across the pulmonary valve
(b p.174) from right ventricular systolic pressure you can calculate
pulmonary artery systolic pressure. Because the gradient is usually small
and right atrial pressure is estimated, right ventricular systolic pressure
is often reported as pulmonary artery systolic pressure.
RIGHT HEART HAEMODYNAMICS
163
Table 3.6 Parameters to help identify fluid status
Suggests
Normal range
Suggests volume
hypovolaemia
overload
IVC diameter
<1cm and collapsing 1-2.5cm, collapsing
>2.5cm, no response
and response
25-75%
to respiration
LVIDd/BSA (cm/m2) <2.4 women
2.4-3.2
>3.2
<2.2 men
2.2-3.1
>3.1
LVEDAI (short axis) <5.5
5.5-10
>10
End point septal
<0.5m
>0.5cm
-
separation
LVESD
Papillary apposition 2.0-4.0cm
-
RV internal dimensions
-
See below
RVIDd >LVIDd
Interventricular
-
No flattening
Diastolic flattening
septum
Right atrium
-
<20cm2
>30cm2
NO RESPIRATORY
VARIATION
AT REST
ON INSPIRATION
NORMAL
ABNORMAL
Fig. 3.34 The 2D images demonstrate normal respiratory variation of the inferior
vena cava and the M-mode trace lack of variation.
Fig. 3.35 The tricuspid valve has been focused on from the apical 4-chamber view
to obtain a continuous wave Doppler trace across the tricuspid valve to measure
peak velocity and derive a pressure gradient.
164
CHAPTER 3 Transthoracic valves
Tricuspid stenosis
General
Tricuspid stenosis is rare. The commonest cause is rheumatic heart disease
with coexistent mitral stenosis. Other causes include: carcinoid (Fig. 3.36),
lupus valvulitis, pacemaker or valvular endocarditis, right atrial tumour,
and obstruction of right ventricle inflow tract (large atrial thrombus or
large vegetations). It is usually associated with tricuspid regurgitation.
Appearance
Comment on:
Leaflet thickening or calcification.
Leaflet motion: classically restricted with diastolic doming of 1 or more
leaflets (especially the anterior leaflet).
Right atrial enlargement.
Dilated IVC.
3D echocardiography provides anatomical detail of leaflets and orifice
area.
Grading severity
Determine severity on the transvalvular gradient (Table 3.7):
• Use CW Doppler aligned across the tricuspid valve in an apical
4-chamber view (averaged throughout the respiratory cycle).
• Measure peak velocity (Fig. 3.37) and calculate peak gradient using
the Bernoulli equation.
Severe tricuspid stenosis is associated with a valve area of <1cm2 or
a peak gradient of >7mmHg (mean >5mmHg) and an inflow time-
velocity integral >60cm.
Pressure half time can not be used to measure valve area as the
appropriate constant for the tricuspid valve has not been determined.
Severity can also be assessed from valve area. This can be calculated
using the continuity equation. A PW Doppler vti can be taken at
the level of the valve annulus and the CSA of the tricuspid annulus
calculated based on the annulus diameter and the assumption that the
orifice is circular. These measurements can then be combined with the
continuous wave vti across the valve.
Tricuspid valve area = (Annulus PW vti area of annulus)/valve CW vti
3D for assessment of tricuspid stenosis?
In mitral stenosis it is possible to accurately planimeter the valve
orifice area in the short axis view with 2D imaging. Due to the
complex geometry of the tricuspid valve it is not possible to
accurately assess the valve orifice area with 2D short axis views.
3D echocardiography allows the tricuspid valve to be rotated
and cropped in any plane and to appreciate the morphology from
short axis views and to also see the valve en face and delineate the
individual leaflets. Both of these 3D tools can be used to planimeter
the orifice.
TRICUSPID STENOSIS
165
Table 3.7 Parameters of TS
Mild
Moderate
Severe
Mean gradient (mmHg)
<4
4-7
>7
Valve area (cm2)
-
-
<1
Stiff, short leaflets,
fixed open during
Mitral valve
systole
closed in
systole
RV
LV
RA
LA
Fig. 3.36 An apical 4-chamber view demonstrating carcinoid heart disease causing
tricuspid stenosis. See W Video 3.23.
Peak velocity across
tricuspid valve
Fig. 3.37 Continuous wave Doppler is used in an apical 4-chamber view to record
peak velocity across the tricuspid valve. This can be used to estimate a gradient in
tricuspid stenosis.
166
CHAPTER 3 Transthoracic valves
Tricuspid valve surgery
Tricuspid valve surgery—replacement or annuloplasty—is considered in
severe tricuspid regurgitation with haemodynamic consequences or when
associated with mitral valve disease.
Carcinoid syndrome
Characterized by the release of 5-hydroxytryptamine from a metastasizing
tumour resulting in thickened and shortened tricuspid leaflets with severe
tricuspid regurgitation. The pulmonary valve may also be involved and the
right atrium and right ventricle are frequently dilated.
Infective endocarditis
Right-sided endocarditis is uncommon except in intravenous drug users,
patients with indwelling catheters, or those with ventricular septal defects.
Vegetations usually occur on the tricuspid valve (Fig. 3.38) in intravenous
drug use, but many have associated left-sided lesions.
Ebstein anomaly
A congenital anomaly of the tricuspid valve with apical displacement of 1
or more leaflets. This diagnosis should be considered when the distance
between the mitral and tricuspid valve planes is >1cm. There is enlarge-
ment of the right atrium and tricuspid regurgitation.
3D transthoracic echocardiography provides detailed anatomical and func-
tional images prior to surgical intervention.
EBSTEIN ANOMALY
167
RV
RA
Vegetation on tricuspid valve
Fig. 3.38 A zoomed apical 4-chamber view to highlight a vegetation on the tricuspid
valve. See W Video 3.24.
168
CHAPTER 3 Transthoracic valves
Pulmonary valve
Normal anatomy
The pulmonary valve consists of 3 leaflets: anterior, left, and right. It
develops alongside the aortic valve and then the right heart and pulmonary
artery twists around the left heart and aorta. The valve lies at the junction
of the right ventricular outflow tract and the pulmonary trunk. It is thinner
than the aortic valve as a result of the lower right heart pressures.
Normal findings
Views
There are limited views of the pulmonary valve (Fig. 3.39). The best
views are the parasternal short axis (aortic valve level) and the right
ventricular outflow. Subcostal short-axis views (at the aortic valve
level) can also be used but are similar to the parasternal short axis
view.
Findings
Parasternal short axis (aortic valve level): this provides a view of the
tricuspid valve, right ventricle, and pulmonary valve wrapped around
the aortic valve. The pulmonary valve lies on the right and this view
can be used to align Doppler through the right ventricle outflow,
pulmonary valve, and pulmonary artery.
Right ventricular outflow: in some people this provides excellent views
of the pulmonary valve, pulmonary artery, and bifurcation. This view
can also be used for alignment of Doppler.
PULMONARY VALVE
169
RV
RV
RA
LA
Right ventricle outflow
Parasternal short axis
Fig. 3.39 Key views to assess the pulmonary valve.
170
CHAPTER 3 Transthoracic valves
Pulmonary regurgitation
General
Colour flow mapping of the pulmonary valve identifies small regur-
gitant jets in most people (Fig. 3.40). These can often be quite eccentric.
Pathological causes of regurgitation are similar to those for tricuspid
regurgitation (Table 3.5, Box 3.2).
Primary valve problems include: rheumatic heart disease, infective endo-
carditis, carcinoid, iatrogenic
(post-valvuloplasty), congenital
(following
surgery for tetralogy of Fallot, leaflet absence). Secondary causes are
due to dilatation of the pulmonary artery (e.g. pulmonary hypertension,
Marfan’s).
Appearance
Examine for anatomic abnormalities to identify mechanism of
regurgitation including anomalies of cusp number, structure or
movement. Comment on any visible valve pathology (e.g. thickening,
vegetation).
Map the regurgitation with colour flow in the parasternal short
axis and right ventricular outflow views. Comment on size, site of
regurgitation, and direction.
Pulmonary regurgitation is commonly at one edge of a commissure
and can appear to lie next to the aorta. This should not be confused
with an aorta-pulmonary communication which would have flow
throughout the cardiac cycle instead of just during diastole.
PULMONARY REGURGITATION
171
RV
RA
PA
LA
Pulmonary regurgitation
RV
RA
PA
LA
Fig. 3.40 Colour flow mapping of pulmonary regurgitation in parasternal short axis
views. Mild (top) and severe (lower) regurgitation. See W Video 3.25.
172
CHAPTER 3 Transthoracic valves
Grading severity
Criteria for assessment are borrowed from aortic regurgitation but
assessment is more qualitative (Table 3.8).
Grade severity as mild, moderate or severe based on:
• Jet length and width relative to outflow tract: Jet diameter is
measured at pulmonary valve leaflets level during early diastole:
jet diameter >0.98cm indicates significant regurgitation. Jet width
>65% of right ventricular outflow tract indicates severe pulmonary
regurgitation.
• Pulmonary regurgitation index (PR Index) is the ratio between
pulmonary regurgitation time and total diastole. An index <0.77
suggests severe PR. The lower the value, the more severe the
regurgitation.
• Vena contracta width lacks validation. 3D vena contracta provides
more quantitative assessment of PR. EROA values mild <20mm2,
moderate 21-115 mm2, and severe >115mm2 have been proposed.1
• Continuous wave regurgitation intensity and shape. Increased
intensity and slope of the Doppler signal (deceleration time)
suggests severe (Fig. 3.41).
(Abnormal pulmonary artery anatomy suggests more severe
regurgitation.)
• Flow across pulmonary valve relative to systemic circulation and
evidence of right ventricle dilatation.
• Holodiastolic flow reversal in the main pulmonary artery
(equivalent to aortic flow reversal) suggests severe regurgitation.
Comment on changes to the right heart—with severe PR, patients
often develop RV dilatation from volume overload and tricuspid
annulus dilatation and tricuspid regurgitation.
Pulmonary artery diastolic pressure
The velocity of the regurgitant jet can be used to quantify the pressure
gradient (using the Bernoulli equation) between the pulmonary artery
and right ventricle during diastole.
Add right ventricular diastolic pressure (assumed to be right atrial
pressure, see Table 3.6) to the pulmonary valve pressure gradient to
calculate pulmonary artery end diastolic pressure.
To calculate mean pulmonary artery end pressure use pulmonary artery
systolic pressure (b p.162) in the equation:
diatolic pressure+ systolic pressure
3
PULMONARY REGURGITATION
173
Table 3.8 Parameters to assess pulmonary regurgitation
Mild
Severe
Pulmonary valve anatomy
Normal
Abnormal
Jet size on colour flow
<10mm long
Large with wide origin
CW density and shape
Soft and slow
Dense and steep
PR Index
<0.77
Jet width of RVOT
>65%
Pulmonary artery flow
Increased
Greatly increased
compared to systemic
Right ventricle size
Normal
Dilated
If features suggest more than mild regurgitation but no features of severe grade as moderate.
Slope of Doppler is
guide to severity
Fig. 3.41 Doppler features to assess pulmonary regurgitation.
Reference
1 Pothineni KR et al. Live/real time three dimensional transthoracic echocardiographic
assessment of pulmonary regurgitation. Echocardiography 2008; 26(8):911–17.
174
CHAPTER 3 Transthoracic valves
Pulmonary stenosis
General
Pulmonary stenosis is usually valvular and congenital
(e.g. related to
rubella, Noonan’s, or tetralogy of Fallot). The valve usually has fusion of
several cusps to form a funnel. Pulmonary stenosis can also occur due to
stenosis of the main pulmonary artery (e.g. following rubella, post-surgical
banding of the pulmonary artery) or subvalvular problems (e.g. congenital
in association with valvular stenosis, tetralogy of Fallot, and transposition
of the great arteries).
Rheumatic pulmonary stenosis is rare. Carcinoid disease is the commonest
cause of acquired pulmonary stenosis. Functional pulmonary stenosis may
arise from RV outflow tract compression by tumours.
Appearance
Comment on the valve:
• Number of leaflets.
• Thickened, dysplastic, calcified leaflets.
• Motion: doming of valve leaflets in systole and restricted motion.
• Measure size of pulmonary annulus.
Comment on associated structures:
• Right ventricular outflow tract and evidence of narrowing, e.g.
infundibular/subvalvar stenosis.
• Post-stenotic dilatation of the pulmonary artery.
• Right ventricular hypertrophy.
• Functional tricuspid regurgitation secondary to pressure overload.
Grading severity
Grade severity based on the peak gradient. This can be supported by
calculating the valve effective orifice area (Table 3.9).
In the parasternal short axis (aortic valve level) or right ventricular
outflow view measure the velocity across the pulmonary valve with
CW Doppler aligned through the right ventricular outflow tract,
pulmonary valve and common pulmonary artery.
Report velocity and gradient across the valve (calculated with the
simplified Bernoulli equation). Mean gradient and pulmonary valve vti
can be obtained by tracing the spectral waveform (Fig. 3.42).
Measure right ventricular systolic pressure.
The continuity equation can be used to measure effective orifice area
of the pulmonary valve. In the parasternal short axis view record a
right ventricular outflow tract (RVOT) PW Doppler peak velocity or
vti (velocity(RVOT)). Measure the outflow tract diameter at this point
and calculate a CSA assuming it is circular (cross sectional area(RVOT)).
Then use the continuity equation including these measures and the
peak velocity or vti from CW across the valve (velocity (pulmonary valve)).
Pulmonary valve CSA equals:
velocity
×cross-sectional area
velocity
(RVOT
)
(RVOT
)
(pulmo
nary value
)
PULMONARY STENOSIS
175
Table 3.9 Parameters to determine severity of pulmonary stenosis
Mild
Moderate
Severe
Peak velocity (m/s)
<3
3-4
>4
Peak gradient (mmHg)
<36
36-64
>64
Valve area (cm2)
>1.0
0.5-1.0
<0.5
Trace spectral
for mean
pressure
gradient and vti
Peak velocity
+
Fig. 3.42 Severity of pulmonary stenosis can be assessed in a similar way to assess-
ment of aortic stenosis. In this example a continuous wave Doppler trace has been
obtained from a parasternal short axis view. The peak velocity can used to calculate
a gradient or be used in the continuity equation.
176
CHAPTER 3 Transthoracic valves
Mechanical prosthetic valves (Fig. 3.43)
All mechanical valves consist of a mobile component (occluder), the
restraining system
(to restrict occluder motion), and the sewing ring
(attaches prosthesis to vessel). Blood flow is restricted through these and
normal pressure gradients are therefore higher across mechanical, com-
pared to native, valves. Valve components are metallic or plastic coated,
with a carbon layer. These cause shadows and reverberations so scanning
from different positions is required to assess the valve. In particular, mitral
prosthesis regurgitation is masked on transthoracic images and if valve
dysfunction is suspected transoesophageal imaging maybe required.
Ball and cage (Starr Edwards)
The ball and cage valve consists of a sewing ring attached to a cage made
of 3 or 4 struts. The blood flows on all sides around a Silastic ball occluder,
which moves within the cage. Blood flow is directed laterally within the
valve and converges downstream (Fig. 3.44, upper image).
Assessment
Use all standard imaging planes adjusted where necessary with slight rota-
tion or tilting to minimize shadows.
Normal appearances
Whether valve is open or closed there will be significant shadows from
the sewing ring and reverberation from the ball. Structures and flows
behind the valve are masked. Physiologic regurgitation is a trivial central jet.
Tilting disc (e.g. Medtronic-Hall, Omniscience)
A single circular disc suspended within a frame, with an off-centre hinge
point. Opening therefore creates 2 orifices, 1 large (major) and 1 small
(minor).
Assessment
Use standard imaging planes with slight rotation or tilting as necessary.
Images are usually best when through the central hinge point or perpen-
dicular to the closed disc. For mitral prostheses use apical windows for
assessment. For aortic prostheses use apical windows for Doppler and
parasternal to differentiate valvular from perivalvular regurgitation.
Normal appearances
There are shadows from the sewing ring and reverberations from the disc
throughout the cardiac cycle.
Valve closed: structures and flow behind the valve are masked.
Physiologic regurgitation is 2 small jets between disc and ring. Some
may have a jet associated with the central strut and some a very long
central jet.
Valve open: disc opens to 55-75°. The strut can be seen in a central
position underneath the sewing ring. 2 colour jets can be displayed.
CW Doppler velocities are similar through minor and major orifice.
MECHANICAL PROSTHETIC VALVES
177
BALL AND CAGE
BILEAFLET
TILTING DISC
STENTED
BIOPROSTHESIS
BLOOD FLOW
CLOSED
OPEN
THROUGH VALVE
Fig. 3.43 Diagram of mechanical prosthesis design and blood flow.
When to use transoesophageal echocardiography?
Transthoracic echocardiography usually provides good alignment with
the transprosthestic flow. Therefore detection of prosthesis stenosis is
not a problem. However, transthoracic assessment of regurgitation is
limited by shadowing and distance to the transducer. Haemodynamic
assessment or an aortic valve prothesis is usually better with a transtho-
racic study. Indications for transoesophageal imaging are:
Transthoracic imaging is inconclusive or non-diagnostic.
Transthoracic findings not in agreement with clinical findings.
Suspected problems of mitral mechanical valve prosthesis.
Suspected prosthetic valve endocarditis.
Suspected prosthetic valve thrombosis.
Intraoperative use (to guide repair, assess success, complications).
178
CHAPTER 3 Transthoracic valves
Bileaflet (e.g. Carbomedics, St. Jude)
These consist of 2 leaflets, separately hinged in the centre of the prosthe-
sis. 3 orifices are created in the open position: 2 large lateral orifices and
1 small central orifice (Fig. 3.44, lower image). If used in the aortic position
a supra-annular placement is often possible and may be used in double
valve replacement in order to achieve greater separation of the valves.
Assessment
As for single tilting disc, use standard imaging planes, mainly apical for
mitral prostheses and both apical and parasternal for aortic valves. Before
making diagnosis of impaired motion of one or both discs, ensure trans-
ducer has been rotated thoroughly to obtain a position in which the cur-
sor (ultrasound beam) is aligned perpendicularly to the central line of the
disc coaptation.
Normal appearances
There will be shadows from the sewing ring and reverberation from discs
throughout the cardiac cycle.
Valve closed: discs close at about 25° and mask structures and flow
behind the valve. Physiologic regurgitation is up to 4 jets originating at
pivot points near the edge of the valve.
Valve open: discs open to 55-75° and 2 separate discs are often seen.
There is more flow acceleration through the narrow central orifice.
Therefore CW measures through the centre may overestimate the
overall pressure gradient, especially for small aortic prosthetic valves.
Use mean rather than peak gradient.
Physiologic regurgitation
Physiologic regurgitation is normal with tilting disc and bileaflet proth-
eses. There are 2 components: (1) an initial backward flow during valve
closure (2) holosystolic flow designed to ‘wash’ the valves and reduce
risk of valve thrombosis. These are referred to as ‘wash’ or ‘closing’
jets.
Differentiation of closing and physiologic jets from pathological
regurgitation?
Physiologic jets:
Flow is contained within the sewing ring.
Colour flow pattern is usually thin and laminar.
Jet length usually less <2-3cm.
Pathologic jets:
Any perivalvular jets (outside the sewing ring).
Different from the expected signature of the physiologic pattern for
the valve.
MECHANICAL PROSTHETIC VALVES
179
Ball and cage in
mitral position
LV
LA
Bileaflet
Closing jets
prosthesis in
mitral
position
LV
LA
Shadowing from valve
Fig. 3.44 Examples of apical views of mitral mechanical prostheses. The top figure
demonstrates a ball and cage valve and the lower figure a bileaflet prosthesis with
two closing jets. Note shadows behind the sewing ring. See W Video 3.26 and
W Video 3.27.
180
CHAPTER 3 Transthoracic valves
Bioprosthetic valves
Bioprosthetic valves are made from porcine aortic valve or bovine pericar-
dium. The leaflets are stiffer than native valve leaflets. Bioprostheses may
be stented or stentless. Stents or struts support the cusps and protrude
downstream (into the aorta with aortic bioprostheses or left ventricle
with mitral bioprostheses). Struts and the ring are metallic so cause shad-
owing (although less than mechanical prostheses). Some models can be
implanted in a supravalvular position. Although their flow profile is similar
to native valves, there is still an increased pressure gradient across the
prosthetic valves, particularly stented bioprostheses.
Stented bioprosthesis (Fig. 3.45)
Assessment
Use standard scan planes. Image prostheses through apical windows with
the beam perpendicular to the closed leaflets. Rotate transducer whilst
using colour flow mapping to assess perivalvular regurgitation.
Normal appearance
There will be shadows from the sewing ring and stents protruding down-
stream throughout the cardiac cycle. In the apical view usually 2 struts are
displayed and, in the short axis, the ring and 3 struts are visible. If the aortic
root is dilated there may be free space between sewing ring and root.
Valve closed: leaflets appear thin like a native valve. Physiologic
regurgitation may be present as small central jet (usually early
postoperatively).
Valve open: valve opens widely with leaflets parallel to the stent
(2-4mm distance).
Stentless bioprosthesis
Assessment
Use standard scan planes. Usually no shadowing.
Normal appearance
Usually very similar to native aortic valve. Leaflets may appear thickened
and junction between valve and annulus may be thickened due to sutures.
Pulmonary valve homografts may have supravalvular thickening and ste-
nosis. Ideally, no regurgitant jet but sometimes minor distortion during
implantation or due to mismatch of prosthesis causes mild central regurgi-
tation. Jet may be eccentric if due to distortion.
Homografts and autografts
May be used in endocarditis or as an autograft in young patients in aortic
valve disease (Ross procedure: native pulmonary valve is used for aortic
valve replacement and a bioprosthesis is implanted as pulmonary valve).
Scan planes and appearances are as for stentless bioprosthesis.
BIOPROSTHETIC VALVES
181
RV
Aorta
LV
LA
Stent of
stented
bioprosthetic
valve in
aortic position
RV
RA
Reverberation
LA
artefact
Fig. 3.45 Examples of stented bioprosthetic valves. The top figure shows a
parasternal long axis view of an aortic prosthesis and the lower figure a parasternal
short axis view. Note the bright struts with artefacts extending away. See W Video
3.28 and W Video 3.29.
182
CHAPTER 3 Transthoracic valves
Prosthetic valve abnormalities
Vegetation, thrombus, pannus
Extended masses on a prosthesis. Pannus is excessive endothelial prolifer-
ation causing obstruction and/or failure in complete valve closure. Pannus
is sometimes difficult to distinguish from thrombus. Both may be present.
No specific texture differentiates masses so to differentiate use:
Appearance: thrombi usually larger, protrude from the sewing ring and
less echocardiographically dense.
Clinical information: suboptimal anticoagulation makes thrombus more
likely, bacteraemia makes vegetation more likely.
Associated abnormalities: vegetations may be associated with
paravalvular abscesses, leaks.
Bioprosthetic valve degeneration
Observed in most prostheses after several years. Infrequent in first 3 years.
Leaflet calcification results in irregular thickening (usually >3mm in thick-
ness). Rigid leaflets have decreased cusp motion, cause stenoses and may
rupture resulting in prolapse (or flail cusp) and valvular regurgitation.
Prosthetic valve dehiscence—‘rocking’ valve (Fig. 3.46)
Exaggerated mobility of valve ring indicates dehiscence. Assess with 2D.
Usually associated with severe paravalvular regurgitation. Valve dehis-
cence is usually preceded by paravalvular leaks.
Valve prolapse In bioprostheses, prolapse of leaflet tissue is possible
and is seen in standard views. Usually leaflets are degenerated (irregular
thickening and calcification) and valvular regurgitation will be present.
Structural damage For example, broken occluder or restraining
system, will be combined with intravalvular regurgitation.
Sutures Seen as immobile, dense structures within the ring. Can
be difficult to differentiate from focal fibrosis. They will be mobile if
dehisced.
Strands Mobile, filamentous strands on normal and abnormal valves
(rarely seen adjacent to native valve). Thought to be fibrin strands
(they can disappear after thrombolysis of thrombosed prostheses).
Poor reproducibility in imaging these structures as visualization is highly
dependent on machine settings.
Pseudo-microbubbles (Fig. 3.47) Look like single contrast microbubbles.
Probably due to micro-cavitation. Found with normal valves but more
often if valve dysfunction. Appear as dots, moving away from prosthesis,
visible only shortly after valve closure (unless valvular or paravalvular leak).
In contrast, spontaneous echo contrast is seen only in areas of low blood
velocity (therefore not at orifices or leakages of prosthetic valves) and is
smoke-like in appearance with swirling patterns.
PROSTHETIC VALVE ABNORMALITIES
183
DIASTOLE
SYSTOLE
Valve dehiscence and ‘rocking’
RV
RV
Ao
Ao
LV
LV
LA
LA
Fig. 3.46 Example of aortic prosthesis rocking.
LV
RV
LA
RA
Pseudo bubbles
Fig. 3.47 Micro-bubbles associated with closure of a mitral prosthesis.
184
CHAPTER 3 Transthoracic valves
Prosthestic valve stenosis
Prosthetic valve stenosis suggests an acceleration of blood through the
prosthetic valve because of some pathology. Pressure gradients may go up
with thrombus/pannus and, rarely, vegetations or degeneration.
Assessment
General
If stenosis is suspected, initial assessment should be to look for pathology
that might explain stenosis (thrombus, vegetation, valve dysfunction) and
check the level of any obstruction (outflow tract, valve level). Then gather
supportive information about severity of any stenosis.
Grading severity
Pressure gradient and velocity (Fig. 3.48)
Techniques are as for native valves (CW Doppler) but mechanical pros-
theses can have 2 or 3 different-sized orifices so application of Bernoulli
equation is not straightforward and calculations can vary depending on
Doppler alignment. With cage-and-ball prostheses it is almost impossible
to get optimal Doppler alignment. In clinical practice, calculation of effec-
tive orifice area is useful.
Orifice area—aortic valve prostheses
Use same technique as for native valve (CW, PW, and LVOT diameter).
Reporting orifice area also avoids problems with variation in cardiac out-
put. For St. Jude bileaflet aortic prosthesis a Doppler velocity index has
been validated:
vti across LVOT/vti across aortic valve <0.23 suggests severe stenosis
Orifice area—mitral valve prostheses
Use techniques as for native valves. The pressure half-time tends to under-
estimate effective orifice area but can be used. Width of the forward flow
may be an alternative, if measured in 2 orthogonal planes.
What is abnormal for prosthetic valves?
Normal mechanical and stented bioprostheses have a pressure gradient
equivalent to mild or moderate stenosis. Normal ranges vary between
manufacturers and valves so refer to published information to give clini-
cal advice. Pressure gradients also vary with haemodynamics, such as
cardiac output, so there is considerable interpatient variability. General
principles about what might need investigation are best based on calcu-
lated orifice area:
Aortic prostheses may be stenotic if calculated valve area is <1cm2
or there has been a >30% change from last follow-up.
Mitral prostheses may be stenotic if pressure half-time >200ms
and peak diastolic velocity >2.5m/s (if only mild regurgitation).
Tricuspid prostheses may be stenotic if peak diastolic velocity
>2.5ms (if only mild regurgitation).
Peak prosthetic aortic jet velocity > 3 m/s
DVI
DVI
DVI
≥ 0.30
0.25-0.29
< 0.25
Jet contour
AT (ms)
>100
<100
>100
<100
Consider PrAV stenosis with
Suggests PrAV
Consider improper
Normal PrAV
• Sub-valve narrowing
stenosis
LVOT velocity**
• Underestimated gradient
• Improper LVOT velocity*
EOA
index
High flow
PPM
Fig 3.48 Algorithm for evaluation of elevated peak prosthetic aortic jet velocity incorporating DVI, jet contour, and acceleration time (AT). *Pulse wave (PW)
Doppler sample too close to the valve (particularly when jet velocity by continuous wave (CW) Doppler is
4m/s). ** PW Doppler sample too far (apical) from
Stenosis further substantiated by estimated orifice area (ERO) derivation compared with reference values if
valve type and size are known. Fluoroscopy and trans esophageal echocardi-ography (TEE) are helpful for further assessment, particularly in bileaf-let valves. Aortic
valve replacement (AVR). Doppler velocity index (DVI) is the ratio of the proximal velocity in the left ventricle out flow tract to that of flow velocity proximal to
the stenosis. Adapted from Figure 10, Recommendations for Evaluation of Prosthetic Valves With Echocardiography and Doppler Ultrasound. American Society of
Echocardiography 2009, 22(0):975-1014.
186
CHAPTER 3 Transthoracic valves
Prosthetic valve regurgitation
Transvalvular regurgitation describes regurgitation within the sewing
ring. This can be caused by leaflet prolapse (bioprostheses),
incomplete disc closure due to clot, pannus (mechanical prostheses)
or structural damage (broken retainment system, dislodged disc).
Paravalvular regurgitation has its origin outside the sewing ring. This
can occur immediately after surgery (usually trivial and resolves after
protamine or with endothelialization during first few postoperative
weeks), be due to dehiscence of the sewing ring, or secondary to
endocarditis.
Assessment
Decide if regurgitation is transvalvular or paravalvular (Fig. 3.48).
When jet is easily displayed it is often paravalvular, as physiologic and
transvalvular regurgitation is shadowed by valve.
Use multiple views and look at jet position with colour flow (use system-
atic approach similar to identification of mitral leaflet scallop prolapse).
Short axis views of rings are very useful to position jets. 3D echocardi-
ography may give further information. If paravalvular, report extent and
localization with figure or reference to ‘clock face’ in parasternal short axis
view (for mitral valve, area adjacent to aortic valve is 12 o’clock).
Transoesophageal echocardiography provides a comprehensive assess-
ment of severity and cause. It should always be performed if transthoracic
screening suggests there may be clinically significant regurgitation.
Grading severity
Pathological regurgitant jets are usually eccentric and often multiple.
Shadowing from sewing ring, struts or disc limit field of view. Therefore,
colour flow area, PISA and vena contracta are not reliable. Assessment
of severity is often qualitative, in which case indirect supportive measures
should also be provided and transoesophageal echocardiography advised.
Supportive measures
Increase in cavity diameters compared to previous studies.
If no prosthetic stenosis, an increase in forward flow velocity (due
to volume overload). For mitral prostheses moderate to severe
regurgitation is suggested by a peak velocity >1.9m/s and mean
gradient >5mmHg. If no aortic stenosis and only mild regurgitation
then a ratio of vti mitral prothesis/vti aortic valve >2.5 suggests
moderate to severe regurgitation.
Pulmonary venous flow for mitral regurgitation (systolic flow reversal).
If left ventricle function is impaired a blunted pulmonary vein flow
pattern is ‘normal’ after mitral valve replacement.
Aortic flow pattern for aortic regurgitation (diastolic flow reversal).
Other techniques
With transvalvular regurgitation (both mitral and aortic) one option is to
measure the proportional area of the sewing ring occupied by the jet in a
short axis view: <10% is mild, 10-25% is moderate, and >25% is severe.
PROSTHETIC VALVE REGURGITATION
187
RV
LV
RA
LA
Paravalvular
regurgitation
LV
RA
LA
Central
regurgitation
RV
LV
LA
Fig. 3.49 Examples of paravalvular and transvalvular regurgitation. See W Video
3.30.
188
CHAPTER 3 Transthoracic valves
Endocarditis
Diagnosis of endocarditis is based on clinical factors
(positive blood
cultures with appropriate organisms, predisposing factors, new valve
dysfunction, peripheral stigmata) supported by echocardiographic abnor-
malities (Duke’s criteria are widely used). A normal echocardiogram never
excludes endocarditis and, if clinical suspicion is high, transoesophageal
echocardiography should always be performed. If normal, repeat imaging
can be considered to monitor for developing pathology.
Assessment
For diagnosis use a full systematic examination with focus on valves (main
site). Bear in mind clinical situation: right-sided valves if intravenous infec-
tion (drugs, lines), known abnormal valves (prosthetic or degenerative),
previous endocarditis (old vegetations). For monitoring use full examina-
tion and make sure you comment on change from previous findings.
For all studies report on: vegetations (location, number, size), abscess
(particularly valve rings), fistulae (e.g. aorta to right heart), valve dysfunc-
tion (including severity, dehiscence, rupture), pericardial effusion.
Vegetation (Fig. 3.49)
Key features to help diagnose: (1) attachment to upstream-side valve;
(2) irregular shape; (3) oscillating motion distinct from valve; (3) related
valve dysfunction. Comment on number of vegetations, attachments, size
(measure in at least 2 directions and provide overall assessment—small,
moderate, large).
Abscess (Fig. 3.50)
Abscesses can be perivalvular or valvular. Appearances initially are often
of a thickening and ‘spongy’ appearance to valve ring (particularly aor-
tic root) or valve leaflet. An echo-free, fluid-filled centre may develop.
Abscesses may open into adjacent cardiac chambers (technically the space
is then no longer an abscess).
For each abscess comment on location with reference to position around
valve (e.g. annulus right coronary cusp). Measure size in different planes
and judge as small, moderate or large. Comment on functional effects of
abscess (e.g. outflow tract or valve distortion).
Fistula
Fistulae usually develop following an abscess and describe an abnormal
connection between 2 cardiac chambers. Use colour flow mapping to
track fistulae and identify jets in cardiac chambers. If aligned, use Doppler
to quantify flow direction and size.
Comment on physical size (length and width) and which chambers are
connected. Give an estimate of haemodynamic significance (e.g. size of
shunt left-to-right heart, change in ventricle size and function, degree of
regurgitation if fistula across valve).
Severity of valvular lesion (see individual valve sections)
Pericardial effusion (see b p.298)
ENDOCARDITIS
189
LV
RV
RA
LA
Tricuspid vegetation
LV
Mitral valve leaflet
LA
vegetation
Fig. 3.50 Top: apical 4-chamber views of tricuspid valve vegetation. Bottom:
parasternal view showing mitral valve vegetation. Note irregular appearance and
valve leaflet attachment. See W Video 3.31 and W Video 3.32.
Aortic root thickening consistent with abscess
RV
RA
AV
PA
LA
Fig. 3.51 Parasternal short axis view that demonstrates thickening of aortic root in
10 o’clock position consistent with an aortic root abscess.
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191
Chapter 4
Transthoracic anatomy
and pathology: chambers
and vessels
Left ventricle
192
Left atrial size
280
Left ventricular
Left atrial function
282
assessment 194
Left and right atria: normal
Left ventricular size
196
ranges 283
Left ventricular size: 2D
Right atrium 284
normal ranges 208
Right atrial size
284
Left ventricular thickness and
Interatrial septum
286
mass 210
Atrial septal defects
288
Left ventricular thickness and
Patent foramen ovale 290
mass: normal ranges 216
Atrial septal aneurysm
290
Left ventricular
Ventricular septum 292
hypertrophy 218
Ventricular septal defects
294
Hypertrophic
Pericardium 296
cardiomyopathy 220
Pericardial effusion
298
Left ventricular non-
Cardiac tamponade 300
compaction 222
Constrictive pericarditis
302
Restrictive
Congenital pericardial
cardiomyopathy 224
disease
306
Dilated cardiomyopathy 224
Pericardial tumours
306
Myocarditis 224
Acute pericarditis
306
Left ventricular function
226
Pericardiocentesis
306
Global systolic function
228
Aorta 308
Regional systolic function
234
Aortic size
310
Left ventricular strain
238
Aortic dilatation
314
Diastolic function
246
Marfan syndrome 316
HFNEF 252
Aortic dissection
318
Left ventricular
Aortic coarctation
320
synchrony 254
Sinus of Valsalva
Optimization 260
aneurysm 322
Right ventricle
262
Aortic atherosclerosis
324
Right ventricular size
264
Cardiac tumours 326
Right ventricular wall
Congenital heart disease 330
thickness
270
Congenital defects 336
Right ventricular function
272
Surgical correction of
Right ventricular
congenital heart
overload 276
disease
340
Left atrium 278
192
CHAPTER 4 Transthoracic chambers and vessels
Left ventricle
Normal anatomy
The left ventricle is a cavity with muscular walls that contains the papillary
muscles and their chordal attachments. The anatomic characteristics of
the chamber size and thickness can vary significantly with pathology, and
many cardiac and systemic processes are associated with cardiac dilatation
or hypertrophy.
Normal findings
2D views
The left ventricle is seen in virtually all windows. The minimal views are
parasternal long and short axis and the apical 4-, 2-, and 3-chamber views
(Fig. 4.1).
2D findings
Parasternal long axis: the basal and mid segments of the septum
and posterior wall (in some publications it is also referred to as the
inferolateral wall) are visible. This view is used for linear measures of
wall thickness and cavity dimensions. The left ventricular outflow tract
can also be assessed.
Parasternal short axis: by angling the probe back and forth, the whole
of the left ventricle can be scanned in cross-section. The key ventricle
views are mid-ventricle (mid-papillary) and apical. The mid-ventricle
level is used for linear and area measures of walls and cavity. Regional
wall motion abnormalities can also be assessed in (in clockwise order)
septum, anterior, lateral, and inferior walls.
Apical 4-chamber: provides best views of apex, septum (on left) and
lateral (on right) walls for regional assessment. Suitable for tracing
ventricle area and left ventricle length.
Apical 2-chamber: focuses on inferior (on left) and anterior walls (on
right).
Apical 3-chamber: the parasternal long axis view but from the apex.
Looks at posterior (inferolateral) wall and septum.
Subcostal provides an alternative view of the left ventricle but is not
essential.
3D views and findings
3D acquisitions of the left ventricle can be obtained from either the
parasternal or apical window.
3D full volume acquisition mode is preferably used to ensure that the
entire left ventricle is imaged.
Following acquisition, the 3D image can be rotated and cut through
any plane to examine any region of interest.
Good 2D endocardial definition is important when deciding on
suitability for 3D LV assessment.
See Chapter 2.
LEFT VENTRICLE
193
SEPTUM
APEX
RV
LV
SEPTUM
LV
LATERAL
RV
POSTERIOR
(INFEROLATERAL)
RA
LA
Parasternal long axis
Apical four chamber
ANTERIOR
SEPTUM
LV
LATERAL
INFERIOR
Parasternal short axis
APEX
APEX
INFERIOR
ANTERIOR
LV
LV
POSTERIOR
SEPTUM
(INFEROLATERAL)
RV
Apical two chamber
Apical three chamber
Fig. 4.1 Key views to assess the left ventricle with walls marked.
194
CHAPTER 4 Transthoracic chambers and vessels
Left ventricular assessment
General
Accurate left ventricular assessment (diameters, volumes, wall thickness,
mass, and function) is critical in clinical practice. Measurements can be
altered by virtually all cardiovascular pathologies. The most common indi-
cation for echocardiography is evaluation of left ventricular function, with
ejection fraction being the most sought parameter. Assessments are fre-
quently visually estimated but there is significant interobserver variability
and dependence on interpreter skill. Quantitative measures are recom-
mended to ensure diagnostic accuracy.
Assessment
Start with an overview of the ventricle in all views (parasternal and
apical) and gather an impression of appearance, size, and function.
Comment on obvious structural changes:
• Ventricular shape, aneurysms, wall thinning, wall hypertrophy, wall
character (‘speckling’ etc.).
Report quantitative measures of size (b p.196) and a general
summary: normal, mild, moderate, or severe dilatation; normal, mild,
moderate, or severe hypertrophy. If hypertrophy, give an idea of the
pattern based on appearance and relative wall thickness, i.e. eccentric,
concentric, asymmetric (septal, apical) (b p.218).
2D and M-mode quantification of left ventricular size and mass has
been well validated but both have advantages and disadvantages.
• M-mode measures in parasternal views are widely used. They
are very dependent on M-mode alignment and take no account
of left ventricle shape or regional wall motion abnormalities.
The alignment problem is reduced with 2D guided or direct 2D
measures.
• In general, left ventricle shape changes are best accounted for by
using the volumetric biplane Simpson’s method for volumes and the
truncated ellipsoid method for left ventricle mass. These methods
should therefore be used to provide accurate assessment of left
ventricle volume and mass respectively.
• Reference ranges are dependent on gender and body habitus.
Ideally, height and weight should be recorded and body surface
area used to correct left ventricular dimensions.
Using the measures of left ventricular size, report a quantitative
assessment of systolic function (e.g. ejection fraction) and summarize
as normal systolic function or mild, moderate, or severe systolic
dysfunction (b p.226).
From apical and parasternal views look at changes in regional wall
motion (normal, hypokinesis, akinesis, dyskinesis, aneurysmal). Report
abnormalities (b p.234).
When relevant, assess and report left ventricular diastolic function from
changes in mitral valve inflow and tissue Doppler imaging (b p.246).
Finally, ensure you have reported fully pathologies that might relate to
the changes you have identified in the left ventricle (e.g. valve disease).
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196
CHAPTER 4 Transthoracic chambers and vessels
Left ventricular size
Because it is difficult to quantify a 3D structure using 2D imaging, the
techniques that developed with 2D echocardiography rely on measuring
the ventricle in standard places. The measures are then reported directly
(linear methods) or used in mathematical equations to model an assumed
shape for the ventricle (volumetric measures). In principle, the more meas-
ures of the left ventricle in the more planes the more accurate the as-
sessment. Conversely, the fewer measures the more assumptions have
to be made and the more likely that regional pathology is overlooked.
Sometimes—such as in a normal heart—simple linear measures are ade-
quate. However, if there is pathology accuracy is required. More recently,
collection of 3D datasets has enabled much more accurate chamber size
quantification.
Linear measures
M-mode
This is based on change in size in a single plane at the mid ventricle level
in a parasternal view (Fig. 4.2). Recent guidelines suggest this should be a
parasternal short axis view.
Optimize a parasternal long axis view with the septum and posterior
wall lying parallel (or a parasternal short axis mid-ventricle view).
Drop the M-mode cursor through opposing walls so that it intersects
both at right angles. In the long axis view the cursor should lie at the
level of the mitral valve tips (some guidelines suggest chordal level).
Look at the M-mode trace and identify the 2 walls. Measure from
edge-to-edge where the walls are closest together (peak systole) and
furthest apart (end diastole). Report the left ventricle systolic and end-
diastolic diameters.
The M-mode trace from a parasternal long axis view can also be used
to measure septal and posterior wall thickness at end diastole.
2D-imaging
This follows the same principle as M-mode but relies on clear 2D images.
Record a loop of an optimized parasternal long axis or short axis (mid
ventricle) view. Identify the end-diastolic frame (largest ventricle).
Measure from endocardial border to border at right angles to each
wall (Fig. 4.3). In the long axis view the line should pass through the
mitral valve tips. Report the left ventricular end-diastolic diameter.
Scroll through the loop to identify the end-systolic frame (smallest
ventricle) and using the same technique measure the left ventricular
end-systolic diameter.
2D vs. 3D volume measurements
Volumes obtained from 3D measurements are significantly larger than
the volumes measured with 2D techniques, contrast enhanced 3D
volumes are larger than corresponding volumes in native 3D echo.
3D LV ejection fraction are lower than in 2D (lower limit 49%).
For longitudinal studies, the same imaging software and postprocessing
units should ideally be used in order to maintain consistency.
LEFT VENTRICULAR SIZE
197
M-mode cursor
PARASTERNAL LONG AXIS
PARASTERNAL SHORT AXIS
M-MODE TRACE
End-systolic
diameter
RV
IVS
LV
PW
End-diastolic
diameter
Fig. 4.2 Measurements using M-mode in parasternal views.
Left ventricle diameter measured
edge-to edge
RV
LV
LA
PARASTERNAL LONG AXIS
Left ventricle diameter measured edge-to-edge
PARASTERNAL SHORT AXIS
Fig. 4.3 Examples of 2D measures in parasternal views.
198
CHAPTER 4 Transthoracic chambers and vessels
2D volumetric measures
Simpson’s method
Simpson’s method (Fig. 4.4) is based on the principle of slicing the left
ventricle from apex down to mitral valve annulus into a series of discs. The
volume of each disc is then calculated (using the diameter and thickness of
each slice). All the disc volumes are added together to provide the total
left ventricular volume. If done in a single plane (based on apical 4-cham-
ber view) it is assumed the left ventricle is circular at each level. Accuracy
is improved by using diameters in 2 perpendicular planes (biplane—apical
4- and 2-chamber) so that the disc surface area is more precisely defined.
Although this can be done ‘by hand’ by measuring the diameter at multiple
levels, in reality, you trace the outline of the ventricle and the machine or
off-line software automatically calculates the volume.
In the apical 4-chamber view obtain a clear image of the left ventricular
cavity with a clear endocardial border.
Record a loop and scroll through to find the end-diastolic image
(usually just before the aortic valve opens or on the R-wave of the
ECG). This image should have the largest left ventricular volume.
Trace around the endocardial border going from one side of the mitral
valve annulus to the other and joining the 2 ends with a straight line.
Record the left ventricular end diastolic volume.
Measure the length of the left ventricle from apex to middle of mitral
valve. Depending on the machine, identification of the apex may be
automatic after tracing the border. Record left ventricular long axis.
Scroll through the loop again and find the smallest left ventricular
volume at end-systole (usually just before the mitral valve opens or
on the T-wave of the ECG). Trace around the endocardial border, as
before, and record left ventricular end systolic volume.
The method described will provide single plane measures of left
ventricular volumes. For biplane measures repeat the process for
diastolic and systolic images using an optimized apical 2-chamber view.
Normal ranges depend on technique, sex and body size
Systematic differences between techniques mean ‘normal’ ranges vary.
For instance, direct 2D measures tend to produce slightly smaller meas-
ures than M-mode. Also, normal ranges depend on the sex and size
of the person. Always report the method you used and demographic
data.
LEFT VENTRICULAR SIZE
199
APICAL FOUR CHAMBER
Left ventricle cavity trace
RV
LV
RA
LA
Left ventricle length
APICAL TWO CHAMBER
Left ventricle cavity trace
LV
LA
Left ventricle length
Fig. 4.4 Biplane Simpson’s method for measurement of left ventricle cavity size.
200
CHAPTER 4 Transthoracic chambers and vessels
Area length equation (Fig. 4.5)
This method can be used if apical definition is poor and it is difficult to
trace the border. It is based on an equation that models a ‘bullet-shaped’
ventricle (and therefore does not take account of regional abnormalities).
For the equation you need the length of the ventricle and the cross-
sectional area at the mid papillary level.
Obtain a clear parasternal short axis (mid ventricle level) view with
good endocardial border definition and record a loop.
Trace around the endocardial border in the end diastolic frame to
obtain the end-diastolic cross sectional area.
In an apical 4-chamber view record the distance from the middle of
the mitral valve annulus to the left ventricle apex at end-diastole and
record the end diastolic left ventricle long axis lengths.
Ventricular volume at end-diastole is then:
(5
cross-sectional area in parasternal short axis ventricle length
• Ventricular volume at end-systole can be measured in exactly the same
way but using parasternal and apical images frozen at end-systole.
Avoid foreshortening—ensure a clear endocardial border
Accurate left ventricular volume measurements require an
unforeshortened ventricle. Foreshortening leads to underestimation
of volume and changes ventricle shape. Foreshortening can usually
be avoided by moving more lateral ± 1 intercostal space further
down. 3 pointers to be confident you have identified the true apex:
Apex is fixed and does not move towards the base in systole.
Apical myocardium is thinner than the rest of the ventricle.
The view is the one with the longest ventricle (if apical view).
If the endocardial border is not clear, volumes will be overestimated.
Clear definition is particularly important to see regional wall motion
abnormalities. Endocardial definition can be enhanced by machine
controls to improve grey levels (such as harmonic imaging, gain,
and contrast) or probe position (increased pressure, better contact,
slight changes in window). If these factors make no difference,
intravascular contrast agents provide excellent border definition.
LEFT VENTRICULAR SIZE
201
Length
LEFT
VENTRICLE
5 x cross sectional area x length
VOLUME
6
Cross sectional area
Trace of
endocardial border
LV length
RV
LV
RA
LA
Fig. 4.5 Area length equation based on measurement of cross-sectional area and
left ventricle length.
202
CHAPTER 4 Transthoracic chambers and vessels
3D volumetric measures
3D echocardiography is an advance on Simpson’s method as it allows con-
touring of the cavity within the 3D space of the echocardiographic volume
acquisition. Therefore there is no need to assume that the short axis view
of the ventricle follows the shape of a circle (or oval) and sum together a
stack of discs’. Instead you can contour the actual shape of the ventricle
in all dimensions.
In order to process full volume data sets, a 4D semi-automated
contour detection program with manual correction options written
specifically for the left ventricle is needed.
Commercially available scanners contain software tools which allow
the assessment of left ventricular volumes and ejection fraction. An
alternative is off-line processing with a commercially available software
package (4D-LV Function, TomTec, Germany) that is able to process
3D datasets from different scanner systems.
After acquisition of a 3D dataset, sliced planes are viewed in
4-chamber view, 2-chamber view, and one or more short axis views
(C-planes) (Figs. 4.6 and 4.7).
The left ventricular volumes are calculated by summing the areas
for each slice through the complete volume data set (volumetric 3D
echo).
How to get optimal 3D volumes
Good image quality on 2D echocardiography is important when
selecting patients to undergo 3D image acquisition.
If the endocardial definition is poor then a left-sided contrast agent
can be used (b p.561).
Full volume datasets are triggered from the ECG trace and so it is
important that the patient has a regular heart rhythm.
To reduce the incidence of stitch artefacts the probe and patient
position should be maintained in a stable position.
Acquisition with the patient holding their breath is advised if the full
volume dataset is going to be acquired over several heartbeats.
LEFT VENTRICULAR SIZE
203
Fig. 4.6 Biplane view during 3D apical LV acquisition showing the 4 -chamber view
(left) and 2-chamber view (right). See W Video 4.1 and W Video 4.2.
Fig. 4.7 3D full volume LV data presentation on Philips QLAB 7.1. Apical
4-chamber view (top left), biplane apical 2-chamber view (top right), short axis
(C plane) view (bottom left), and representation of the 3 displayed planes (bottom
right).
204
CHAPTER 4 Transthoracic chambers and vessels
Acquisition of 3D volume for assessment of LV
Position the probe at the apex in the same position as for acquisition
of 2D 4-chamber view. Modified windows may be used if selected
parts of the left ventricle need to be assessed.
A biplane preview screen is used so that the 4- and 2-chamber views
can be seen simultaneously to help avoid foreshortening, see Fig. 4.6.
Depth, gain, and TGC are adjusted in 2D imaging in order to achieve
the best possible endocardial definition.
For full volume datasets maximize the number of subvolumes (beats)
used to generate the 3D image according to patient breath holding
capabilities and the regularity of the heart rhythm. The greater the
number of subvolumes that can be acquired and effectively stitched
together without artefacts, the greater the temporal and spatial
resolution.
Acquire a 3D dataset and then evaluate it for quality.
Commercially available 3D scanners allow the acquired image to
be viewed on the machine in several short axis planes as well as
a rendered 3D volume. This is important in order to identify any
stitching artefacts which may have occurred.
Assess endocardial visualization using the cropping tools of the
scanner.
If not adequate, discard and acquire another. Keep doing this until you
are happy that you have a volume you will be able to post-process
effectively.
Preparing the dataset
Postprocessing systems will normally automatically display an apical
4-chamber view, 2-chamber view, and C-planes (short axis view). How
you then handle the images varies with the different software packages
but typically:
The planes can then be adjusted by the operator to ensure the
4-chamber plane has been accurately identified and is unforeshortened.
Similarly the plane used to create the 2-chamber view can also be
adjusted.
Once happy that the long axes of the heart have been identified the
ventricular volumes and ejection fraction can then be calculated. To do
this typically the operator is asked to:
• Identify the end-diastolic and end-systolic frame (some software
will require you to mark these frames).
• Identify anatomical points on the 4- and 2-chamber left ventricular
views (e.g. left ventricular walls, left ventricular apex, or mitral
valve, see Fig. 4.8) so that the semi automated programme can
delineate the left ventricular contour. The software then will
delineate the contours in the other slices and frames, see Fig. 4.9.
LEFT VENTRICULAR SIZE
205
Fig. 4.8 Setting anatomical landmarks for estimation of 3D end-diastolic volume
(Phillips QLAB). Once the appropriate frame for end diastole has been selected
and the image has been orientated to reduce foreshortening the post processing
programme prompts the operator to mark the basal septum (yellow dot), basal
lateral wall (red dot), basal anterior wall (purple dot), basal inferior wall (black dot),
and the apex (blue dot).
Fig. 4.9 Once the initial anatomical landmarks have been set, the post processing
programme will delineate the LV contour for view in the 4 chamber (top right),
2 chamber (top left) and short axis or C-Plane views (bottom left). In doing this a
17 segment model of the LV is created (bottom right). See W Video 4.3.
206
CHAPTER 4 Transthoracic chambers and vessels
Review of contouring and calculation of volumes
Once the postprocessing package has completed contouring the left
ventricle (Fig. 4.10), check that it has accurately delineated the true
left ventricular border by slicing through the left ventricular cavity
in the short axis planes and make corrections if you observe major
deviations.
The end-diastolic, end-systolic volumes, stroke volume, and ejection
fraction are judged as in 2D echocardiography.
Visually assess the regional left ventricular wall motion in the standard
apical and serial short axis views to ensure that the calculated ejection
fraction is similar to what the operator would expect visually.
The left ventricular volume can be subdivided into 16 or 17
subvolumes. These create a pyramid volume with the peak in the
centre of the left ventricle, which is often coloured in by the software
(Fig. 4.11).
The end-diastolic, end-systolic volumes and ejection fraction can
be assessed for each of the subvolumes, but the generally accepted
normal values are not yet available. At present the display of the
subvolumes helps to visualize regional wall motion abnormalities in
conjunction to the findings in the 2D cut planes.
The timing of peak contraction can be assessed using the subvolume
curves (Fig. 4.11).
The 3D analysis software measures the time from end-diastole until
the smallest left ventricular volume is recorded (lowest point of the
curve) and calculates the mean and standard deviation.
Left ventricular size: 3D normal ranges
Upper normal values (mean + 2 standard deviations [SD])
LV end-diastolic volume index (LVEDVI): 82mL/m2
LV end-systolic volume index (LVESVI): 38mL/m2
Lower limit (mean – 2 SD)
LVEF: 49%
For left ventricular subvolumes no generally approved normal values
have been established.
EF, ejection fraction; LVEDVI, LV end-diastolic volume index; LVESVI, LV end-
systolic volume index.
LEFT VENTRICULAR SIZE
207
Fig. 4.10 Following initial placement of the required landmarks on the apical
4- and 2-chamber views the post processing programme will contour the volume.
The accuracy of this automatic process can be checked by slicing down the short
axis planes and checking if the delineated contour (yellow line) tracks the LV
endocardial border well. Adjustments can then be made if there are discrepancies.
See W Video 4.4.
Fig. 4.11 17 segment 3D LV volume shell at end diastole (left) and at end systole
(right) with diastolic volume represented as a wire frame. A = anterior, S = septum,
L = lateral, I = inferior. 16 segment 3D LV volume curves during a cardiac cycle.
See W Video 4.5.
208
CHAPTER 4 Transthoracic chambers and vessels
Left ventricular size:
2D normal ranges (Table 4.1)
Table 4.1 Ranges for measurement of left ventricular size. (Adapted
from Recommendations for Chamber Quantification: A Report
of the American Society of Echocardiography Guidelines and
Standards Committee and the Chamber Quantification Writing
Group, Developed in Conjunction with the European Association of
Echocardiography. J Am Soc Echocardiogr 2005; 18: 1440-1463.)
Part 1, Values for women
Women
Normal
Mild
Moderate
Severe
LV dimension
LV d diameter, cm
3.9-5.3
5.4-5.7 5.8-6.1
>6.1
LV d diameter/BSA, cm/m2 2.4-3.2
3.3-3.4 3.5-3.7
>3.7
LV d diam/height, cm/m
2.5-3.2
3.3-3.4 3.5-3.6
>3.7
LV volume
LV d vol, mL
56-104
105-117 118-130
>130
LV d vol/BSA, mL/m2
35-75
76-86 87-96
>96
LV s vol, mL
19-49
50-59 60-69
>69
LV s vol/BSA, mL/m2
12-30
31-36 37-42
>42
Linear method: fractional shortening
Endocardial, %
27-45
22-26 17-21
<17
Mid wall, %
15-23
13-14 11-12
<11
2D method
Ejection fraction, %
>54
45-54 30-44
<30
BSA, Body surface area; d, diastolic; s, systolic.
Bold rows identify best validated measures.
LEFT VENTRICULAR SIZE: 2D NORMAL RANGES
209
Table 4.1 (Contd.)
Part 2, Values for men
Men
Normal
Mild
Moderate
Severe
LV dimension
LV d diameter, cm
4.2-5.9
6.0-6.3 6.4-6.8
>6.8
LV d diameter/BSA, cm/m2 2.2-3.1
3.2-3.4 3.5-3.6
>3.6
LV d diameter/height, cm/m 2.4-3.3
3.4-3.5 3.6-3.7
>3.7
LV volume
LV d vol, mL
67-155
156-178 179-201
>201
LV d vol/BSA, mL/m2
35-75
76-86 87-96
>96
LV s vol, mL
22-58
59-70 71-82
>82
LV s vol/BSA, mL/m2
12-30
31-36 37-42
>42
Linear method: fractional shortening
Endocardial, %
25-43
20-24 15-19
<15
Mid wall, %
14-22
12-13 10-11
<10
2D method
Ejection fraction, %
>54
45-54 30-44
<30
BSA, Body surface area; d, diastolic; s, systolic.
Bold rows identify best validated measures.
210
CHAPTER 4 Transthoracic chambers and vessels
Left ventricular thickness and mass
All measurements of left ventricular mass are based on the principle of
estimating the difference between the epicardial and endocardial left
ventricular volumes and then calculating the mass of this ‘shell’ using the
known myocardial density (i.e. multiplication of the volume by 1.05). The
measurement techniques are the same as for quantification of left ven-
tricular size (b p.196). However, they are applied to obtain both a cavity
volume and a total volume. Measurements are done at end-diastole.
Linear measures of wall thickness can be reported directly or used
to estimate mass based on simple formulae but do not take account of
changes in left ventricular geometry. Volume measures are preferred and
3D echocardiography can also be used to assess mass as long as there is
good epicardial border definition.
Linear measures
Interventricular septum and posterior wall thickness
The simplest and most widely used assessments of left ventricular thick-
ness are interventricular septum and posterior wall thickness from M-mode
or 2D images (Fig. 4.12).
In a parasternal long axis or parasternal short axis (mid papillary level)
drop an M-mode cursor through the ventricle perpendicular to the
walls at the level of the mitral valve leaflet tips.
Identify the lines that relate to the septum and posterior wall and
measure the thinnest part (end-diastole).
Report wall thickness and if increased consider further characterization
of hypertrophy (b p.218)
Measurements can also be done directly from parasternal 2D images,
frozen in end-diastole. Measure with calipers from edge to edge.
Volume measures from linear measures
Teichholz method or prolate ellipse of revolution
Left ventricular mass can be estimated from linear dimensions (see b
‘Linear Measures’, p.210) using a ‘prolate ellipse of revolution’ formula.
Traditionally, this was based on M-mode measures. The equation uses
cubed measurements so slightly off-axis views or small errors in diam-
eter are amplified into large differences in volume. The method takes no
account of abnormal left ventricular morphology and is rarely used now.
In parasternal long or short axis (mid papillary level) views obtain
measures of left ventricular end-diastolic diameter (LVEDD),
interventricular septum thickness (IVS) and posterior wall thickness (PWT).
In an apical 4-chamber view obtain a measure of end-diastolic left
ventricular length (from apex to middle of mitral valve annulus).
Left ventricular mass is automatically calculated using the formula:
0 8× 1 05
0.6
g
(the constants (0.8 and 0.6) improve the accuracy of the basic equation
(in bold) in studies based on postmortem hearts).
LEFT VENTRICULAR THICKNESS AND MASS
211
M-mode cursor
PARASTERNAL LONG AXIS
PARASTERNAL SHORT AXIS
M-MODE TRACE
Interventricular
septum
RV
IVS
LV
PW
Posterior wall
Interventricular
septum
Posterior wall
Fig. 4.12 Position for linear measures of left ventricle thickness.
212
CHAPTER 4 Transthoracic chambers and vessels
2D volume measures (Fig. 4.13)
Area-length and ellipsoid models
There are two validated methods available for estimating left ventricular
mass based on the area-length formula (b p.200) and the truncated
ellipsoid model. Both methods use the same set of measurements in end-
diastole—total and cavity myocardial area (short axis view, mid-papillary
level) and left ventricle length (apical 2 chamber view)—and only vary in the
equation they use to estimate volumes.
Obtain a clear parasternal short axis view (mid ventricle level) with
good endocardial and epicardial border definition.
Record a loop and scroll through to the end-diastolic frame.
Trace around the endocardial border and record the endocardial or
left ventricular cavity cross sectional area. Do not include the papillary
muscles in the tracing.
Trace around the epicardial border and record the epicardial or total
cross sectional area.
Myocardial area is the difference between the total cross-sectional area
and the cavity cross sectional area.
In a non-foreshortened apical 2-chamber view record a loop and
identify the end-diastolic frame (when the ventricle is largest). Measure
the distance from apex to the middle of the mitral valve annulus.
Record the left ventricular length.
The machine or off-line software will automatically calculate left
ventricular mass from these measurements.
The truncated ellipsoid equation for a volume is:
8
cross-sectional area in parasternal short axis 2 3
ventricle lenght
Biplane Simpson’s model
It is possible to use a biplane Simpson’s method (b p.198) to calculate
mass from 2D images as long as epicardial border definition is good. The
accuracy of the technique is dependent on obtaining a clear epicardial bor-
der in both planes but, unlike other methods, will take account of regional
wall motion abnormalities or asymmetric variation in wall thickness. The
principle behind this technique is also the basis for how mass is measured
in 3D echocardiography. To undertake this with 2D:
Measure total end-diastolic left ventricular volume using Simpson’s
method by tracing the epicardial border in apical 4- and 2-chamber
views.
Subtract left ventricular end-diastolic volume assessed with Simpson’s
method from this total volume. Multiply the difference by 1.05 to
obtain a left ventricular mass.
LEFT VENTRICULAR THICKNESS AND MASS
213
ALL MEASURES AT END DIASTOLE
LEFT
EPICARDIAL
LEFT
VENTRICLE
VOLUME
VENTRICLE
WALL
VOLUME
VOLUME
LEFT VENTRICLE WALL VOLUME MYOCARDIAL DENSITY (1.05) = LEFT VENTRICLE MASS
Traced endocardial border
LV
Traced epicardial border
APICAL TWO CHAMBER
LV length
LV
LA
Fig. 4.13 Measures for volume assessment for left ventricular mass.
214
CHAPTER 4 Transthoracic chambers and vessels
3D volume measures
3D assessment of mass is an improvement on the 2D biplane Simpson’s
approach to assessment of mass but instead of just using 2 planes the
contours of the epicardial and endocardial ‘shells’ are identified in 3D
by automated software. This technique of measuring the volume in 3D
is a key reason why left ventricular mass can be measured so accurately
with cardiovascular magnetic resonance. With good image quality, 3D left
ventricular mass measures with echocardiography are now as good as gold
standard techniques. To measure left ventricular mass with 3D:
Acquire a 3D apical full volume data set, see b p.202.
Continue to discard and acquire full volumes until you are happy
you have the best quality 3D dataset without artefact and with good
border definition.
Load the dataset into postprocessing software. This will display the left
ventricle in the standard views, typically, 4-chamber, 2-chamber, and
short axis stack.
The exact approach to analysis depends on the software package.
However, typically (Fig. 4.14).
• In the 4-chamber view the operator will have to mark the mitral
valve hinge points and contour the end diastolic endocardial
border.
• The operator then identifies the contour of the outer ventricular
wall.
• This procedure is repeated for the 2-chamber view.
• The software package then automatically estimates the end-
diastolic volumes and, base to apical length to generate a measure
of left ventricular mass.
LEFT VENTRICULAR THICKNESS AND MASS
215
Fig. 4.14 3D estimation of LV mass using Phillips QLAB. End-diastolic frames in the
apical 4-chamber and apical 2-chamber views are selected. The mitral valve insertion
points and endocardial border is contoured (yellow line). Following this the outer
LV wall is contoured (green line). The software will then calculate the end diastolic
volume, base to apical length and LV mass.
216
CHAPTER 4 Transthoracic chambers and vessels
Left ventricular thickness and mass:
normal ranges (Table 4.2)
Table 4.2 Ranges for measurement of left ventricular mass.
(Adapted from Recommendations for Chamber Quantification:
A Report of the American Society of Echocardiography Guidelines
and Standards Committee and the Chamber Quantification Writing
Group, Developed in Conjunction with the European Association of
Echocardiography. J Am Soc Echocardiogr 2005; 18: 1440-1463.)
Part 1, Values for Women
Women
Normal Mild
Moderate Severe
Linear method
LV mass, g
67-162
163-186
187-210
>210
LV mass/BSA g/m2
43-95
96-108
109-121
>121
LV mass/height, g/m
41-99
100-115
116-128
>128
LV mass/height2, g/m2
18-44
45-51
52-58
>58
Relative wall thickness, cm
0.22-0.42 0.43-0.47 0.48-0.52
>0.52
Septal thickness, cm
0.6-0.9
1.0-1.2
1.3-1.5
>1.5
Posterior wall thickness, cm 0.6-0.9
1.0-1.2
1.3-1.5
>1.5
2D method
LV mass, g
66-150
151-171
172-182
>182
LV mass/BSA, g/m2
44-s88
89-100
101-112
>112
BSA, Body surface area.
Bold rows identify best validated measures.
LEFT VENTRICULAR THICKNESS AND MASS: NORMAL RANGES
217
Table 4.2 (Contd.)
Part 2, Values for men
Men
Normal Mild
Moderate Severe
Linear method
LV mass, g
88-224
225-258
259-292
>292
LV mass/BSA g/m2
49-115
116-131 132-148
>148
LV mass/height, g/m
52-126
127-144
145-162
>163
LV mass/height2, g/m2
20-48
49-55
56-63
>63
Relative wall thickness, cm
0.24-0.42 0.43-0.46 0.47-0.51
>0.51
Septal thickness, cm
0.6-1.0
1.1-1.3
1.4-1.6
>1.6
Posterior wall thickness, cm 0.6-1.0
1.1-1.3
1.4-1.6
>1.6
2D method
LV mass, g
96-200
201-227
228-254
>254
LV mass/BSA, g/m2
50-102
103-116 117-130
>130
BSA, Body surface area.
Bold rows identify best validated measures.
218
CHAPTER 4 Transthoracic chambers and vessels
Left ventricular hypertrophy
General
The clinical importance of left ventricular mass relates to identification of
pathological left ventricular hypertrophy. Left ventricular hypertrophy can
occur secondary to other pathology (e.g. aortic valve disease or hyperten-
sion), or be a primary problem with the myocardium (e.g. hypertrophic
cardiomyopathy, infiltrative cardiomyopathy). With hypertrophic cardio-
myopathy there may be asymmetric changes with septal or apical changes.
Physiological hypertrophy is also found (e.g. athletes or in pregnancy) that
is thought to be reversible. In the elderly there is sometimes septal angula-
tion and thickening which creates the impression of septal hypertrophy
but left ventricle mass is usually unchanged.
Assessment
If hypertrophy is present base further assessment on: (1) a description of
the pattern (global or asymmetric) (Fig. 4.15), (2) a description of severity
using overall mass and mass relative to ventricular size, (3) characteri-
zation of related pathology (e.g. valve disease or outflow tract obstruc-
tion) and unusual appearances (e.g. speckling texture of amyloid, localized
hypertrophy of tumour).
Appearance
Using all views make a qualitative judgement of hypertrophy.
Parasternal short axis view is good for seeing concentric hypertrophy.
Parasternal long axis and apical 5-chamber views pick up septal
hypertrophy. Apical and subcostal views can look for apical
hypertrophy. Report the pattern and, if asymmetric, wall thickness
measures at different points.
A common reported abnormal texture is amyloid ‘speckling’. This can
be influenced by contrast and gain settings. Localized hypertrophy with
abnormal echolucency might suggest malignant infiltration.
Grading severity
Left ventricular mass can be clinically graded into 4 categories: (1) normal,
(2) increased relative wall thickness with increased mass (concentric left
ventricular hypertrophy), (3) increased mass with normal relative wall
thickness (eccentric left ventricular hypertrophy) or (4) normal mass with
increased relative wall thickness
(concentric remodelling). Concentric
changes suggest pressure overload (e.g. due to aortic stenosis or hyper-
tension). Eccentric changes suggest volume overload (e.g. due to aortic
regurgitation). Grade severity by reporting overall mass and/or wall thick-
ness, and relative wall thickness.
Overall severity: Fig. 4.15 provides a guide to grading hypertrophy
based on mass and wall thickness measures.
Relative wall thickness: use left ventricular posterior wall thickness
(PWT) and left ventricular end diastolic diameter (LVEDD). Relative
wall thickness is calculated as: (2 × PWT)/LVEDD.
• If relative wall thickness is >0.42 report concentric hypertrophy.
• If relative wall thickness is <0.42 report eccentric hypertrophy.
LEFT VENTRICULAR HYPERTROPHY
219
NORMAL
ECCENTRIC
CONCENTRIC
HYPERTROPHY
HYPERTROPHY
ASYMETRIC
HYPERTROPHY
e.g. pressure overload—
aortic stenosis,
e.g. volume overload
hypertension
e.g. hypertrophic
cardiomyopathy
>0.42
CONCENTRIC
CONCENTRIC LVH
REMODELLING
RELATIVE
WALL
THICKNESS
<0.42
NORMAL
ECCENTRIC LVH
NORMAL
HYPERTOPHY
LV MASS
Fig. 4.15 Patterns of hypertrophy.
220
CHAPTER 4 Transthoracic chambers and vessels
Hypertrophic cardiomyopathy
General
Hypertrophic cardiomyopathy describes marked left ventricular hyper-
trophy secondary to specific genetic abnormalities. There are multiple
gene defects that lead to hypertrophy and more are being identified. The
responsible genes commonly control muscle fibre function. The hypertro-
phy can be of many different patterns and towards the end of the disease
process left ventricular failure can develop (in 10% of cases). The classic
pattern is of marked septal hypertrophy (Fig. 4.16) associated with sig-
nificant outflow obstruction. LVOT obstruction occurs in about a quarter
of patients. Symptoms of breathlessness may be due to any or a com-
bination of: reduced diastolic or systolic left ventricular function, mitral
regurgitation, left LVOT obstruction or microvascular dysfunction.
Assessment
If hypertrophic cardiomyopathy is suspected report the pattern and
measures of wall thickness, relative wall thickness and mass.
Assess the LVOT at rest and consider exercise-induced gradients.
Report left ventricular systolic and diastolic function and look at mitral
valve function and regurgitation.
Assessment of strain or myocardial velocities using TDI or speckle
tracking may help identify impaired cardiac function prior to cardiac
hypertrophy.
Left ventricular outflow
Historically, M-mode has been used to demonstrate outflow obstruction.
Systolic anterior motion of mitral valve is seen with M-mode placed
through the mitral leaflets. It is considered severe (i.e. obstructive)
if the leaflet touches the ventricular septum or the outflow tract is
narrowed by the anterior mitral valve leaflet for >40% of systole.
Obstruction tends to be in mid to late systole leading to a drop in
flow through the aortic valve towards the end of systole. Therefore,
an M-mode trace through the aortic leaflets can demonstrate early
closure of the valve and the valve may appear to flutter as flow drops.
Doppler should be used as the main method to quantify obstruction.
In an apical 5- or 3-chamber view place colour flow mapping over the
outflow tract. This may demonstrate turbulent, high velocity, flow (an
irregular scattering) in the outflow tract.
In the apical 5-chamber view align the CW Doppler through the
outflow tract, aortic valve, and aorta. Record a spectral trace to obtain
peak and mean velocities. The trace may appear as a scimitar shape
demonstrating the classic, late, dynamic obstruction (Fig. 4.17).
Place PW Doppler at the bottom of the outflow tract and move it
towards the valve. If the gradient is due to hypertrophy the peak
velocities will be present in the outflow tract below the valve and the
trace will start aliasing due to the high velocities.
In a symptomatic patient—particularly if symptomatic on exercise—
without obstruction, an exercise stress protocol can be used and
outflow tract gradient measured at peak exercise.
HYPERTROPHIC CARDIOMYOPATHY
221
Asymetric septal
hypertrophy
RV
LV
LA
Fig. 4.16 Parasternal long axis view demonstrates septal hypertrophy.
See W Video 4.6.
Systolic anterior
motion of
mitral valve
LV
LA
Late systolic acceleration
—‘scimitar’ curve
Normal shape
Fig. 4.17 Top: apical 4-chamber view demonstrates systolic anterior motion of
mitral valve. Bottom: scimitar-shaped spectral trace characteristic of late systolic
acceleration.
222
CHAPTER 4 Transthoracic chambers and vessels
Left ventricular non-compaction
Left ventricular non-compaction is an inherited condition characterized
by marked left ventricular trabeculation (Fig. 4.18) within the left
ventricular apex and if more pronounced extending towards the
midventricular or even basal segments.
The inferior and lateral segments are more commonly affected than
the septum.
Left ventricular non-compaction may lead to impaired ventricular
function and can be a substrate for left-sided thrombi and arrhythmias.
To identify non-compaction left-sided contrast agents are helpful. In
apical views the trabeculation is seen as a partially contrast-filled layer.
Report the thickness of the trabeculation relative to the myocardium.
A ratio of >2:1 of the non-compacted (trabeculations) myocardium
to compacted (normal) myocardium at end-systole suggests left
ventricular non-compaction. Colour Doppler often demonstrates
flow between the trabeculations. Cardiovascular magnetic resonance
imaging aids diagnosis.
LEFT VENTRICULAR NON-COMPACTION
223
2D IMAGE
CONTRAST IMAGE
Marked
lateral wall
trabeculation
Fig. 4.18 An apical 4-chamber view demonstrating lateral wall trabeculation. The
abnormal trabeculations of left ventricular non-compaction can be highlighted with
contrast (note improved image quality between native and contrast images) or
colour flow mapping. See W Video 4.7 and W Video 4.8.
224
CHAPTER 4 Transthoracic chambers and vessels
Restrictive cardiomyopathy
True restrictive cardiomyopathy is rare and tends to occur due to infiltra-
tive disease such as amyloidosis. Symptoms develop due to myocardial
thickening and stiffening leading to diastolic dysfunction. Late in the disease
systolic dysfunction can develop as contractile function diminishes.
A full assessment of the left ventricle (size and mass, systolic
and diastolic function; b p.246) is needed for diagnosis. Classic
appearance is normal systolic function and cavity dimensions but
abnormal diastolic function with varying increases in wall thickness.
The usual diagnostic conundrum is differentiation from constrictive
pericarditis. Techniques such as tissue Doppler imaging and mitral
inflow are useful and described in the pericardium section on b p.302.
Dilated cardiomyopathy
Dilated cardiomyopathy describes left ventricular dilatation and impaired
function and can be accompanied by right ventricular dilatation. There can
be many underlying causes, such as ischaemic heart disease, tachycardia-
induced, metabolic conditions (e.g. hyperthyroidism, phaeochromocytomas),
postpartum, or post-myocarditis. The term idiopathic dilated cardiomyop-
athy is used if no underlying cause is identified. Echocardiography should
provide information on ventricle size and function and, be used for follow-
up to gauge recovery or deterioration.
Myocarditis
Myocarditis occurs due to a viral infection either acutely or as a post-viral
phenomenon. It can affect left ventricular global systolic function with or
without left ventricular dilatation and can range from mild to severe. A peri-
cardial effusion may also develop. LV dysfunction can resolve, stabilize, or
deteriorate and myocarditis is a common cause for dilated cardiomyopathy.
Recovery is assessed by repeated echocardiography to determine changes
in left ventricular function. Cardiovascular magnetic resonance imaging may
be useful to determine the degree of myocardial damage.
MYOCARDITIS
225
3D echocardiography in cardiomyopathies?
Real-time 3D echocardiography has advantages over 2D echocardiog-
raphy which may be helpful in the assessment of patients with cardio-
myopathies:
It permits more accurate assessment of ventricular volumes.
3D imaging allows detection of early changes in myocardial
mechanics prior to changes in conventional measures of ventricular
function with the use of 3D speckle tracking. This has been shown
to provide results similar to that for 2D speckle tracking although as
real-time 3D uses only one apical view rather than multiple views,
post-processing is less time consuming.
For the assessment of cardiomyopathies with poor ventricular
function, real-time 3D has been used to quantify left ventricular
mechanical dyssynchrony to identify patients who may be suitable for
cardiac resynchronization therapy.
In patients with hypertrophic cardiomyopathy, 3D echocardiography
has been shown to provide important insights into the mechanics
and deformational geometry of the left ventricular outflow tract.
3D echocardiography has helped to show that in patients with
hypertrophic cardiomyopathy and systolic anterior motion of the
mitral valve the anterior segment of the anterior mitral valve leaflet
causes the development of the left ventricular outflow tract gradient.
In patients with apical hypertrophic cardiomyopathy, 3D
echocardiography allows cropping to visualize the left ventricular
apex in multiple directions planes to help assess for hypertrophy.
The use of 3D echocardiography in the diagnosis of left ventricular
non-compaction has also been reported. By rotating and cropping
the dataset it allows the extent of non compaction to be determined
in a segmental approach.
226
CHAPTER 4 Transthoracic chambers and vessels
Left ventricular function
Assessment of left ventricular function is one of the most frequently
requested echocardiography studies, with ejection fraction the most
sought after parameter. This is driven by several issues:
The number of patients presenting with dyspnoea and possible
congestive heart failure is increasing, there is clear prognostic
significance to the parameter of ejection fraction.
To help guide therapy (especially decisions for device therapy in heart
failure and surgery for valve disease). Remember that congestive
heart failure is a clinical diagnosis and even before clinical signs are
evident abnormalities of left ventricle function may be apparent. Early
detection is critical to prevent progression of heart failure.
Assessment
An assessment of left ventricle function should be comprehensive. Box 4.1
outlines the techniques for a complete examination. Not all will be felt nec-
essary for all patients and selection should be based on the clinical indication
for the study. However, the minimal requirements are an assessment of:
Left ventricle size and shape.
Systolic function, including regional differences.
Diastolic function.
LEFT VENTRICULAR FUNCTION
227
Box 4.1 Assessment of left ventricular function
Global systolic function:
Subjective evaluation of size, shape, regional and global function.
Measurement of left ventricle volumes/dimensions, ejection
fraction (Simpson’s or 3D).
Doppler: volumetric measurements, dP/dt in patients with mitral
regurgitation.
New techniques for myocardial function (strain, strain rate).
LV response to exercise stress.
Left ventricle shape and wall stress.
Regional systolic function:
Subjective evaluation of segmental function, wall motion score.
Myocardial contrast enhancement.
Diastolic function:
Transmitral flow categorization.
Strategies for recognition of pseudonormal filling.
LA size (area or volume).
Annular tissue Doppler (E/E’).
Response to Valsalva manoeuvre.
Others (pulmonary vein flow, mitral flow propagation).
Synchrony:
M-mode intraventricular delay.
Doppler assessment of interventricular delay.
Tissue Doppler imaging.
228
CHAPTER 4 Transthoracic chambers and vessels
Global systolic function
Left ventricular systolic evaluation is commonly performed by eye. Although
the eyeball of an experienced reader is equivalent to the trackball, the
desirability of visual assessment is dependent on the circumstances. Visual
assessment alone is appropriate in an emergency but inappropriate in
most circumstances when elective decisions are being made. Global systo-
lic function should be quantified. The standard approaches are detailed
here and the most accurate (and therefore the preferred methods) are
based on volumetric measures (b p.198).
2D measures
Ejection fraction
This represents the fraction of blood within the left ventricle which is eject-
ed in 1 cardiac cycle (Fig. 4.19). To calculate, use the end-diastolic (LVEDV)
and end-systolic (LVESV) volumes (b p.198). The ejection fraction is:
LVEDV LVESV
×100%
LVEDV
EF can be calculated from linear measures (b p.196) using Teicholz’ equa-
tion, but this is notoriously inaccurate, especially if regional function is
reduced. If apical images are suboptimal, use of LV opacification may per-
mit measurement using Simpson’s rule, and 3D imaging may be performed
from the parasternal window. Teicholtz equation:
LVEDD LVESD3
3
×100%
LVEDD
Fractional shortening (fractional area change)
Fractional shortening and fractional area change represent summary meas-
ures of changes in left ventricle size in mid cavity. Fractional shortening is
based on the standard linear measures (Fig. 4.20 and b p.196):
LVEDD LVESD
×100%
LVEDD
Fractional area change (Fig. 4.21) uses end-diastolic (LVEDA) and end-
systolic (LVESA) cavity cross-sectional area traced in parasternal short
axis (mid-ventricle level) view (to measure area see b p.199):
LVEDA LVESA
×100%
LVEDA
GLOBAL SYSTOLIC FUNCTION
229
END
END
STROKE VOLUME
DIASTOLIC
SYSTOLIC
VOLUME
VOLUME
EJECTION
STROKE VOLUME
× 100% =
END DIASTOLIC VOLUME
FRACTION
Fig. 4.19 Principle of ejection fraction. This can also be estimated from linear
measures.
End diastolic diameter
End systolic diameter
FRACTIONAL
× 100% =
SHORTENING
End diastolic diameter
Fig. 4.20 Principle of fractional shortening based on linear measures.
DIASTOLIC
SYSTOLIC
AREA
AREA
FRACTIONAL
× 100% =
AREA CHANGE
DIASTOLIC
AREA
Fig. 4.21 Principle of fractional area change.
230
CHAPTER 4 Transthoracic chambers and vessels
3D measures
Inaccuracy of the earlier described measurements is inherent in
the projection of the 3D structure of the heart in 1D or 2D, which
necessitates both geometric assumptions and appropriate plane
location.
These considerations are especially important for repeat imaging,
for which exact plane duplication is almost impossible. A wealth of
evidence supports 3D to be a more accurate means of obtaining LV
volumes than standard imaging—although the benefit is less marked
for EF.
Patients most likely to benefit are those with ischaemic cardiomyopathy
and those having repeat studies. There remains some underestimation
of LV volumes due to suboptimal resolution of trabeculations.
Further technical developments are needed to improve imaging quality
and frame rate, but the technique is ready for routine use.
Doppler evaluation
Stroke volume and cardiac output
Doppler measurements of stroke volume are more commonly written
about than performed.
The volume of blood that forms the ejection fraction (LVEDV − LVESV)
represents the stroke volume. Normally this is around 75-100mL.
These measures vary with body size and should be divided by body
surface area (body surface area = sq root(height (m) × weight
(kg)/36)) to give a stroke volume index (normally 40-70mL/m2) and
cardiac index (normally 2.5-4L/min/m2) respectively.
If the mitral valve is competent then this can be multiplied by heart
rate to calculate cardiac output. Normally this is around 4-8L/min.
Stroke volume may be derived from EDV and ESV measures, but this
depends on good image orientation.
Doppler may be useful for stroke volume assessment (Fig. 4.22), but
depends on accurate outflow tract measures (errors of which are
squared to calculate area).
Measurement of dP/dt can be a useful extra measure in patients with
severe mitral regurgitation.
Calculating stroke volume
In apical 5-chamber view record a PW Doppler in the outflow tract
and trace the shape. Record the velocity time integral (vti).
In a parasternal long axis view, zoom the LVOT and measure the
width (edge to edge, just below aortic valve).
Stroke volume is the area of the outflow tract (π x [LVOT
diameter/2]2) multiplied by the outflow tract vti.
Cardiac output is stroke volume multiplied by heart rate.
GLOBAL SYSTOLIC FUNCTION
231
AORTA
LV
LV
LA
LA
LVOT cross sectional area × LVOT vti = stroke volume
stroke volume × heart rate = cardiac output
Fig. 4.22 Stroke volume can be used as a Doppler-based assessment of left
ventricle function.
232
CHAPTER 4 Transthoracic chambers and vessels
dP/dt
dP/dt describes the rise in intraventricular pressure during early systole
(Fig. 4.23). The change in pressure is determined by systolic contrac-
tion so the faster the rise the better the left ventricular systolic function.
Theoretically this should be less dependent than ejection fraction on the
loading condition of the heart. It can only be measured if there is signifi-
cant mitral regurgitation.
In an apical 4-chamber view align the CW Doppler through the mitral
valve and the associated regurgitant jet.
Record a spectral trace at a sweep speed of 100mm/s to broaden the
tracing. Set the scale to focus on the 0 to 4m/s range.
Measure the time taken for the velocity of the regurgitant jet to rise
from 1 to 3m/s (the measure has been standardized for this pressure
rise from 4 to 36mmHg). The machine or software will normally
automatically calculate dP/dt if the 1m/s and 3m/s points are marked
although it can be calculated by hand.
dP/dt >1200mmHg/s (roughly <27ms between points) relates to
normal function and <800mmHg/s (roughly >40ms) is severely
depressed function.
Left ventricular outflow vti
To gain an impression of whether cardiac output is normal, low, or high
measure vti in the left ventricular outflow tract using PW Doppler from
an apical 5-chamber view. In the general population if the heart rate is
between 60-100 then normal range is 18-22. This technique can also be
applied to assess right ventricular output using PW Doppler in the right
ventricular outflow tract in a parasternal short axis view. Normal values
should be 76% (or three-quarters) of left ventricle outflow vti.
GLOBAL SYSTOLIC FUNCTION
233
LV
RV
RA LA
dt
100
0
100
200
dP = 36 - 4mmHg
300
400 cm/s
dt < 27ms = normal function
dt > 40ms = severely impaired function
Fig. 4.23 dP/dt measures the rise in intraventricular pressure. A mitral regurgitant
jet has been assessed with continuous wave Doppler in an apical 4-chamber view.
234
CHAPTER 4 Transthoracic chambers and vessels
Regional systolic function
Although regional changes can occur in cardiomyopathies, the most com-
mon cause of regional left ventricle dysfunction is coronary artery disease.
Regional abnormalities are usually assessed by eye and are dependent on
operator experience. Basic assessment is of wall movement in coronary
artery territories. This should be refined to gauge movement of wall seg-
ments and can then be semi-quantified with wall motion scores. There are
fully quantitative methods although not yet in routine clinical practice.
Qualitative assessment
The key to reporting regional dysfunction is to use a standard system
to segment the heart. The standard 16-segment model of the American
Society of Echocardiography (septal, lateral, anterior, and inferior at the
apex, as well as anteroseptal and posterior segments at the base and mid-
papillary muscle level) is still widely used, although the American Heart
Association has moved to a 17-segment model (which includes a true
apical segment) to encourage similar segment models between imaging
techniques (Fig. 4.25).
Wall motion
Record parasternal long and short axis and, apical 4-, 3-, and
2-chamber views. Avoid foreshortening and ensure a clear endocardial
border. Enhance the border with left-sided contrast agents if needed
(see b p.561).
Generally: anterior wall, apex, and septum are supplied by the left
anterior descending artery; lateral and posterior (inferolateral) walls
by the circumflex artery; and inferior wall by the right coronary artery.
However, basal septum in an apical 4-chamber view is right coronary
artery territory and supply of the apex and posterior wall varies
slightly depending on which coronary system is dominant (left or right)
(Fig. 4.24).
In each loop look at each segment and score as normal, hypokinetic
(endocardial excursion <5mm), akinetic (endocardial excursion
<2mm), or dyskinetic (endocardium moves out in systole).
As movement may be passive, look for thickening in segments you are
unsure about. Normal segments will thicken by >50% between diastole
and systole. If present, report as normal or hypokinetic.
Present the findings as a diagram.
Wall motion scores
Wall motion scoring permits semi-quantitative evaluation of the regional
function assessment.
Score normal regions as 1; hypokinestic as 2; akinetic as 3; and
dyskinetic as 4. Score aneurysms as 5; and thinning with akinesis as 6;
or thinning with dyskinesis as 7.
Calculate (or let the software calculate) a wall motion score index by
averaging scores of all individual segments. This is a semi-quantitative
index of global systolic function analogous to ejection fraction.
REGIONAL SYSTOLIC FUNCTION
235
LAD
RCA
LCX (or LAD)
RCA
LAD
Apical four chamber
Apical two chamber
LAD
LAD
LCX
RCA
RCA
(or RCA)
LCX
Apical three chamber or
Parasternal short axis
parasternal long axis
Left anterior descending artery (LAD)
Left circumflex artery (LCX)
Right coronary artery (RCA)
Boundaries between artery territories
will vary slightly with coronary anatomy
Fig. 4.24 Coronary artery supply to walls of left and right ventricle.
236
CHAPTER 4 Transthoracic chambers and vessels
Quantitative assessment
Concordance of wall motion assessment between centres may be improved
with the use of standard reading criteria, but remains imperfect. The benefit
of a suitable objective measure would be to supplement wall motion scoring
and help less expert readers.
Quantitation of regional function has been performed with a number of
echocardiographic and Doppler modalities (Table 4.3). Although some are
encouraging, none have entered mainstream practice.
Table 4.3 Assessment techniques for regional function
Radial
Longitudinal
Displacement and
Centre-line (from 2D)
Annular M-mode
thickening
Color kinesis
Tissue tracking
Anatomical M-mode
Speckle
Speckle or TDI
Velocity
Speckle
TDI or speckle
Deformation
Speckle
TDI or speckle
Timing
TDI (time to peak systole
TDI (time to peak systole
or onset of diastole)
or onset of diastole)
APICAL CAP
APICAL CAP
X
APICAL INFERIOR
APICAL ANTERIOR
APICAL SEPTUM
APICAL LATERAL
X
X
(ANTEROSEPTUM)
X
X
LV
MID SEPTUM
MID LATERAL
MID INFERIOR
X
X
MID ANTERIOR
X
X
(INFEROSEPTUM)
(ANTEROLATERAL)
BASAL SEPTUM
X
X
BASAL LATERAL
BASAL INFERIOR
X
X
BASAL ANTERIOR
(INFEROSEPTUM)
(ANTEROLATERAL)
Apical Two Chamber
Apical Four Chamber
APICAL CAP
ANTEROSEPTUM
ANTERIOR
APICAL LATERAL
APICAL SEPTUM
(ANTEROSEPTUM)
ANTEROLATERAL
MID INFEROLATERAL
MID SEPTUM
X
X
(POSTERIOR)
(ANTEROSEPTUM)
INFEROSEPTUM
BASAL INFEROLATERAL
X
X
BASAL SEPTUM
(POSTERIOR)
(ANTEROSEPTUM)
INFERIOR
INFEROLATERAL
Parasternal Short Axis
Apical Three Chamber or
(all MID Segments)
Parasternal Long Axis
X marks the distinct seventeen segments (some are seen in multiple views)
Fig. 4.25 17-segment model (16-segment is the same without the apical cap). Note that some segments are seen in multiple views. The posterior wall can also
be referred to as the inferolateral wall. ‘X’s mark the 17 different segments of the ventricle, some of which are seen in the other views (unmarked segments).
238
CHAPTER 4 Transthoracic chambers and vessels
Left ventricular strain
Background
Strain is a fundamental physical property of myocardium that reflects its
deformation under an applied force. Two methods are used: (1) tissue
Doppler—which derives strain from strain rate, a gradient of adjacent
velocities over a sampling distance, and
(2) speckle tracking—which
derives strain from excursion of the speckles.
Complete assessment of strain—radial, longitudinal, circumferential, and
the shear stress—may be achievable but is likely to be too much informa-
tion for routine clinical use. The most robust and reproducible measure is
longitudinal strain, for which there is the most clinical data. Circumferential
strain (Figs. 4.26 and 4.27) can be assessed with speckle tracking but radial
strain is difficult to measure by any method.
Which technique?
Speckle strain is simpler and provides strain in multiple dimensions—
potentially in 3D. Speckle strain is the preferred option apart
from when high frame-rate is needed (e.g. for strain rate or stress
imaging), in which case tissue velocity is likely superior.
Neither tissue velocity nor speckle techniques are perfect and
require further development—for example, studies suggest strain
values in the same myocardium differ depending on the machine.
Global strain
Although ejection fraction is simple and intuitive, as well as being
supported by a wealth of prognostic information, it has important
limitations including image quality dependence, geometric assumptions,
load dependence, and insensitivity to early disease (which is
characterized by disturbances of longitudinal function).
Global strain avoids inaccuracy due to inaccurate border tracing, but is
dependent on both loading conditions and image quality.
Global strain is an analogue of ejection fraction, and can be measured
as either longitudinal (GLS) or circumferential strain (GCS), derived
as the mean of interpretable regional strains. These parameters have
predicted outcome in two studies.
Global strain is likely to be of value for sequential studies (e.g. left
ventricular response to therapy), and the detection of early disease
(e.g. infiltration, cardiotoxicity).
Global strain is the average of the strain measurements in all 16 or 17
myocardial segments (or the segments where strain measurements are
available).
LEFT VENTRICULAR STRAIN
239
Normal values for strain measurements
By convention, shortening is described by a negative value and lengthening
by positive strain. If the myocardium did not contract then strain would
be 0. Longitudinal strain is the most robust clinically and normal regional
peak systolic strain in the longitudinal direction is approximately −18%.
Longitudinal strain values of −14% or even closer to 0 are probably
abnormal and a global longitudinal strain of −12% corresponds to an EF
<35%. So far there is only very limited data available on normal ranges
for all the parameters but the values given here have been published as
normal ranges (mean ± SD) for the different types of strain (modified
from Saito K et al.1). Note longitudinal and circumferential strain are
negatives as the left ventricle reduces in size during systole, whereas,
because radial strain describes thickening of the myocardium in systole,
it is positive.
3D speckle tracking*
2D speckle tracking
Longitudinal, %
−17.0±5.5
−19.9±5.3
Circumferential, %
−31.6±8.0
−27.8±6.9
Radial, %
34.4±11.4
35.1±11.8
3DT=3D speckle tracking; 2DT=2D speckle tracking, *Artida (Toshiba)
Reference
1 Saito K et al. Comprehensive evaluation of left ventricular strain using speckle tracking
echocardiography in normal adults: comparison of three dimensional and two dimensional
approaches. Am Soc Echocardiogr 2009; 22(9): 1025–30.
240
CHAPTER 4 Transthoracic chambers and vessels
Regional strain
The most important application of regional strain is to the recognition
of ischaemic heart disease. The recognition of scar (resting imaging),
viability (low-dose response), and ischaemia (peak dose imaging) is
subjective and depends on image quality and observer expertise. Strain
may offer a sensitive and reproducible alternative.
The use of strain to recognize resting wall motion abnormalities may
improve the detection of coronary disease in the ICU, operating room,
and Chest Pain Unit (cut-offs of −0.83/s for strain rate and −17.4% for
strain have been proposed).
Diastolic strain disturbance may persist for hours and represent a
potential ‘ischaemic memory’ signal. Strain has also been used to
anticipate the transmural extent of scar.
The augmentation of viable segments in response to dobutamine may
also be quantified with strain. Speckle strain appears to be inferior to
Doppler-based strain, especially in the basal segments, possibly due to
image quality.
The assessment of strain during ischaemia remains extremely difficult.
A human study has shown an increment of both sensitivity and
specificity by combination of strain rate with wall motion. However,
Doppler-based strain rate is onerous and subject to artefact, and
speckle-based imaging is limited by image quality and frame-rate.
The application of strain to the timing of regional contraction
(mechanical dispersion) has potential applications in cardiac
resynchronization therapy and possibly in the prediction of ventricular
arrhythmias.
Other strain applications that will likely assume importance are RV and
atrial strain.
Advantages and disadvantages of strain imaging
The advantages of strain include:
A sensitive and automated marker of regional and global function.
It is relatively homogeneous in different LV segments.
It is a marker of contractility.
It is independent of tethering.
The disadvantages of strain include:
Methods are time-consuming, complex, and require a knowledgeable
user to avoid misleading results due to artefact.
Speckle strain is dependent on good image quality.
Tissue velocity requires imaging of the structure as close as possible
to the ultrasound beam.
LEFT VENTRICULAR STRAIN
241
Fig. 4.26 2D circumferential strain. Postprocessing to delineate endocardial and
epicardial borders (Toshiba Artida 2D wall motion tracking software).
Fig. 4.27 2D circumferential strain with post processing on QLAB demonstrating
regional circumferential strain at basal LV short axis level (Phillips QLAB 8.1). See
W Video 4.9.
242
CHAPTER 4 Transthoracic chambers and vessels
Strain assessment by 2D speckle tracking
Image acquisition
Good 2D image quality is necessary to ensure clear visualization of the
endocardium.
For complete 2D strain analysis all of the standard views for
assessment of left ventricular regional wall motion will need to be
acquired: left ventricular parasternal view; left ventricular short axis
view (basal, mid and apical level) and left ventricular apical 4-, 3-, and
2-chamber views.
Optimize the 2D image, adjusting the sector size, and depth to focus
on the left ventricle.
Ensure the frame rate is between 50-90 frames/s.
Acquire images at end expiration.
Postprocessing
A number of postprocessing software packages exist.
After loading the appropriate view of the left ventricle the software
package will ask the operator to confirm which view it is.
Some software packages allow the gain of the image to be altered
again if necessary.
The operator will be prompted to identify specific points on the image
to mark (usually up to 3 points). From this the software automatically
will delineate the endocardial and epicardial borders (Fig. 4.26).
The image can then be played. It is important that the operator
visually assesses how well the automated borders are tracking the true
endocardium/epicardium through the cardiac cycle.
If the tracking is poor it will be necessary to adjust the automated
border as required.
When happy, the operator can then select which type of strain is to be
analysed (Fig. 4.27).
A colour overlay which corresponds to the colour bar on the left of
the screen will be seen (see Fig. 4.28).
Each image of the left ventricle which is being assessed will be displayed
segmentally and also displayed on a segmental strain graph.
LEFT VENTRICULAR STRAIN
243
Fig. 4.28 2D speckle tracking post processing using Toshiba Artida 2D wall motion
tracking. The LV in each view is segmented and has a colour overlay which cor-
responds to the strain value on the colour bar (far left of each image). Segmental
strain curves also shown (right). Top: normal circumferential strain basal LV level.
Middle: normal radial strain basal LV level. Bottom: normal longitudinal strain apical
LV 4-chamber view. See W Video 4.10 and W Video 4.11.
244
CHAPTER 4 Transthoracic chambers and vessels
Strain assessment by 3D speckle tracking
Image acquisition
For adequate 3D speckle tracking analysis it is important that the 2D
windows are good so that the endocardial border can be seen.
Once the optimal 2D left ventricular apical 4-chamber view has been
obtained, select 3D view.
3D full volume acquisition mode should be used.
In the biplane view, adjust the depth and sector width to ensure you
focus on the left ventricle.
For 3D speckle tracking the image resolution should be optimized so
that an adequate frame rate is achieved. Adjust the line density and
use the maximal number of subvolumes (beats) possible depending on
patient breath-holding capabilities.
Acquire a full volume at end expiration.
Check for the presence of stitching artefacts in the 4-chamber view
and also by slicing the left ventricle to view in several short axis planes.
If adequate, accept the image or else delete and start acquisition again.
Postprocessing
Several different postprocessing software packages exist and whilst
there may be some variation in individual algorithms, the general
principles of estimating 3D strain are similar.
Select the 3D full volume left ventricular acquisition to be used.
The left ventricle will then be displayed in a number of planes—usually
an apical 4-chamber view, apical 2-chamber view, and 3 short axis
slices (Fig. 4.29).
The left ventricular orientation in the biplane view can be adjusted to
correct for foreshortening.
The level of the 3 short axis planes can also be adjusted to ensure that
the left ventricular apex, mid left ventricle (papillary muscle view), and
basal left ventricle are being displayed.
The software package will then prompt the operator to identify
and mark anatomical landmarks (usually between 3-5) on the left
ventricular biplane view. The automated software will then delineate
the endocardium and epicardium in all of the on-screen left ventricular
views.
The operator can then play the loop of the cardiac cycle to see
whether the epicardial and endocardial borders are being tracked
appropriately.
In addition to end-diastolic volume, end-systolic volume, and ejection
fraction, the software calculates left ventricular mass. The left
ventricular mass is measured during the cardiac cycle and a flat curve
is an indicator for good tracking of the endocardium and epicardium
as it is consistent with mass being constant. The following values are
available within 30 seconds after initiating the analysis:
• Global and segmental displacement.
• Global and segmental strain strain rate, displacement.
• A special feature is 3D strain which probably comes closest to the
real movement of speckles.
• Rotation and twist.
LEFT VENTRICULAR STRAIN
245
Fig. 4.29 3D strain acquisition and postprocessing on Toshiba Artida system. Top:
from the apical LV window, the LV is displayed in two apical views and three short
axis views. Middle: contouring of the epicardial and endocardial border. Bottom:
normal LV 3D circumferential strain analysis. See W Video 4.12.
246
CHAPTER 4 Transthoracic chambers and vessels
Diastolic function
Diastolic dysfunction is increasingly recognized as an important influence
on symptoms and haemodynamic status. Diastole extends from aortic
valve closure to mitral valve closure and has 4 distinct phases:
Isovolumetric relaxation—before the mitral valve opens.
Early filling—accounting for up to 80% of ventricular filling.
Diastasis—as left atria and left ventricle pressures equalize.
Atrial systole—accounting for the remainder of ventricular filling.
Diastolic dysfunction during the early phases is due to problems with
active myocardial relaxation. This is usually present early in disease devel-
opment (e.g. ischaemia, aortic stenosis, hypertension, hypertrophy) and
is termed abnormal relaxation. With disease progression, fibrosis devel-
ops and chamber compliance reduces (also seen with infiltrative disease).
These changes affect later diastole and lead to restrictive filling. During the
transition there is a period of apparently pseudonormal filling on some
echocardiographic parameters at the mitral valve although diastolic func-
tion remains impaired.
Assessment
Measurement of transmitral flow (left ventricular filling) is the cornerstone
of diastolic function evaluation (i.e. E/A ratio). This measure is refined with:
(1) pulmonary vein flow and left atrial size (to understand left atrial pres-
sure) and (2) tissue Doppler imaging of the mitral annulus (to study changes
in myocardial movement) (see Fig. 4.16). Colour M-mode propagation has
also been used. The report should comment on the presence and pat-
tern of diastolic dysfunction (abnormal relaxation, pseudonormal filling or
restrictive filling). Also comment on likely underlying pathology, if identified,
during the examination.
Mitral valve inflow
In the apical 4-chamber view position the PW Doppler sample volume
at the mitral leaflet tips (Fig. 4.30). Use colour Doppler if necessary to
optimize beam alignment with mitral inflow. Record a tracing.
E/A ratio: measure peak E-wave velocity and peak A-wave velocity.
Normal filling is generally characterized by an E/A ratio of 0.75-1.5.
Other measures:
Deceleration time: measure the distance from start to end of the
E-wave. If the end is obscured by the A-wave extrapolate the slope
to the baseline. A deceleration time of 160-260ms is normal.
Isovolumetric relaxation time: measure the time from the end of the
aortic outflow trace to the start of the mitral inflow trace. This
normally requires two different Doppler recordings (one of aortic
outflow and one of the mitral inflow) with timings taken relative to
a fixed point on the ECG. Normal range for 21-40yrs is 67 ± 8ms;
41-60yrs is 74 ± 7ms; over 60yrs is 87 ± 7ms.
Valsalva manoeuvre: the mitral inflow pattern can be recorded again
with the patient performing a Valsalva. If there is pseudonormal
or reversible restrictive filling the trace will revert to an abnormal
relaxation pattern.
DIASTOLIC FUNCTION
247
1
E/A ratio = E peak vel/A peak vel
E peak velocity A peak velocity
+
+
Pulse wave
Doppler signal
at mitral valve
2
Deceleration time
a
isovolumetric
Pulse wave
a - b =
3
relaxation time
Doppler signal
b
from left
ventricular
outflow
Fig. 4.30 Doppler measures of diastolic function. E/A ratio uses peak of E and A
wave velocities from PW Doppler at mitral valve tips. Deceleration time is time
from peak of E wave to baseline. Isovolumetric relaxation time: a = time from R
wave on ECG to start of mitral valve inflow, b = time from R wave to end of aortic
outflow.
248
CHAPTER 4 Transthoracic chambers and vessels
Left atrial size
• Determine left atrial size by standard methods (b p.280). Increased
left atrial size implies raised left atrial pressure.
Pulmonary vein flow
In the apical 4-chamber view ensure there is enough depth to see the
pulmonary vein inflow. The easiest vein to see (and best aligned for
Doppler) is the right upper pulmonary vein near the atrial septum.
Placement can be optimized with colour flow mapping to demonstrate
the pulmonary vein flow.
Place the PW Doppler sample volume just inside the pulmonary vein
and record a spectral tracing. A good tracing confirms a satisfactory
position.
The tracing will consist of 2 forward flow phases, systolic and diastolic,
followed by an atrial reversal (due to atrial systole). Normally the
systolic wave is dominant or equal to the diastolic wave.
A prominent atrial reversal (>30cm/s peak velocity of the atrial wave
and >20-30ms longer duration of the atrial wave compared to the
duration of the A wave on the mitral inflow) is a specific but not very
sensitive marker of raised filling pressure. Blunting of the systolic flow
wave is a reliable marker of raised filling pressure in patients with
systolic dysfunction, but not normal function.
Tissue Doppler imaging
In apical 4-chamber views place the PW tissue Doppler on the septal
or lateral annulus of the mitral valve (there is no clear consensus about
which is optimal). The tissue Doppler spectrum can be optimized by
decreasing the sample volume and optimizing gain settings (excessive
gain causes spectral broadening). Ensure it is aligned with the long axis
of the ventricle.
The Doppler pattern should be the same as the mitral valve inflow
with an E wave and A wave (but below the baseline away from the
probe). Measure the peak velocity of both. They are usually referred
to as E’ and A’ (see Tables 4.4 and 4.5).
E/E’ can also be calculated and relates to left atrial pressure. E/E’ <8
suggests normal left atrial pressure and E/E’ >15 suggests elevated left
atrial pressure.
E/E’ is central to recent recommendations for the diagnosis of heart
failure with a normal ejection fraction (HFNEF) (see Fig. 4.32).
DIASTOLIC FUNCTION
249
Diastolic function: tips and measures
Transmitral flow categorization (see Figs. 4.16 and 4.31)
1. Impaired relaxation This is characterized by reduction of the peak
transmitral pressure gradient (hence lower E velocity and E/A ratio
[<1 in young, <0.5 in elderly]) and prolongation of the E deceleration
slope (>220ms in young, >280ms in elderly). Cardiac pacing, left bundle
branch block, and RV overload may provoke the same changes.
2. Pseudonormal filling As left atrial pressure increases with progressive
left ventricle disease, E velocity and deceleration time return to
normal. With exception of patients with more marked elevations
of filling pressure and low heart rate, who may show a mid-diastolic
(‘L’) wave, transmitral flow patterns cannot be distinguished from
normal without the performance of other steps. The first step is to
suspect the condition—‘normal’ transmitral flow in the setting of left
ventricle enlargement, hypertrophy, or systolic dysfunction is likely to
be pseudonormal. The second step is to assess left atrial size, followed
by estimation of filling pressure (as E/E’) and tissue Doppler of the mitral
annulus. Note that when left ventricle ejection fraction is preserved,
E deceleration time, the Valsalva response, blunting of the pulmonary
venous S wave (and S/D ratio), and flow propagation velocity may be
unreliable indicators of diastolic dysfunction.
3. Restrictive filling Continued elevation of filling pressure leads to
increased E velocity (increase in E/A ratio >2) and shorter E deceleration
time (<150ms). This finding is unusual with normal ejection fraction
(indicating a restrictive cardiomyopathy, e.g. amyloidosis), and is more
commonly associated with left ventricle dilatation and severe systolic
dysfunction. The presence of reversibility
(i.e. normalization with
Valsalva or after diuresis) is prognostically very important.
250
CHAPTER 4 Transthoracic chambers and vessels
Table 4.4 Age-adjusted normal cut-offs for selected diastolic
parameters
<40 years 40-60 years >60 years
E deceleration time (ms)
<220
140-250
140-275
Septal E’ velocity (cm/s)
>9
>7
>6
Lateral E’ velocity (cm/s)
>11
>10
>7
Table 4.5 Useful criteria for differentiating normal from pseudonormal
filling in adult subjects with normal left ventricular systolic function
Normal
Pseudo-normal
Lateral E’ velocity (depending on age)
>7-11
<7-11
Lateral E/E’
<10
>10
PV A velocity (cm/s)
<35
>35
PV A duration - transmitral
<30
>30
A duration (ms)
Valsalva manoeuvre
No significant
E/A <1 or
change in E/A
E/A decrease
ratio
by >50%
PV = pulmonary venous.
NORMAL
IMPAIRED
PSEUDO-
REVERSIBLE
FIXED
RELAXATION
NORMAL
RESTRICTIVE
RESTRICTIVE
MITRAL VALVE
0.75< E/A <1.5
E/A 0.75
0.75< E/A <1.5
E/A >1.5
INFLOW
Decel time >140ms
Decel time >140ms
Decel time <140ms
E
A
Adur
PULMONARY
S>D
S<D or
VEIN FLOW
ARdur<Adur
ARdur >Adur+30ms
S
D
AR
ARdur
TISSUE DOPPLER
E/E’ <10
E/E’ 10
MITRAL ANNULUS
A'
E'
Fig. 4.31 Doppler patterns for mitral valve, pulmonary vein, and mitral annulus to characterize diastolic function. The mitral inflow can be repeated with
a Valsalva manoeuvre and if there is pseudonormal filling the mitral inflow will change to an impaired relaxation pattern. Reversible restrictive describes a
restrictive pattern in which the mitral valve inflow also changes to an impaired relaxation pattern on Valsalva. Mitral: E = peak E wave velocity, A = peak
A wave velocity, Adur = duration of A wave. Tissue Doppler mitral annulus: E’ = peak velocity; A’ = peak velocity. Pulmonary vein flow: S = peak systolic
wave; D = peak diastolic flow; AR = peak atrial reversal flow; ARdur = duration of atrial reversal wave.
252
CHAPTER 4 Transthoracic chambers and vessels
HFNEF
Clinically, it is increasingly recognized that there is a group of patients
who require treatment for symptoms of heart failure (shortness of breath
etc.) but who have normal systolic cardiac function. These symptoms
appear to relate to underlying diastolic dysfunction and they are increas-
ingly referred to as patients with heart failure with a normal ejection frac-
tion (HFNEF). HFNEF could be a precursor of heart failure with reduced
ejection fraction. Guidelines have been established to help guide diagnosis
and treatment of this group of patients.
The diagnosis of HFNEF requires the following conditions to be fulfilled:
Signs or symptoms of heart failure.
Normal or mildly reduced LV systolic function (LVEF >50% and LV end
diastolic volume index <97mL/m2.
Evidence of diastolic dysfunction.
Assessment for a diagnosis of HFNEF (Fig. 4.32)
Left ventricular end-systolic and end-diastolic volumes should be
calculated from standard views to obtain a Simpson’s biplane or 3D
evaluation (b p.228).
If left ventricular ejection fraction is >50% and the left ventricle is
not dilated (<97mL/m2) then proceed on to obtain an assessment
of diastolic function based on both tissue Doppler imaging of the
mitral annulus and transmitral inflow velocities by PW Doppler
(Fig. 4.30).
Using these Doppler measures calculate the ratio of E/E’. This
correlates closely with left ventricular filling pressure and if E/E’ is
>15 then this is considered diagnostic for HFNEF. If E/E’ <8 then,
conversely, HFNEF is excluded.
If E/E’ is between 8 and 15 then further echocardiographic evaluation is
required. Any of the following are considered to support a diagnosis of
HFNEF:
• E/A <0.5 and deceleration time >280ms (age >50 years).
• LA indexed volume >40mL/m2.
• LV mass index >122g/m2 (female) or >149g/m2 (male).
• Duration of reverse pulmonary vein atrial flow—duration of mitral
valve atrial wave flow >30ms.
HFNEF
253
How to diagnose HFNEF
Symptoms or signs of heart failure
Normal or mildly reduced left ventricular systolic function
LVEF > 50%
and
LVEDVI < 97 mL/m2
Evidence of abnormal LV relaxation, filling
diastolic distensibility, and diastolic stiffness
Invasive Haemodynamic
TD
Biomarkers
measurements
E/E > 15
15 > E/E > 8
NT-proBNP
mPCW > 12 mmHg
> 220pg/mL
or
or
LVEDP > 16 mmHg
BNP > 200pg/mL
or
τ > 48 ms
or
b > 0.27
Biomarkers
Echo - Bloodflow Doppler
TD
NT-proBNP
E/A>50yr < 0.5 and
E/E > 8
> 220pg/mL
DT>50yr > 280 ms
or
or
BNP > 200pg/mL
Ard-Ad > 30 ms
or
LAVI > 40 mL/m2
or
LVMI > 122 g/m2 (5):
149 g/m (4)
or
Atrial fibrillation
HFNEF
Fig. 4.32 Diagnostic flowchart on ‘How to diagnose HFNEF’ in a patient suspected
of HFNEF. LVEDVI, left ventricular end-diastolic volume index; mPCW, mean
pulmonary capillary wedge pressure; LVEDP, left ventricular end-diastolic pressure;
t, time constant of left ventricular relaxation; b, constant of left ventricular chamber
stiffness; TD, tissue Doppler; E, early mitral valve flow velocity; E0, early TD
lengthening velocity; NT-proBNP, N-terminal-pro brain natriuretic peptide; BNP,
brain natriuretic peptide; E/A, ratio of early (E) to late (A) mitral valve flow velocity;
DT, deceleration time; LVMI, left ventricular mass index; LAVI, left atrial volume
index; Ard, duration of reverse pulmonary vein atrial systole flow; Ad, duration of
mitral valve atrial wave flow. Paulus WJ et al. Eur Heart J 2007. 28(20):2359-550.
254
CHAPTER 4 Transthoracic chambers and vessels
Left ventricular synchrony
The current selection criteria for cardiac resynchronization therapy
include NYHA class III or IV heart failure symptoms and left ventricle
ejection fraction <35% on maximal medical therapy, in the setting of a
widened QRS (the relevant QRS width varies between trials, but usually
is >120ms (usually left bundle branch block)). Despite using these criteria
20-30% do not respond and it may be that others with heart failure would
benefit.
Markers of dyssynchrony (Fig. 4.33)
Echocardiographic assessment of synchrony can be used for patient
selection, pacing site selection, or both. Synchrony can be assessed be-
tween right ventricle and left ventricle (interventricular dyssynchrony—
electromechanical delay in right ventricular outflow tract and left ventricular
outflow tract) or within the left ventricle (intraventricular dyssynchrony—
M-mode, tissue Doppler, strain, 3D). There are few comparisons between
the markers and centres often offer a ‘menu’ of measurements. A list
follows, with findings that would suggest dyssynchrony:
M-mode septum to posterior delay >130ms.
Inter-ventricular delay >40ms.
Systolic strain (% delayed contraction >30).
Septal to posterior wall delay >65ms by tissue Doppler imaging.
Dyssynchrony index >32.6ms.
Parametric markers: tissue strain index, tissue tracking.
Interventricular dyssynchrony
Interventricular dyssynchrony is the difference in time between onset of
pulmonary flow and onset of aortic flow ( 40ms suggests dyssynchrony).
Because separate views are needed for each measurement the onset of
flow in each view is timed relative to the ECG trace.
Obtain a parasternal short axis view (aortic valve level). Record a PW
Doppler tracing through the pulmonary valve. Ensure there is a surface
ECG recording.
In an apical 4-chamber view place a PW Doppler in the outflow tract
and record a tracing. Ensure there is a surface ECG trace.
Measure the distance from the start of the QRS to the start of the
pulmonary valve flow on the first view then measure the distance
from the start of the QRS to the start of the aortic valve flow on the
second view. The difference is the interventricular delay.
Intraventricular dyssynchrony (septal vs. lateral wall)
Intraventricular dyssynchrony is the delay between the septal and poste-
rior wall peak contraction ( 130ms suggests dyssynchrony), i.e. the delay
between the opposite walls of the left ventricle being fully contracted.
• In a parasternal long axis view drop the M-mode cursor perpendicular
to the septal and posterior wall. On the tracing identify the peak of
septal and posterior wall systolic motion. Measure the time difference
between the 2 walls and this is the intraventricular delay.
LEFT VENTRICULAR SYNCHRONY
255
Time delay between septal and
inferolateral wall contraction
RV
LV
INTRAVENTRICULAR DELAY = DELAY BETWEEN SEPTUM AND INFEROLATERAL WALL
RV
LV
RA
LA
LA
TIME DELAY TO
TIME DELAY TO AORTIC
PULMONARY OUTFLOW
OUTFLOW
INTERVENTRICULAR DELAY = DELAY TO AORTIC OUTFLOW - DELAY TO PULMONARY OUTFLOW
Fig. 4.33 Measurement of inter- and intraventricular dyssynchrony.
256
CHAPTER 4 Transthoracic chambers and vessels
Tissue Doppler measures
Differences in movement of the mid and basal segments of each wall of
the left ventricle can be assessed by tissue Doppler imaging to provide
some impression of the coordination of the ventricle. The assessment can
be based on 8 measures from apical 4- and 2-chamber views, or 12 meas-
ures, which include measures in the apical 3-chamber view (Fig. 4.34).
In apical 4-chamber place the tissue Doppler sample volume on each
side of the mitral valve annulus and in the mid segments of the septum
and lateral wall. Record tracings in each position.
Repeat the process in the apical 2-chamber view on each side of the
annulus and the mid segments of the inferior and anterior walls.
This can then be repeated in the apical 3-chamber view in all 4 basal
and mid segments.
Measure the time from the start of the QRS to the systolic phase of
motion on each tracing.
The standard deviation of the 8 (or 12) measures provides a global
index of dyssynchrony (>33ms suggests dyssynchrony).
An alternative measure is the delay between the basal septum and
basal lateral wall in the apical 4-chamber view (>60ms suggests
dyssynchrony).
Finally if any of the 8 (or 12) measures are >100ms different then this
suggests dyssynchrony.
Use in follow-up: how to define success?
The most widely used markers include clinical improvement (formalized
as improvement in heart failure class or quality of life score) and improved
exercise capacity (e.g. lengthening of a 6-minute walk). Echocardiographic
markers include 15% decrease in left ventricle volumes, 5% increase
in ejection fraction, any decrease in left ventricle mass, or a decrease in
mitral regurgitation severity.
Unresolved issues
Current guidelines for CRT therapy do not include dysynchrony meas-
urements. There are controversial studies on the value of routine syn-
chrony studies for decision on CRT treatment. A number of potential
contributions from echocardiography remain unresolved:
What is the optimal synchrony marker to predict recovery?
Predicting response to CRT using 2D echocardiography has been
seen with varying degrees of success.
Should echocardiography be used to assess ischaemia/viability?
Is guidance regarding optimal pacing site useful?
Should echocardiography be used to make adjustments to pacing
parameters over time as cardiac function varies?
LEFT VENTRICULAR SYNCHRONY
257
RV LV
RV LV
RV
LV
LV
RV
RA
LA
RA
LA
RA
LA
RA
LA
Time delay to systolic
motion of wall
LV
LV
LV
LV
Fig. 4.34 Tissue Doppler imaging in basal and mid segments of left ventricle walls
from apical 4- and 2-chamber views. For a 12-segment model the apical 3-chamber
view is used as well.
258
CHAPTER 4 Transthoracic chambers and vessels
3D for assessment of dyssynchrony? (Fig. 4.35)
Real-time 3D echocardiography has been used to quantify global LV
mechanical dyssynchrony in patients with and without prolonged
QRS duration.
Using real-time 3D echocardiography, data sets for global and
segmental LV volumes can be processed to analyse the time-volume
relationship during the cardiac cycle.
From 3D LV acquisition, a series of volume curves can be obtained
to show the variation of segmental volume during the cardiac cycle.
In a synchronous ventricle, the individual segmental volume curves
should reach their minimum volumes at a similar time at end systole.
With a dyssynchronous LV, the segmental volume traces vary with
respect to time.
A systolic dyssynchrony index (SDI) has been proposed which
can be used to identify chronic heart failure patients who may not
otherwise be considered for CRT. Here, the SDI is defined as the
standard deviation of the time taken to reach minimal regional
volume using a 16-segment model and expressed as a percentage
of the cardiac cycle. It has been shown that clinical responders to
CRT had larger SDI at baseline versus non-responders and that an
SDI >6.4% had a sensitivity of 88% and a specificity of 86% to predict
acute volumetric response to CRT.
Advantages and disadvantages of 3D for dyssynchrony
The use of real-time 3D imaging has advantages over 2D echocardiography:
There is simultaneous acquisition of all LV segments during the same
cardiac cycles.
All LV segments are recorded simultaneously and thus avoid
problems with heart rate variability which may be seen in 2D
echocardiography.
The use of real-time 3D imaging has the disadvantages:
The image quality of real time 3D echocardiography is lower than
that for 2D echocardiography with lower temporal resolution than
2D tissue Doppler imaging.
Stitching artefacts may be more prevalent in the population of
patients being assessed due to breath-holding problems and also
rhythm disturbances.
LEFT VENTRICULAR SYNCHRONY
259
Fig. 4.35 Example of segmental volume traces in a patient with LV dyssynchrony.
Bottom: segmental volume curves varying with time during the cardiac cycle. In each
curve, the red triangle is a marker of the minimum systolic volume.
260
CHAPTER 4 Transthoracic chambers and vessels
Optimization
Optimization procedures often do not lead to clinical improvement but
two pacing parameters can be altered to test for benefit. Delay between
pacing atrium and ventricle (AV delay) and delay between pacing left and
right ventricle (VV delay).
Assessment
Start
Ensure you have the appropriate pacemaker programmer and a technician.
Start by collecting the standard baseline dyssynchrony measures (b p.254)
and record the current programmed AV and VV delay.
AV delay (Fig. 4.36)
The aim is to choose the shortest AV delay that still allows complete
ventricular filling. There are 2 approaches. Both use apical 4-chamber view
with a PW Doppler profile of mitral valve inflow.
Iterative method
Program a short AV delay (e.g. 50ms) on the pacemaker. Look at the
A-wave and decrease the delay in 20ms steps until the A-wave starts
to be truncated. Then gradually extend the delay by 10ms steps until
the A-wave is just complete (Fig. 4.36).
Ritter method
Program a short AV delay (e.g. short delay = 50ms) and measure
distance from start of QRS to end of A wave (QAshort).
Program a long AV delay (e.g. long delay = 150ms) and measure
distance from start of QRS to end of A wave (QA long).
Calculate optimal delay as = long delay + QAlong - QAshort.
VV delay (Fig. 4.37)
In an apical 5-chamber view place PW Doppler in left ventricular outflow
tract. Keep it in the same position throughout the study.
Start the VV delay with left ventricle paced 80ms before the right.
Record a spectral profile and annotate with the VV delay.
Calculate the vti by tracing the spectral profile.
Reduce the delay by 20ms to 60ms and record another vti.
Repeat, reducing delay by 20ms until there is no delay (0ms).
Then start pacing right ventricle first, increasing in 20ms increments
up to 80ms.
Also, try left and right ventricle pacing alone.
Look at results and identify parameter with maximal vti. There should
be a graded pattern away from the optimal delay. Choose this as the
new VV delay.
If decision is to pace right ventricle first AV delay should be reset.
new optimal AV delay = previous optimal AV delay − VV delay.
Finish
Program new AV and VV delay. Finish study with full re-evaluation of
synchrony to ensure improvement following reprogramming.
OPTIMIZATION
261
ITERATIVE METHOD
RITTER METHOD
150ms
AVlong = 150ms
MITRAL INFLOW
QAlong
MITRAL INFLOW
Reduce AV delay in 20ms steps until A wave truncates
AVshort = 50ms
AV delay too short
QAshort
Increase AV delay in 10ms steps until optimal A wave
AVopt = AVlong + QAlong QAshort
AV delay optimal
Fig. 4.36 Two methods to measure AV delay.
80
60
40
20
0
20
40
60
80
LV first
RV first
Choose VV delay that produces
maximal aortic vti
Fig. 4.37 VV delay assessed from recordings of aortic vti at different programmed
delays. The VV delay with maximal aortic vti is selected.
262
CHAPTER 4 Transthoracic chambers and vessels
Right ventricle
Normal anatomy
The right ventricle is made up of inflow (sinus), apical trabecular, and
outflow (conus) regions though there is no clear demarcation between
each. Towards the apex a muscular moderator band connects the free wall
and septum. The combination of a thin free wall and thick septum leads
to an irregular crescent shape when viewed in short axis with asymmetric
contraction. The right ventricle maintains blood flow from the venous
system to the pulmonary vasculature and from there to the left atrium
and left ventricle. Size and function can therefore be affected by pulmo-
nary problems (e.g. pulmonary hypertension, embolism), left-sided heart
disease (e.g. left ventricle failure, mitral valve disease), and right ventricular
disorders (e.g. infarction, dysplasia). Septal defects have important effects
on right ventricular function because the right heart is exposed to systemic
pressures.
Normal findings
Views
Key views are: parasternal long axis; parasternal right ventricular inflow
and outflow; parasternal short axis (aortic valve, mitral valve and mid-
papillary levels); apical 4- and 3-chamber; subcostal (Fig. 4.38).
Findings
Parasternal long axis: right ventricle nearest probe. View can be used
for M-mode measures of the proximal RVOT.
Parasternal right ventricular inflow and outflow: these give excellent
views of tricuspid and pulmonary valves. TR jet velocity can be
measured if there is good alignment.
Parasternal short axis (aortic valve, mitral valve, and mid-papillary
levels): right ventricle wraps around the left ventricle and therefore
can be scanned through at multiple levels (as for the left ventricle).
At the aortic valve it can be seen with both tricuspid and pulmonary
valves and Doppler measures can be performed. As the plane moves
towards the apex, the right ventricle is seen as a crescent to the left
of the left ventricle. These views can give an impression of size and, in
combination with septal appearance, of right ventricular pressure.
Apical views: this can be used to assess function based on tricuspid
annulus movement. Cranial tilt of probe may demonstrate right
ventricular outflow. Visualization of TR jet is improved by medial and
cranial displacement of the probe.
Subcostal view: right ventricle nearest probe with ventricular
septum horizontal. Best view for septal defects (colour flow) as well
as measuring wall thickness. A short axis view of basal right ventricle
can be achieved in certain patients, particularly if thin. Doppler
interrogation of outflow and main pulmonary artery can
be undertaken.
RIGHT VENTRICLE
263
LATERAL(FREE) WALL
RV
RV
LV
RA
LA
PULMONARY
ARTERY
Parasternal long axis
Parasternal short axis
TRICUSPID VALVE
RV
PULMONARY VALVE
RV
RA
Right ventricle outflow
Right ventricle inflow
LV
RV
RV
LV
RA
LA
Parasternal short axis
Apical four chamber
RA
RV
LV
LA
LV
RV
Apical three chamber
Subcostal
Fig. 4.38 Key views to assess the right ventricle.
264
CHAPTER 4 Transthoracic chambers and vessels
Right ventricular size
The right ventricle has a complex shape so assessment of size is often
performed qualitatively. However, the right ventricle has significant clinical
relevance and a more thorough quantitative assessment is now warranted.
This task has been aided by recent guidelines which have provided guid-
ance on quantification and normal values.
Assessment
Assess the right ventricle in several views. If it does not appear normal
comment on cavity size, as well as wall thickness, outflow tract size, and
right atrial area.
2D measures of size
Right ventricular cavity size
The apical 4-chamber view should be focused to maximize the size
of the RV such that it transects the acute margin of the RV while
keeping the LV apex in view. The latter is key since it is easy artificially
to make the RV form the apex and be bigger than the LV.
A useful rule of thumb is that the normal RV should be two-thirds the
size of the LV. However this relies on the LV being normal sized itself.
Appearances of the cardiac apex can be instructive: with moderate
amounts of dilatation, the acute angle formed by the RV free wall and
septum increases. In severe RV dilatation, the RV apex can dominate
over the left.
Overall, it is more helpful to assess RV size quantitatively using the
diameter at the tricuspid annulus and mid cavity diameter which should
be less than 4.2cm and 3.5cm respectively.
If so this can be reported as apex forming.
The RVOT can be measured in the left parasternal (and subcostal
views if necessary). The proximal RVOT is seen in the PLAX and
PSAX at the level of the aortic valve (RVOT1) where a value >33mm
is abnormal, but it is preferred to take the distal RVOT (RVOT2)
where the PV and infundibulum meet. The RVOT is dilated here if
>27mm. (See Fig. 4.39 and Table 4.6.)
Right atrial area can be measured from planimetry in the apical 4-chamber
considered to reflect RA enlargement.
RIGHT VENTRICULAR SIZE
265
Fig. 4.39 Six standard measures of right ventricle size from apical 4-chamber (top)
and parasternal short axis (bottom) views.
Table 4.6 2D parameters to assess right ventricle size and function
(ASE guidelines)
Measure
Abnormal
Chamber dimensions
RV basal diameter (RVD1)
>4.2cm
RV subcostal wall thickness
>0.5cm
RVOT PSAX distal diameter (RVOT2)
>2.7cm
RVOT PSAX proximal diameter (RVOT1)
>3.3cm
Systolic function
TAPSE
<1.6cm
Tissue Doppler peak velocity at the annulus
<10cm/s
Pulsed Doppler myocardial performance index
>0.40
Tissue Doppler myocardial performance index
>0.55
Fractional area change (%)
>35%
266
CHAPTER 4 Transthoracic chambers and vessels
3D measures of size
Analysis of 3D right ventricular views is currently possible with a commer-
cially available software package (4D-RV Function, TomTec, Germany). Only
patients with very good image quality should be considered for 3D echocar-
diography of the right heart. Also, for accurate assessment there should
be no arrhythmia, and breath-holding capacity should be good. Following
initial acquisition of the 3D dataset, cut planes are reviewed in the short axis
view (in order to outline the tricuspid valve in the optimal position), apical
4-chamber plane (to outline the apex) and the coronal plane (to outline the
RVOT). The right ventricular volumes are calculated by summing the areas
for each slice through the complete volume data set (Table 4.7).
Acquisition of 3D volume for assessment of RV and RA volumes
Position the probe at the apex in the same position as for acquisition
of 2D 4 chamber views.
The biplane preview (Fig. 4.40) screen is used so that the 4- and
2- chamber views can be seen simultaneously to help avoid
foreshortening.
Sometimes the probe will need to be tilted anteriorly towards the
RVOT.
Depth, gain, and TGC are adjusted in 2D imaging in order to achieve
the best possible endocardial definition.
For full volume datasets maximize the number of subvolumes (beats)
used to generate the 3D image according to patient breath-holding
capabilities. The greater the number of subvolumes, the greater the
temporal resolution.
Acquire 2D or more 3D datasets as artefacts are common and then
inspect the dataset.
Use short axis planes to make sure there are no stitching artefacts.
Use the cropping tool to ensure there is good endocardial delineation
and that the right ventricular outflow tract is included in the dataset.
If the listed criteria are not adequate delete and reacquire.
Table 4.7 Normal values for 3D RV volumes and ejection fraction
LRV (95% CI) Mean (95% CI) URV (95% CI)
3D RV EF (%)
44 (39-49)
57 (53-61)
69 (65-74)
3D RV EDV indexed (mL/m2) 40 (28-52)
65 (54-76)
89 (77-101)
3D RV ESV indexed (mL/m2) 12 (1-23)
28 (18-38)
45 (34-56)
CI, confidence interval; EF, ejection fraction; EDV, end-diastolic volume; ESV, end-systolic
volume; LRV, lower reference value; URV, upper reference value.
RIGHT VENTRICULAR SIZE
267
Fig. 4.40 Acquisition of full volume RV 3D dataset showing initial biplane view
used to optimize the RV and to avoid foreshortening. 4-chamber view (left) and
2-chamber view (right).
Fig. 4.41 Image orientation and setting of anatomical landmarks. The initial 3D
dataset is displayed as three 2D images: 4-chamber (top left), 2-chamber (top
right), and 2 short axis (sagittal) views (bottom). Moving the blue dashed cursor up
and down the ventricle will allow the coronal view to be altered accordingly. The
program prompts the operator to mark the centre of the tricuspid valve (blue dot),
centre of the mitral valve (red dot) and centre of the LV apex (green dot). Once
this has been completed, then RV contouring can be performed. See W Video 4.13.
268
CHAPTER 4 Transthoracic chambers and vessels
Processing the dataset
Image orientation and setting of anatomical landmarks
TomTec (Germany) allows post processing of full volume 3D right
ventricular datasets. Initially the operator is prompted to select the
orientation from which the image was acquired (apical-lateral, apical-
medial or subcostal).
Play the dataset initially and confirm that the chosen end-systolic and
end-diastolic frames are correct or adjust if needed.
The initial display shows the 3D volume as a sequence of three 2D
slices: the apical window, the 2-chamber window (coronal view), and
the short axis window (sagittal view).
When the cropping mode is activated these views usually are displayed
but often have to be adjusted in order to obtain the right ventricle in
full length, to include RVOT and to get the sagittal mid right ventricle
view around 90° angulated to the apical 4-chamber view.
The postprocessing system will prompt you to identify certain
anatomical landmarks on the sagittal (e.g. centre of tricuspid valve,
centre of mitral valve, and the left ventricular apex), Fig. 4.41. The
landmarks are obtained by slicing the apical view using the slice prompt
(see Fig. 4.42 blue dashed line). When the centre of the tricuspid valve
is located the position is marked on the sagittal view (see Fig. 4.41,
blue dot). The centre of the mitral valve is then marked (see Fig. 4.41,
red dot). Finally the horizontal cutting plane (yellow dashed line) is
moved so that the sagittal view is cutting the left ventricular apex and
again this is marked on the sagittal view (see Fig. 4.41, green dot).
RV contouring
The initial contours are then set in the apical 4-chamber view; sagittal
and coronal cut planes in end-systole and end-diastole, see Fig. 4.42.
During contouring of the sagittal and coronal planes, the program
helps the operator to delineate the endocardial border by showing
circular targets which the contour should pass through (see Fig. 4.42).
Trabeculations are included in the endocardial rim, but the apical
component of the RV moderator band is excluded from the cavity.
The software then will calculate the contours in the other slices and
frames.
After the 3 planes have been contoured, check the calculated contours
with reference to the true anatomical structure of the right ventricle
by slicing through the right ventricular cavity and making corrections if
major deviations are observed.
The TomTec programme will then estimate the right ventricular end-
diastolic, end-systolic, and stroke volumes as well as calculating the
right ventricular ejection fraction.
The right ventricular motion can be reviewed in a 3D model and
rotated to be seen from different angles (Fig. 4.43).
The right ventricular motion can also be viewed, for instance with a
static wire frame, see Fig. 4.43.
RIGHT VENTRICULAR SIZE
269
Fig. 4.42 RV contouring (green line) in the 3 cut planes: apical (top left), sagittal
(top right), coronal (bottom left). Circular yellow targets created by the program to
help the operator contour the RV (bottom right). See W Video 4.14, W Video 4.15,
W Video 4.16.
Fig. 4.43 On left, 3D solid display of RV. This is described as a Beutel display.
On right, Beutel display with a static wire frame representing the end-diastolic
Beutel overlaps a dynamic 3D surface model (green). See W Video 4.17.
270
CHAPTER 4 Transthoracic chambers and vessels
Right ventricular wall thickness
This can be assessed at end-diastole using M-mode imaging in the parasternal
long axis view, or more consistently from the subcostal view (Fig. 4.44).
Normal is <0.5 cm.
In the subcostal view use a clear 2D image frozen in end-diastole (or
perpendicular M-mode trace). Measure from edge-to-edge of the free
wall at the level of the of the tip of the anterior tricuspid valve leaflet.
In the parasternal view use a 2D image or M-mode trace with cursor
perpendicular to the ventricle wall at the mitral valve tip level.
In either view take care not to include epicardial fat, coarse
trabeculations, or papillary muscles in the measurement.
RIGHT VENTRICULAR WALL THICKNESS
271
2D measures in subcostal view
RV
RA
LV
LA
Thickened RV wall measured in
subcostal 2D view
M-mode of parasternal long axis
End-diastolic wall
thickness
RV
IVS
End-diastolic cavity
LV
diameter
PW
Fig. 4.44 Measurement of RV wall thickness from a 2D subcostal view (top) and
M-mode in parasternal long axis view (bottom).
272
CHAPTER 4 Transthoracic chambers and vessels
Right ventricular function
Although it can be evaluated qualitatively by studying the movement of
the right ventricle free wall and assigning a label of normal or impaired
to right ventricular systolic function, quantitation of right ventricular
systolic function is now recommended.
A number of measures of right ventricular systolic function have
evolved whose purpose is to sidestep the difficulties of using
volumetric techniques established in the left ventricle for the
geometrically complex right ventricle.
The number of surrogates for right ventricular systolic function is a
reminder that no single index predominates. More recently, quantifying
right ventricular systolic function using volumetric techniques has been
simplified by advances in 3D imaging acquisition and analysis.
Assessment
Assess right ventricular function from the apical 4-chamber view.
Confirm your impression in parasternal and subcostal views.
Concentrate on movement of the tricuspid annulus to get an overall
impression of function.
Support this by looking at regional wall motion abnormalities and
thickening along the free wall to the apex, note whether areas are
normal, akinetic or dyskinetic (use same criteria as left ventricle regional
assessment, b p.234).
When assessing regional wall motion abnormalities, bear in mind that the
right ventricular free wall is predominantly supplied by the right coronary
artery and that the septum, apex, and, in some patients, the distal free
wall is supplied by the left anterior descending artery. Where possible,
use the 4 methods described in this section to quantify right ventricular
systolic function:
Myocardial Performance Index (MPI) or TEI index
Considered a cumulative measure of right ventricular systolic and
diastolic dysfunction.
It is calculated by dividing the isolvolumic time by ejection time.
These measures can be derived using pulsed Doppler. The ejection
time is derived from the spectral trace in the RVOT and the
isovolumic time from the pulsed Doppler of inflow across the tricuspid
valve. Ensure heart rates are similar when each pulsed Doppler
measure is recorded as variation in cardiac cycle length will make the
measures inaccurate. This means it is particularly unreliable in atrial
fibrillation.
Alternatively, both indices can be derived at the same time from the
TDI trace of the tricuspid annulus (Fig. 4.45).
A value >0.40 for the pulsed Doppler method and 0.55 for the TDI are
abnormal.
RIGHT VENTRICULAR FUNCTION
273
IVCT
IVRT
S
A’
E’
a
b
Fig. 4.45 Tei index. A’ = myocardial lengthening velocity during atrial contraction;
E’ = myocardial velocity during early diastole; a = time interval from the end of the
A’ wave to the beginning of the E’ wave; S = myocardial shortening velocity during
ventricular systole; b = time interval from beginning to the end of the S wave;
IVCT = isovolumic contraction time; IVRT = isovolumic relaxation time. Myocardial
performance index (TEI) index: (a—b)/b.
274
CHAPTER 4 Transthoracic chambers and vessels
Tricuspid annular plane systolic excursion (TAPSE)
In the normal right ventricle, the lateral side of the tricuspid annulus moves
towards the apex during systole reflecting right ventricular longitudinal
function. TAPSE is a way of measuring how much it moves.
Obtain an apical 4-chamber view.
Place the M-mode cursor through the lateral annulus of the tricuspid
valve and record a trace (Fig. 4.46).
Measure the maximum excursion.
A value <16mm indicates right ventricular systolic dysfunction.
Although a simple, reproducible measure it relies on the assumption that
longitudinal motion is a surrogate for right ventricular systolic function as
a whole.
Peak systolic velocity of right ventricular basal free wall TDI (Fig. 4.45)
Similar to TAPSE this measure assesses movement of the right ventricular
free wall. However, instead of looking at the distance the tricuspid an-
nulus moves it uses tissue Doppler imaging to measure how quickly the
annulus moves.
Obtain an apical 4-chamber view.
Place the pulse wave TDI cursor either on the lateral edge of the
tricuspid annulus or basal segment of the right ventricular free wall
close to the annulus (normally well seen with transthoracic echo).
Obtain a tissue Doppler trace and measure the maximal systolic
velocity of the basal right ventricular free wall. This is referred to as S’.
S’ velocity <10cm/s reflects right ventricular systolic dysfunction.
Ejection fraction and fractional area change (FAC)
Right ventricular ejection fraction is difficult to measure on 2D because of
complex geometry but, if available, 3D volume acquisitions can be post-
processed using dedicated software to calculate volumes over the cardiac
cycle and derive an ejection fraction.
On 2D imaging fractional area change can be assessed from an apical
4-chamber view (Fig. 4.47). To perform this measure
Obtain a clear apical 4-chamber view.
Identify the end-diastolic frame (largest ventricle). Trace around
the endocardial border being careful to exclude right ventricular
trabeculae and obtain an area.
Identify the end-systolic frame and repeat the process to obtain the
end-systolic area.
The difference between the 2 measures can be reported as a
percentage relative to the end-diastolic area.
A 2D fractional area change of <35% indicates right ventricular systolic
dysfunction.
RIGHT VENTRICULAR FUNCTION
275
Fig. 4.46 Calculation of TAPSE: M-mode cursor is aligned with the tricuspid valve
annulus in the 4 chamber view and the systolic excursion measured (yellow arrow).
FRACTIONAL AREA CHANGE = CHANGE IN AREA
x100%
AREA IN DIASTOLE
LV
RV
LV
RV
LA
AREA IN
LA
SYSTOLE
AREA IN
DIASTOLE
Tricuspid annulus
movement in
LV
RV
systole
RV
RA
LA
RA
LA
Fig. 4.47 Right ventricle function assessed by fractional area change or (more
commonly) movement of tricuspid annulus.
276
CHAPTER 4 Transthoracic chambers and vessels
Right ventricular overload
Identifying volume or pressure overload in the right ventricle can aid
clinical assessment of right heart function. Although often considered
together they usually represent 2 different initial pathologies. Right volume
overload suggests a left-to-right shunt or right-sided valvular regurgitation.
Pressure overload suggests pulmonary hypertension or pulmonary stenosis.
Pressure overload can develop from volume overload, and occasionally vice
versa, in which cases features of both will be present.
Assessment
The key points to look at when evaluating the 2 situations are:
What happens to right ventricle size and thickness (b pp.264-71)?
Volume overload leads to increased cavity size and pressure overload
leads to increased wall thickness. However, one can lead to the
other and the two findings will coexist.
How does the interventricular septum behave during the cardiac cycle?
• Simply, volume overload is related to a flattened septum in diastole
whereas pressure overload is associated with a flattened septum in
both diastole and systole.
Assess right ventricular systolic pressure (b p.162) to help support your
impression of right ventricle pressure or volume overload.
Volume overload (Fig. 4.48)
Obtain a clear parasternal short axis (mid papillary level) view.
Ventricle size and wall thickness: in volume overload the right ventricle
should be dilated (the same size or bigger than the left ventricle) so
comment on size. In chronic overload the right ventricle may start to
hypertrophy but this will be eccentric as there will still be dilatation.
Septum: the septum will flatten in diastole due to the large right
ventricular volume and create a D-shaped ventricle (as volume
overload worsens it will start to bow into the left ventricle). But then
in systole the left ventricle reverts to a circular shape. This creates
abnormal septal motion towards the left ventricle in diastole and
towards the right ventricle in systole.
Pressure overload
Use the same parasternal short axis (mid papillary level) view.
Ventricle size and wall thickness: in chronic pressure overload the right
ventricle free wall thickens (normally half left ventricle thickness) but
the cavity will remain the same until the right ventricle starts to fail.
Septum: as pressure increases the septum will flatten out towards the
left ventricle through both diastole and systole. With chronic pressure
overload and increase in wall thickness the right ventricle will start
to behave more like a left ventricle, the septum will bow into the left
ventricle and contract towards the right ventricle during systole. This
also creates paradoxical septal motion (but for a different reason from
volume overload).
RIGHT VENTRICULAR OVERLOAD
277
Dilated RV
Flattened septum
with D-shaped LV
Fig. 4.48 Example of right ventricle volume overload in a parasternal short axis
view. Note dilated right ventricle and flattened septum in diastole. See W Video 4.18.
278
CHAPTER 4 Transthoracic chambers and vessels
Left atrium
Normal anatomy
The left atrium receives blood from the 4 pulmonary veins. It acts as a
reservoir and as a conduit to transport blood to the left ventricle. It has
contractile function and atrial systole contributes approximately 25% of left
ventricle filling. Morphologically the atrium can be considered as having a
body and an appendage. The common anatomical variations related to
the atrium are those associated with the atrial septum, such as aneurysm,
patent foramen ovale, atrial septal defect, or lipomatous hypertrophy. Rare
anatomic variants can occur within the atrium such as cor triatum, in which
the left atrium is separated into a superior and an inferior chamber.
Normal findings
Views
The key views for the left atrium are: parasternal long axis, and apical
4- and 2-chamber (Fig. 4.49). The apical views are the most useful to
assess left atrial volume and left atrial haemodynamics.
The parasternal short axis (aortic valve level) includes the left atrium
and can be useful to look at the septum. The subcostal view aligns the
left and right atrium perpendicular to the probe so can be useful for
Doppler assessment of the septum.
Findings
Parasternal long axis: the left atrium lies below the aortic root and the
view is used for simple linear measures of left atrial size.
Parasternal short axis (aortic valve level): the left atrium lies below the
aortic valve. The interatrial septum is seen on the left and the left atrial
appendage can occasionally be seen on the right.
Apical 4- and 2-chamber: the left atrium lies at the bottom of the
images and the views allow assessment of left atrial volume. The
septum can also be studied. However, it lies vertically in the image and
it is difficult to identify defects or do Doppler measures. Pulmonary
veins are seen at the back of the atrium in the apical 4-chamber
(particularly the right upper vein that lies by the septum). In the apical
2-chamber the left atrial appendage can sometimes be seen pointing
out to the right. Generally, the left atrial appendage is only rarely
visualized by transthoracic imaging.
Subcostal view: the septum lies horizontal in the image and this is the
best view to look for septal defects with colour flow and Doppler.
LEFT ATRIUM
279
RV
RV
LV
LA
RA
LA
PULMONARY
ARTERY
Parasternal long axis
Parasternal short axis
LV
RV
RA
LA
Right upper
pulmonary vein
Apical four chamber
LV
LV
RV
Left atrial
LA
LA
appendage
Apical two chamber
Apical three chamber
Fig. 4.49 Key views to assess left atrium.
280
CHAPTER 4 Transthoracic chambers and vessels
Left atrial size
Left atrial enlargement is of clinical importance as it is associated with
adverse cardiovascular outcome from a range of pathologies including
myocardial infarction, stroke, dilated cardiomyopathy, and diastolic left
ventricular failure with increased filling pressure. Atrial enlargement is also
associated with atrial fibrillation.
Assessment
Preferred assessment is with volumes measured in apical views. Historically
linear measures in parasternal views are quoted. This is the anteroposterior
diameter. If the atrium has enlarged along the long axis of the heart this may
be missed with single anteroposterior linear measures.
Volumetric measures
Volume measures use the same principles and equations as for left ventricle
volume assessment (b p.196). The left atrium can be modelled with the
area-length formula, Simpson’s method (that cuts the atrium into a series
of disks and adds up the volumes of each disk), and the ellipsoid method.
All calculations are usually done automatically by the machine software
but require measurement of atrial length and diameters or planimetry
of cross-sectional area. If measures are done in the 4-chamber view it is
assumed that the atrium is spherical. Use of both 4- and 2-chamber views
allow 3D assessment.
Obtain a clear apical 4-chamber view with enough depth to include the
whole of the left atrium.
Record a loop and scroll through to identify end-systole.
Planimeter around left atrium excluding the junction of the pulmonary
veins and left atrial appendage (if visible). Record the area.
Measure the length from back of the left atrium to the midpoint of a
line across the mitral annulus (Fig. 4.51).
Repeat the process in the apical 2-chamber view.
Use the shorter of the 2 lengths as the measure of atrial length.
The machine will calculate volumes by Simpson’s method.
The area length formula for left atrial volume is calculated as:
8
4
×
area in
2-chamber
3×
× atrial length
The ellipsoid formula is:
4
2)×(
2)× apical view diameter 2)
3
Linear measures
In a parasternal long axis view, record a 2D loop and identify end-
systole. Measure perpendicularly across the atrium from edge-to-edge.
Alternatively, drop the M-mode cursor across the atrium at the level
of the aortic valve tips, perpendicular to the walls. Measure left atrial
size at end-systole (maximal size) (Fig 4.50).
LEFT ATRIAL SIZE
281
Aortic
root
LA
Left atrial diameter at end systole
Fig. 4.50 M-mode measures of anteroposterior left atrial size in parasternal long
axis view.
Left atrial length
RV
LV
RA
LA
Traced left atrium (end systole)
LV
LA
Left atrial length
Fig. 4.51 Area tracing of left atrium in apical views to provide a more accurate
assessment of left atrial size.
282
CHAPTER 4 Transthoracic chambers and vessels
Left atrial function
Indices of left atrial function, that incorporate left atrial ejection fraction
corrected for cardiac output and body surface area have been reported in
the literature, but are not in clinical use.
Indirect measures of atrial function include the presence of P waves on
the ECG, a transmitral A wave on pulse wave Doppler (the best way
to demonstrate normal atrial contraction) and the presence of an atrial
reversal wave on PW Doppler of the pulmonary vein. The presence of
a P-wave on ECG but absent A-wave on mitral inflow suggests atrial
dysfunction. This can occur, for example, early after cardioversion from
atrial fibrillation.
LEFT AND RIGHT ATRIA: NORMAL RANGES
283
Left and right atria: normal ranges (Table 4.8)
Table 4.8 Parameters to assess left and right atria
WOMEN
NORMAL
MILD MODERATE
SEVERE
Atrial dimension
LA diameter, cm
2.7-3.8
3.9-4.2 4.3-4.6
>4.6
LA diameter, BSA, cm/m2
1.5-2.3
2.4-2.6 2.7-2.9
>2.9
RA minor axis, cm
2.9-4.5
4.6-4.9 5.0-5.4
>5.4
RA minor axis/BSA, cm/m2
1.7-2.5
2.6-2.8 2.9-3.1
>3.1
Atrial area
LA area, cm2
<20
20-30 31-40
>40
Atrial volume
LA volume, mL
22-52
53-62 63-72
>72
LA volume/BSA, mL/m2
<29
29-33 34-39
>39
MEN
NORMAL
MILD MODERATE
SEVERE
Atrial dimension
LA diameter, cm
3.0-4.0
4.1-4.6 4.7-5.2
>5.2
LA diameter, BSA, cm/m2
1.5-2.3
2.4-2.6 2.7-2.9
>2.9
RA minor axis, cm
2.9-4.5
4.6-4.9 5.0-5.4
>5.4
RA minor axis/BSA, cm/m2
1.7-2.5
2.6-2.8 2.9-3.1
>3.1
Atrial area
LA area, cm2
<20
20-30 31-40
>40
Atrial volume
LA volume, mL
18-58
59-68 69-78
>78
LA volume/BSA, mL/m2
<29
29-33 34-39
>39
BSA, Body surface area.
Bold rows identify best validated measures.
284
CHAPTER 4 Transthoracic chambers and vessels
Right atrium
The right atrium acts as reservoir for blood from the coronary sinus, and
inferior and superior vena cava. It has some unique anatomical features
that can be mistaken for pathology. These include the Eustachian valve,
which in utero directs blood from the inferior vena cava through the
foramen ovale but becomes redundant after birth. If it does not regress
it is seen attached to the right atrial wall between the inferior vena cava
and border of the fossa ovalis. A Chiari network is a remnant from the
embryological stage before the Eustachian valve forms and is a thin mem-
brane, typically fenestrated, near the orifice of the inferior vena cava and
extending further across the right atrium than the Eustachian valve.
Normal views and findings
The right atrium can be seen in a modified right ventricle inflow view
and parasternal short axis view (aortic valve level) (Fig. 4.52).
The apical 4-chamber view is useful for volume measurements and
Doppler interrogation of tricuspid valve inflow.
The subcostal view often provides excellent views of the right atrium
and right atrial inflow from the inferior vena cava.
Right atrial size
Techniques to measure right atrial size are borrowed from those for the
left atrium but assessment is less clinically relevant. Right atrial size meas-
urements are most often used in assessment of right ventricular systolic
pressure (b p.264). There is little research or clinical data so normal
ranges are fairly simplistic without reference to sex or body size.
Qualitative measures
The simplest assessment is to compare the left and right atria in an
apical 4-chamber view (Fig. 4.53). If the right atrium appears larger than
the left it is dilated.
Quantitative measures
Minor axis is a simple linear measure. On an apical 4-chamber view
measure across the middle of the atrium from lateral wall to septum.
Ranges are in Table 4.8.
Area can be reported. Trace around the right atrium joining the lateral
and septal sides of the tricuspid annulus with a straight line.
A volume can be calculated using the area length equation (b p.196)
with measures from an apical 4-chamber view. Right atrial length is
required and can be measured from the back of the atrium to the
middle of the annulus.
RIGHT ATRIAL SIZE
285
TRICUSPID VALVE
RV
RV
RA
RA
LA
PULMONARY
ARTERY
Parasternal short axis
Right ventricle inflow
LV
RV
RA
RV
LV
LA
RA
LA
Eustachian valve
Apical four chamber
Subcostal
Fig. 4.52 Key views to assess right atrium.
RV
LV
RA area trace
RA
LA
Minor axis
Fig. 4.53 Assessment of right atrial size from area measures in apical views.
286
CHAPTER 4 Transthoracic chambers and vessels
Interatrial septum
Normal anatomy
The atrial septum divides the left and right atrium. Embryologically it develops
as two distinct sheets, the primum and secundum septum. In utero the
septum, specifically the foramen ovale, acts as a portal for blood to pass
from the inferior vena cava, directed by the Eustachian valve, to the left side
of the heart, bypassing the lungs. After birth the foramen closes. In around
80% of people it seals but remains evident as a depression in the septum
called the fossa ovalis. In 20% it remains as a potential communication
between right and left heart.
Normal findings
Views
The atrial septum is best assessed in a subcostal view (Fig. 4.54). This is the
only view that has the septum perpendicular to the probe and therefore
aligns the septum for Doppler or colour flow assessment. The atrium can
also be assessed in the parasternal short axis (aortic valve level) and apical
4-chamber view. Agitated saline contrast can be used to investigate the
possibility of a patent foramen ovale.
Findings
Parasternal short axis (aortic valve level): the septum lies in the far
field extending from the aortic ring (usually at the bottom left) with
the left atrium on the right and right atrium on the left.
Apical 4-chamber: the septum can be seen lying between the atria in
the far field. Because it is in line with the probe there may be areas
of ultrasound dropout that can be confused for defects. Colour flow
mapping in this view can be tried.
Subcostal view: the right atrium lies nearest the probe and the septum
lies across the screen. This view can be used for colour flow mapping
and Doppler alignment through the septum.
INTERATRIAL SEPTUM
287
RV
LV
RV
RA
LA
RA
PULMONARY
ARTERY
LA
ATRIAL SEPTUM
Parasternal short axis
Apical four chamber
RA
RV
LV
LA
ATRIAL SEPTUM
Subcostal
Fig. 4.54 Key views to assess the atrial septum.
288
CHAPTER 4 Transthoracic chambers and vessels
Atrial septal defects
Atrial septal defects are the commonest congenital heart defect. Although
they can occur on their own they are frequently associated with other
defects and a full echocardiographic assessment should be performed. They
can also be iatrogenic (e.g. after cardiac surgery and transseptal puncture)
or accidental (e.g. after pacing). There are 4 types of congenital defect:
Secundum atrial septal defect (65%)—fossa ovalis/central septum.
Primum atrial septal defect (15%)—more muscular septum by valves.
Sinus venosus defect (10%)—near the superior vena cava/posterior
and superior septum.
Coronary sinus defects are much rarer.
Assessment
Initial assessment should be with 2D imaging, followed by colour flow map-
ping to study direction of flow (Fig. 4.55) and then Doppler to quantify the
size of the shunt. Where suspicion of a defect remains high, a contrast study
can be performed with Valsalva to identify a left-to-right shunt (b p.572).
Full assessment may require a transoesophageal study (see Chapters 5 and 7).
2D and colour flow mapping
Study the septum in all the standard views and look for gaps in the septum.
To avoid overcalling septal dropout the defect should be apparent in differ-
ent planes. There may be indirect evidence of a problem that prompts more
careful study, in particular: right atrial and right ventricular enlargement
without other cause; an abnormally directed colour flow jet in the right
atrium on colour flow mapping; abnormal septal motion or an aneurysmal
septum. Comment on:
The position of the defect and, therefore, likely classification.
Any associated defects (particularly relevant for primum defects).
The size of the defect in two directions if possible (this can be done in
subcostal views with long axis and sagittal planes through the defect).
Direction and timing of flow from colour flow mapping. Usually
predominantly left to right during systole but with chronic right
ventricle overload flow starts to occur right to left.
RV size and function.
RV systolic pressure.
Doppler quantification of shunt
The principle of shunt quantification is comparison of right and left
ventricle stroke volumes. Their ratio (called Qp/Qs) should be 1 but with
shunting to the right the ratio increases and to the left the ratio declines.
Accuracy depends on accurate measures of outflow tract diameter.
Obtain LVOT PW Doppler vti from apical 5-chamber view and
diameter from parasternal long axis.
2
Qs =
×(
)
× aortic vti
Measure RVOT PW Doppler vti and diameter from a parasternal short
axis (aortic valve level) view.
2
Qp =
×(
)
× pulmonary vti
Report the ratio Qp/Qs.
ATRIAL SEPTAL DEFECTS
289
ASD with colour flow
demonstrating left to
right flow
RA
LV
LA
Fig. 4.55 Colour flow mapping of atrial septum in subcostal view. See W Video 4.19,
W Video 4.20, W Video 4.21, W Video 4.22.
Primum atrial septal defects and associated defects
Primum defects occur when there is failed development of the primum
septum. To make the diagnosis there must be no atrial septal tissue
extending from the base of the atrio-ventricular valves.
The atrial septal defect on its own is a partial atrio-ventricular canal
defect. If extending to involve the ventricular septum and atrio-ventriular
valves it forms a complete atrio-ventricular canal or endocardial cushion
defect. The valves often have abnormal atrio-ventricular valve rings and
lie in the same plane in apical views (instead of the usual apical displace-
ment of the tricuspid valve i.e. loss of off-setting).
If there is a primum septal defect look for and comment on:
Inlet ventricular septal defect.
Cleft mitral valve leaflet—generally involving the anterior mitral
valve leaflet at around ‘12 o’clock’ in the parasternal short axis
(mitral valve level) view. Invariably associated with regurgitation,
often eccentric.
Mitral and tricuspid regurgitation.
Partial attachment of the anterior mitral valve leaflet to the
ventricular septum—best seen from the parasternal long axis view
after forward and backward displacement of the probe.
290
CHAPTER 4 Transthoracic chambers and vessels
Patent foramen ovale
If the foramen ovale fails to seal after birth (~20-30% of the popula-
tion) it remains possible for pressure changes in the left and right atria to
reopen the hole. This is of clinical interest because patent foramen ovale
are amenable to percutaneous closure and their presence raise the
possibility that emboli, e.g. clots or fat, could pass from the right heart to
the systemic circulation and cause strokes. Furthermore foramen ovale
are associated with decompression illness and, possibly, migraines.
To identify a patent foramen ovale right-to-left flow needs to be identified
for a short period during the cardiac cycle (flow throughout the cardiac
cycle identifies a septal defect). Sometimes this can be done with colour
flow but usually means contrast is needed (see Chapter 9).
Atrial septal aneurysm
Atrial septal aneurysms are an area of excessive mobility of the atrial
septum and in 75% of cases are associated with patent foramen ovale. The
technical definition is movement of the septum (at least 10mm in width)
away from the normal plane of the septum (to left or right) by 10mm
(Fig. 4.56). Usually the septum will move back and forth as the relative
pressure gradient between atria varies, but may be fixed. Comment on
presence and look for underlying reasons.
ATRIAL SEPTAL ANEURYSM
291
Atrial
septal
LV
aneurysm
RV
RA
LA
Width and displacement of septum >10mm
Fig. 4.56 Demonstration of septal aneurysm. At least 10mm wide with at least
10mm movement. See W Video 4.23.
292
CHAPTER 4 Transthoracic chambers and vessels
Ventricular septum
Normal anatomy
The ventricular septum divides the left and right ventricle. The ventricular
septum can be divided simply into: (1) a small membranous portion below
the aortic valve and forming part of the left ventricular outflow tract, and
(2) a muscular septum, spreading inferiorly, anteriorly and apically. These
have separate embryological origins.
The muscular septum can be subdivided into 3 areas: the inlet septum
between the mitral and tricuspid valves; the trabecular septum extending
to the apex and forming the bulk of the septum on echocardiographic
views; and the outlet septum close to the aortic and pulmonary valves.
These subdivisions are used to classify ventricular septal defects.
Normal findings
Views
Any view that studies the ventricles can also be used to study the ventricular
septum. Therefore, parasternal long and short axis views, apical 4-, 5-, and
3-chamber and subcostal are all useful (Fig. 4.57).
Findings
Parasternal long axis: the membranous septum (or sometimes part
of the muscular outlet septum) is seen in the LVOT, with the mid
segments of the trabecular (muscular) septum lying to the left.
Parasternal short axis (aortic valve level): the membranous and outlet
septum are seen around the aortic ring.
Parasternal short axis (midpapillary muscle level): the septum lies
between the right and left ventricle and mainly consists of the
muscular (trabecular) septum. The muscular inlet septum may be seen
at the bottom of the septum.
Apical 4- and 5-chamber: the trabeculated (muscular) septum can be
viewed right up to the apex. In a 4-chamber view the muscular inlet
septum is seen between mitral and tricuspid valves. In the 5-chamber
view the membranous septum by the aortic valve comes into view.
Subcostal view: the septum lies perpendicular to the probe and this
view provides an opportunity for aligning colour flow mapping and
Doppler through the septum.
VENTRICULAR SEPTUM
293
LV
RV
RV
LV
RA
LA
Parasternal long axis
Apical four chamber
Membranous septum
LV
Muscular septum
Outlet (or membranous) septum
Outlet septum
Parasternal short axis
Inlet septum
Trabecular septum
RV
RV
LV
RA
RA
LA
LA
Apical five chamber
Parasternal short axis
Fig. 4.57 Key views to assess the ventricular septum and areas of septum.
294
CHAPTER 4 Transthoracic chambers and vessels
Ventricular septal defects
Ventricular septal defects are one of the common congenital heart defects.
They can occur anywhere within the septum and are named according to
their location—membranous or muscular (inlet, outlet, or trabeculated)
(Fig. 4.58). If they involve both the membranous and muscular septum
they are called peri-membranous. Gerbode defects are a specific type from
left ventricle to right atrium. As well as being congenital they can occur
due to ischaemia (post infarction, often quite apical in trabecular septum
with multiple holes) or be iatrogenic following cardiac surgery or pacing.
Membranous (and peri-membranous) are easiest to identify, with muscular
defects the most often missed because the defect is small or altered in
shape by ventricular contraction.
Assessment
Initial assessment should be with 2D imaging, followed by colour flow.
Doppler can quantify the size of any shunt.
2D and colour flow imaging
Study the septum in all views and look for gaps. To avoid overcalling
septal drop-out the defect should be apparent in different planes.
Colour flow imaging over the septum, particularly in the subcostal and
parasternal views, is essential to scan for abnormal colour flow jets
appearing in the right ventricle and originating from the septum.
The septum is curved and can not be seen entirely in one plane.
Peri-membranous defects are easiest to see in parasternal long axis
and short axis (aortic valve level) views with tilting to scan through
the septum. These views also identify outlet defects, which can be
differentiated from peri-membranous defects because they lie nearer
the pulmonary valve. The inlet and trabecular defects are better seen
in apical and subcostal views but may need probe tilting to scan the
septum.
Comment on
Position of the defect and, therefore, likely classification.
Characteristics of the defect, e.g. multiple small defects.
Size of the defect (in 2 directions if possible, e.g. subcostal views with
long axis and sagittal planes through the defect). Measure size from 2D
images or colour flow jet.
Direction and timing of flow from colour flow mapping. With large
chronic defects right ventricular pressure will increase and the left-
to-right flow will reduce. Colour flow may be less evident.
If possible, use PW or CW Doppler aligned across the defect to
measure the pressure gradient between ventricles using the Bernouli
equation (= 4 × velocity2). Right ventricular pressure can be measured
from the pressure gradient. If the aortic valve is normal then systolic
blood pressure will equal left ventricular systolic pressure. Right
ventricular systolic pressure = systolic blood pressure—gradient
across the defect.
Left and right ventricle size and function, as well as evidence of right
ventricle pressure or volume overload (b p.276).
Associated problems, e.g. aortic valve dysfunction and regurgitation.
VENTRICULAR SEPTAL DEFECTS
295
Colour flow
mapping
demonstrates
flow
LV
Large
membranous
septal defect
RV
LA
Large
muscular
septal defect
RV
RA
LV
LA
Fig. 4.58 Examples of ventricular septal defects. The top figure shows a large
congenital peri-membranous defect in an apical view. The lower figure demonstrates
a trabecular muscular defect secondary to ischaemia seen in a subcostal view.
See W Video 4.24, W Video 4.25, W Video 4.26, W Video 4.27.
296
CHAPTER 4 Transthoracic chambers and vessels
Pericardium
Normal anatomy
The pericardium surrounds the heart. An outer, supportive, fibrous peri-
cardium blends superiorly into the aorta and pulmonary arteries and infe-
riorly attaches by ligaments to the diaphragm, sternum and vertebrae. On
the inside of the fibrous layer and the outer surface of the heart are two
serous membranes which allow the heart to move. There are two irregular
holes through the membranes; one around the aorta and pulmonary
arteries, and the other around the pulmonary veins and vena cavae. The
membranes join around the edges of the holes to create an enclosed,
‘deflated’ sac which can fill with fluid. Because they wrap round the blood
vessels two pockets (or sinuses) are created; the transverse sinus between
aorta and pulmonary artery, and the oblique sinus between the pulmonary
veins on the back of the left atrium. These are important because localized
collections can form in the pockets.
Normal findings
Views
Part of the pericardium can be seen in all views and should be studied
in all scan planes—only part of the pericardium may be affected in
disease or there may be a localized collection.
The best views are: parasternal long and short axis, apical 4-chamber,
and subcostal (Fig. 4.59).
Pericardium
The pericardial surfaces are difficult to see because they adhere to
surrounding structures but may appear as a thin, slightly brighter line
around the heart.
Measures of pericardial thickness do not correlate well with pathology
specimens but the pericardium is normally 1-2mm thick. CT or
magnetic resonance imaging should be used to measure thickness.
Pericardial space
The pericardial space is seen as a black line around the heart. It is
normal to have a few millimetres of fluid.
Distinguishing pericardial from pleural fluid
In the parasternal long axis view use the descending aorta as a landmark.
The pericardial sac tucks in between the aorta and left atrium, so peri-
cardial fluid will extend up to the gap and lie in front of the aorta. Pleural
fluid will track behind the aorta and over the left atrium.
If both pericardial and pleural fluid are suspected look for the pericardium
lying as a continuous dividing line within the fluid in an apical view.
PERICARDIUM
297
ANTERIOR PERICARDIAL FLUID
RV
LV
LA
POSTERIOR PERICARDIAL FLUID
PLEURAL FLUID WOULD LIE
BEHIND AORTA
Fig. 4.59 Parasternal long axis view showing heart lying in global pericardial
effusion. Measure depth on 2D (double ended arrow) or M-mode and report
measurement site. See W Video 4.28 and W Video 4.29.
298
CHAPTER 4 Transthoracic chambers and vessels
Pericardial effusion
Amount of pericardial fluid
Measure fluid thickness using 2D or M-mode in several places and
views. Report the depth and where the measurement was made.
For global effusions, grade as mild, moderate, or large based on depth
(depth also approximates to volume of fluid).
<0.5cm
Minimal
50-100mL
0.5-1cm
Mild
100-250mL
1-2cm
Moderate
250-500mL
• >2cm
Large
>500mL
More accurate volume measures can be made with planimetry from
traced pericardial and heart borders in apical views. It is possible to
produce even more accurate measures with 3D echocardiography,
although there is not usually any clinical indication.
Thickness does not relate to clinical severity
Rapid accumulation of a small quantity can have as severe a haemodynamic
effect as slow accumulation of a large quantity. Look for features of
tamponade.
Appearance of pericardial space
Fluid is the black echolucent area and will be serous, blood, or pus. It is
difficult to differentiate with echocardiography.
Strands (fibrin) can occur in any condition which causes inflammation
(infection, haemorrhage, or uraemia) (Fig. 4.60).
Masses are more unusual and could be haematoma, tumour,
cyst, or related to infection, e.g. fungus. Comment on size, shape,
appearance, movement, attachments to surfaces, e.g. pericardium,
ventricle. Haematoma is usually the same echocardiographic
density as myocardium—so may be difficult to see—but suggests a
haemopericardium.
Localization Look at effusion in all views and comment whether global
(most common) or localized. Specify where the effusion is localized.
Problems with localized effusions
Suspect localized effusions after cardiac surgery (blood) or infections
(loculation). Localized effusions may only be evident because
of restricted pulmonary vein flow (oblique sinus) or unusual
compression of a cardiac chamber. Consider transoesophageal
echocardiography in patients with haemodynamic problems after
cardiac surgery to look for localized effusions.
Apparent posterior localization may be because a small effusion has
shifted posteriorly due to gravity in a supine patient.
A localized anterior space in parasternal views may actually be
mediastinal (e.g. fat, fibrosis, thymus).
Evidence of cardiac tamponade see b p.300.
PERICARDIAL EFFUSION
299
Best site for pericardiocentesis
GLOBAL PERICARDIAL
FIRBRIN STRANDS
EFUSION
LV
RV
LA
RA
Fig. 4.60 Apical 4-chamber view with global pericardial effusion and fibrin strands.
Comment on strands and attachment to ventricle.
300
CHAPTER 4 Transthoracic chambers and vessels
Cardiac tamponade
Cardiac tamponade is a clinical diagnosis based on tachycardia (>100bpm),
hypotension (<100mmHg systolic), pulsus paradoxus (>10mmHg drop
in blood pressure on inspiration), raised JVP with prominent x descent.
Echocardiography provides supporting evidence.
2D findings suggestive of tamponade (Fig. 4.61)
As intrapericardial pressure rises and begins to exceed right heart pres-
sure, parts of the cardiac chambers collapse during the cardiac cycle.
Clinical signs usually appear before the left heart is affected.
Right atrium appears to collapse faster than usual in atrial systole.
Parts of right ventricle start to collapse during ventricular diastole. First
the right ventricular outflow during early diastole (at lowest pressure)
then as intrapericardial pressure increases collapse extends to involve
whole of right ventricle and whole of diastole.
Combination of rapid atrial collapse in atrial systole followed by rapid
ventricular collapse in ventricular diastole creates the appearance of a
‘swinging right atrium and ventricle’.
Doppler findings suggestive of tamponade
Doppler findings in tamponade are the echocardiographic demonstration
of the exaggerated variation in right and left ventricle inflow during
respiration—clinically demonstrated as pulsus paradoxus.
In an apical 4-chamber view place PW Doppler at tricuspid valve
inflow. Switch on physiological respiration trace (if available) and slow
sweep speed to 25cm/s.
Acquire a tracing and measure maximum and minimum E-wave
velocities (these correspond with respiration: maximum in inspiration).
Do the same at the mitral valve (E-wave maximum in expiration).
Normal variation is <15% at mitral valve and <25% at tricuspid valve.
Greater than this supports tamponade but clinical signs are usually
associated with ~40% variation at the mitral valve.
Exaggerated flow changes through the heart during respiration can also be
demonstrated in the left and right ventricle outflow tracts (increased flow
in inspiration on the right and in expiration on the left).
Use PW Doppler in RVOT in parasternal short axis. Record vti and
peak velocity in inspiration and expiration.
Do the same at the LVOT in apical 5-chamber.
Normally vti and peak velocity vary <10% during respiration.
Problems with assessment of tamponade
2D and Doppler measures are only accurate with ‘normal’ relations
between intrapericardial, intrathoracic, and intraventricular pressures.
Increased ventricular ‘stiffness’ (ventricular hypertrophy, intraventricular
haematoma) or increased right ventricular pressure (pulmonary hyper-
tension) makes the ventricle less likely to collapse. Low volume states
mean the change in ventricular inflow on Doppler is less pronounced.
Doppler indices are not validated in ventilated patients.
CARDIAC TAMPONADE
301
Pulsus paradoxus
There is normally a swing of 5mmH2O in intrathoracic pressure with res-
piration. Inspiration leads to an increase in blood flow into the lungs and
therefore an increase in flow into the right heart and reduced flow into
the left heart. Expiration forces blood out of the lungs and increases flow
into the left heart and reduces flow into the right heart. This accounts for
the normal variation in blood pressure (‘left-sided pressures’) with respi-
ration. Increased pericardial fluid increases intrapericardial pressure. Left
and right ventricular filling is impaired and this filling is exacerbated on
the left on inspiration leading to an exaggerated drop in blood pressure
on inspiration.
Changes in 2D and Doppler with increasing tamponade
1. Tricuspid valve inflow pattern.
2. Mitral valve inflow pattern.
3. Abnormal right atrial collapse in atrial systole.
4. Right ventricular outflow collapse in ventricular diastole.
5. Left ventricular outflow collapse in ventricular diastole.
Start of right atrial collapse
in atrial systole
RA
LV
LA
Right ventricular collapse in
ventricular diastole
Fig. 4.61 Subcostal long axis view showing early atrial systolic collapse and
ventricular diastolic collapse.
302
CHAPTER 4 Transthoracic chambers and vessels
Constrictive pericarditis
Constrictive pericarditis is uncommon and often has vague signs and
symptoms with a long history. It can be due to chronic inflammation
as a result of infection (classically tuberculosis), cardiothoracic surgery,
radiation, or connective tissue disease. It can be transient with pericardial
inflammation. Diagnosis is clinical. Echocardiography can be supportive
and differentiate from restrictive cardiomyopathy. Magnetic resonance
imaging or CT are also usually required to assess the pericardium.
2D findings suggestive of constriction
Look for the pericardium: may appear normal thickness (1-2mm) or
thickened (up to 10mm) (measurements are inaccurate so use other
modalities for actual measures). May appear bright or there may be
shadowing from calcium (a marker of chronic inflammation).
Assess the left ventricle: usually normal systolic function—consider
other causes if not. Assess septal motion in parasternal views with 2D
and M-mode. Classically, septum appears to ‘flutter’ as left and right
ventricles fill during diastole. Probably due to waves of competitive
filling of the 2 ventricles. Seen as early diastolic notching on M-mode,
or paradoxical and then normal motion on 2D.
CONSTRICTIVE PERICARDITIS
303
Differentiation from restrictive cardiomyopathy (Table 4.9)
Table 4.9 Clinical features of constrictive pericarditis and restrictive
cardiomyopathy are similar. Echocardiography is useful to differentiate
Restrictive
Constrictive pericarditis
cardiomyopathy
Similarities between conditions:
E/A ratio
Increased
Increased
Deceleration time
Decreased
Decreased
Differences between conditions:
LV function
May be abnormal
Usually normal
Pericardium
Normal
May be bright or thick
Septal motion
Usually normal
May be abnormal
Atria
Biatrial enlargement Usually normal size
Mitral annulus velocity Decreased
Normal
Ventricular inflow
Normal variation
Increased variation on respiration
304
CHAPTER 4 Transthoracic chambers and vessels
Doppler findings suggestive of constriction
Assess mitral and tricuspid inflow during respiration just as for
tamponade (Fig. 4.62). Constrictive pericarditis causes the same
changes as tamponade (>25% variation at tricuspid and >15% at
mitral). As the ventricles are supported by ‘stiff’ pericardium no
ventricular collapse.
Look for features of diastolic dysfunction (b p.246). Exaggerated E/A
ratio on mitral inflow and shortened deceleration time (time from
peak to end of E-wave: normal >160ms).
Use tissue Doppler (if available). In apical 4-chamber place cursor on
lateral mitral annulus. In constrictive pericarditis myocardial function is
normal and peak mitral annulus velocity is therefore normal (>10mm/s).
If reduced, consider restrictive cardiomyopathy (Fig. 4.63).
CONSTRICTIVE PERICARDITIS
305
INSPIRATION
EXPIRATION
INSPIRATION
PHYSIO TRACE
MAXIMUM E-WAVE VELOCITY
MINIMUM E-WAVE VELOCITY
Fig. 4.62 Diagram representing pulsed wave Doppler trace at tricuspid valve. There
is significant variation in tricuspid valve inflow (>25%) consistent with cardiac tam-
ponade or constrictive pericarditis. The same recording can be done at mitral valve
but maximum E-wave velocity will be in expiration and normal variation is <15%.
LV
LV
RV
RV
LA
LA
RA
RA
Fig. 4.63 Tissue Doppler imaging of lateral mitral annulus showing reduced
movement in restrictive cardiomyopathy (left) compared to normal myocardial
function (right). Normal motion is >10cm/s.
306
CHAPTER 4 Transthoracic chambers and vessels
Congenital pericardial disease
Congenital absence of pericardium is rare. Usually suspected in 2D because
of an obvious gap or herniation of part of the heart (often left or right
atrial appendage or parts of ventricle). The heart may be abnormally
positioned with right atrial or ventricular dilatation and paradoxical septal
motion. Record where the pericardium is missing and any functional
effects of herniation.
Congenital pericardial cysts are more common. Usually benign. Comment
on size, mobility, position, attachment, appearance (fluid, masses).
Pericardial tumours
Primary cardiac tumours or metastatic tumours can involve the pericardium.
Comment on any masses, reporting the position, size, appearance, attach-
ments, and functional effects on cardiac function.
Acute pericarditis
There are no echocardiographic features diagnostic of acute pericarditis.
Echocardiography should be used in suspected pericarditis to look for:
Complications (e.g. effusions).
Left ventricular function (e.g. abnormal function may suggest
myocarditis).
Underlying causes (e.g. tumour or regional wall motion abnormalities
suggestive of myocardial infarction).
Other causes for clinical signs (e.g. endocarditis, pericardial effusion).
Pericardiocentesis
Echocardiography is very useful during pericardiocentesis. Pericardio-
centesis is usually done from subcostal or apical positions so assess
pericardial fluid in both views (Fig. 4.64).
Before the procedure record:
Depth of fluid in each position.
Depth from skin to the outer boundary of fluid (a guide as to how far
to introduce the needle).
During the procedure:
Angle of the echo probe to achieve images can be a guide to the angle
to be used for the needle.
The needle can sometimes be seen advancing into pericardial space.
If unclear whether needle is in pericardial space, inject agitated saline
contrast down needle. Contrast should be seen clearly filling the
pericardial space if needle is correctly positioned . . . or filling another
cardiac chamber if not!
PERICARDIOCENTESIS
307
RV
LV
AGITATED SALINE
RA
CONTRAST IN
LA
PERICARDIAL SPACE
Fig. 4.64 Pericardiocentesis from subcostal position monitored by echocardiography
from apex. Agitated saline contrast has been injected down the pericardiocentesis
needle and is seen circulating in the pericardial space. This confirms the correct
location of the needle.
308
CHAPTER 4 Transthoracic chambers and vessels
Aorta
Normal anatomy
The aorta is the main conductance artery of the body, carrying blood
from the heart to all major branch vessels. It has a functional role, distend-
ing during systole and recoiling in diastole, to propel blood. The aortic
wall has 3 layers: tunica intima, a thin inner layer, lined by endothelium;
tunica media, a thicker middle layer of elastic tissue for tensile strength and
elasticity; tunica adventitia, a thin outer layer, predominantly collagen,
housing the vasa vasorum and lymphatics.
There are 4 major sections: (1) ascending aorta from aortic valve annulus
including sinuses of Valsalva, sinotubular junction (the narrowest point)
and up to right brachiocephalic artery; (2) aortic arch from brachiocephalic
to aortic isthmus (just distal to left subclavian artery); (3) descending aorta
from isthmus to diaphragm; (4) abdominal aorta from diaphragm to aortic
bifurcation and origin of iliac arteries.
Normal findings
Views
Parts of the aorta can be seen in all windows (Fig. 4.65). Full evaluation
requires a combination of views and additional, non-standard transducer
positions.
Proximal ascending aorta
Proximal ascending aorta is best seen in the parasternal long axis view.
Additional views include, particularly if dilated, the right parasternal
views or left parasternal views from higher intercostal spaces for
ascending aorta, (particularly with patient in extreme left lateral
position to bring aorta more anterior). Doppler interrogation is limited
to qualitative assessment of flow and aortic regurgitation severity.
Apical views: the ascending aorta can also be visualized in apical
5- and 3-chamber views. 2D image quality is limited at this depth but
orientation is optimal for Doppler to assess aortic regurgitation.
Aortic arch
Suprasternal views (and supraclavicular views) allow assessment
of aortic arch and brachiocephalic vessels. Both transverse and
longitudinal views are possible but the latter is most useful to identify
head and neck vessels. Descending aorta is only partially in plane and,
artefactually, appears to taper. Descending aorta blood flow can be
used to assess aortic regurgitation severity and aortic coarctation.
Descending thoracic aorta
Descending thoracic aorta is seen in cross-section posterior to
the left atrium in the parasternal views. The proximal segment of
descending aorta is seen in the suprasternal view. Additional views of
the longitudinal section of the descending thoracic aorta can normally
be visualized from an apical 2-chamber view with lateral angulation and
clockwise rotation of probe. The distal thoracic aorta and proximal
abdominal aorta can be visualized from the subcostal view.
AORTA
309
PROXIMAL
RV
AORTA
LV
LV
RV
DESCENDING
PROXIMAL
AORTA
AORTA
Parasternal long axis
Apical three chamber
AORTIC ARCH
RV
LV
ASCENDING
AORTA
DESCENDING
RA
LA
AORTA
PROXIMAL
AORTA
Apical five chamber
Suprasternal
Fig. 4.65 Key views to assess the aorta.
The pathological significance of the aortic isthmus
The isthmus is the point where the relatively mobile ascending aorta
and arch become fixed to the thorax and thus the aorta is vulnerable
to trauma at this point. Coarctations also commonly develop here. The
isthmus is just distal to the left subclavian.
310
CHAPTER 4 Transthoracic chambers and vessels
Aortic size
The terms proximal aorta or aortic root refer to the aortic annulus,
sinuses of Valsalva, sinotubular junction, and proximal ascending aorta.
Measurement of the aortic root is of crucial importance in the diagnosis of
Marfan syndrome, and in the serial monitoring of patients with, or at risk
of, progressive dilation of the ascending aorta. While a single measure-
ment of the proximal aorta may suffice in the normal examination, when
monitoring aortic root dilatation a minimum of 4 measurements should be
routinely made and recorded from the parasternal long axis view.
Different methods for assessing aortic root dilation are quoted in the
literature (e.g. systolic versus diastolic measurement; inner to inner or
leading edge to leading edge dimensions). Normative data in adults were
calculated using leading edge methodology in diastole. However, to try
and achieve consistency with both other chamber measurements and
other imaging methods it is now more common to measure inner edge to
inner edge at the widest diameter, i.e. in systole. Differences are likely to
be small but it is important that the method used is stated and consistent
methodology used in follow-up.
Assessment (Fig. 4.66)
Make measurements from a parasternal long axis view in systole (with
valve leaflet tips open to their maximum).
2D measurement at the sinuses gives higher values than M-mode
measurements and are preferred. Make measurements parallel to
aortic annular plane from inner edge to inner edge.
A complete assessment includes measurement of:
• Annulus (normal 2.3 ± 0.3cm).
• Sinus of Valsalva, at aortic leaflet tip level (normal 3.4 ± 0.3cm;
<2.1cm/m2).
• Sinotubular junction.
• Proximal ascending aorta (normal 2.6 ± 0.3cm).
Comment on how the measurements were made and use the
appropriate normal values. In a normal study a single aortic diameter
may be sufficient. When possible, report size relative to body
surface area.
Where needed, continue the assessment by providing measurements
of the arch from suprasternal views, descending aorta from parasternal
views and, for completeness, abdominal aorta from subcostal views.
• Aortic arch.
• Descending thoracic aorta (normal <1.6 cm/m2).
• Abdominal aorta (normal <3 cm; <1.6 cm/m2).
AORTIC SIZE
311
Serial measurements and identification of dilatation
In serial measurements the annulus is not prone to dilation. Any
significant change should raise suspicion of methodological error and
caution over interpreting measurements elsewhere. In effect, the
annulus acts as a control for serial studies.
Measurements at the sinus of Valsalva are the key. They tend to be
the site of initial ectasia when the aortic root does dilate in Marfan
syndrome. In the normal adult it measures <3.7cm but can vary
with body surface area (Fig. 4.67). Normograms that adjust for body
surface area maximize sensitivity for the detection of aortic dilation
in adults, but for practical purposes the upper normal limit in the
adult is 2.1cm/m2 and anything below this can be reported as normal.
Aortic
Sinus of
Sinotubular
Ascending
annulus
valsalva
junction
aorta
Aortic arch
Descending aorta
Fig. 4.66 Measurement of aortic size at key locations from parasternal long axis
(top) and suprasternal (bottom) views.
312
CHAPTER 4 Transthoracic chambers and vessels
Calculating a z-score: Cornell data-based formulae for
children and adults in different ranges of age
Z-scores for aortic root size are used extensively in the new Ghent
criteria for Marfan syndrome. Therefore it is important to know what
they are.
A z-score is a way to take account of expected variability in a measure
so that you can assess how abnormal the value you have obtained really
is. The z-score represents the proportion of a standard deviation that
the value you have measured lies away from the expected mean for that
measure, given the level of another factor. For example, the distribution
of aortic root size varies with age. Therefore, you can not know if the
aortic root size you measure is abnormal unless you know what the
normal range is for the age group of patient you are studying. For aortic
root size this is further complicated by the fact that aortic root size also
varies with body surface area so this also needs to be taken into account
in the z-score. The formulae listed here allow you to calculate an ‘aortic
root size’ z-score for different age groups based on what the predicated
aortic root size would be for the patient body surface area. To use these
formulae you need to know for your patient their: 1) age, 2) body surface
area 3) measured aortic root diameter (originally measured in diastole—
leading edge to leading edge; inner edge measurements in systole now
recommended). Then, choose the formulae below that suit the age of
the patient and calculate their predicted aortic root size using the patient’s
body surface area. Then, calculate the z-score using the measured root
diameter and the predicted root diameter. This number tells you how
many standard deviations the patient lies away from the mean.
Age up to 15:
Mean predicted aortic root (cm) = 1.02 + 0.98 × BSA
Z = (Measured root diameter - predicted aortic root diameter)/0.18
Age 20 to 40:
Mean predicted aortic root (cm) = 0.97 + 1.12 × BSA
Z = (Measured root diameter - predicted aortic root diameter)/0.24
Age >40
Mean predicted aortic root (cm) = 1.92 + 0.74 × BSA
Z = (Measured root diameter - predicted aortic root diameter)/0.37.
Mean predicted aortic root size is based on Dubois formula.
AGED 20-39 years
AGED >40 years
4.2
4.4
4.0
4.2
3.8
4.0
3.6
3.8
3.4
3.6
3.2
3.4
3.0
3.2
2.8
3.0
2.6
2.8
2.4
2.6
2.2
2.4
2.0
2.2
1.2
1.4
1.6
1.8
2.0
2.2
2.4
1.2
1.4
1.6
1.8
2.0
2.2
2.4
Body surface area (m2)
Body surface area (m2)
Fig. 4.67 Ranges of normal sinus of Valsalva size according to age.
314
CHAPTER 4 Transthoracic chambers and vessels
Aortic dilatation
General (Fig. 4.68)
Dilatation of the aorta is an increase in diameter more than expected for
age and body size and is the most commonly identified aortic abnormality.
When localized to the sinus of Valsalva the risk of complications is
significantly lower than when there is generalized aortic dilatation but still
higher than no dilatation! Causes include: degenerative disease (hyper-
tension, atherosclerosis, cystic medical necrosis, post-stenotic); collagen
vascular disease (Marfan syndrome, Ehlers-Danlos, Loeys-Dietz, familial
aortic aneurysm); inflammatory disorders (rheumatoid, systemic lupus
erythematosus, ankylosing spondylitis, Reiter syndrome, syphilis, aortic
arteritis); trauma (blunt or penetrating).
Assessment
Measure the degree of dilatation at multiple positions and report where
and how the measurements were made.
Differentiation of degenerative dilatation from Marfan
When the aorta dilates due to degenerative disease, the contours of the
sinuses of Valsalva and the normal slight narrowing at the sinotubular
junction are maintained. In contrast, dilatation of the aorta in Marfan
syndrome is characterized by enlargement of the sinuses of Valsalva,
resulting in loss of narrowing at the sinotubular junction.
Indications for considering elective aortic root
replacement
Aortic diameter 45mm in adults with connective tissue disease,
especially if a family history of aortic dissection.
Aortic diameter 50mm in patients with bicuspid aortic valve
disease.
Aortic diameter 55mm in adults without connective tissue
(atherosclerotic aneurysm).
Rapid change in the aortic root size: >5mm per year.
If there is an indication for aortic valve replacement, lower thresholds
can be used: concomitant root replacement should be considered if
aortic diameter 40 mm.
There is an increased risk in pregnancy. If the aortic diameter is 40 mm,
monitoring with echocardiography and clinical examination should be
considered monthly. Progressive root dilatation to 45 mm should lead
to consideration of surgery prior to, or contemporaneous with, delivery
of the child. Special precautions would also be required at the time of
delivery which should take place under the care of a specialist team
managing complex pregnancy with cardiac disease.
AORTIC DILATATION
315
Ascending aorta aneurysm
Fig. 4.68 Example of dilatation of the proximal ascending aorta seen in a
parasternal long axis view.
316
CHAPTER 4 Transthoracic chambers and vessels
Marfan syndrome
Marfan syndrome is an autosomal dominant connective tissue disorder due
to mutation in the Fibrillin 1 gene. It is a multisystem disorder that affects
both locomotor and cardiovascular systems, and the eyes. The incidence
is approximately 1 in 10,000 births of whom approximately 26% are a spon-
taneous mutation, i.e. have no family history. Many individuals have some
of the skeletal features of Marfan syndrome without the actual condition
and the diagnosis is dependent on diagnostic criteria (Ghent criteria).
Assessment
Echocardiography is key for the criteria and should concentrate on aortic
root dimensions (Fig. 4.69). To correct for body size, either a Z-score
should be calculated using a validated formula, with the Cornell formula
the most commonly used, or aortic root dimensions plotted on a validated
nomogram against body surface area. An aortic Z-score of 2 supports
diagnosis of Marfan syndrome. Previous or newly diagnosed aortic root
dissection carries the same weight.
The presence of mitral valve prolapse, diagnosed as per standard practice
(see b p.128), scores 1 in the systemic score (which has replaced minor
criteria) and its presence and severity should therefore also be reported.
2010 Revised Ghent Nosology for Marfan syndrome
Marfan syndrome should be diagnosed if any 1 of these 7 rules is fulfilled:
If no family history of Marfan syndrome:
1. Aortic Z 2 and Ectopia lentis
2. Aortic Z 2 and Fibrillin 1 gene mutation
3. Aortic Z 2 and Systemic score 7
4. Ectopia lentis and Fibrillin 1 gene mutation with known aortic
aneurysm
If positive family history of Marfan syndrome:
5. Ectopia Lentis and confirmed family history
6. Systemic score 7 and confirmed family history
7. Aortic Z score 2 if over 20 years, 3 if below 20 years, and
confirmed family history.
For explanation of Z-score see b p.312.
MARFAN SYNDROME
317
Aortic root
dilation
AV cusps
LV
MV leaflets
Fig. 4.69 Parasternal long axis view of dilation of the aortic root in a patient with
Marfan syndrome. See W Video 4.30.
318
CHAPTER 4 Transthoracic chambers and vessels
Aortic dissection
General
Aortic dissection originates from an intimal tear, leading to subintimal
haemorrhage which can extend within a false lumen back to the aortic valve
or forwards, throughout the aorta. Aortic dissection is life threatening,
with an early mortality of 1% per hour. Presentation is usually with severe
chest pain. The differential includes other causes of chest pain such as
acute myocardial infarction or chest wall pain, and aortic intramural
haemorrhage or expanding thoracic aneurysm. Risk factors for dissection
include: Marfan syndrome, aortic dilatation/aneurysm, hypertension, aortic
valve disease—particularly bicuspid valve (risk 5× normal).
The Stanford classification is the simplest and most pragmatic.
Type A: involvement of the ascending aorta irrespective of
involvement elsewhere.
Type B: limited to the arch and/or descending thoracic aorta.
Assessment
Prompt diagnosis is crucial and transthoracic echocardiography is of value
in initial management. Examine for diagnostic features and for secondary
complications. A negative transthoracic study does not exclude aortic dis-
section and where there is a high index of suspicion further imaging with
TOE, CT, or magnetic resonance imaging will be required.
Diagnostic features
Look for the presence or absence of any possible dissection flap in all
aortic views (parasternal, suprasternal, subcostal) (Fig. 4.70). A flap will
appear as a linear mobile structure with motion independent of the
aortic wall.
3D echocardiography can confirm presence of dissection flap—which
will appear as sheet-like structure—and extent, helping to exclude or
confirm involvement of coronary ostia.
Look for a false lumen using colour flow Doppler placed over the
aorta in all aortic views. There will be different patterns of flow in the
true and false lumen.
Beam-width artefact and reverberation
Beam-width artefact and reverberation can mimic a dissection flap.
M-mode of aortic wall motion and a suspected flap will demonstrate
flap motion which is different from aortic wall movement, whereas a
reverberation artefact will move with the wall.
Secondary complications
Measure aortic root size from parasternal views, size of arch and
descending aorta from suprasternal views, and size of descending
thoracic and abdominal aorta from subcostal views.
Comment on and quantify aortic regurgitation.
AORTIC DISSECTION
319
Comment on pericardial fluid and perform Doppler analysis of
transmitral and transtricuspid blood flow to diagnose tamponade.
A small acute collection can cause tamponade without obvious
pericardial fluid.
Assess left ventricular systolic function, and comment on any regional
wall motion abnormalities which might suggest coronary artery
involvement.
Dilated ascending aorta
RV
Dissection flap
LV
LA
PARASTERNAL LONG AXIS VIEW
Dissection flap
Ascending
Descending
aorta
aorta
SUPRASTERNAL VIEW
Fig. 4.70 Examples of aortic dissection flap seen in parasternal long axis and
suprasternal views. See W Video 4.31, W Video 4.32, W Video 4.33.
320
CHAPTER 4 Transthoracic chambers and vessels
Aortic coarctation
General
Aortic coarctation is a congenital narrowing in the proximal descending
thoracic aorta, usually located immediately proximal to the entry site of
the ductus arteriosus. It may be suspected in a patient with hypertension
and a weak femoral pulse, radiofemoral delay or systolic murmur. Aortic
coarctation first diagnosed in adulthood is usually asymptomatic as the
stenosis is not usually severe and collaterals are present. 50-80% will have
a bicuspid aortic valve and other cardiac abnormalities (e.g. subaortic
membrane, supravalvular aortic stenosis).
Assessment
Echocardiography is required in diagnosis and follow-up. Aortic coarctation
can be relatively complex and further imaging (usually magnetic resonance
imaging) is performed if intervention is being considered.
Diagnosis
The suprasternal view is the most useful.
Identify the brachiocephalic vessels—coarctation usually occurs just
distal to the left subclavian with post-stenotic dilatation common.
Use colour flow mapping of the descending aorta to identify a high-
velocity narrowed flow stream with turbulence (even if 2D poor).
Place CW Doppler through the point of maximum colour flow
turbulence to measure a typical systolic velocity gradient. The gradient
will typically persist to end diastole (‘diastolic tail’) (Fig. 4.71).
CW Doppler tends to overestimate the gradient and better
correlation with catheter gradients can be obtained if the proximal
velocity is measured with PW Doppler and the modified Bernoulli
equation used to calculate flow.
If coarctation is suspected but difficult to image, CW Doppler using a
pencil probe in the suprasternal position will often allow measurement
of a gradient in the descending aorta.
Follow-up
All patients with previous repair of coarctation of the aorta should be
followed up throughout adult life. Echocardiography should be repeated
annually. Where visualization is inadequate alternative imaging such as CT
or magnetic resonance imaging may be needed.
Examine and report the residual gradient.
Look for abnormalities in the aorta and comment on development of
any aneurysm at the site of previous repair.
Reassess the aortic valve annually: early degenerative disease is
common (sometimes in previously unrecognized bicuspid valve).
AORTIC COARCTATION
321
Aorta
Suprasternal view with CW
+
Peak velocity
Diastolic tail
Fig. 4.71 Doppler profile in coarctation of the aorta from a suprasternal view.
Note the increased peak velocity and prolonged flow throughout diastole
(‘diastolic tail’).
322
CHAPTER 4 Transthoracic chambers and vessels
Sinus of Valsalva aneurysm
Sinus of Valsalva aneurysms can be congenital resulting from incomplete
fusion of the distal bulbar septum that divides the aorta and pulmonary
arteries. They tend to have a long sac of mobile tissue projecting into ad-
jacent structures, forming a ‘wind sock’ appearance. Acquired aneurysms,
usually due to endocarditis, lead to more symmetrical dilation, with no
excess tissue. If rupture occurs, a fistula develops between aorta and adja-
cent chamber, with left-to-right shunting and clinical features that can vary
in severity from acute haemodynamic compromise to a new continuous
murmur. 85% affect right coronary sinus and project/rupture into the right
ventricle; 10% affect non-coronary sinus and project/rupture into the right
atrium; 5% affect left coronary sinus and project/rupture into the left atrium.
Assessment
Use parasternal long and short axis views to diagnose and measure
(Fig. 4.72).
If rupture suspected, use parasternal short axis view at and above
the aortic valve. Colour flow mapping will usually confirm site of
communication and continuous flow. If possible the coronary artery
should be visualized to exclude coronary artery fistulae.
CW Doppler will show a high velocity systolic and diastolic signal.
Comment on the size of the right atrium (which reflects acute right
atrial overload) and left atrial and left ventricular size (which will
reflect the extent of chronic volume overload).
3D echocardiography may be helpful in planning particular surgical or
percutaneous approach to repair. Image the aortic valve in parasternal
long axis view before acquiring a full 3D volume set.
SINUS OF VALSALVA ANEURYSM
323
RV
Sinus of Valsalva aneurysm
LV
LA
Fig. 4.72 Parasternal long axis left ventricle (LV) showing sinus of Valsalva
aneurysm. RV right ventricle, LA left atrium. See W Video 4.34.
324
CHAPTER 4 Transthoracic chambers and vessels
Aortic atherosclerosis
General
Atherosclerosis of the aorta can result in dilatation, aneurysm, or dissection
and is a risk factor for coexisting coronary artery disease and cerebrovascular
disease.
Assessment
Aortic atheroma can be visualized with transthoracic echocardiography
(although transoesophageal is more appropriate) in either the proximal
ascending aorta or, more commonly, in the descending abdominal aorta.
Atherosclerotic thoracic aortic aneurysm may also be detected by tran-
sthoracic imaging, either at the aortic root or behind the left atrium in
the descending thoracic aorta (parasternal long axis view). More rarely,
descending abdominal aortic aneurysm may be picked up in subcostal
views (Fig. 4.73). The extent of the aneurysm cannot usually be accurately
quantified, but the extent of dilatation and presence or absence of laminar
thrombus can be commented upon. Further imaging will frequently be
required.
AORTIC ATHEROSCLEROSIS
325
Modified subcostal view
Aortic atheroma
Fig. 4.73 A subcostal view aligned to view the abdominal aorta. Note the thickening
of the wall and irregular appearance consistent with an atherosclerotic plaque.
326
CHAPTER 4 Transthoracic chambers and vessels
Cardiac tumours
One of the most ‘exciting’ things to see in echocardiography is a cardiac
mass that should not be there. Once seen it is easy to forget about con-
tinuing with the systematic collection of information but this is essential in
order to understand what effect any mass may be having. Masses will be
vegetations, cysts, tumours (benign and malignant), or thrombus (Figs. 4.74
and 4.75).
Primary tumours—benign (80%)
Myxoma
Myxoma is the most common primary tumour (30% of tumours: 74% left
atrium, 18% right atrium, 4% left ventricle free wall). 10% are familial so
family counselling should be considered if other familial cases.
Appearances and assessment
Globular, finely speckled mass with well-defined edges. May prolapse into
left ventricle. Usually attached to interatrial septum (fossa ovalis 90%).
Attachment best visualized in apical and subcostal
4-chamber views.
Tumour calcification may be seen infrequently. Determine length and
diameter of myxoma. Quantify severity of coexisting mitral regurgitation
or effective stenosis caused by myxoma.
Myxoma or thrombus?
No specific finding differentiates the two but thrombus is more often
irregular, layered, immobile, broad-based (myxoma typically has a stalk)
and located near the posterior wall of the left atrium. The left atrium is
more likely to be dilated with an abnormal mitral valve.
Papillary fibroelastoma
10% of primary tumours. Found attached most commonly to mitral and aortic
valves with small pedicles. Rarely attach to LVOT or papillary muscles.
Appearances and assessment
Small (rarely >1cm in diameter), mobile, pedunculated, echocardiograph-
ically-dense mass. May mimic vegetation or Lambl’s excrescences. Usually
no other valve abnormalities. Comment on size, location, and functional
effects.
Other tumours
Lipoma (10%), fibroma (4%), rhabdomyoma (9%—children more common).
Primary tumours—malignant (20%)
Typical tumours are sarcomas, angiosarcomas and rhabdomyosarcomas.
Primary lymphomas also reported. Final diagnosis often requires biopsy.
Appearances and assessment
Often irregular and invade into myocardium. Can be recognized as unusual,
localized myocardial thickening. Report location, extent, and functional
effects (valve or ventricle dysfunction, restrictive or constrictive physiology,
pericardial fluid). Comment on concerns about cause.
CARDIAC TUMOURS
327
MYXOMA
LV
RV
RA
LA
FIBROELASTOMA
LV
RV
RA
LA
INFILTRATION
RV
RA
LV
LA
Fig. 4.74 Examples of primary cardiac tumours. Top figure demonstrates a myxoma
prolapsing through the mitral valve. The middle figure is an apical 5-chamber view
that demonstrates a fibroelastoma on the aortic valve. The bottom figure is a
subcostal view of an infiltrative mass, probably malignant tumour.
See W Video 4.35.
328
CHAPTER 4 Transthoracic chambers and vessels
Secondary tumours—metastases
40 times more common than primary malignant tumours. Cardiac metas-
tases occur in 5% of patients who die of malignant tumours. Most common
tumours to metastasize to heart are: melanoma, bronchogenic carcinoma,
breast cancer, lymphoma, gastrointestinal adenocarcinoma, laryngeal car-
cinoma, pancreatic cancer, mucinous adenocarcinoma of cervix/ovary.
Often clinical presentation is with tachycardia, arrhythmias, or heart failure
and most common finding is a pericardial effusion.
Appearances and assessment
Usually seen as wall thickening and there may be an associated pericardial
effusion. Tumour mass may protrude into a cardiac chamber. Comment
on size, location, and functional effects.
Valve cysts
Fluid-filled cysts can be found on valves often due to myxomatous degen-
eration. They appear as round structures, often with a pedicle attachment.
The cyst has a fluid-filled appearance and there may be floating structures
inside. Comment on location, size, and functional effects.
Pericardial cyst
Cysts can form in pleura or pericardium. Most commonly cysts are seen
around the right costophrenic location (70%), then left costophrenic angle
(30%) and rarely in upper mediastinum, hila, or left cardiac border.
Appearances and assessment
Pericardial cysts appear as an ovoid space adjacent to a cardiac chamber.
The differential is between cyst and loculated pericardial effusion, dilated
coronary sinus or ventricular pseudo-aneurysm.
Extra-cardiac tumours
Tumours within the thorax, but separate from the heart, can be incidentally
picked up during echocardiography. Parasternal views identify mediastinal
cysts or thymomas. Other extra-cardiac tumours include haematoma,
teratoma, diaphragmatic hernia, and pancreatic cysts.
Appearances and assessment
Comment on location, suspected cause, and functional effects. Key effects
are displacement of the heart, compression of cardiac chambers, evidence
of superior vena cava obstruction, cardiac tamponade, constrictive peri-
carditis, pulmonary or tricuspid stenosis.
CARDIAC TUMOURS
329
CYST
RV
RA
LV
LA
RV
LV
LA
EXTRA CARDIAC
MASS
LV
THROMBUS
Fig. 4.75 Examples of tumours. Top figure is a subcostal view of a mitral valve cyst.
The middle figure demonstrates a large extra-cardiac mass causing chamber
compression. The bottom figure shows an apical left ventricle thrombus.
See W Video 4.36 and W Video 4.37.
330
CHAPTER 4 Transthoracic chambers and vessels
Congenital heart disease
Background
Common congenital heart defects, such as atrial and ventricular septal
defects (b pp.288, 292) and coarctation of the aorta (b p.320) have
distinct methods of assessment using standard techniques. More complex
congenital disease is dealt with in specialist texts. Imaging of any congenital
heart disease, simple or complex, relies on the same basic echocardio-
graphic principles and should not be alarming. All images must be acquired
and assessed. If complex, liaise closely with a specialist congenital centre.
It is also worth remembering that echocardiography complements other
imaging tools and a range of imaging modalities are required in the
management of patients with congenital heart disease.
Assessment
Try to obtain as much patient detail as possible prior to scanning such
as operation notes, previous procedures and results of previous imaging
investigations. This will immediately tell you what you might expect to be
seeing and what views may be most useful or required. When starting to
image remember:
Do not be scared: apply basic principles of transthoracic
echocardiography—assessment of ventricular function, valvular
function, and presence of a pericardial effusion is usually possible in
all patients (Fig. 4.76).
However, experience is essential for imaging of patients with complex
congenital heart disease and, in particular, interpretation of imaging can
be operator dependent. Therefore, if you are not experienced do not
hesitate to ask for advice or support from seniors or a specialist Adult
Congenital Heart Disease Centre.
Beware of endocarditis in the congenital patient.
CONGENITAL HEART DISEASE
331
Particular advantages of echocardiography in congenital
heart disease
Non-invasive detailed anatomical information with serial assessment.
Doppler assessment of valves, aortic arch (coarctation), shunt
calculation (rarely used), baffle obstruction (atrial switch TGA
patients).
Contrast bubble echo for the identification of shunts, e.g. PFOs (see
b p.572).
Assisting with percutaneous interventional procedures.
Dobutamine stress echo for arterial switch TGA patients (ischaemia).
Advanced techniques: tissue Doppler for ventricular function, 3D
for detailed anatomical information (e.g. Ebstein’s, AVSD), speckle
tracking and dyssynchrony assessment.
332
CHAPTER 4 Transthoracic chambers and vessels
Key views and findings
A standard dataset acquisition can be undertaken. However, additionally,
abdominal views from the subcostal window can be very helpful and
therefore 9 key views are recommended to ensure a systematic approach.
It should also be remembered that because of the unusual features of
congenital heart disease it is also important to be opportunistic if good
images appear in unusual positions. The key 9 views are:
1. Abdominal transverse
Subcostal window with probe marker at ~3 o’clock: provides
information on abdominal situs (liver/stomach) and relationship of
aorta and IVC (right) to the spine.
2. Abdominal longitudinal
Subcostal window with the probe marker towards head ~12 o’clock:
used to identify the pulsatile aorta and coeliac axis. If the probe is
angled towards the liver it will be possible to identify hepatic veins and
inferior vena cava draining to a right-sided atrium.
3. Parasternal long axis including the inflow and outflow views
Useful for assessment of right ventricular outflow tract and right
ventricular inflow.
4. Parasternal short axis
Especially looking for a perimembranous VSD (at 10 o’clock),
LPA/RPA, origins of coronary arteries, mitral valve and LV/RV.
5. Apical 4/3/2 chamber:
Look for normal off-setting of atrio-ventricular valves (tricuspid should
be more apical). Identify the moderator band at apex of right ventricle
to establish a morphological right ventricle. Assess for any associated
lesions.
6. Apical 5 chamber:
Detailed assessment of the aorta and valve.
7. Subcostal (epigastric):
Scan systematically the liver, right atrium, atrial septum, left atrium, and
pulmonary veins entering left atrium.
8. Arch view/suprasternal:
Neck extension may optimize views. Identify ascending aorta, neck
vessels and PA. Look for any coarctation or PDA.
9. Right parasternal long axis:
May provide further information on aortic valves.
CONGENITAL HEART DISEASE
333
Subcostal situs solitus/AV and VA concordance
Acquire full examination and
Are there 1 or 2 ventricles?
assess the:
Identify the LV and RV
Valves
Assess ventricles in standard
Parasternal and apical
manner
ventricular views
Look for shunts and
Subcostal views for
communications
pulmonary veins, IVC
Continue with full data set of
Suprasternal view for ?PDA
images
/?aortic coarctation
Fig. 4.76 Basic questions to ask during transthoracic examination.
334
CHAPTER 4 Transthoracic chambers and vessels
Sequential segmental analysis
There is some key information that needs to be established in order to
evaluate a patient with congenital heart disease. This information relates to
how the heart and blood vessels connect together. The sequence given here
can be used to gather all this key information (see also Table 4.10).
Establish arrangement of atrial chambers (situs)
The atria are defined by the appendages (right-broad, left-narrow) and
by the systemic and pulmonary connections. Normal is situs solitus and
abnormal situs inversus (morphological left atrium on right). Abdominal
organs usually match atria (liver on left suggests inversus). Use subcostal
views and look for the features:
Left atrium has long, thin atrial appendage and rounded shape.
Right atrium has broad, short appendage, and Eustachian valve.
Identify where inferior vena cava and pulmonary vein connect (vein
inflow does not identify atria as connections vary).
Determine ventricular morphology and arrangement: atrioventricular
(AV) connections
Normally the heart tube folds to the right and heart lies in left chest with
right ventricle anteriorly. If the tube folds to the left the right ventricle
lies on the other side of left ventricle. Atrio-ventricular valves stay with
ventricles. Use the following features to identify the ventricles:
Identify right ventricle from trabeculations, 3 papillary muscles,
tri-leaflet valve, moderator band, and triangular cavity.
Left ventricle has smooth surface, 2 papillary muscles, bileaflet valve,
and bullet-shape.
Establish right ventricle from moderator band and tricuspid valve. Left
ventricle is bullet-shaped and associated with mitral valve.
Determine morphology of great arteries
This identifies arterial transposition and can occur if valves are in ‘right’
position but folding rotates ventricles, or if ventricles are right but arteries
are switched.
Use parasternal short axis and modified long axis views to identify
pulmonary artery from orientation (heading posteriorly) and
bifurcation. Ascending aorta heads superiorly.
Use suprasternal views to see if the arch goes to left (normal) or right.
Ventriculoarterial (VA) connections
Morphology of arterial valves, arterial relations, and infundibular
morphology can be established from parasternal and apical windows.
Assess for any associated intracardiac lesions
Patients may have >1 lesion. A full data set is required looking for flow
abnormalities and shunts.
Establish cardiac position in the chest and orientation of cardiac apex
Use subcostal view. The usual arrangement of the heart and body
organs is situs solitus (left-sided heart, left-sided stomach and spleen
and a right-sided liver).
CONGENITAL HEART DISEASE
335
Table 4.10 Sequential segmental analysis used in congenital heart
disease
Abdominal situs
Solitus (liver on right, stomach on Left)
Inversus (liver on left/transverse, stomach on right)
Atrial anatomy and
Solitus (RA on right)
systemic venous
Inversus (RA on left)
connections
Ambiguous/indeterminate
Atrioventricular
2 AV valves
connections
Common AV valve
AV valve atresia
Straddling or overriding AV valve
Morphology of
Right ventricle on right
Ventricles
Right ventricle on left
Univentricular heart
Morphology of
Concordant (normal)
great arteries
Discordant (transposition)
Double outlet (left or right ventricle)
Common outlet (truncus arteriosus)
Single artery atresia
336
CHAPTER 4 Transthoracic chambers and vessels
Congenital defects
Some of the disorders that may be seen during routine echocardiography
include:
Patent ductus arteriosus
Patent ductus arteriosus connects aorta to pulmonary artery and can be
identified as follows:
Identify the aortic end in descending aorta using a suprasternal view
focusing just distal to left subclavian.
The pulmonary end empties into left pulmonary artery just to left of
pulmonary trunk and can usually be seen from a modified parasternal
short axis views.
Colour flow will demonstrate a jet directed the wrong way in the
pulmonary trunk (towards the pulmonary valve).
Report functional effects of the left-to-right shunt.
Persistent left superior vena cava
A persistent left superior vena cava drains into the coronary sinus. Usually
the right superior vena cava is also present although it is possible only to
have a left superior vena cava. To identify these abnormalities:
Use an apical 4-chamber view adjusted to cut below the mitral valve.
This will demonstrate the coronary sinus. It is usually dilated.
Agitated saline contrast injected into a vein in the left arm will opacify
the coronary sinus before the right atrium.
Then inject agitated saline into a vein in the right arm. If the right
superior vena cava is still present contrast will appear in the right
atrium first, as normal. If the right superior vena cava is absent the
saline will appear in the coronary sinus first.
There is usually no significant haemodynamic effects but it complicates
pacemaker placement.
Anomalous pulmonary drainage
This describes drainage of pulmonary veins into right atrium. Total drain-
age requires a septal defect for oxygenated blood to reach systemic circu-
lation. In partial drainage 1 or 2 pulmonary veins still drain to left.
Most easily assessed with TOE.
Right upper pulmonary vein may drain to right atrium or superior vena
cava.
Right lower pulmonary vein may connect to inferior vena cava.
Left pulmonary veins may connect to innominate vein.
CONGENITAL DEFECTS
337
SINGLE
VENTRICLE
RA
LA
Fig. 4.77 Apical 4 chamber view of a single ventricle.
Displaced tricuspid
valve leaflets
Dilated RA
Displaced tricuspid
valve leaflet
Small LV
Atrialised RV
Fig. 4.78 Apical 4-chamber view of Ebstein’s anomaly. See W Video 4.38 and
W Video 4.39.
338
CHAPTER 4 Transthoracic chambers and vessels
Tetralogy of Fallot
Combination of right ventricle outflow obstruction, ventricular septal
defect, right ventricular hypertrophy, and aorta overriding the septum.
Assessment preoperatively should focus on, and quantify, each aspect.
Double outlet right ventricle
Both aorta and pulmonary artery arise from right ventricle. Ventricular
septal defect allows oxygenated blood to reach systemic circulation.
Persistent truncus arteriosus
Single trunk divides into systemic and pulmonary arteries. Associated with
ventricular septal defect and single valve in trunk.
Hypoplastic left ventricle
Usually involves whole of left heart with disordered valve development
and small left atrium and ventricle.
Single ventricle
Single ventricle with mitral, tricuspid, aortic and pulmonary valves con-
nected. Chamber can be of left or right origin with remnants of other
ventricle seen (Fig. 4.77).
Obstructive congenital disorders
Many congenital defects can be organized, and assessed, according to their
restriction or obstruction to blood flow. They can be demonstrated using
standard 2D imaging and Doppler quantifications.
Right ventricular inflow:
Ebstein’s anomaly and tricuspid atresia (Fig. 4.78 and b p.122).
Right ventricular outflow:
Subvalvular—outflow tract (use short axis views).
Pulmonary valve—pulmonary stenosis (b p.156).
Supravalvular—pulmonary artery (use short axis views).
Left ventricular inflow:
Pulmonary veins—stenosis or obstruction. Usually requires
transoesophageal echocardiography to document.
Atrium—atrial membranes (either across the middle of atrium—cor
triatum or supravalvular).
Mitral valve—congenital stenosis (b p.101), double inlet valve.
Left ventricular outflow:
Subvalvular—fibromuscular (wall thickening) or membranous (discrete
membrane present) (use parasternal and apical views).
Aortic valve—bicuspid valve (b p.134).
Supravalvular level—membranous or fibromuscular thickening (use
parasternal views).
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340
CHAPTER 4 Transthoracic chambers and vessels
Surgical correction of congenital
heart disease
Complete repairs
With effective correction there may be little echocardiographic evidence
of repair. A full systematic study should be used and reports made of any
residual functional effects on valve function, as well as disorders of left
or right ventricle appearance or function. Residual shunts or abnormal
vascular connections should be commented upon.
Shunts (Fig. 4.79)
These were designed to increase blood flow into the pulmonary artery to
improve oxygenation but nowadays full repairs of defects are preferred.
Blalock-Taussig shunt
This shunt connects the subclavian or innominate artery to a branch of
the pulmonary artery. The shunt can be made on the left or right. It can
be seen in suprasternal views and both colour flow mapping and Doppler
assessment can be attempted to identify stenosis or changes in flow.
Glenn shunt
The Glenn shunt (may be bilateral) anastomized the superior vena cava to
the pulmonary artery either completely or to allow two-way flow.
Fontan procedure
This was used to bypass an abnormal right ventricle by directing flow from
the systemic atrium to the pulmonary circulation. In fact there are a range
of Fontan procedures and it can be difficult to evaluate with echocardiog-
raphy without knowing the surgical details although assessing ventricular
SURGICAL CORRECTION OF CONGENITAL HEART DISEASE
341
(a) Total cavopulmonary connection
TCPC (Extracardiac conduit)
(TCPC, lateral tunnel)
SVC
SVC
PA
PA
RA
RA
IVC
IVC
Atriopulmonary Fontan
PA
RA
IVC
(b)
A
B
C
SVC
SVC
RSVC
LSVC
RPA
LPA
PA
PA
RA
RA
RA
IVC
IVC
Hepatic veins
Fig. 4.79 (a) Types of Fontan operation. (b) Diagrams illustrating various types
of Glenn shunt. A) Classical Glenn. B) Bidirectional Glenn. C) Bilateral bidirectional
Glenn.
Reproduced from Myerson S, Choudhury Rand Mitchell A (2009) Emergencies in Cardiology,
2nd edn, Oxford University Press, Figures 16.10 and 16.11.
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343
Chapter 5
Transoesophageal
examination
Introduction 344
Indications
346
Contraindications and complications 348
Information for the patient 350
Preparing for the study 352
Preparing and cleaning the probe 354
Probe movements 356
Anaesthetic, sedation, and analgesia
358
Sedation complications 360
Intubation
362
Image acquisition 364
Four chamber view 368
Five chamber view 370
Short axis (aortic valve) view
372
Short axis (right ventricle) view
374
Long axis (aortic valve) view
376
Long axis (mitral valve) view
378
Atrial septum (bicaval) view 380
Two chamber (atrial appendage) view 382
Pulmonary vein views 384
Coronary sinus view 386
Transgastric short axis views
388
Transgastric long axis view 390
Transgastric long axis (aortic) view
392
Transgastric right ventricular view
394
Deep transgastric view 396
Pulmonary artery view 398
Aortic views 400
3D oesophageal views 402
3D mitral valve 404
3D aortic valve 406
3D aorta 406
3D tricuspid valve 408
3D pulmonary valve 408
3D left ventricle
410
3D interatrial septum 412
X-plane 414
344
CHAPTER 5 Transoesophageal examination
Introduction
Transoesophageal echocardiography (TOE) has emerged over only
the last 30 years. The first M-mode transoesophageal images were
published in the 1970s by Dr Frazin, a cardiologist in Chicago, who
attached a traditional probe onto the end of an endoscope. It did
not catch on as a technique because the patient found it difficult to
swallow the probe.
By the early 1980s 2D imaging with superior, smaller probe technology
had become realistic, significantly advanced by the introduction of the
electronic, phased-array probe. The early probes were single plane and
it was not until the 1990s that biplane probes became a reality. These
were finally superseded by multiplane imaging, a move that provided
the leap in functionality that we take for granted today.
TOE uses all the same technology as transthoracic imaging.
2D echocardiography, colour and spectral Doppler can all be
performed as well as tissue Doppler imaging and 3D reconstructions.
However, transoesophageal imaging possesses a major advantage in
that there is little tissue between the probe and the heart to degrade
the image. This also means the probe virtually touches the heart so the
ultrasound beam does not need to penetrate as far. Higher ultrasound
frequencies can therefore be used (typically 5-7.5MHz) which
enhances spatial resolution.
A lot of the clinical applications have been driven by interest in
intraoperative monitoring and this remains a key application of the
technique. However, real-time imaging with unparalleled spatial and
temporal resolution makes the image quality superior to all other
modalities within the imaging window provided by the oesophagus.
As the procedure is well tolerated, TOE has guaranteed usefulness
for cardiology studies, particularly where detailed anatomical and
functional imaging is needed.
During the last few years real-time 3D transoesophageal
echocardiography has become an important tool in particular to guide
interventions.
INTRODUCTION
345
Performing the study
There are many different patients in whom TOE is requested, from
patients who require elective monitoring of stable clinical problems
such as aortic dissection to those with emergency haemodynamic
problems. The background and approach to each study will
therefore vary considerably. This chapter is written to provide a
framework to perform an elective, or planned, transoesophageal
echocardiogram in an awake patient.
For intraoperative studies or those on Intensive Care Units the
patient is already sedated or anaesthetized and, unless planned
before an operation, may not have given consent. However, even
in these situations the majority of the framework for performing
a study is still relevant. All aspects of assessing indications and
contraindications should be carried out, as well as preparation of
machine, probe, and monitoring. The only real differences are usually
the patient position (lying on their back), the presence of other
things in the mouth (tracheal tubes), and depth of sedation
(general anaesthetic or deep sedation).
346
CHAPTER 5 Transoesophageal examination
Indications
There are generally accepted, evidence-based uses of TOE which have
evolved in clinical situations where there is a need for high spatial and
temporal resolution to assess pathology.
Haemodynamic monitoring in anaesthetized patient:
• Perioperative monitoring.
• Intensive care monitoring.
Evaluation of valve pathology:
• Pre-surgical evaluation for repair of mitral or aortic valves.
• Evaluation of cause of dysfunction.
Intracardiac shunts.
Cardiac embolic source:
• Intracardiac shunts.
• Left-sided thrombus—ventricle, left atrial appendage.
• Left-sided valve abnormalities/masses/vegetations.
• Aortic atheroma.
Endocarditis:
• Diagnosis.
• Monitoring.
Evaluation of prosthetic valve dysfunction.
Congenital heart disease.
Aortic dissection and aortic pathology.
Cardiac masses (where transthoracic imaging inadequate).
Imaging during procedures:
• Percutaneous procedures—ASD/PFO closure, mitral balloon
valvuloplasty.
• Electrophysiology and pacing—transseptal puncture, lead
placement.
• Cardiothoracic surgery.1
Transcatheter aortic valve implantation (TAVI).
Poor transthoracic windows or inadequate image quality.
Reference
1 American Society of Anesthesiologists. Practice guidelines for perioperative transesophageal
echocardiography. Anesthesiology 1996; 84:986–1006.
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348
CHAPTER 5 Transoesophageal examination
Contraindications and complications
Consider contraindications before starting. Absolute contraindications
tend to be oesophageal problems that make the procedure technically
impossible and increase the risk of traumatic injury. The decision to go
ahead despite relative contraindications depends on the importance of
the clinical information to be gathered, whether there are alternative ways
to gather the data and operator experience. During and after the proce-
dure be vigilant for possible complications and ensure the patient is fully
informed of these risks when taking consent.
Absolute contraindications
Oesophageal tumours causing obstruction of the lumen.
Oesophageal strictures.
Oesophageal diverticula.
Patient not cooperative.
Relative contraindications
Oesophageal reflux refractory to medical therapy.
Hiatal hernia.
Odynophagia or dysphagia.
Previous oesophageal or gastric surgery.
Previous oesophageal or gastric bleed.
Oesophageal varices: using a sheath is said to reduce the risk as the gel
reduces the pressure of the probe tip. However, transgastric views are
not advised and there must not have been a bleed in the preceding
4 weeks.
Severe cervical arthritis.
Profound oesophageal distortion.
Recent radiation to head and neck.
Significant dental pathology.
Complications
A study of complications in around 10,000 patients showed a very low
incidence.1 Failed intubation occurred in around 2%. All other complications
had an incidence of <1%.
Intubation problems—termination because of choking.
Pulmonary problems—bronchospasm, hypoxia.
Cardiac problems—ventricular extrasystole, tachycardia, atrial
fibrillation, AV block, angina.
Bleeding—from pharynx, related to vomiting, from oesophagus.
Perforation—risk of perforation increases in small patients and in all
conditions that make the oesophagus friable, e.g. prior radiation to
head, neck or oesophagus, steroid treatment, gastro-oesophageal
reflux disease, prolonged duration of probe in patient.
Probe failure.
CONTRAINDICATIONS AND COMPLICATIONS
349
Antibiotic prophylaxis for TOE?
Antibiotic prophylaxis is not recommended for any indication under
current guidelines.
It remains reasonable to consider antibiotics in occasional cases, for
example a patient with a prosthetic heart valve and evidence of poor
oral hygiene, in whom the study is being performed for an indication
other than suspected endocarditis. In these individual cases, practice
is governed by clinical common sense rather than evidence.
Reference
1 Daniel WG et al. Safety of transesophageal echocardiography. A multicenter survey of 10,419
examinations. Circulation 1991; 83:817–21.
350
CHAPTER 5 Transoesophageal examination
Information for the patient
For elective or planned studies patients should be provided with informa-
tion or have a detailed verbal explanation. Informed consent is essential as
it is a semi-invasive procedure and sedation is used.
Example information sheet
You have been asked to attend for transoesophageal echocardiography
(TOE). A TOE is a test that allows the doctor to look closely at the
heart without other organs obscuring the view. In order to carry out
the procedure, the scope, which is a long flexible tube, is passed through
the mouth and down the gullet.
Before the procedure
You should not have anything to eat or drink for at least 6 hours before
the procedure. When you arrive you will be seen by a doctor who will
take a medical history and after explaining the procedure, ask you to sign
a consent form. If you have any concerns, please do not hesitate to ask,
as we would like you to be as relaxed as possible. We will be pleased
to answer any queries.
What happens during the procedure?
A blood pressure cuff will be attached to your arm and a small moni-
tor placed on your finger to monitor the oxygen levels in the blood.
The doctor will spray your throat with some local anaesthetic. A mouth
guard is placed between your teeth to protect the tube and your teeth.
You will be asked to turn onto your left side and the room’s main lights
will be turned off. Your sedation is then given through a small tube
(cannula) which will be inserted into your arm. When you are sleepy
the procedure will start. There will be several people looking after you
including the doctor, a nurse and a technician. The procedure takes
10-20min to examine all areas carefully.
Benefits The benefits from TOE are that it can: define the nature of
cardiac symptoms; decide which further therapeutic and diagnostic pro-
cedures you may have to undergo.
Risks
Risks from TOE are tiny. Usually the investigation is tolerated well; some
patients may have some mild symptoms during the test (mostly coughing).
Serious risks are very rare and include palpitations 0.75% (7 patients in
every 1000), angina 0.1% (1 patient in every 1000), bronchospasm/hypoxia
0.8% (8 patients in every 1000), bleeding 0.2% (2 patients in every 1000),
oesophagus perforation, extremely rare less than 0.01% (1 in every
10 000 patients). Your doctor would not recommend that you have a
transoesophageal echocardiogram unless they felt that the benefits of
the procedure outweighed these small risks.
After the procedure The sedation may last up to an hour. Your blood
pressure and respiration will be checked and you may have an oxygen
mask on while you are awake. The sedation has an amnesic effect so you
should remember little of the procedure when you wake up.
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352
CHAPTER 5 Transoesophageal examination
Preparing for the study
Setting up the environment
With the patient on their bed, ensure there is a blood pressure cuff
on the arm and set to automatic monitoring every 5-10min. Check a
baseline blood pressure.
Set up stable ECG monitor on the machine.
Monitor oxygen saturations and check a baseline saturation level.
Provide supplemental oxygen, usually via nasal specs at 2L/min.
Ensure suction is available and working.
Check bed height and position so operator and nursing staff are not
bending over the patient but stand upright during the procedure.
Check relative position of machine, patient, and operator to ensure
operator has a clear view of images.
Nursing
The nurse should talk to the patient and check identity and consent.
The nurse stands behind the patient or at the head of the bed to
reassure the patient and support the head and mouth guard.
During the procedure they should monitor haemodynamics and
saturations and inform the operator if they change.
They should monitor for secretions and give suction as required.
After the procedure they should stay with the patient to ensure
adequate recovery from the sedation.
Operator
Check notes for indications and purpose of study. Check past medical
history, allergies, and any contraindications.
Make sure patient has been starved for at least 6 hours and has taken
out any false teeth/loose bridges/loose teeth.
Ensure the apparatus is ready: probe prepared (b p.354), attached,
and selected; probe steering works; transoesophageal machine presets
selected, ECG tracing and patient details on machine.
Sedation drawn up (b p.358), local anaesthetic spray available, and IV
cannula in arm ready for sedation.
Ensure gel ready to be applied to probe.
Then give local anaesthetic spray (b p.358).
For the awake patient, ask them to roll onto their left side and ensure
a stable position—often achieved if the patient brings their right leg
over their left in a ‘recovery position’ arrangement. If in an ITU setting,
ask if the patient is able to be rolled onto their left.
Ensure the head of the bed is flat, the patient has their head on a
pillow, and there is a mat under the head to absorb any secretions.
For the awake patient, ask them to drop their chin onto their chest.
Place the mouth guard between their teeth.
Give sedation (b p.358) and start the intubation (b p.362).
PREPARING FOR THE STUDY
353
Preparing for TOE—a 10-point plan
1. Put sheath on the probe.
2. Review referral form/notes for indication, contraindications.
3. Ask patient when was last meal (should be >6 hours before),
previous problems with swallowing, known oesophageal disease,
allergies.
4. Insert patient name and hospital number on scanner and ask
patient to confirm.
5. Insert IV cannula.
6. Attach probe to the scanner, test steering and whether probe is
accepted by the scanner.
7. Start blood pressure monitoring and pulse oximetry, nasal specs
for oxygen supply (2L/min).
8. Apply local anaesthesia to patient’s throat, then rotate patient into
a left lateral decubitus position.
9. Put in mouth guard.
10. Give sedation.
354
CHAPTER 5 Transoesophageal examination
Preparing and cleaning the probe
The probe can easily be damaged either externally (by chemicals or mis-
use) or by the patient (beware teeth!). There are also important health
and safety issues about protecting the patient from the probe.
Checking the probe
Check over the probe at the start of the procedure. Look for evidence
of damage to the coating and layers. There may be breaks or ‘bubbling’
in the coating. In extreme situations the underlying wire shielding may
be exposed with a risk of current leak or heating to the patient. If you
are concerned about the integrity of the probe use a different probe and
contact the manufacturer.
Preparing and cleaning
There are 2 options for probe preparation and cleaning.
The probe is used without a cover
Glutaraladehyde
In this case it is essential it is sterilized between cases. After the
investigation the probe should be washed down with water and
then immersed in a tube containing glutaraldehyde solution (licensed
for endoscope disinfection) for a fixed period of time according to
manufacturer guidelines.
Glultaraldehyde can cause allergies or breathing problems. Therefore
ensure regular fresh air in the room where the probe is cleaned.
Furthermore, the probe needs to be rewashed with water to ensure
the solution is removed before the probe is used on the next patient.
The handgrips and controls of the probe should be wiped with an
alcohol-based agent. Alcohol should not normally be used to clean the
transducer face at the tip of the probe.
The probe is used with a purpose-designed sheath
Sheaths protect the probe from infection and provide electrical
isolation from the patient.
There are both latex and latex-free versions.
To prepare, fill the sheath tip with the supplied gel using a syringe.
Then feed the probe all the way into the sheath and fix the upper end
with the supplied plastic clip.
Avoid air bubbles in the gel around the transducer as these degrade
image quality. Press them further up the sheath or pull and release the
sheath tip to expel them away from the transducer.
When performing a series of studies there is no need to carry out
a complete disinfection between patients. After each investigation
remove the sheath and wipe off any gel left on the probe. Then clean
the probe with water and an alcohol-based agent.
If the sheath breaks during the procedure or a perforation is seen
afterwards, immerse the probe in disinfectant solution.
In patients with a high infection risk (HIV, hepatitis B, etc.) disinfect the
probe with a commercial solution after sheath removal and sterilize
the controls with alcohol-based solutions.
PREPARING AND CLEANING THE PROBE
355
Tristel sporicidal wipe
This is a rapid action sporicidal wipe (Fig. 5.1) which is used to clean
probes that have been used with sheaths.
After removing the sheath, the first step is to clean the probe with
the pre-clean sporicidal wipe. It is impregnated with a low-foaming
surfactant system combined with triple enzymes, producing ultra-low
surface tension for rapid cleaning.
Then apply the sporicidal wipe which is initially activated with a foam
pump.
Next, application of the rinse wipe is the final step in the
decontamination process. It is impregnated with deionized water and
a low level of antioxidant which will remove and neutralize chemical
residues from the probe surface.
Fig. 5.1 Tristel sporicidal wipes. Following the procedure the probe is initially
cleaned with the pre-clean wipe. The sporicidal wipe is then activated with a foam
pump and used to clean the probe. Finally the rinse wipe is used to wipe the probe,
neutralizing any remaining chemical residues.
356
CHAPTER 5 Transoesophageal examination
Probe movements
A combination of probe movements is required to gather all the images
(Fig. 5.2). For many of the views, changes in sector angle are the primary
control, with physical movements used to optimize the image.
Withdrawal and advance
Moving the probe forward and backwards in the oesophagus is the sim-
plest manoeuvre. The depth of the probe is best controlled with the hand
nearest the patient’s mouth. This hand can also judge the size of small
movements forward and back relative to the mouth guard. The depth
of probe insertion is marked on the probe in centimetres. This number
should be used when images need to be annotated to record probe depth.
It measures the distance from probe tip to front incisors.
Rotation (or turning)
The probe can be rotated clockwise or anti-clockwise within the oesopha-
gus. This is achieved by twisting the handheld control section with one
hand, and the probe near the mouth guard with your other hand. This
movement is usually used to orientate the heart in the image plane and to
look at the descending aorta.
Sector angle
On the controls there are usually 2 buttons side by side. These rotate the
angle of the imaging plane forward and backward between 0° and 180°.
The angle plane can also sometimes be changed directly from the ultra-
sound machine. The current angle plane is displayed on the screen.
Angulation (or retro-/ante-flexion)
The large wheel on the control panel moves a few centimetres of the
transducer tip forwards and backwards. Angulation forwards is usually
used to press the transducer against the oesophagus wall or stomach to
improve contact and image quality. Angulation backwards can be effective
at lengthening out the left ventricle.
Lateral motion
The small wheel on the control panel causes movement of the transducer
tip from side-to-side. This is very rarely used and for the most part can
be ignored. Occasionally with difficult images or abnormally positioned
hearts small lateral motions may be helpful.
Position lock
Most probes have a lever behind the control wheels that locks the probe in
position. For most studies this is not required and can be ignored. For long
periods of monitoring—particularly in transgastric views intraoperatively—
the lock can be used. However, there is an increased risk of traumatic
injury with movement of the probe with the lock on. Care must be taken
to remove the lock before the probe is repositioned.
CONTROL WHEELS
PHYSICAL MOVEMENTS
BUTTONS
OF PROBE
ANGULATION
SECTOR ANGLE
WITHDRAW AND ADVANCE
LOCK
LATERAL MOTION
ROTATION
Fig. 5.2 Probe movements and the controls on the handset that allow motion. The main controls are the large wheel (angulation) and the buttons (sector angle).
The small wheel and lock are rarely needed.
358
CHAPTER 5 Transoesophageal examination
Anaesthetic, sedation, and analgesia
Local anaesthetic
Start with a local anaesthetic Xylocaine® (lignocaine) spray.
With the patient sitting up, spray several times onto the back of
their throat. Ask them to hold the liquid for a few seconds and then
swallow. Repeat the spray to ensure good anaesthesia.
Warn the patient that the spray has an unusual taste, their mouth and
throat will feel numb, and their swallow may feel strange or difficult.
The spray will need 2-3min to have an effect.
Sedation and analgesia
There are no standard guidelines for TOE and it is possible to perform the
study with no sedation. However, the following routines (see also Fig. 5.3)
can be used (borrowed from other endoscopic procedures). A benzodi-
azepine provides sedation and amnesia, and an opioid analgesia. Remember
that ‘the difference between good and bad sedation is around three minutes’,
i.e. wait for the sedation to work.
Ensure reversal agents are available and accessible (flumazenil for
midazolam and naloxone for pethidine or fentanyl). Life support
equipment should be accessible.
Start with 25microgram IV fentanyl (or 25mg IV pethidine)—then
give 2mg IV midazolam and this is usually sufficient for most patients.
Aim for the patient to be ‘drowsy but rousable’. In certain patients
and situations lower starting doses are advisable (see b ‘Specific
situations’ p.358).
Wait 3-5min then assess level of sedation (patient response,
haemodynamics). If not adequate, give further bolus of 2mg IV
midazolam.
Repeat the ‘wait and bolus’ regime until adequate sedation.
Total sedation should not exceed 10mg midazolam and/or 75mg
pethidine (or 100microgram fentanyl). Stop and consider a general
anaesthetic at a later date.
Once sedation is appropriate start intubation. If intubation is difficult
because the patient is awake return to the sedation routine.
During the procedure (after intubation) if the patient becomes
distressed consider giving further boluses of sedation.
Specific situations
In younger patients (and some older patients) increasing doses
of midazolam can increase agitation and be counterproductive.
Consider using more analgesia and less sedation from the outset.
In older patients (particularly >80 years) oversedation is a problem
so start with 1mg IV midazolam, withhold the opioid, and wait longer
between boluses as the sedation may be slower to circulate.
Use lower starting doses for those with significant left ventricular
failure or respiratory disease, hypotension, or neurological
impairment.
ANAESTHETIC, SEDATION, AND ANALGESIA
359
Patient assessment (allergies, IV access,
consent).
BP, ECG and oxygen monitoring.
Supplemental oxygen.
Equipment prepared.
Sedation drawn up and antidotes present.
Local anaesthetic throat spray
Give 25microgram fentanyl (or pethidine 25mg)
Give 2mg midazolam
(1mg if >75 yrs or depressed respiratory, cardiac or
neurological function)
Wait 3 to 5
minutes
YES
Assess sedation level (aim for drowsy but rousable)
Less than 10mg
NO
Adequate
midazolam given?
sedation?
YES
NO
Continue with intubation and/or
investigation
Stop and
consider
alternative
approaches
NO
Adequate
Stop and reverse
sedation for
agents
intubation?
YES
YES
NO
Adequate
YES
Oversedated
sedation during
haemodynamic
procedure?
problems, not
rousable?
End of
NO
procedure
NO
YES
Post procedure
care
Fig. 5.3 Flow chart for sedation protocol.
360
CHAPTER 5 Transoesophageal examination
Sedation complications
Although by using low-dose conscious sedation with up-titration com-
plications are relatively infrequent, it is always essential to be vigilant.
Monitoring of the patient during the procedure is mandatory. Several
expert bodies have produced guidelines for how to give sedation if you
are not an anaesthetist. It is advisable to have a local policy for how to use
sedation for TOE and an audit process so that problems or adverse events
associated with the procedure are identified.
Peri-procedure
Monitor for drops in blood pressure and saturations throughout the
procedure. These are the commonest side effects of sedation.
If hypotensive, patients may be mildly dehydrated as they are nil by
mouth so consider IV fluids.
Drops in saturations may be temporary at the start of sedation and
can be corrected with increased supplemental oxygen.
If there are ever any concerns about the level of sedation or degree of
haemodynamic or respiratory changes, reverse the sedation and stop
the procedure (if still ongoing).
To reverse the midazolam give flumazenil. This is relatively short acting
so after a period of time, if the sedative effects return, consider further
boluses or even an infusion.
To reverse the opioid give naloxone.
In those with left ventricular failure, lying flat with sedation can
precipitate acute failure so be alert for clinical signs and treat with
diuretics etc. if necessary.
Allergic reactions can occur with sedation so treat as appropriate.
Post-procedure
After the procedure, the patient should be monitored until they are
fully awake.
If the procedure has been elective and the patient is going home
afterwards they should be advised not to drive or operate heavy
machinery for 24 hours.
Further reading
Mankia K et al. Safe combined intravenous opiate/benzodiazepine sedation for transoesophageal
echocardiography. Br J Cardiol 2010; 17:125–7.
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362
CHAPTER 5 Transoesophageal examination
Intubation
Intubation is a key skill to learn. Unless you intubate successfully the pro-
cedure can not start. The skills to perform successful intubation in elective
studies with light sedation are broadly similar to those skills for intubation
in intraoperative or Intensive Care settings. Everyone develops their own
techniques but a standard procedure is as follows.
Intubation with light sedation
General
Ideally have two people, one to hold the controls, and the other to
hold the end of the probe and intubate. If on your own, lie the probe
along the bed and concentrate on intubation. Some people can hold
the controls in one hand and feed the probe with the other, but this
requires an uncomplicated passage of the probe.
Talk confidently and calmly to the patient. Guide them through the
procedure and the swallows. After intubation reassure them and
tell them to take gentle breaths through the nose. The attitude of
the operator and how they relate to—and relax—the patient often
determines the success of the procedure.
The routine
The patient should be lying on their left side with their chin towards
their chest. This encourages the probe to pass into the oesophagus
(exactly what you try to avoid with chin-lift during resuscitation).
Check the mouth guard is in position between the teeth.
Wipe gel over the probe tip to about 40cm. Too much increases the
risk of aspiration and too little makes probe movement difficult and
uncomfortable for the patient.
Check probe controls and put a curve on the end of the probe.
Ensure the curve on the tip lines up with the expected curve into the
back of the mouth then pass the probe through the mouth guard and
onto the tongue.
Ask the patient to swallow once to get the probe to the back of the
mouth and then a second time to pass it into the oesophagus. The
second step should be timed to coincide with the swallow.
To direct the probe a finger can be placed in the mouth beside the
mouth guard. This guides the probe into the back of the mouth. It
is especially useful when learning, when the probe is not passing
smoothly, or in the anaesthetized patient.
When the probe is in the oesophagus stop and do not move anything
for a few minutes while the patient settles.
The operator should then remove one glove and get into position.
One gloved hand controls the probe at the mouth guard and the other
holds the controls. The operator usually stands facing the patient with
their right hand at the patient’s mouth and looks over their shoulder at
the images. An alternative arrangement is to stand at right angles, with
the left hand at the patient’s mouth, facing the machine.
INTUBATION
363
Intubation in the anaesthetized patient
Use the same probe preparation and use a mouth guard.
Ensure there is a curve on the probe, then use a finger to guide the tip
into the back of the mouth.
If the patient is on their back get someone to lift the chin towards the
chest.
The probe may pass smoothly into the oesophagus with light pressure.
If there is resistance induce a reflex swallow with some forward
pressure on the back of the tongue.
If a tracheal tube is in place, passage of the probe into the oesophagus
may be restricted by the tracheal tube. To overcome this, ask for the
assistance of the anaesthetist, either to temporarily deflate the cuff or
to manipulate the tracheal tube.
What to do if the probe does not pass or patient is
agitated?
You should not need to give more than a gentle steady force to the
probe. If resistance is felt assume it has gone the wrong way.
If you are not already using your finger to guide the probe, do so.
Feel where the tip of the probe has gone. It may have doubled
back on itself in the mouth or you may feel it heading up or down.
Withdraw slightly, adjust the rotation and then try to advance again,
with a swallow.
If it is not clear where the probe has gone, withdraw entirely, check
the curve on the probe and its direction, then restart.
If the patient cannot swallow because they are too sedated use a
finger to direct the probe.
If the patient starts coughing think whether you may have passed the
probe into the trachea. Withdraw the probe and start again.
If the patient becomes very agitated, stop and consider whether to
try again after more sedation and/or analgesia.
In around 2% of cases intubation fails. Know when to stop. After two
or three attempts have been unsuccessful consider getting help from
a more experienced operator, if available. If the patient is becoming
very agitated despite adequate sedation and analgesia, stop. If
the investigation is essential, the study can always be rearranged
with a general anaesthetic to ensure patient compliance and/or an
anaesthetist to aid intubation.
364
CHAPTER 5 Transoesophageal examination
Image acquisition
Standard acquisition
Acquisition of transoesophageal images should always be performed in a
standardized way—with a set sequence of views. Virtually all the views
have corresponding transthoracic views and therefore if you have prior
training in transthoracic imaging think about these views to identify struc-
tures. As with performing a transthoracic study, all the views should be
recorded for comprehensive data collection. Even when there is a specific
question (e.g. exclusion of atrial clots before cardioversion) a full dataset
should be acquired to ensure nothing is missed.
IMAGE ACQUISITION
365
Optimize the views using small changes in transducer
position
Adjust by angulation, moving the transducer up and down, and rotating
the sector (tips will be given for each of the views). Don’t move too fast
and too much. Slight changes have a big impact on the image!
Most scan planes have several different structures
All structures cannot always be viewed in a single recorded loop. Slight
adjustments of the probe position and/or sector may be needed and
loops recorded for each structure.
If you get lost
If during a transoesophageal investigation you become disoriented find
the 4-chamber view again. Reset the rotation to 0° and then try some
rotation and repositioning of the probe until the 4 chambers come back
into view.
366
CHAPTER 5 Transoesophageal examination
The ‘screenwiper’ principle
The best initial sequence of views (scan planes) is summarized by the
screenwiper principle (Fig. 5.4). This section describes how to collect tran-
soesophageal data following the screenwiper principle.
Starting from 0° the sector is moved across in steps to around 135°
and then back again in a series of steps.
At each step the view needs only minor modifications of probe
position to optimize the image. This reduces major probe movements
and minimizes patient discomfort.
Each view is examined in:
2D imaging.
Then colour flow Doppler recordings.
And, if needed, spectral Doppler recordings (PW and/or CW).
3D imaging allows the acquisition of real-time 3D information about car-
diac structures and improves spatial orientation. 3D can be performed
in selected views for example of the mitral valve. As with transthoracic
echocardiography, a variety of acquisition modes can be used depending
on the size of the volume of interest.
Live 3D acquisition: allows the generation of live 3D images
which are displayed in a pyramidal volume without the need for
electrocardiographic gating.
Live 3D zoom: allows the display of a magnified pyramidal volume
(smaller than live 3D mode).
Full volume acquisition: allows the segmental build up of a 3D image
over several consecutive cardiac cycles and gives the largest volume
images.
3D full volume colour acquisition.
X-plane imaging: this provides 2 orthogonal views from the same heart
beat. The initial image on the left is the baseline reference whilst the
image on the right can be electronically rotated to any angle between
0-180°.
After the screenwiper is complete, additional views can then be used, as
required, to look at pulmonary veins, transgastric views, the aorta, or any
abnormal findings.
IMAGE ACQUISITION
367
4 chamber
1
view
2
5 chamber
view
50º
Short axis
Long axis
3
135º
4
aortic view
75º
aortic view
110º
2 chamber
Bicaval
view
view
6
5
Fig. 5.4 ‘Screenwiper’ principle showing sequence of sector angles for first 6 views.
Once in position, the image can be optimized with slight variation in sector angle
(usually <5°) followed by slight adjustments in depth and tilting as necessary.
Basic screenwiper study
1.
4-chamber view.
2.
5-chamber view.
3. Short axis aortic view (± right ventricle inflow/outflow).
4. Long axis aortic view.
5. Interatrial septal view.
6. Left atrial appendage view.
then further views
7. Left pulmonary venous view.
8. Right pulmonary venous view.
9. Pulmonary artery view.
10. Transgastric views.*
11. Descending aorta view.
12. Aortic arch view.
* Not necessary in all patients.
368
CHAPTER 5 Transoesophageal examination
Four chamber view
This is the first view to acquire (Fig. 5.5) and is similar to the transthoracic
4-chamber view (but upside down). After intubation, advance the probe
to around 35cm from the teeth.
Finding the view
Rotation should be set at 0°.
The atria will probably be the first feature you see.
Turn the probe to swing all 4 chambers into view.
Withdraw and advance the probe slightly to avoid the LVOT but keep
a clear view of the mitral valve.
If the LVOT is still seen, try adding up to 15°.
If necessary, improve contact by probe angulation.
What do you see?
Use this view to assess
Global and regional left ventricle function, and wall thickness.
Right ventricle size and function.
Mitral valve morphology (orifice, prolapse).
Tricuspid valve morphology.
Use this view to measure
Right and left ventricle size (although beware foreshortening).
Mitral Doppler measurements.
Key features of view
Mitral valve: key view for mitral valve to assess morphology and
haemodynamics. A2 segment of anterior mitral leaflet (aML) and
P3 segment of the posterior mitral leaflet (pML) seen. Colour flow
mapping will show stenosis and/or regurgitation. Supplement with CW
or PW Doppler as for transthoracic echocardiography.
Tricuspid valve: lateral leaflet is better displayed than septal.
Assessment is often limited by foreshortening. To get a better view
of the tricuspid valve advance the probe slightly deeper into the
oesophagus. Supplement with Doppler as required.
Left and right atrium: the main cavity of both atria and the interatrial
septum can be seen. However, fossa ovalis is not usually seen. Turn
the probe slightly left and right to scan through the atria.
Left ventricle: parts of the interventricular septum and the lateral wall
are displayed. Often left ventricle is foreshortened and measurement
of end-diastolic and end-systolic volumes may be inaccurate. Retroflex
the probe to lengthen out the left ventricle but beware contact may
be lost.
Right ventricle: an impression of size and function of the right
ventricle relative to the left is obtained, although there is a risk of
foreshortening, as with the left ventricle.
FOUR CHAMBER VIEW
369
POST
ANT
AO
LA
LV
STOMACH
MV
A2 leaflet
P2 leaflet
LA
0
0
180
RA
LV
RV
TV
Lateral leaflet
Septal leaflet
Fig. 5.5 Position of probe and classical image for a 4-chamber view. Without
ante- or retro-angulation of the probe the left ventricle is usually foreshortened.
See W Video 5.1.
370
CHAPTER 5 Transoesophageal examination
Five chamber view
This is the second view and is similar to the transthoracic apical 5-chamber
view (Fig. 5.6). The main purpose is to get to the appropriate level for the
aortic short axis view. However, an initial view of the LVOT is provided.
Finding the view
Rotation should be set at 0°.
From the 4-chamber view withdraw the probe very slightly until the
LVOT comes into plane.
What do you see?
Use this view to assess
LVOT obstruction.
Aortic regurgitation.
Use this view to measure
No specific measurements.
Key features of view
Most of the features are as for the 4-chamber view.
LVOT: look at the size of the outflow tract and use colour flow
mapping within the tract to look for aortic regurgitation or flow
turbulence due to obstruction.
FIVE CHAMBER VIEW
371
POST
ANT
AO
LA
LV
STOMACH
MV
0
0
180
AV
LA
LVOT
RA
LV
RV
Fig. 5.6 Probe position for 5-chamber view with classic image. See W Video 5.2.
372
CHAPTER 5 Transoesophageal examination
Short axis (aortic valve) view
An essential view. The perfect short axis view of the aortic valve, it
can also provide information on the right heart and interatrial septum
(Fig. 5.7). It is equivalent to the parasternal short axis.
Finding the view
From the apical 5-chamber rotate the sector to around 50°.
Optimize further with slight clockwise rotation of the probe.
The probe may need to be withdrawn or advanced slightly to get the
right scan plane. Focus on a clear view of the aortic valve.
What do you see?
Use this view to assess
Aortic valve morphology and pathology.
Perivalvular processes.
Sometimes, tricuspid and pulmonary valves.
Coronary artery origins can also be seen.
Interatrial septum for patent foramen ovale.
Use this view to measure
Left atrial diameter.
Aortic valve orifice area and aortic root diameter.
Key features of view
Aortic valve: the valve lies in the centre: left coronary cusp on the
right, right coronary cusp at the bottom and non-coronary on the left.
Colour flow identifies regurgitation and, by adjusting the image to go
through the tips of valve, planimetry can be used to measure aortic
valve orifice area.
Aortic root: around the valve is the aortic root. Infection or aortic
surgery can make this thickened or ‘boggy’. Abscesses may also be
seen.
Transverse sinus: between the aortic root and the left atrium is the
transverse sinus (part of the pericardial space). This may contain fluid.
Coronary arteries: to display the coronary ostia withdraw the probe
a few millimetres. Left main stem is at 2 o’clock and right coronary
artery at 6 o’clock. The left coronary system can sometimes be
tracked to, and beyond, the bifurcation. Colour flow and Doppler
demonstrates flow.
Left atrium: lying between the probe and the aortic valve, this is a
standard view for linear measures of left atrial size.
Tricuspid valve: this can sometimes be seen below and to the left of
the aortic valve. Better views are obtained from the right ventricular
inflow/outflow view.
Pulmonary valve: this lies below and to the right of the aortic valve.
Interatrial septum: the interatrial septum abuts the aortic root in the
10 o’clock position. The fossa ovalis is not usually seen but when
looking for a patent foramen ovale this view is often very stable for
shunt studies using colour flow or contrast.
SHORT AXIS (AORTIC VALVE) VIEW
373
POST
ANT
AO
LA
LV
STOMACH
Atrial septum
AV
0
55
180
LA
LMS
RA
NCC
LCC
PA
RCC
RV
PV
TV
Fig. 5.7 Short axis view of aortic valve. See W Video 5.3.
374
CHAPTER 5 Transoesophageal examination
Short axis (right ventricle) view
This view may be included for better display of the pulmonary valve and is
also called the right ventricle inflow-outflow view (Fig. 5.8).
It is very similar to the aortic view and can be skipped if the pulmonary
valve has already been adequately displayed. It is equivalent to the par-
asternal short axis transthoracic view.
Finding the view
From the short axis aortic view rotate the sector to around 70-80°.
The probe may need to be withdrawn or advanced slightly to get the
right scan plane. Focus on a clear view of the pulmonary valve.
The optimal view will include the tricuspid and pulmonary valve with
the right ventricle wrapped around the aortic valve—a right ventricular
inflow-outflow view.
What do you see?
Use this view to assess
Pulmonary valve morphology and pathology.
Tricuspid valve morphology and pathology.
Base of right ventricle.
Use this view to measure
Right ventricle and outflow tract size.
Key features of view
Pulmonary valve: this lies below and to the right of the aortic valve. Use
colour flow to assess for regurgitation.
Tricuspid valve: lies below and to the left of the aortic valve. Use colour
flow to assess regurgitation and sometimes the valve is sufficiently
aligned for CW Doppler measures.
Right ventricle: the ventricle wraps around below the aortic valve
and measurements of size at the base and in the outflow tract are
sometimes possible.
SHORT AXIS (RIGHT VENTRICLE) VIEW
375
ANT
POST
AO
RA
RV
STOMACH
0
66
180
RA
AV
PA
RV
TV
PV
Fig. 5.8 Short axis view focused on right heart with change in sector. See W Video 5.4.
376
CHAPTER 5 Transoesophageal examination
Long axis (aortic valve) view
This view is equivalent to a transthoracic apical 3-chamber view or par-
asternal long axis view (Fig. 5.9). It is used to assess the aortic and mitral
valves as well as left ventricle, outflow tract, and left atrium. In some peo-
ple the mitral valve is not seen well as it lies more inferiorly. An adjusted
long axis view will then be needed to assess the mitral valve (b p.418).
Finding the view
From the short axis views rotate the sector to around 135°.
Withdraw, advance, and turn the probe slightly to get the scan plane.
Focus on a clear view of the aortic valve and ascending aorta.
The optimal view will include 2 clear valve leaflets and a straight
ascending aorta.
What do you see?
Use this view to assess
Aortic valve morphology and pathology.
Mitral valve morphology and pathology.
Perivalvular processes.
LVOT and membranous septum.
Ascending aorta.
Use this view to measure
Aortic root, sinuses, and ascending aorta.
Left atrial size.
Key features of view
Aortic valve: the right coronary cusp is seen at the bottom and non-
coronary cusp at the top. Colour flow will demonstrate regurgitation
and this can be a good view for identifying vegetations or masses.
Aortic root: the entire aortic root, including sinuses of Valsalva,
sinotubular junction, and ascending aorta should be visible for
measurement.
Ascending aorta: slight adjustment can often bring into view a lot of the
proximal portion of the ascending aorta.
Mitral valve: A2 and P2 segments of the valve are seen and can be used
for colour flow and other Doppler measures. However, for proper
visualization the probe may need to be advanced slightly.
Left atrium: the atrium lies nearest the probe and linear size can be
measured from probe to aortic root.
Left ventricle: the septum (including the membranous septum below
the aortic valve) and inferolateral wall can usually be seen to assess
wall motion abnormalities.
Right ventricle: the right ventricle outflow is just seen below the aortic
valve and sometimes the pulmonary valve is partially visible.
Transverse sinus: This lies between aortic root and left atrium and may
contain fluid.
LONG AXIS (AORTIC VALVE) VIEW
377
POST
ANT
AO
LA
LV
STOMACH
MV
A2 leaflet
0
135
180
LA
P2 leaflet
NCC
Aorta
RCC
Lateral
LV
wall
RV
Septum
Fig. 5.9 Long axis view demonstrates aortic valve and left ventricle. See W Video 5.5.
378
CHAPTER 5 Transoesophageal examination
Long axis (mitral valve) view
This view is a slight adjustment of the long axis aortic view but focused on
the mitral valve. If the views of the mitral valve were already optimal in the
aortic long axis image this view can be skipped.
Finding the view
From the long axis aortic view, at around 135°, advance the probe
slightly.
Focus on a clear view of the mitral valve and try and get an
unforeshortened left ventricle.
The optimal view will include 2 clear mitral valve leaflets.
What do you see?
Use this view to assess
Mitral valve morphology and pathology.
Left ventricular global and regional function.
Use view to measure
Doppler measures of mitral regurgitation and stenosis.
Key features of view
The features are similar to the long axis aortic view (except the aortic
valve may be less clear).
Mitral valve: A2 and P2 segments of the valve are seen. Colour
flow can map regurgitation and assess flow convergence and vena
contracta. The valve is also usually aligned for Doppler measures.
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380
CHAPTER 5 Transoesophageal examination
Atrial septum (bicaval) view
This is a unique transoesophageal view with no equivalent transthoracic
image (Fig. 5.10). It is perfect for studying both atria and the septum.
Finding the view
From the long axis views rotate the sector to around 110°.
Turn the probe clockwise away from the left ventricle. You will see
the septum come into view as a line across the screen.
Withdraw, advance and turn the probe. Focus on a clear view of the
septum, with the ‘dip’ of the fossa ovalis in the centre.
The optimal view includes inferior and superior vena cavae on either
side with the right atrial appendage visible on the right.
What do you see?
Use this view to assess
Drainage of superior and inferior vena cava.
Assessment for atrial septal defect and patent foramen ovale.
Drainage of right upper pulmonary vein.
Eustachian valve.
Use this view to measure
The tricuspid regurgitation jet may be aligned for Doppler measures.
A slightly adjusted view can be used to look at the right upper
pulmonary vein flow.
Key features of view
Left and right atria: the left atrium is nearest the probe.
Interatrial septum: this is the most prominent feature and can be
qualitatively assessed for thickness and atrial septal defects. Colour
flow mapping and contrast provide more detailed information on
interatrial shunts.
Inferior vena cava and Eustachian valve: these lie on the left of the
image and flow can be mapped with colour flow. The Eustachian valve
is seen as a mobile strand originating from the orifice of the inferior
vena cava.
Superior vena cava and christa terminalis: these lie on the right of the
image with the christa terminalis usually seen as a bright bar below the
superior vena cava separating it from the right atrial appendage.
Right atrial appendage: this is a wide-mouthed, shallow, trabeculated
appendage lying on the right of the image below the superior vena
cava. Atrial pacing wires may be seen hooking into the appendage.
Tricuspid valve: the tricuspid valve may be seen in the far field. To
optimize the valve image advance the probe. Colour flow can assess
regurgitation and the valve is often aligned for Doppler measures.
Right upper pulmonary vein: to see the vein the probe needs to be
turned anticlockwise slightly to focus on the superior vena cava. The
right upper pulmonary vein lies parallel to the superior vena cava. The
vein is often aligned for Doppler measures. This view is used to look
for abnormal pulmonary venous drainage.
ATRIAL SEPTUM (BICAVAL) VIEW
381
POST
ANT
AO
LA
RA
STOMACH
0
111
180
LA
Atrial septum
IVC
SVC
Christa terminalis
Fossa ovalis
Eustachian valve
RA
Right atrial appendage
Fig. 5.10 Bicaval view with unusually prominent tricuspid valve. See W Video 5.6.
382
CHAPTER 5 Transoesophageal examination
Two chamber (atrial appendage) view
This view is important for several features of the left heart: mitral valve,
left ventricular function and left atrial appendage (Fig. 5.11). The view is
equivalent to the transthoracic apical 2-chamber view.
Finding the view
Rotate back from the bicaval view to see mitral valve and left ventricle.
Change the sector to around 75°.
Withdraw and advance the probe to focus on a clear view of the
mitral valve and left ventricle. Turn the probe to obtain the longest
(unforeshortened) view of the left ventricle.
To see the left atrial appendage clearly you may need to adjust the
sector angle between 90° and 50°.
The optimal view includes mitral valve, left atrial appendage, and an
unforeshortened left ventricle. An unforeshortened left ventricle and
left atrial appendage may not be visible in the same view and in this
case separate images should be stored for each feature.
What do you see?
Use this view to assess
Global and regional left ventricle function, wall thickness.
Mitral valve morphology (orifice, prolapse).
Left atrial appendage.
Left upper pulmonary vein.
Use this view to measure
Left ventricle diastolic and systolic dimensions.
Ejection fraction.
Mitral valve.
Key features of view
Left ventricle: the inferior wall is on the left and anterior wall on the
right. This is the preferred view for measurement of left ventricle
size because the ventricle is less likely to be foreshortened with the
sector at 70-90° (the plane can be made to cut through the apex by
turning the probe). Regional abnormalities and papillary muscles can
be assessed.
Mitral valve: often a commissural view i.e. valve is cut along its
commissure so that P1, A2, and P3 segments are seen. Colour flow and
Doppler measures are possible. Long axis of valve ring can be assessed.
Left atrial appendage: a curved finger heading down from the left
atrium to the left of the mitral valve. Beware of variation in anatomy,
multiple lobes or retroverted appendages. These will need assessment
with atypical scan planes. Get an optimal image will slight variation in
sector angle and probe position. The appendage is aligned for Doppler
measures.
Left upper pulmonary vein and ‘warfarin’ ridge: this lies above the left
atrial appendage and is divided from it by the warfarin (or coumadin)
ridge (seen as a bright bar on the right of the screen). Probe may
need to be withdrawn slightly to view vein. Vein is aligned for Doppler
measures.
TWO CHAMBER (ATRIAL APPENDAGE) VIEW
383
POST
ANT
AO
LA
LV
STOMACH
0
75
180
MV
Left upper
LA
pulmonary vein
Coronary sinus
P3
orifice (not seen)
A2
P1
but parallel to
appendage
LV
Inferior
wall
LA appendage
Anterior
wall
Fig. 5.11 2-chamber view cutting across mitral valve commissure. See W Video 5.7.
384
CHAPTER 5 Transoesophageal examination
Pulmonary vein views
Each pulmonary vein requires a separate view (Fig. 5.12).
Finding the views
Right upper pulmonary vein
The right upper pulmonary vein is best seen in the adjusted atrial
septal (bicaval) view (b p.380) lying parallel to the superior vena cava.
This view also allows Doppler alignment.
The vein can be identified starting from the apical 4-chamber 0° view.
Rotate the probe to the right hand side of the image and withdraw
slightly. The right upper pulmonary vein is seen adjacent to, and
wrapping around, the superior vena cava. Varying the sector angle may
between 0-20° can be useful to lengthen out the vein.
Right lower pulmonary vein
The right lower pulmonary vein is best identified starting from the
apical 4-chamber 0° view. Rotate the probe to focus on the right hand
side of the image (as when finding the right upper pulmonary vein) and
then advance the probe slightly. The vein should be seen just below
the right upper pulmonary vein.
Left upper pulmonary vein
The left upper pulmonary vein is best seen in the adjusted 2-chamber
view (b p.382) lying parallel to, and above, the left atrial appendage.
This view also allows Doppler alignment.
The vein is also seen with sector set to 0°. Rotate the probe to focus
on the left hand side of the image and withdraw slightly. Look for the
vein orifice.
Left lower pulmonary vein
To identify the left lower pulmonary vein start from the apical
4-chamber 0° view. Rotate the probe to focus on the left hand side of
the image. The vein should be seen below the left upper pulmonary
vein orifice.
What do you see?
Use these views to assess
All 4 pulmonary veins.
Use these views to measure
Pulmonary vein flow in upper pulmonary veins.
Identifying pulmonary veins
At 0° the lower veins lie roughly perpendicular to the ultrasound
beam (across the screen) while the upper veins lie parallel with the
beam (pointing towards the probe).
As the names suggest, the lower veins lie below the upper veins. If
an upper vein is identified then advance the probe slightly to see the
lower vein and vice versa.
Colour flow mapping is very useful to identify the veins. The colour
flow will demonstrate blood flow out of the veins into the atrium.
PULMONARY VEIN VIEWS
385
RIGHT PULMONARY VEINS
0
110
180
LA
Septum
RIGHT UPPER
RA
RAA
SVC
0
0
180
RIGHT LOWER
LA
SVC
RIGHT UPPER
LEFT PULMONARY VEINS
0
75
180
Warfarin
ridge
LA
LEFT UPPER
LV
LAA
0
0
180
LEFT LOWER
LA
LEFT UPPER
Fig. 5.12 Different viewing positions to identify pulmonary veins.
386
CHAPTER 5 Transoesophageal examination
Coronary sinus view
Seeing the coronary sinus can be useful in some procedures such as elec-
trophysiology studies or pacing device placement. It also allows assess-
ment of congenital abnormalities such as a persistent left superior vena
cava (Fig. 5.13).
Finding the view
Start from a 4-chamber view at 0°.
The coronary sinus wraps around and below the mitral valve, opening
into the right atrium. Therefore advance the probe so that the image
plane cuts below the mitral valve. This may be helped by some
retroflexion of the probe.
The optimal view has the coronary sinus perpendicular across the
screen opening into the right atrium.
CORONARY SINUS VIEW
387
POST
ANT
AO
LA
LV
CORONARY
SINUS
Coronary sinus
RA
LV
RV
Fig. 5.13 Coronary sinus view. See W Video 5.8.
388
CHAPTER 5 Transoesophageal examination
Transgastric short axis views
Transgastric scanning can be quite uncomfortable to the conscious and
mildly sedated patient. Transgastric views should be performed in well-
sedated, compliant patients when further information is required. They can
also be routinely performed intraoperatively. Short axis views are equiva-
lent to transthoracic parasternal short axis views and can often be adjusted
to create mid-papillary and mitral valve level views (Fig. 5.14). They can be
particularly useful intraoperatively to monitor left ventricle function.
Finding the view
From the 4-chamber view, with sector angle at 0°, advance the probe
several centimetres. The patient may rouse slightly as you enter the
stomach.
Angulate the probe forwards hard to try and get it at right angles.
Withdraw the probe so the transducer tip presses on the upper
stomach wall, against the diaphragm, underneath the heart.
Make slight adjustments by turning the probe, as well as withdrawing
and advancing until the left ventricle is seen in short axis.
Keep the probe angulated forward.
By withdrawing and advancing the probe along the bottom of the heart
it is theoretically possible to see the left ventricle at several levels,
e.g. mid-papillary, mitral valve.
The optimal view is an on-axis cross-section through the left ventricle.
What do you see?
Use this view to assess
Global and regional left ventricle function, wall thickness.
Mitral valve morphology.
Can provide information on right ventricle size and function.
Pericardial effusions may be seen.
Use this view to measure
Left ventricle size and wall thickness.
Key features of view
Left ventricle (mid-papillary level): with a clear short axis cut through
the ventricle the septum, anterior, lateral, and inferior walls of the
ventricle can be reviewed. This is an ideal view for measures of left
ventricle size and thickness.
Mitral valve (mitral valve level): a slight withdrawal of the probe from
the mid-papillary level should bring the image plane up to the mitral
valve. You should be able to scan through the chordae up to the
leaflet tips. Use colour flow to highlight regurgitation jets.
Right ventricle: the right ventricle can be seen as a crescent around
one side of the left ventricle. This view can give an impression of right
ventricle size and function.
TRANSGASTRIC SHORT AXIS VIEWS
389
POST
ANT
AO
LA
LV
STOMACH
INFERIOR WALL
Posterior leaflet
Posteromedial
Anterior leaflet
SEPTUM
papillary muscle
LV
LATERAL
WALL
RV
Mitral valve opening
Anterolateral
ANTERIOR WALL
papillary muscle
Fig. 5.14 Transgastric short axis views at mitral valve (left) and mid ventricle (right)
levels. See W Video 5.9 and W Video 5.10.
390
CHAPTER 5 Transoesophageal examination
Transgastric long axis view
The long axis view provides an unparalleled view of the mitral subvalvular
apparatus (Fig. 5.15).
Finding the view
From the short view rotate the sector angle to 90°.
Keep hard probe angulation.
Make slight adjustments by turning the probe until the left ventricle is
seen in long axis.
The optimal view should include the mitral valve, subvalvular
apparatus, and left ventricle.
What do you see?
Use this view to assess
Global and regional left ventricle function, wall thickness.
Mitral valve morphology.
Subvalvular mitral apparatus.
Use this view to measure
Left ventricle size and wall thickness.
Key features of view
Left ventricle: similar to the 2-chamber view the inferior wall is nearest
the probe and anterior walls in the far field. Foreshortening occurs
easily. This can provide information on wall thickness as well as global
and regional function.
Mitral valve and subvalvular apparatus: a commissural view, the leaflet
anatomy is not always clear but the subvalvular apparatus can be
incredibly detailed. The different order chordae tendinae as well
as both papillary muscles can be reviewed. Colour flow can map
regurgitation.
Left atrium and left atrial appendage: the left atrium is present but not
usually in great detail. You may notice the left atrial appendage in the
far field.
TRANSGASTRIC LONG AXIS VIEW
391
POST
ANT
LA
LV
STOMACH
Posteromedial papillary muscle
Inferior wall
0
90
180
LV
Mitral valve
Anterior wall
Mitral valve chordae
Fig. 5.15 Transgastric long axis view of left ventricle. See W Video 5.11.
392
CHAPTER 5 Transoesophageal examination
Transgastric long axis (aortic) view
The long axis view can be modified slightly to bring the LVOT into the
image for Doppler measures across the aortic valve (Fig. 5.16).
Finding the view
From the long axis view rotate the sector angle to 110°.
Keep hard probe angulation.
Make slight adjustments by turning the probe until the LVOT is seen in
the far field. Colour flow may help to identify flow through the aortic
valve.
The optimal view should include the LVOT aligned in the far field
aligned for Doppler measures.
What do you see?
Use this view to assess
Doppler measures of aortic valve velocities.
Use this view to measure
Aortic and LVOT velocities.
Key features of view
Aortic valve and LVOT: the aortic valve may be seen close to the
mitral valve in the far field. Colour flow mapping may make this
more apparent. The valve and outflow tract is aligned in this view for
Doppler measures.
TRANSGASTRIC LONG AXIS (AORTIC) VIEW
393
POST
ANT
AO
LA
LV
STOMACH
0
110
180
LV
Aortic valve
CW Doppler
Fig. 5.16 Transgastric long axis view of LVOT. See W Video 5.12.
394
CHAPTER 5 Transoesophageal examination
Transgastric right ventricular view
This is similar to the left ventricular long axis view but can be difficult
to find. However, if available it can give a useful assessment of the right
ventricle and inflow (Fig. 5.17).
Finding the view
From the transgastric long axis left ventricle view turn the probe
clockwise.
The right ventricle should appear in long axis similar to the left
ventricle.
The optimal view should include the tricuspid valve, subvalvular
apparatus, and right ventricle.
What do you see?
Use this view to assess
Tricuspid valve morphology.
Subvalvular tricuspid apparatus.
Use this view to measure:
No specific measurements.
Key features of view
Right ventricle: this is an unusual 2-chamber view of the right ventricle
and atrium but can give an impression of right-sided chamber size.
Tricuspid valve and subvalvular apparatus: as with the mitral views
the subvalvular apparatus is usually detailed. Colour flow can map
regurgitation and there can be a qualitative assessment of tricuspid
valve function. As the right ventricle is relatively difficult to see with
transoesophageal imaging this may provide a good window to look for
tricuspid valve pathology, e.g. vegetations and masses.
Right atrium: the right atrium can be viewed.
TRANSGASTRIC RIGHT VENTRICULAR VIEW
395
0
126
180
RV
RA
TV
POST
ANT
RA
RV
STOMACH
Fig. 5.17 Transgastric right ventricle view. See W Video 5.13.
396
CHAPTER 5 Transoesophageal examination
Deep transgastric view
Deep transgastric views are only really required when Doppler information
is needed about the aortic valve and transthoracic imaging is not possible.
The view tries to recreate a transthoracic apical 5-chamber view (Fig. 5.18).
Finding the view
From the transgastric long axis view advance the probe further into
the stomach.
Set the sector to 0°.
Ensure full angulation of the probe and good contact with the stomach
wall.
What do you see?
Use this view to assess
Global and regional left ventricle function.
LVOT and aortic valve.
Use this view to measure
Left ventricle function.
Aortic and LVOT velocities (if seen - may need some sector angle
adjustment).
Key features of view
Aortic valve and LVOT: the aortic valve lies in the far field and may be
highlighted by colour flow mapping. The primary purpose of this view
is to align the valve and outflow tract for Doppler measures.
Left ventricle: similar to the 4-chamber view. The septum and lateral
wall are seen.
DEEP TRANSGASTRIC VIEW
397
POST
ANT
AO
LA
LV
STOMACH
0
0
180
LV
LVOT
MV
AV
LA
Fig. 5.18 Deep transgastric view. See W Video 5.14.
398
CHAPTER 5 Transoesophageal examination
Pulmonary artery view
A view to study the pulmonary arteries. Can be useful to assess size of
artery or look for large pulmonary emboli (Fig. 5.19).
Finding the view
Start from the short axis aortic view. The sector may need to be
reduced slightly to 40°.
Withdraw the probe slowly until you have a short axis view of the
ascending aorta.
The probe may need to be angulated forward gently to demonstrate
the pulmonary artery.
What do you see?
Use this view to assess
Ascending aorta for dissection or dilatation.
Pulmonary artery.
Use this view to measure:
Aortic and pulmonary artery size.
Key features of view
Pulmonary arteries: the right pulmonary artery is seen wrapping around
the aorta and lies between the aorta and probe. The main pulmonary
artery is seen to the side of the aorta. The left pulmonary artery is not
visible.
Ascending aorta: a short segment of the ascending aorta can usually be
seen to assess dilatation, dissection, and atheroma.
Superior vena cava: the superior vena cava is seen in cross-section close
to the aorta and right pulmonary artery.
PULMONARY ARTERY VIEW
399
POST
ANT
AO
PA
RA
RV
STOMACH
RIGHT
PULMONARY
0
40
180
ARTERY
SUPERIOR VENA
CAVA
DILATED
ASCENDING
AORTA
MAIN
PULMONARY
ARTERY
Fig. 5.19 View of the pulmonary artery.
400
CHAPTER 5 Transoesophageal examination
Aortic views
The final views are usually the aortic views (Fig. 5.20). They can be
important for monitoring dissection or studying atheroma. They can also
be used to assess aortic flow in aortic regurgitation. The only limitation is
that TOE can not see the distal ascending aorta and proximal part of the
aortic arch as the air-filled left bronchus obscures the view.
Finding the view
The ascending aorta is seen in the pulmonary artery view. Obtain the
short axis aortic view at 50° and then withdraw the probe slowly to
scan up the aorta as far as images are maintained.
For descending aorta and aortic arch, start from the 4-chamber view
with a sector angle of 0° and turn the probe slowly so that it starts to
face posteriorly.
It is usually best to turn the probe anti-clockwise until the circular
aorta is seen.
Decrease the depth so that the aorta fills the screen and you usually
also need to reduce the gain slightly.
The probe may then be withdrawn slowly to scan up the aorta. As the
aorta curls around the oesophagus some slight turning will be required
as the probe is withdrawn.
The optimal view is a cross-section through the aorta. A long axis view
can also be useful and is achieved by changing the sector angle to 90°.
What do you see?
Use this view to assess
Aortic dissection or dilatation.
Atheroma and thrombus.
Aortic flow, e.g. in aortic regurgitation.
Use this view to measure:
Aortic size.
Aortic flow.
Key features of view
Descending aorta: there is good depiction of the aortic walls and their
layers as well as thickening and gross atherosclerosis. If measurements
are made, annotate images with the depth of the probe so that serial
measures are possible.
Aortic arch: at the top of the descending aorta the aortic cross-section
will disappear and the vessel opens out into the arch. The origin of the
left subclavian artery may be seen. By changing the sector angle to 90°
at this point a cross-section can be maintained.
Ascending aorta: a short segment of the ascending aorta can usually be
seen to assess dilatation, dissection, and atheroma.
AORTIC VIEWS
401
POST
ANT
AO
LA
LV
STOMACH
0
0
180
0
90
180
AORTA
AORTA
Atherosclerosis
Fig. 5.20 Aortic short (on left) and long (on right) axis views. See W Video 5.15
and W Video 5.16.
402
CHAPTER 5 Transoesophageal examination
3D oesophageal views
3D oesophageal views allow the spatial orientation of anatomy and pathol-
ogy to be fully appreciated from multiple positions and in different imaging
planes (Fig. 5.21). In principle all views used for 2D imaging are also suit-
able for 3D recordings.
Finding the view
Optimize the 2D image by adjusting the sector width, depth, and gain
settings appropriately.
Decide on which 3D image acquisition mode you would like to use.
For larger volumes of interest then full volume acquisition provides the
largest volume of imaging. For smaller regions of interest (e.g. valves)
then live 3D or 3D zoom modes may be preferable to improve the
balance between temporal and spatial resolution, see Table 5.1.
Full volume acquisition
This mode records over 4 cardiac cycles and then stitches these
together to form a full volume.
After the 2D image has been optimized, select 3D/full volume.
A biplane display will appear allowing the operator to view the region
of interest to ensure that it is being adequately imaged without
foreshortening.
Adjust the line density and sector width appropriately to optimize the
region of interest.
Ensure that the ECG gating is adequate.
Acquire the 3D image.
Check for the presence of stitching artefacts and when happy accept
the acquisition.
This mode also allows full volume colour acquisition.
Live 3D acquisition
Optimize the 2D image and view in biplane mode to ensure optimal
probe position and adjust sector accordingly.
Acquire live 3D.
3D zoom acquisition
Optimize the 2D image.
Select 3D zoom mode to show the image in a biplane view.
A box will appear to delineate the area which will be shown in 3D
zoom. Adjust the position of the box whilst still in biplane mode to
ensure the region of interest seen in both orthogonal views is within
the guide box.
Acquire 3D zoom.
3D OESOPHAGEAL VIEWS
403
Table 5.1 Properties of the 3D image acquisition modes
Full volume
Live
Zoom
Dimensions
90° × 90°×
60° × 30° × depth
20° × 20°–90° ×
depth of
of 2D image
90° × variable height
2D image
Real time?
No
Yes
Yes
Frame rate
20-40Hz
20-30 Hz
5-10Hz
(4 beats);
40-50Hz
(7 beats)
Cardiac
Left ventricle,
Any 2D image
Cardiac valves, left
structure of
mitral valve
atrial appendage
interest
Clinical
LV function.
Examine anatomy
Examine anatomy
application
colour
and guide
Doppler
interventional
procedures
Possible
Yes
No
No
presence of
stitch artefacts?
Temporal
Best
Mid
Worst
resolution
Spatial
Worst
Mid
Best
resolution
Fig. 5.21 Full volume 3D acquisition with subsequent rotation and cropping to
reveal the 3D spatial relationship between the cardiac valves. See W Video 5.17.
404
CHAPTER 5 Transoesophageal examination
3D mitral valve
The mitral valve views are usually acquired from the same views used for
2D imaging of the mitral valve and are excellent for assessing mitral valve
pathology such as mitral valve prolapse.
Finding the view
From the mid oesophageal position obtain the optimal image of
the mitral valve using from the 4-chamber 0°, 2-chamber 75°, or
3-chamber 135° views.
Once the image has been optimized, select the appropriate acquisition
mode.
Image acquisition modes
The mitral valve can be easily imaged using all 3D acquisition modes:
full volume, live, and zoom.
In full volume mode, colour Doppler can be used to acquire a 3D
colour image across the valve.
3D zoom allows the mitral valve anatomy to be examined in detail
with adequate spatial and temporal resolution.
What do you see?
Use mitral valve views to assess
Mitral valve morphology (Figs. 5.22 and 5.23) and pathology.
3D applications for imaging the mitral valve
Acquisition of 3D datasets allows post processing and the mitral valve
to be rotated to be viewed from the surgical view of the left atrium.
3D TOE allows a visually superior understanding of normal MV
anatomy and causes of valvular dysfunction. It allows detailed analysis
of MV anatomy to view the annulus, leaflets, and subvalvular apparatus
from different orientations and planes.
It is becoming increasingly used to guide mitral valve repair (b p.446).
Imaging of prosthetic mitral valves using 3D acquisition modes
can be very useful, allowing a detailed assessment of the valve and
any coexisting pathology (e.g. site of paravalvular regurgitation or
dehiscence).
Use view to measure
3D colour full volume data sets can be rotated and cut in different
planes and used to quantify the origin of the regurgitant jet(s) as well
as estimate the vena contracta and regurgitant orifice area.
As 3D datasets can be viewed from multiple angles and cropped in
different planes, it allows estimation of the smallest true MV orifice by
planimetry.
Off line reconstruction packages allow 3D MV models to be generated
from original TOE datasets (Figs. 5.22 and 5.23).
Key features of view
Rotation and viewing through different planes allow all the valve
leaflets, annulus and subvalvular apparatus to be viewed.
3D MITRAL VALVE
405
Fig. 5.22 Live 3D acquisition of mitral valve. Subsequent rotation and cropping
to allow visualization of the valve from the LV apex. AMVL = anterior mitral valve
leaflet; PMVL = posterior mitral valve leaflet. See W Video 5.18.
Fig. 5.23 Live 3D acquisition of mitral valve. Subsequent rotation and cropping to
allow visualization of the valve from the left atrium and identification of the anterior
(A) mitral valve leaflet scallops and posterior (P) mitral valve leaflet scallops;
Ao = aorta. See W Video 5.19.
406
CHAPTER 5 Transoesophageal examination
3D aortic valve
3D imaging of the aortic valve is useful for highlighting the mechanism of pa-
thology and also to guide aortic valve interventional procedures (Fig. 5.24).
Finding the view
From the mid oesophageal the short axis 50-70° view is used.
Image acquisition modes
3D imaging of the aortic valve can be difficult because of its anterior
position and thin pliable cusps.
All 3D acquisition modes can be used although multiple images
may need to be recorded when using zoom mode to ensure entire
coverage of the valve.
In full volume mode, colour Doppler can be used to acquire a 3D
colour image across the valve.
What do you see?
Use aortic valve views to assess
Aortic valve morphology and pathology.
3D applications for imaging the aortic valve
It is becoming increasingly used to guide TAVI (b p.464).
Imaging of prosthetic aortic valves using 3D acquisition modes can
be very useful, allowing a detailed assessment of the valve and any
coexisting pathology (e.g. areas of dehiscence).
Use view to measure
3D colour full volume data sets can be rotated and cut in different
planes and used to quantify the origin of the regurgitant jet(s) as well
as estimate the vena contracta and regurgitant orifice area.
As 3D datasets can be viewed from multiple angles and cropped in
different planes, it allows estimation of the smallest true AV orifice by
planimetry (Fig. 5.25), aortic ring, LVOT, and proximal aorta.
Key features of view
Anatomy of aortic valve
3D aorta
Image acquisition modes
All 3D imaging modes can be used depending on the size of the region
of interest which is being examined.
What do you see?
Use aortic valve views to assess
Aorta and root pathology e.g. dissection/atheroma.
3D applications for imaging the aorta
3D imaging of the aortic root can provide detailed assessment of
complex anatomical pathologies, e.g. aneurysm, aortic dissection.
3D AORTA
407
Use view to measure
The extent of dissection/thrombus/atheroma if present.
Fig. 5.24 Live 3D TOE short axis view of the aortic valve when closed. View shows
non-coronary cusp (NCC), right coronary cusp (RCC), left coronary cusp (LCC),
LA (left atrium), inter atrial septum (IAS), right atrium (RA), tricuspid valve (TV),
and pulmonary valve (PV). See W Video 5.20 and W Video 5.21.
Fig. 5.25 Post-processing systems such as Phillips QLAB allow the 3D view to be
sliced down over several planes. Multiple slices seen here from aortic valve short
axis view. See W Video 5.22.
408
CHAPTER 5 Transoesophageal examination
3D tricuspid valve
3D imaging of the tricuspid valve can be difficult because of the valve’s thin
leaflets and also its anterior position (Fig. 5.26).
Finding the view
From the 4-chamber 0° view or transgastric RV view, rotate the probe
so that the tricuspid valve is focused on.
Image acquisition modes
From the 4-chamber view, 3D datasets of the tricuspid valve can be
acquired.
All 3D acquisition modes can be used although multiple images
may need to be recorded when using zoom mode to ensure entire
coverage of the valve.
In full volume mode, colour Doppler can be used to acquire a 3D
colour image across the valve.
What do you see?
Use view to assess
Tricuspid valve and annulus morphology and pathology.
3D applications for imaging the tricuspid valve
Acquisition of 3D datasets allows post-processing and the tricuspid
valve to be rotated to be viewed from the surgical view of the right
atrium.
3D imaging allows the TV to be viewed from the atria and gives an
appreciation of its relationship to the MV and AV.
Use view to measure
3D colour full volume data sets can be rotated and cut in different
planes and used to quantify the origin of the regurgitant jet(s) as well
as estimate the vena contracta and regurgitant orifice area.
As 3D datasets can be viewed from multiple angles and cropped in
different planes, it allows estimation of the smallest true TV orifice by
planimetry.
Key features of view
Rotation and viewing through different planes allow all the valve
leaflets and to be viewed.
3D pulmonary valve
As the pulmonary valve is the most anterior of all valves and also the
thinnest, 3D TOE is limited and it is difficult to obtain adequate 3D
views.
3D PULMONARY VALVE
409
Fig. 5.26 Full volume 3D 4-chamber acquisition showing closed tricuspid valve
(TV), right atrium (RA), right ventricle (RV), left atrium (LA), and left ventricle (LV).
See W Video 5.23.
410
CHAPTER 5 Transoesophageal examination
3D left ventricle
3D imaging of the left ventricle can be used to help quantify LV function or
to confirm the presence of pathology (e.g. apical thrombus) (Fig. 5.27).
Finding the view
From the 4 chamber 0° view or 2 chamber 90° view, optimize the
depth settings and ensure that the ventricle is not foreshortened.
Image acquisition modes
Full volume acquisition mode is used to enable the best chance of
capturing the entire ventricle.
Close inspection of the full volume datasets is necessary following
acquisition to review the image quality and to also exclude the
presence of stitch artefacts.
What do you see?
Use view to assess
Left ventricle
3D applications for imaging the left ventricle
Post-processing packages allow the ventricular volumes and ejection
fraction to be estimated from the 3D datasets (Fig. 5.28).
The 3D datasets can be rotated and cropped to review images of the
left ventricle from the short axis plane.
Assessment of regional LV function and synchrony.
Use view to measure
Left ventricular volumes.
Ejection fraction.
Key features of view
Left ventricle.
3D LEFT VENTRICLE
411
Fig. 5.27 Full volume 3D LV 4-chamber acquisition showing closed tricuspid valve
(TV), right atrium (RA), right ventricle (RV), left atrium (LA), mitral valve (MV), and
left ventricle (LV).
Fig. 5.28 Full volume 3D LV 4-chamber acquisition with post-processing on Phillips
QLAB islice. iSlice allows the LV to be viewed in 2 orthogonal views with multiple
short axis slices taken over regular intervals (bottom right panel).
412
CHAPTER 5 Transoesophageal examination
3D interatrial septum
3D imaging of the interatrial septum has become invaluable not only for
confirming dimensions of atrial septal defects but also to demonstrate the
spatial relationship of defects to surrounding structures (Fig. 5.29). These
views are also used to guide percutaneous atrial septal interventional
procedures.
Finding the view
The optimal view is obtained from the bicaval 110° view.
Image acquisition modes
Using full volume or zoom modes allows detailed assessment of the
interatrial septum from the bicaval view.
What do you see?
Use views to assess
Interatrial septum.
Right atrium.
Left atrium.
SVC.
IVC.
3D applications for imaging the interatrial septum
Acquisition of 3D datasets allows post-processing and the interatrial
septum to be rotated to be viewed from either the left or the right
atrium.
3D TOE allows a visually superior understanding of the atrial septal
anatomy and of pathology compared to 2D TOE.
It is becoming increasingly used to guide percutaneous closure of atrial
septal defects.
Use view to measure
As 3D datasets can be viewed from multiple angles and cropped in
different planes, it allows the size of defects and their relationship to
surround structures to be better appreciated.
3D colour full volume data sets can be used to view the flow of blood
across defects.
Key features of view
Interatrial septum and defects.
The relationship of the interatrial septal defects to the MV, AV,
SVC, IVC.
3D INTERATRIAL SEPTUM
413
Fig. 5.29 Top: full volume 3D acquisition of atrial septum from bicaval view
showing interatrial septum (IAS), fossa ovalis (FO), left atrium (LA), inferior vena
cava (IVC), superior vena cava (SVC), and right atrium (RA). Bottom: En face view
of the interatrial septum which has been rotated and cropped to show its orienta-
tion with regards to the IVC. See W Video 5.24.
414
CHAPTER 5 Transoesophageal examination
X-plane
The use of X-plane imaging during TOE provides the operator with further
anatomical information and can also be useful as guidance during interven-
tional procedures. X-plane allows 2 high resolution images of the heart to
be displayed simultaneously in real time (Fig. 5.30).
Finding the view
Obtain the appropriate 2D view.
Optimize the 2D image settings.
Select X-plane mode. Live imaging provides 2 orthogonal views from
the same heart beat. The initial image on the left is the baseline
reference whilst the image on the right can be electronically rotated to
any angle between 0-180°.
When happy acquire the image.
X-plane images can be acquired with and without the use of colour
Doppler.
Use this view to
Examine the left atrial appendage anatomy and for pathology
(e.g. thrombus).
When high spatial and temporal resolution is needed e.g. valve
vegetations.
X-PLANE
415
Fig. 5.30 X-plane image acquisition of the aortic valve. After selecting X-plane, the
left hand image will display the current live image. Adjusting the angle cursor (red
dashed line) will alter the angle of acquisition of the second image on the left hand
side. See W Video 5.25.
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417
Chapter 6
Transoesophageal
anatomy and pathology:
valves
Mitral valve
418
Mitral regurgitation
420
Mitral valve prolapse
426
Mitral stenosis
432
Mitral valve preoperative assessment 436
440
Mitral valve balloon valvotomy 444
Mitral valve repair
446
Mitral valve replacement 448
Aortic valve
452
Aortic stenosis
454
Aortic regurgitation
456
Aortic valve preoperative assessment 460
Aortic valve replacement 462
TAVI 464
Assessment during TAVI 466
Tricuspid valve
468
Tricuspid regurgitation and stenosis
468
Pulmonary valve 470
Pulmonary regurgitation and stenosis 470
Endocarditis 472
418
CHAPTER 6 Transoesophageal anatomy and pathology
Mitral valve
TOE is one of the most important tools for the assessment of mitral valve
disease and allows superb visualization of the mitral valve. The modality is
particularly good for systematic reviews of the different valve segments.
Mitral valve anatomy is described on b p.106. Briefly, there are 2 leaflets
each with 3 segments (or scallops)—a large anterior and a crescent-shaped
posterior leaflet. Assessment of stenosis and regurgitation follows the
same criteria as for transthoracic imaging (b pp.110 and 116) but TOE
allows a more detailed study of the pathology underlying regurgitation or
stenosis.
Normal findings
Views
The mitral valve is sliced through in virtually all the mid-oesophageal
views and the ‘screenwiper’ principle allows rotation through the valve
in multiple planes (Fig. 6.1). The mid-oesophageal views also allow
alignment of Doppler and colour flow across the valve. The minimum
views are the mid-oesophageal views at around 0°, 135°, 90°, and 80°.
The transgastric views provide additional information in both the
short axis 0° (pulled back slightly) and the long axis 90° view for the
subvalvular apparatus.
Normal findings
4-chamber 0° view: this classically includes A2, A1, and P1 segments of
the valve (however, there is a tendency to cut more through A2 and
P2 if the LVOT is seen and the papillary muscles are not evident).
Long axis 135° view: equivalent to the apical 3-chamber view this gives
a good stable view of A2 and P2.
2-chamber 75° view: stable ‘commissural’ view to see P1 and P3 either
side of A2. Rotation of the probe allows you to swing more towards
the anterior or posterior leaflet. Slight adjustment of sector angle
will bring in the left atrial appendage and localize A1/P1 next to the
appendage.
Transgastric short axis view or ‘fish mouth’ view has the A3/P3
segments nearest the probe. The 90° view can be used to look at the
papillary muscles and chordae.
Identifying mitral valve leaflets and segments
There are rigorous descriptions of which leaflets are seen in which view.
Initially standard views allow good orientation but as you become more
familiar you can play with these by slight adjustments of the probe to cut
through the 3D structure at any point. There are 2 tips to identify the
segments and leaflets:
The anterior leaflet is nearest the septum/LVOT and usually appears
larger than the posterior leaflet.
The segments are numbered so that A1 and P1 are nearest the left
atrial appendage.
MITRAL VALVE
419
4 Chamber view—0-15º
Commissural view—60-80º
LA
RA
LA
A2 A1 P1
P3
A2
P1
RV
LV
LV
Transgastric short axis view—0º
70º-90º
135º
2 Chamber view—90º
Long axis view—135º
LA
LA
AO
P3
A3
A2
A1
P2
A2
RV
LAA
LV
LV
Fig. 6.1 Key views to assess mitral valve.
420
CHAPTER 6 Transoesophageal anatomy and pathology
Mitral regurgitation
TOE should be used to assess mitral regurgitation when:
TTE is inconclusive or technically difficult.
To define the underlying mechanism for planning mitral valve surgery.
TOE is particularly useful to visualize where the regurgitant jet passes
through the valve. Higher transducer frequencies and multiple views
result in more reliable measurements of both vena contracta and flow
convergence. However, the different transducer frequency, pulse repetition
frequency, and gain also mean they appear larger on transoesophageal images
than transthoracic images.
Assessment
Appearance
Start in the 4-chamber 0° view and map the regurgitation with colour
flow. Scan through the valve at different angles to establish the shape,
direction, and pattern of the jet. Comment on:
• Where the regurgitation passes through the valve, e.g. perforation,
failure of coaptation, prolapse of a leaflet scallop.
• Direction of eccentric jets (anterior or posterior). Remember
anteriorly-directed suggests posterior valve pathology and vice
versa.
• How far back the jet extends (involving pulmonary veins?).
• If there are several jets comment on each.
Use transgastric long axis 90° view to look at subvalvular apparatus
(Fig. 6.2). Comment on: papillary muscle and chordae with reference
to shortening and rupture.
Report associated features, e.g. atrial size, ventricle size, and function.
3D TOE MR
As the probe is much closer in TOE and with higher resolution, live
imaging can often be used rather than full-volume acquisition.
Studies have demonstrated greater accuracy than 2D TOE in
identifying the position of the prolapse (see b p.428).
Excellent resolution is possible.
As well as being used for assessment of regurgitation, 3D TOE can
guide placement of clips for transcutaneous treatment of mitral
regurgitation.
3D colour flow Doppler
This allows assessment of MR especially eccentric jets (Fig. 6.5).
Acquisition does require multiple cycles and there may be problems
with artefacts on reconstruction, especially with AF.
2D PISA assessment is based on the assumption of a hemispherical
3D shape. However, this is not always the case and all planes can be
assessed with 3D TOE (Fig. 6.3).
The origin of paravalvular leaks can be difficult to identify. However,
this can be made easier using 3D TOE.
MITRAL REGURGITATION
421
Partially ruptured
papillary muscle
0
90
180
Fig. 6.2 Transgastric long axis view demonstrates subvalvular apparatus. In this
example there is a partial papillary muscle rupture.
80
40
DOPPLER
BASELINE
SHIFT
-80
-120
Flow convergence zone becomes
larger and more clearly defined
Fig. 6.3 Flow convergence radius is more clearly defined with Doppler baseline shift.
422
CHAPTER 6 Transoesophageal anatomy and pathology
Grading severity
Assess severity on vena contracta, flow convergence, pulmonary venous
flow, and valve structure. Colour jet area can also be used (Table 6.1).
Colour Doppler jet area
This can be difficult to assess with TOE because sector width often does
not include the whole of the atrium. Proportional jet area is therefore
difficult to judge. 4-chamber 0° and long axis 135° views may give the best
impression.
Vena contracta
TOE provides excellent views and resolution for measurement of colour
flow through the valve.
In mid-oesophageal views choose the plane which cuts through the jet.
Zoom in on the colour flow through the mitral valve and record a
loop. Identify the image with maximal flow through the valve.
The vena contracta is the narrowest region of the regurgitant jet
(usually as it passes through the valve). Report the diameter.
Pulmonary venous flow
TOE provides a unique opportunity to visualize directly all 4 pulmonary
veins and measure pulmonary vein flow (Fig. 6.4). The contralateral pul-
monary vein to an eccentric jet (i.e. left pulmonary veins for an anteriorly-
directed jet and vice versa) should be used to avoid changes in flow due
to washing of the jet into the vein.
In 4-chamber 0° view rotate to the left to identify the left-sided veins
(b p.384). Advance or withdraw the probe to bring them into view.
The left upper pulmonary vein usually points towards the probe and
left lower pulmonary vein is perpendicular. To help with identification
place colour flow by the edge of the atrium and look for the jets of
the veins draining into the atrium. Slight changes in the plane angle can
optimize the view. Right-sided veins are identified in the same way but
with rotation to the right. Again the right upper pulmonary vein points
towards the probe and lower vein is perpendicular.
Alternative views are: (1) 110° bicaval view rotated to the left - right
upper pulmonary vein lies parallel to the septum (2) 2-chamber 75°
(left atrial appendage) view, in which the left upper pulmonary vein lies
parallel to the left atrial appendage.
Place the pulsed wave Doppler sample volume around 1 cm into the
chosen vein (Fig. 6.4).
Look at the systolic and diastolic components of the spectral trace and
comment if the systolic wave is blunted or reversed relative to the
diastolic wave (normally the same direction, with systolic dominant).
Supportive measures
These can be measured as for transthoracic imaging (b p.122).
MITRAL REGURGITATION
423
PW in pulmonary vein
Systolic
flow
reversal
Fig. 6.4 Pulmonary venous flow with an example of abnormal systolic flow reversal.
Fig. 6.5 Live 3D acquisition of mitral valve with P1 prolapse. The image has been
cropped and rotated to be seen from the left atrium. AV aortic valve, the anterior
(A) mitral valve scallops and posterior (P) mitral valve leaflet scallops are seen.
See W Video 6.1.
424
CHAPTER 6 Transoesophageal anatomy and pathology
Carpentier (functional) classification
The Carpentier classification (Type 1 to 3) is sometimes used to report
the functional basis for mitral regurgitation. This categorizes cause accord-
ing to leaflet motion. It is relevant to different surgical approaches.
Normal leaflet motion (Type 1):
Annular dilatation causes regurgitation due to failed coaptation.
Leaflet perforation (e.g. from endocarditis).
Excessive leaflet motion (Type 2):
Prolapse of leaflet edge beyond the plane of the annulus.
Mitral valve prolapse, rupture/dysfunction of the papillary muscle.
Restricted leaflet motion (Type 3):
Leaflet edge remains below the plane of the annulus during
systole. Usually secondary to rheumatic disease, left ventricle
dilatation, posterior wall infarction.
MITRAL REGURGITATION
425
Table 6.1 Parameters to assess mitral regurgitation
Specific signs of severity
Mild
Severe
Vena contracta
<0.3cm
>0.7cm
Jet (Nyquist 50-60cm/s)
<4cm or <20% left
>40% left atrium large &
atrium
central or wall impinging
Small & central
and swirling
PISA r (Nyquist 40cm/s)
(<0.4cm)
Large (>1cm)
None/minimal
Pulmonary vein flow
-
Systolic reversal
Valve structure
-
Flail or rupture
Supportive signs of severity
Mild
Severe
Pulmonary vein flow
Systolic dominant
Mitral inflow
A-wave dominant
E-wave dominant
(>1.2 m/s)
CW trace
Soft & parabolic
Dense & triangular
LV and LA
Normal size LV
Enlarged LV & LA
if chronic MR
if no other cause
Report as moderate if signs of regurgitation are greater than mild but there are no features of
severe regurgitation.
426
CHAPTER 6 Transoesophageal anatomy and pathology
Mitral valve prolapse
The clear images of valve leaflets allow identification of the morphology
of mitral valve prolapse. Description of mitral valve prolapse is a common
indication for TOE because of its clinical importance to determine whether a
valve can be repaired or will need to be replaced. The commonest prolapse
is of the P2 segment of the posterior leaflet. This is amenable to a standard
repair procedure.
Assessment of prolapse
Start by studying the regurgitation. Comment on appearance and
severity. Take particular note of the direction of the jet as a guide
to the predominant leaflet prolapse (Fig. 6.6). Anteriorly-directed
suggests posterior leaflet prolapse and vice versa. Also comment on
changes in left atrial and ventricular size and function.
Then use the ‘screenwiper’ principle to scan through the mitral valve
at 0°, 135°, 110°, 80° (Fig. 6.7). Ensure each segment has been studied
(Fig. 6.6). Comment on which segments prolapse. If the tips of the
segment reflect back into the left atrium then report this as ‘flail’
(important when planning the operation).
Remember that both leaflets, or more than one segment, may be
prolapsing. Report all the abnormalities.
A transgastric 0° short axis view can be used to confirm the segment
prolapse and the long axis 90° view should be used to look at the
subvalvular apparatus to identify chordae or papillary muscle rupture.
MITRAL VALVE PROLAPSE
427
LONG AXIS VIEW
0 140 180
0 135 180
LA
LA
Aorta
LV
LV
Anteriorly-directed jet
Posteriorly-directed jet
Fig. 6.6 Examples of mitral valve prolapse in 135° long axis views. Left figure shows
an anteriorly-directed jet due to posterior leaflet prolapse and the right figure a
posteriorly-directed jet.
70-90º
135º
Fig. 6.7 The short axis figure demonstrates which scallops are seen in the three key
views. The 4-chamber 0° and long axis 135° views are particularly good for studying
the central scallops (A2 and P2). The 2-chamber view with sector variation between
70-90° can be very useful for looking at the side scallops (A1/P1, A3/P3).
428
CHAPTER 6 Transoesophageal anatomy and pathology
3D assessment of prolapse
The use of 3D echocardiography has lead to improvements in the
understanding of normal MV anatomy and the cause for mitral valvular
pathology.
Set up a 3D volume from the oesophageal position. Ensure from the
biplane view that it includes all the mitral valve and in particular the
area you suspect is prolapsing.
Once the volume position and image quality is optimized, acquire a 3D
dataset. Live 3D or 3D zoom image mode acquisition is ideally suited
to imaging of the mitral valve as the image volume usually is sufficient
for good coverage of the valve and there is adequate spatial and
temporal resolution without the limitation of stitching artefacts seen
with full volume acquisition. However, you may want to acquire a full
volume as well for later post-processing.
Rotate, crop, and set gain settings to focus on the mitral valve.
View the valve from the left atrium and assess valvular morphology in
detail. Identify individual scallops (remember A1 and P1 lie near the
left atrial appendage, which should be visible as a round opening in the
left atrial wall) (Figs. 6.8, 6.11).
Confirm your impression from the 2D images of the extent of
prolapse (number of scallops, width of prolapsing scallop) and confirm
the cause of the prolapse e.g. ruptured chordae.
In particular, use the global 3D view to resolve any uncertainties about
the number of affected scallops and position of pathology, as well as
ensuring there are no other areas of pathology on the mitral valve that
were missed on the 2D sequential views.
3D colour flow mapping may be useful to confirm the position of small
areas of prolapse (Fig. 6.9).
The images can then be post-processed to create a model of the
mitral valve to aid surgery.
MITRAL VALVE PROLAPSE
429
Fig. 6.8 Live 3D acquisition of mitral valve with P1 prolapse (above) and P2
prolapse (below). The image has been cropped and rotated to be seen from the
left atrium. AV aortic valve, the anterior (A) mitral valve scallops and posterior (P)
mitral valve leaflet scallops are seen. See W Video 6.2, W Video 6.3, W Video 6.4.
Mitral regurgitation
colour Doppler
Mitral Valve Leaflet
Prolapse
Fig. 6.9 3D colour Doppler acquisition of mitral regurgitation due to mitral valve
leaflet prolapse. See W Video 6.5.
430
CHAPTER 6 Transoesophageal anatomy and pathology
Post-processing of 3D datasets to create mitral valve
model
2D echocardiography only allows the mitral valve annulus to be
measured in 2 perpendicular planes. There may be difficulties in
choosing the appropriate sites for annulus measurement due to poor
spatial resolution.
The advent of complex post-processing software such as TomTec
and Phillips mitral valve quantification have allowed extraction of
modelling data from 3D volumes (Fig. 6.10).
A series of 2D sections are obtained from the 3D data and the
operator defines the annulus and commissures and traces the
leaflets. The post processing software then generates a valve model.
Different parameters of the mitral valve can then be quantified
according to a number of presets.
These advances have improved the understanding of the complex geom-
etry of the mitral annulus and has added to the surgical decision-making
process.
MITRAL VALVE PROLAPSE
431
Fig. 6.10 Reconstructed 3D image of mitral valve prolapse. The areas of maximal
prolapse are shown in red. A = anterior; P = posterior; PM = posteromedial;
AL = anterolateral; Ao = aorta.
Fig. 6.11 Live 3D view showing left atrial appendage (LAA) and surgical view of
mitral valve from left atrium.
432
CHAPTER 6 Transoesophageal anatomy and pathology
Mitral stenosis
TOE is not routinely used to assess mitral stenosis but stenosis should be
commented upon and graded if seen during a study. Assessment may be
needed if there are poor transthoracic windows or if the valve is being
assessed for percutaneous intervention with balloon valvotomy (b p.444).
TOE is also used intraoperatively during percutaneous interventions on
the mitral valve.
Appearance
Remember to comment on mobility, calcification, and chordae. Comment
on associated valvular lesions, left atrium, and right heart.
Grading severity
Grade severity on planimetered area (b p.434) supported by pressure
half time and pressure gradient, see Table 6.2.
Pressure half-time and pressure gradient:
In any oesophageal view with good alignment through the valve align
the CW Doppler through the mitral valve orifice.
For pressure half-time, measure the slope of the E-wave diastolic
flow on the spectral trace (Fig. 6.12). Trace the Doppler waveform to
obtain mean pressure gradient. Remember:
Table 6.2 Parameters to assess mitral stenosis
Mild
Moderate
Severe
MV area (cm2)
>1.5
1.0-1.5
<1.0
MV pressure half-time (ms)
<150
150-220
>220
Mean pressure gradient (mmHg)
<5
Variable
>10
TR velocity (m/s)
<2.7
Variable
>3
MITRAL STENOSIS
433
CW across MV for pressure
half time
Fig. 6.12 Pressure half-time measured in a long axis view.
PMVL
AMVL
AV
Fig. 6.13 3D live image of mitral valve in a patient with mitral stenosis. Image
captured at end-diastole highlighting the small central mitral valve orifice.
PMVL = posterior mitral valve leaflet; AMVL = anterior mitral valve leaflet;
AV = aortic valve. See W Video 6.6.
434
CHAPTER 6 Transoesophageal anatomy and pathology
Mitral valve area = 220/pressure half-time
Planimetry
A transgastric 0° view provides a short axis ‘fish mouth’ view of the
mitral valve. The probe may need to be withdrawn and advanced
slightly to optimize the image and ensure the leaflet tips are being
imaged. Identify the maximum opening in diastole and trace along the
inner edge of the leaflets. Report the surface area of the orifice.
3D planimetry
3D TOE can aid in mitral stenosis assessment as planimetry of the
mitral valve orifice can be performed on a 3D acquisition whereby
the true leaflet tip orifice can be selected within a multiplanar
reconstruction (Fig. 6.13).
Set up a 3D volume from the oesophageal position ensuring that all of
the mitral valve is seen in the biplane view. Minor adjustments may be
needed to find the optimal view especially in the presence of drop out
shadowing which can be seen in calcific mitral stenosis (Fig. 6.14).
When happy with the probe position, acquire the 3D image.
Rotate, crop, and set gain settings to focus on the mitral valve and
view the valve from the left atrium.
The dataset can be exported for post-processing. The mitral valve will be
displayed in 2 orthogonal views. The cropping plane can then be adjusted
to cut through the narrowest end-diastolic MV orifice (Fig. 6.15).
MITRAL STENOSIS
435
0
135
180
LA
Aorta
LV
Bright, calcified,
elbow-shaped
valve leaflets
Planimetered valve area in
transgastric view
Fig. 6.14 Examples of mitral stenosis in 4-chamber and transgastric views.
Note planimetered surface area in short axis view.
Fig. 6.15 Calculation of mitral valve area by QLAB 7.1 (Phillips). Two orthogonal
views of the mitral valve (top left quadrant and top right quadrant) following 3D
zoom mode live acquisition (bottom right quadrant). Following alignment of the
mitral valve orifice, the valve area can be traced (bottom left quadrant).
436
CHAPTER 6 Transoesophageal anatomy and pathology
Mitral valve preoperative assessment
Transoesophageal echocardiographic assessment of the mitral valve is
essential before surgery. The key surgical decision in the patient with mitral
regurgitation is whether the valve is to be repaired or replaced. With
mitral stenosis the request for imaging is usually to assess suitability for
valvotomy or to determine severity of stenosis and effects on the left
ventricle and other valves.
What the surgeon wants to know
Mitral regurgitation
The main objectives prior to mitral valve surgery are to define:
Underlying anatomic details of the mitral regurgitation. Include a full
assessment (b p.420) and ensure comments on:
• Severity.
• Central or eccentric.
• If prolapse, which scallops are affected and whether flail elements.
Size of annuloplasty ring likely to be needed if repaired or size of valve
if replaced. Report:
• Mitral annulus size in 2 orthogonal planes.
• Leaflet length.
Presence and location of annulus calcification. There is a risk of
annulus leak if in an area of repair.
If regurgitation secondary to endocarditis, comment on complications
of the endocarditis: fistulae from left ventricle to aorta, right ventricle
or left atrium; mitral valve annulus abscess; other valve involvement in
endocarditis (typically aortic or tricuspid valve).
3D mitral valve preoperative assessment
3D TOE is eminently suited to mitral valve assessment (Fig. 6.16). Both
a 3D zoom and full volume acquisition can be used to precisely quantify
leaflet anatomy, annulus geometry, and region of prolapse, which can aid
surgical planning.
3D image acquisition of the mitral valve has the applications:
Allows the visualization of the mitral valve from both the atrial and
ventricular aspect providing views familiar to the surgeon.
In the assessment of certain types of mitral valve prolapse 3D TOE
accurately identifies involved segments.
In mitral stenosis 3D TOE can provide detailed assessment of the
leaflets and their commissures as well as subvalvular apparatus.
MITRAL VALVE PREOPERATIVE ASSESSMENT
437
Paravalvular Leak, 2 Jets
2 Paravalvular Leaks
Left Atrial Appendage
Two Occluder Devices
Fig. 6.16 3D TOE prosthetic valve assessment. See W Video 6.7, W Video 6.8,
W Video 6.9. Surgical view showing bioprosthesis in mitral position with
paravalvular leak (top and middle). Same value with 2 Amplatz occluder devices
(bottom) to close leaks.
438
CHAPTER 6 Transoesophageal anatomy and pathology
Mitral stenosis
Underlying anatomical details of the mitral stenosis. Include a full
assessment (b p.432) and ensure comments on:
• Severity.
• Pathological basis: rheumatic or degenerative.
Assess suitability for valvuloplasty (b p.444).
Size of replacement valve likely to be needed. Report:
• Mitral annulus size (in both valve axes if possible).
For all mitral surgery
Left atrial size. A dilated left atrium (>50 mm) provides good surgical
exposure of mitral valve directly through a left atrial incision. If the left
atrium is normal size or only mildly increased the surgeon may need
an alternative surgical approach (e.g. transatrial septum).
Assessment of cardiac function. Significant left ventricle dysfunction
caused by mitral regurgitation encourages mitral valve repair rather
than replacement.
Reports of other valve disease, particularly the aortic valve.
Preoperative versus intraoperative assessment
The severity of mitral regurgitation may be underestimated during intra-
operative TOE. Preload, afterload, and inotropic state of the heart are
reduced during general anaesthesia. Therefore, all patients undergoing
valve surgery should have transoesophageal imaging prior to surgery.
Assessment of the valve intraoperatively should take into account the
preoperative information and changes in conditions due to the anaesthesia.
Volume loading and inotropic agents can sometimes be used to mimic
haemodynamics comparable to those without anaesthesia.
MITRAL VALVE PREOPERATIVE ASSESSMENT
439
Factors that make mitral valve repair unfavourable
Annular calcification. It is most common in the posterior annulus and
can extend into the myocardium and leaflets.
Marked mitral ring dilatation (>5cm in the 2-chamber view).
Extensive leaflet disease (3 or greater prolapsed or flail segments seen).
Risk of systolic anterior motion of mitral valve post-repair
If repair is planned then it is important to assess, before surgery, the
risk of postoperative systolic anterior motion of the anterior leaflet and
consequent obstruction of the LVOT. This causes obstruction in 715% of
patients after mitral valve repair. The following findings in the preopera-
tive examination are associated with an increased risk of postoperative
systolic anterior motion of the anterior leaflet and should be reported
if present:
Excess mitral leaflet tissue. Particularly elongated anterior leaflet
causing an increase in slack leaflet available to obstruct the outflow
tract.
Anteriorly-displaced papillary muscles.
Non-dilated left ventricle.
Narrow mitral-aortic angle.
More anterior position of the leaflet coaptation point due to
relatively large posterior mitral leaflet: Anterior to posterior leaflet
ratio <1.
Distance from the coaptation point to the septum <2.5cm.
In high-risk cases the surgical approach may be modified. In patients with
an excessive posterior leaflet a sliding leaflet plasty can be carried out after
resection of the P2 segment. Another option is the use of a rigid ring to
increase the anterior-posterior diameter—in particular if the coaptation
line is displaced anteriorly after resection of excessive tissue.
440
CHAPTER 6 Transoesophageal anatomy and pathology
is a device which allows percutaneous edge-to-edge repair
for mitral regurgitation (Fig. 6.17). There are several anatomical features
which are assessed echocardiographically when determining the suitability
Contraindications
Mitral valve orifice <4cm2 with secondary mitral regurgitation.
Endocarditis.
Cardiac mass/thrombus.
Active rheumatic valve disease.
Mitral stenosis.
Previous mitral valve replacement.
Unsuitable leaflet anatomy (calcification and/or cleft affecting leaflets in
the potential deployment zone).
The presence of a flail leaflet when: the width of the flail segment
t15mm or the flail gap is t10mm; bileaflet flail.
Anatomic suitability
A TOE is carried out pre device deployment to carefully analyse the
anatomy of the interatrial septum and the mitral valve leaflets, annulus,
chordae, and subvalvular apparatus (Fig. 6.18).
The presence of an atrial septal defect/patent foramen ovale and the
thickness of the atrial septum should be noted. These will determine the
ease with which the transseptal puncture is performed.
All standard mitral valve views should be obtained with and without
colour Doppler in order to identify the area of maximal MR as well as
the anatomy of each leaflet at that position.
is ideally at the junction of A2:P2.
Adverse factors which may hinder device deployment should be noted:
leaflet thickness; leaflet calcification; chordal fusion/calcification or
calcification of the subvalvular apparatus below the maximal area of MR.
Degenerative MR (see Fig. 6.18)
Flail gap: should be taken in the 135* long axis, 0* 4-chamber or 90*
2-chamber view where the flail gap is largest. (Needs to be <10mm.)
Flail width: should be taken in transgastric short axis where the flail
width is largest. (Needs to be <15mm.)
Functional MR
Coaption depth: should be taken in 0* 4-chamber view where
coaption depth is greatest. (Needs to be <11mm.)
Coaption length: should be taken in 0* 4-chamber view where length
is shortest. (Needs to be >2mm.)
MITRACLIP
®
441
a. transoesophageal echocar-
diogram with the clip across the mitral valve leaflets (LVOT view) and the leaflets
inserted into the V between the arms of the clip (ventricular aspect of the valve, A)
and the grippers (atrial aspect of the valve, G). Both leaflet tips should be clearly
seen in this position (*) prior to closure of the clip and grasping the leaflet.
DEGENERATIVE MR
FLAIL GAP
FLAIL WIDTH
FUNCTIONAL MR
COAPTION DEPTH
COAPTION LENGTH
suitability.
442
CHAPTER 6 Transoesophageal anatomy and pathology
Procedure
Transseptal puncture
The bicaval view, short axis view and 4-chamber view of the atrial
septum should all be obtained to demonstrate the anatomy. The
trans-septal catheter tip can be watched moving into the fossa ovalis
causing tenting (Fig. 6.19).
Generally the puncture should be 3-4cm from the mitral valve
although this should be modified according to the site and mechanism
of the pathology.
Following successful puncture, views are obtained to help the safe
navigation of the catheter and then guidewire into the left upper
pulmonary vein (avoiding the left atrial appendage).
Introduction of guide catheter and MitraClip®
Using a modified short axis view the guide catheter/dilator are
introduced. The guide catheter has echogenic markers on it helping to
identify when it has crossed the interatrial septum.
inserted
until visible in the mid LA.
is navigated to a position where it straddles the MV.
above the MV.
Crossing the mitral valve
Using a combination of the LVOT and bicommissural views the
clip is positioned directly over the target area of the MV. Biplane
echocardiography can be useful to confirm this position in 2
orthogonal views.
Correct position is confirmed using colour Doppler and the clip
should ideally bisect the regurgitant jet equally.
The clip is advanced into the LV and the superior aspect of the gripper
arms should be clearly identified below the MV leaflets.
Live 3D TOE images can also help confirm the positioning and that the
clip is perpendicular to the closure line of the valves (Fig. 6.20).
MitraClip® insertion and grasping
Once the positioning of the clip has been confirmed it is retracted
towards the MV leaflets. Echocardiography is pivotal to ensure that
there is no distortion to the valvar/subvalvar apparatus and that
perpendicularity is maintained.
The moment of grasp should be recorded to ensure that a suitable
amount of leaflet is held within each arm of the clip.
Confirmation of leaflet grasping and device deployment
Adequate grasp is confirmed by visualizing the anterior and posterior
mitral valve leaflets from the LVOT and 4-chamber views.
It is important to note the leaflet insertion point and leaflet movement
is adequate.
When happy with adequate leaflet grasping the clip arms are closed to
approximately 60° and final images are performed to demonstrate the
accurate placement of the clip, the reduction in the degree of MR and
the absence of mitral stenosis.
MITRACLIP®
443
The MitraClip® is then fully deployed and the valve reassessed to
determine the haemodynamic success of the procedure, any potential
requirement for a second clip, and the size of the residual defect from
the transeptal puncture.
Fig. 6.19 Positioning of catheter for transseptal puncture. Tenting (T) of the
inter-atrial septum at the fossa ovalis caused by the transseptal catheter is clearly
seen, with the two views allowing superoinferior adjustment (a, bicaval) and
antero-posterior adjustment (b, modified short axis aortic). LA = left atrium,
RA = right atrium, T = tenting.
Fig. 6.20 3D TOE of the mitral valve visualized from the left atrial aspect during
above the valve leaflets to ensure perpendicularity
with the closure line of the valve.
444
CHAPTER 6 Transoesophageal anatomy and pathology
Mitral valve balloon valvotomy
TOE is performed routinely to assess suitability for percutaneous valvotomy
for treatment of mitral stenosis. Contraindications to intervention that should
be reported include:
Left atrial appendage thrombus.
Moderate mitral regurgitation or greater.
Severe aortic or tricuspid valvular disease.
Echocardiographic scoring of mitral valve morphology can be preformed
to predict successful outcome. The commonest is the Wilkin’s scoring
based on 4 features each scored 1-4, giving a minimum score of 4 and
maximum of 16. The lower the score the more suitable the valve for
balloon valvotomy. A score of >8 suggests poor long-term outcome with
percutaneous intervention.
Leaflet mobility
1 Highly mobile with restriction of leaflet tips only.
2 Mid portion and base of leaflets have reduced mobility.
3 Valve leaflets move forward in diastole mainly at the base.
4 No or minimal forward movement of the leaflets in diastole.
Valvar thickening
1 Leaflets near normal (4-5mm).
2 Mid leaflet thickening, pronounced thickening of the margins.
3 Thickening extends through entire leaflet (5-8mm).
4 Pronounced thickening of all leaflet tissue (8-10mm).
Subvalvar thickening
1 Minimal thickening of chordal structure just below the valve.
2 Tickening of chordae extending up to 1/3 of chordal length.
3 Thickening extending to the distal 1/3 of chordae.
4 Extensive thickening and shortening of all chorda extending down to
the papillary muscles.
Valve calcification
1 A single area of increased echo brightness.
2 Scattered areas of brightness confined to the leaflet margins.
3 Brightness extending into the mid portion of the leaflets.
4 Extensive brightness through most of the leaflet tissue.
MITRAL VALVE BALLOON VALVOTOMY
445
3D TOE during balloon valvotomy?
Balloon mitral valvuloplasty is usually performed with echocardiography
guidance—3D TOE is ideal for monitoring transseptal puncture, balloon
placement, inflation, and effects on the valve.
Doppler indices are inaccurate post-valvuloplasty and 3D planimetry
allows a more accurate assessment of procedural success (with the best
correlation with invasive monitoring) or immediate complications.
446
CHAPTER 6 Transoesophageal anatomy and pathology
Mitral valve repair
Postoperative assessment
Assessment of mitral valve repair should be based on:
Residual regurgitation
Despite competent valve at surgical inspection and leak test by the sur-
geon there may still be significant valvular regurgitation in the beating,
volume-loaded heart. This may be due to ischaemic wall dysfunction or
systolic anterior motion of the mitral leaflet. Use standard 2D and colour
images to assess severity, location, and likely underlying mechanism.
3D image can provide much more precise location and mechanisms of
residual regurgitation.
Moderate to severe residual regurgitation usually requires surgical
revision or conversion to valve replacement.
Para-annulus leak can occur after repair if there was a large posterior
leaflet resection. Even mild degrees of para-annulus leak usually
require further surgical revision to avoid postoperative haemolysis.
New stenosis
After repair of the mitral valve the repaired leaflet usually appears thickened,
shortened, and almost immobile. Use CW Doppler to assess trans-mitral pres-
sure gradient and pressure half-time. However, pressure half-time method
may be inaccurate immediately postoperative (the method assumes that
the left atrial and ventricular compliance do not affect the pressure decline,
but up to 72 hours after surgery compliance is altered). Interpret orifice
area taking into account heart rate and stroke volume. Stenosis is often
due to under-sized annuloplasty.
Systolic anterior leaflet motion/left ventricle outflow obstruction
Systolic anterior leaflet motion/left ventricle outflow obstruction can be
due to mitral valve repair with or without concomitant basal septal hyper-
trophy, but also can be caused by haemodynamic factors. Inotropic agents,
vasodilators, and low volume states provoke systolic anterior leaflet motion/
left ventricle outflow obstruction in susceptible patients and have to be
discontinued before considering re-intervention. In some patients beta-
blockers may be useful. To demonstrate systolic anterior motion of the
mitral leaflet use the aortic long axis 135° view. 2D and M-mode images
can demonstrate abnormal leaflet movement. However, Doppler measure-
ments have to be performed in gastric views, which may be difficult in
theatre and the peak gradient of outflow tract should be differentiated
from the mitral regurgitation jet.
Consider whether effects can be reduced by changes in cardiac physiology
(improved left ventricle cavity size and diastolic filling): increase left ventri-
cle filling, stop/reduce positive inotropic drugs, commence beta-blockade,
pace the ventricle. Monitor effectiveness of medical treatments with repeat
echocardiography. If medical management fails surgical revision of repair or
valve replacement may be indicated.
MITRAL VALVE REPAIR
447
Left ventricular function
Hypo- or akinesis of the lateral and inferoposterior wall can be due
to circumflex artery injury if sutures are too deep into the mitral ring.
New impaired posterior wall contraction is most likely due to air embo-
lism into the right coronary which is usually reversible with or without
additional cardiopulmonary bypass support.
Aortic valve
Aortic valve competence can be impaired by deep suture placement in
the mitral anterior annulus or significant reduction of mitral annulus in
patients who has minimal aortic cusp coaptation reserve before the mitral
valve repair.
De-airing
During cardiopulmonary bypass air can be trapped in pulmonary veins,
the left ventricle apex, or left atrial appendage. This air is mobilized by the
surgeon before coming off bypass and enters the left ventricle and aorta.
As it is expelled it resembles the typical pattern of agitated saline (as might
happen if there was a massive right-to-left shunt during contrast echocar-
diography). Remaining air can be scanned for after de-airing.
448
CHAPTER 6 Transoesophageal anatomy and pathology
Mitral valve replacement
Post-operative assessment
Mechanical valve dysfunction is more likely with: over-sized prosthesis;
small left ventricle cavity; excessive subvalvular apparatus, double valve
replacement; anatomical mechanical prosthesis orientation. Bioprostheses
dysfunction may be due to: distorted annulus due to over sizing or suture
looping of cusps. The key features to assess immediately after replacement
are:
Valve prosthesis regurgitation
Use colour flow to look for normal prosthesis wash jets (closing jets) and
differentiate from paravalvular regurgitation. If present consider:
Severity: for biological valves mild central jet is normal. Small
degrees of paraprosthetic regurgitation (mechanical and biological
valves) immediately after surgery often improve with protamine
administration. If moderate to severe central regurgitation and
restricted prosthetic cusp opening/closing, surgical intervention is
normally indicated. 3D image is highly recommended for identifying
the location and mechanism of regurgitation.
Valve prosthesis opening
Use 2D and 3D imaging to look for symmetrical, synchronized opening
and closing of prosthesis leaflets (Figs. 6.21 and 6.22). Look for functional
stenosis (measure prosthesis mean gradient and effective orifice area).
If abnormal opening consider:
Relation between prosthetic valve and subvalvular apparatus: with
mechanical bileaflet prostheses, opening and closing may be reduced
or restricted because the leaflets impinge on the subvalvular apparatus
(posterior leaflet may be preserved in valve replacement).
Left ventricle filling and contraction: If not adequately filled or poorly
contracting, re-evaulate when filling status and contraction are brought
to normal level. If prosthesis still dysfunctional surgical intervention is
advisable.
LVOT obstruction
Assess valve movement with 2D and 3D imaging and colour flow map-
ping in the outflow tract. PW Doppler in the outflow tract can be used
in transgastric views. Obstruction may be due to septal hypertrophy
combined with a high profile prosthesis intruding into the outflow tract.
MITRAL VALVE REPLACEMENT
449
BILEAFLET VALVE (LONG AXIS VIEW)—MITRAL POSITION
Shadowing from valve
BILEAFLET VALVE (2 CHAMBER VIEW)—MITRAL POSITION
Fig. 6.21 Examples of mechanical mitral valve prostheses in long axis and
2-chamber views. See W Video 6.10.
450
CHAPTER 6 Transoesophageal anatomy and pathology
Cardiac function
After mitral surgery use 2D imaging to re-assess global and regional left
and right ventricular function. With acute correction of regurgitation, left
ventricular ejection fraction can be expected to drop (e.g. from 60-70% to
40%) due to sudden reduction in left ventricular stroke volume, without pro-
portional reduction in left ventricular cavity size, combined with a variable
degree of underlying impaired contractile function. Mitral valve replace-
ment for mitral regurgitation has more adverse physiological effects on left
ventricular function than repair.
If left ventricular filling is adequate but cavity is dilated and global
ejection fraction is <30% consider inotropic support and monitor
response with echocardiography until stable haemodynamics.
If there is a new lateral or inferoposterior wall motion abnormality,
consider whether the circumflex artery could have been damaged.
Large posterior wall hypokinesis can be caused by air embolism,
additional support may be required.
Always consider other general causes for acute severe deterioration in
global cardiac dysfunction after cardiopulmonary bypass.
MITRAL VALVE REPLACEMENT
451
Bioprosthetic MVR
Viewed from LA (open)
Bioprosthetic MVR
Viewed from LV
Three struts visible
Fig. 6.22 3D prosthetic valve views. See W Video 6.11 and W Video 6.12.
452
CHAPTER 6 Transoesophageal anatomy and pathology
Aortic valve
Very good views of the aortic valve can be obtained with TOE because
there is only the left atrium, which is a clear fluid-filled window, between
the valve and the probe. Aortic valve anatomy is described on b p.132
but essentially comprises of 3 cusps and associated sinuses of Valsalva,
named after the coronary arteries that derive from them (right, left, non-
coronary).
TOE is indicated to study the aortic valve when transthoracic images are
of insufficient quality or better spatial resolution is needed to provide
complete assessment of valve pathology, for example vegetations, aortic
root abscesses, aortic valve area and prosthetic valve function.
Normal findings
Views
The best views to see the aortic valve are the 50° short axis view
and 135° long axis view (Fig. 6.23). These can be supported by the
5-chamber 0° left ventricular outflow view.
Additional information is obtained from transgastric views which
provide better alignment for Doppler. The aortic valve can be studied
with a transgastric long axis 110° view and the deep transgastric 0°
view.
Aortic valve
5-chamber 0° left ventricular outflow view: this provides a limited first
view of the left ventricular outflow and with colour flow can be used
to judge whether there is any aortic regurgitation.
Short axis 50° view: this is the first clear view and is similar to the
transthoracic parasternal short axis but upside down. A classic
Y-shaped cross-sectional view of the cusps is seen (left on the right,
right on the left and non nearest the probe). To optimize the image
try slight rotation or movement of the probe up and down. Get all
3 cusps in view, of equal size. Withdraw the probe further to bring
the coronary arteries, sinotubular junction, and then ascending aorta
into view. Advance the probe to see the LVOT. Colour flow mapping
allows positioning of aortic regurgitant jets. This view also allows the
stenotic valve area to be measured.
Long axis 135° view: this view is similar to the transthoracic parasternal
long axis. Right and non-coronary cusps are seen (non-coronary
nearest the probe and right nearest the right ventricle). Use the view
to measure aortic root, sinotubular junction, and valve annulus.
Transgastric 110° long axis view: this view allows the outflow tract to
be aligned with Doppler. The aortic cusps are sometimes seen in the
far field but it can be difficult to get a clear image. Colour flow can
help to pick out the outflow tract.
Deep transgastric view: this is an alternative to align the Doppler with
the outflow tract and valve. It provides an equivalent view to the
transthoracic apical 5-chamber but is difficult to obtain. If there are
good transthoracic windows it will not add more information.
AORTIC VALVE
453
Short axis view—50º
Long axis view—135º
AORTA
PULMONARY
LA
ARTERY
LA
LCC
NCC
RA
LV
RCC
NCC
RV
RCC
Transgastric view—110º
Deep transgastric view — 0º
LV
LV
AORTA
Fig. 6.23 Key views to assess the aortic valve (NCC = non-coronary cusp;
RCC = right coronary cusp; LCC = left coronary cusp).
454
CHAPTER 6 Transoesophageal anatomy and pathology
Aortic stenosis
Evaluation of aortic stenosis with TOE follows the same routine as for
transthoracic but with more emphasis on 2D imaging to assess valve
pathology. The criteria to determine severity (Table 6.3) are the same as
transthoracic echocardiography (Table 3.3).
Assessment
Bear in mind the potential causes of aortic stenosis:
In all the views look for evidence of calcification.
In the 50° short axis view look at number of cusps.
Look at associated structures—aortic root dilatation etc.
Grading severity
2D-imaging
In 50° short axis view and 135° long axis view look at valve motion. If the
valve appears to open normally aortic stenosis is unlikely to be present.
In the 135° long axis view, if the cusps separate by >12mm aortic stenosis
is mild or better.
Planimetered valve orifice
In 135° long axis view obtain a clear image of all cusp edges.
Move the probe back and forth until the cusp tips in systole are seen
in plane.
Zoom onto the valve and store a loop. Scroll through the loop and try
and identify the largest opening during systole.
Trace along the inner edge of the cusps.
Report the surface area of the orifice.
Problems with planimetered measures:
Shadowing from heavy calcification can make it difficult to get an accurate
area or it may be difficult to the get the open tips in systole in plane with
the probe.
Doppler assessment
Both the velocity across the valve and continuity equation require aortic
valve vti (or peak flow), LVOT vti (or peak flow), and LVOT dimension.
It is often easier and more accurate to do this with TTE but can also be
done during a transoesophageal examination.
Use a transgastric 110° long axis or deep transgastric view to line up
the CW Doppler with the aortic valve and aorta (Fig. 6.24).
Acquire a spectral recording and trace the aortic vti.
In the same view acquire a PW Doppler in the LVOT and trace the vti.
Measure the LVOT diameter in the 135° long axis view.
Report the peak velocity or use the standard continuity equation:
valve area = LVOT area × LVOT vti/aortic vti
AORTIC STENOSIS
455
Table 6.3 Parameters to assess aortic stenosis
Mild
Moderate
Severe
Peak velocity (m/s)
2.0-2.9
3.0-4.0
>4.0
Peak gradient (mmHg)
<35
35-65
>65
Mean gradient (mmHg)
<20
20-40
>40
Valve area (cm2)
>1.5
1.0-1.5
<1.0
LV
Aorta
Peak velocity across aortic valve
in transgastric 110º view
+
0
57
180
LA
Bicuspid valve—with planimetered area
Fig. 6.24 Measurement of aortic stenosis severity from Doppler in a transgastric
110° view (top) and planimetered area in a short axis 50° view (bottom).
456
CHAPTER 6 Transoesophageal anatomy and pathology
Aortic regurgitation
In evaluation of aortic regurgitation with TOE there is more emphasis
on 2D imaging to assess cause. Doppler criteria to determine severity
(Table 6.4) are as for transthoracic (Table 3.4).
Assessment
Bear in mind potential causes of regurgitation and study both valve and
aortic root (b p.310).
In all the views look for evidence of abnormal valve motion.
In the 50° short axis view look at the valve and position of
regurgitation. Study the sinuses and aortic root.
In the 135° long axis view look at the aortic root dimension and check
for dissection.
Comment on the location and direction of jet. 3D imaging can be of
use for identification of the origin of regurgitation jets around the
aortic valve. For this 3D colour flow mapping is required.
Grading severity
Colour flow Doppler
Aortic regurgitation can first be identified in the 5-chamber 0° view
although this may not give you an idea of severity.
The 50° short axis view with colour flow provides an impression of
where the regurgitation is and the area of the jet relative to the LVOT.
The 135° long axis view with colour flow provides the most
information to assess severity. This view can be used to assess vena
contracta and jet width relative to LVOT (Fig. 6.25).
3D colour flow mapping
To collect a 3D colour flow dataset (Fig. 6.26) use the oesophageal
window with the 3D volume optimized to include the aortic valve.
It is often easiest to start with your optimized 2D long axis 135° view
or 50° short axis view of the aortic valve before switching to the
biplane view to set up the 3D volume.
Remember that the colour flow mapping full volume acquisitions tend
to be over more heartbeats and therefore are more prone to stitching
artefacts.
Large jets are often more complex and therefore more difficult to
characterize on 3D. The easiest jets to localize are thin, long jets or
multiple small jets. 3D can be very useful to identify the presence of
multiple jets in a single global view that may have been missed, or
thought to be the same jet, on sequential 2D views.
AORTIC REGURGITATION
457
0
135 180
Severe AR with jet filling
ventricular outflow tract
Fig. 6.25 Broad vena contracta filling outflow tract (bottom) consistent with severe
regurgitation. See W Video 6.13.
Fig. 6.26 3D colour Doppler of paraprosthetic aortic regurgitation.
See W Video 6.14.
458
CHAPTER 6 Transoesophageal anatomy and pathology
Aortic flow reversal
In the 90° long axis aortic view PW Doppler with some correction for
angle will allow assessment of aortic flow in diastole. Some diastolic
flow reversal is normal. Holodiastolic flow reversal is associated with
severe aortic regurgitation (Fig. 6.27).
Continuous wave Doppler
For CW assessment of aortic regurgitation a transgastric 110° long axis
view or deep transgastric view is required to align the Doppler signal.
Look at density of signal, deceleration slope and peak velocity.
However, these are less accurate with TOE because of technical
limitations in alignment.
Table 6.4 Parameters to assess severity of aortic regurgitation
Specific signs of severity
Mild
Severe
Vena contracta
<0.3cm
>0.6cm
Jet (Nyquist 50-60cm/s)
central, <25%
central, >65% of LVOT
of LVOT
Descending aorta
No or brief early
Holodiastolic flow reversal
diastolic flow reversal
Supportive signs of severity
Mild
Severe
Pressure half-time
>500ms
<200ms
Left ventricle
Normal LV
Moderate or greater (only
for chronic lesions) LV
enlargement (no other cause)
Report as moderate if signs of regurgitation are greater than mild but there are no features of
severe regurgitation.
AORTIC REGURGITATION
459
Diastolic flow reversal in aorta
Fig. 6.27 Abnormal aortic flow reversal consistent with severe regurgitation.
460
CHAPTER 6 Transoesophageal anatomy and pathology
Aortic valve preoperative assessment
Thorough preoperative assessment allows careful planning of surgery
on the aortic valve. Aortic valve replacement is the most frequently per-
formed valve surgery with an increasingly elderly population. Preoperative
information should include data on the valve, the left ventricle, and the
aorta.
What the surgeon wants to know
General
Before all types of aortic surgery the basic information needed is:
Aortic valve cusp morphology and function.
Aortic root size (look for abscesses if endocarditis present).
Aortic annulus size (to judge prostheses size if replacement planned).
Evidence of sinotubular junction dilatation (if >25% bigger than aortic
annulus then aortic homograft or stentless bioprosthesis may be
contraindicated).
Ascending aortic dimension and geometry (ascending aorta dilatation
>45mm may require replacement).
Descending aorta size and flow velocity.
Anatomy and dynamics of LVOT (in surgery for stenosis check for a
subaortic stenosis to account for gradient).
Coronary ostia size, location, and flow velocity (check for ostial
stenoses and coronary sinus calcification that might complicate
coronary reimplantation in aortic root replacement).
Left ventricle cavity size, function, and degree of hypertrophy.
Bicuspid valves
In young patient with bicuspid aortic valve pay particular attention to:
Concomitant abnormalities in LVOT.
Coronary anatomy.
Aortic root, arch, and descending aortic structure.
Aortic remodelling
In aortic root remodelling check native valve can be preserved. Look at:
Aortic cusp morphology and mobility.
Aortic sinus geometry.
3D aortic valve preoperative assessment
Assessment for suitability and guiding transcatheter aortic valve
implantation, see b p.464.
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462
CHAPTER 6 Transoesophageal anatomy and pathology
Aortic valve replacement
Postoperative assessment
Assessment of an aortic valve replacement should be based on:
Valve prosthesis opening
With 2D, 3D imaging (and if appropriate M-mode) look at valve opening
and closing (Fig. 6.28). Assess velocity across the aortic valve with CW
Doppler from a transgastric view. Expect a mean gradient of <15mmHg.
Valve prosthesis regurgitation
Check for regurgitation with colour flow. There may be small closing jets
or some mild paraprosthetic regurgitation particularly before protamine
is given. If regurgitation is seen, determine severity and location (trans- or
paraprosthetic). If bioprosthetic valve implanted, consider whether due to
annulus distortion. Paravalvular regurgitation is more likely with a severely
calcified aortic annulus, infected aortic valve or redo aortic valve surgery.
Endocarditis
If surgery was for endocarditis ensure any abscesses or fistulae that were
present have been excluded or closed.
Cardiac function
For all surgery, determine global and regional cardiac function using standard
techniques (b p.480). Expect an ejection fraction of 40-60% if normal
before surgery. If significant impairment consider causes as for mitral valve
surgery (b p.447) and in particular consider whether there has been
damage to coronary artery ostia.
Coronary arteries
Check for proximal coronary obstruction or occlusion. In short axis views
assess proximal coronary lumen size and flow velocity. Acute coronary
obstruction can be due to acute thrombus, emboli, prosthesis mal-position
and/or oversizing, or abnormal coronary anatomy in congenital aortic
valve disease. Depending on the degree and location of coronary ostia
obstruction, it can cause failure to wean off cardiopulmonary bypass at the
outset or delayed onset of cardiac arrest by the time of chest closure.
De-airing
During cardiopulmonary bypass air can be trapped in pulmonary veins,
the left ventricle apex, or left atrial appendage. This air is mobilized by the
surgeon before coming off bypass and enters the left ventricle and aorta.
As it is expelled it resembles the typical pattern of agitated saline (as might
happen if there was a massive right-to-left shunt during contrast echocar-
diography). Remaining air can be scanned for after de-airing.
Other
Monitor for LVOT obstruction and systolic anterior motion of mitral valve
(see b p.446). If there has been septal myoectomy check for a ventricular
septal defect.
AORTIC VALVE REPLACEMENT
463
BALL AND CAGE VALVE—AORTIC POSITION
SINGLE DISC VALVE—AORTIC POSITION
STENTED BIOPROSTHESIS
STENTS
Fig. 6.28 Examples of prosthetic valves in the aortic position. Top figure is a long
axis view of a ball-and-cage valve and the middle figure of a single disc valve. The
bottom figure is a short axis view of a stented bioprosthesis. See W Video 6.15
and W Video 6.16.
464
CHAPTER 6 Transoesophageal anatomy and pathology
TAVI
Assessment of patient suitability for transcatheter aortic valve implantation
(TAVI) requires detailed imaging including echocardiography. A full study
is performed either with TTE or TOE but often both.
Assessment before TAVI
The study needs to include information on:
Aortic valve
The information needed by the operator relates to the severity of aortic
stenosis to confirm that TAVI is required, the anatomy to determine whether
the valve is suitable for percutaneous closure, and the presence of other
pathology that may influence patient outcome. The report should include:
Whether the valve is tricuspid valve or bicuspid (bicuspid valve
currently a contraindication).
The true severity of aortic stenosis: aortic valve area <1cm2 or
<0.6cm2/m2. Accurate planimetry of the valve based on careful 2D or
3D alignment with leaflet tips should be included.
Extent and location of valve calcification: possibility of coronary
obstruction by displaced calcification.
Size and shape of aortic sinuses and sinotubular junction.
Aortic annulus size: measure annulus size in a parasternal long axis
view or from a 3D dataset from hinge point to hinge point of valve
leaflets—crucial for correct device sizing (Fig. 6.29).
Report on the presence of left ventricular septal hypertrophy:
prominent septal bulge may complicate device positioning.
Try and determine location of coronary ostia and height from annulus
(coronary height). Table 6.5: assess risk of coronary obstruction by
device.
General
Assess ventricle and other valves:
Assess left ventricular hypertrophy and function and cavity size:
particularly important for transapical approach.
Assess right ventricular function and estimate pulmonary pressure: risk
of RV deterioration during procedure.
Mitral valve anatomy and function: significant mitral regurgitation is a
relative contraindication.
Aortic calcification: extensive descending aorta atheroma may increase
embolic risk.
Presence of pleural and pericardial effusions: to allow early
identification of any complications.
In patients with significant left ventricular dysfunction and aortic stenosis
a dobutamine stress echo may be helpful in clarifying both the severity of
the aortic stenosis and the degree of left ventricular hibernation.
TAVI
465
Importance of annulus size
)
are suitable for annulus sizes ranging from 18-27mm (Table 6.5). If there
is concern over measurement accuracy then comparison with data from
angiography, computed tomography, and magnetic resonance aortography
may be required to decide on eventual device size.
The degree of valvular calcification and LVOT size are also important
factors in correct device sizing. Undersizing the prosthesis may lead to
paravalvular regurgitation, oversizing may lead to poor stent expansion,
coronary obstruction or root rupture.
Table 6.5 TAVI devices
Device
Annulus
Sinus of Sinotubular Coronary
range
Valsalva junction
height
26mm
20-23mm
t27mm d40mm
t14mm
29mm
24-27mm
t28mm d43mm
t14mm
23mm 18-21.5mm
N/A
N/A
t10mm
21.5-24.5mm N/A
N/A
t11mm
Fig. 6.29 Measurement of aortic annulus size by 2D (left) and 3D (right) TOE.
466
CHAPTER 6 Transoesophageal anatomy and pathology
Assessment during TAVI
Peri-procedural echocardiography, usually with TOE (although both ICE
and TTE have been used), is key to ensuring accurate valve deployment
and excluding any complications (Fig. 6.30).
TAVI procedure steps
Crossing the aortic valve
Assess position of wire across valve—usually in commissure between
non- and right-coronary cusps.
Exclude pericardial effusion due to wire perforation of left ventricle.
Assess degree of aortic regurgitation once wire and catheter across
valve.
Balloon aortic valvuloplasty
Confirm balloon position across aortic valve.
Assess degree of expansion of balloon.
Quantify aortic regurgitation post valvuloplasty.
Assess change in aortic valve motion—sufficient to allow passage of
prosthesis?
Prosthesis positioning and deployment
The exact position of the prosthesis depends on the type used but
both require precise placement to within 1mm to ensure correct
function.
Full expansion of the balloon during deployment should be noted.
Degree and extent of any paravalvular regurgitation post
deployment—rarely a second balloon inflation may be needed.
Assessment of any complications
The echocardiographer must be alert to potential complications and con-
tinuously monitor for:
Decline in left or right ventricular function following rapid pacing or
prosthesis deployment.
Pericardial effusion and tamponade due to ventricular or annulus
perforation.
Prosthetic dysfunction due to stuck leaflets.
Paravalvular regurgitation.
Aortic injury or dissection.
Coronary obstruction.
Thrombus formation on wires and sheaths.
ASSESSMENT DURING TAVI
467
Valvuloplasty balloon
positioned across aortic
valve pre inflation.
Balloon inflated across
aortic valve
Positioning TAVI device pre
deployment
Fig. 6.30 The use of TOE during TAVI. See W Video 6.17, W Video 6.18,
W Video 6.19, and W Video 6.20.
468
CHAPTER 6 Transoesophageal anatomy and pathology
Tricuspid valve
The tricuspid valve is often included in a transoesophageal study but,
unless the indication is a study of endocarditis, is not the primary focus.
Generally the right heart is more difficult to study with TOE because it lies
furthest from the probe.
Normal findings
Views
The best views are: 4-chamber 0°; bicaval 110°; short axis 80° (right
ventricular inflow/outflow); and right ventricle transgastric 90°.
Findings
4-chamber 0° view: the tricuspid valve lies on the left and the probe
may need to be advanced slightly to optimize the image.
Bicaval 110° view: usually used to study the atrial septum, if the probe
is advanced slightly, the tricuspid valve often comes into view in the far
field. This view usually gives good alignment for Doppler studies.
Right ventricle 80° short axis view: the aortic valve appears in cross-
section in the centre of the view with the right ventricle wrapped
around in the far field. This view gives a good image of both tricuspid
and pulmonary valves with tricuspid valve on the left.
Transgastric 90° long axis view: from a standard long axis view of
the left ventricle, clockwise rotation of the probe to the right can
sometimes bring the right ventricle with the tricuspid valve and
subvalvular apparatus clearly into view.
Tricuspid regurgitation and stenosis
Assessment of regurgitation
Assess regurgitation on appearance and severity according to the standard
transthoracic guidelines (b p.158). Vena contracta (Fig. 6.31), PISA, CW
tracing, valve structure, and right heart size are usually possible with TOE,
whereas jet area and hepatic vein flow are not. See Table 6.6.
Assessment of stenosis
Assess stenosis on appearance (leaflet thickening or restriction) and severity
according to the transvalvular gradient. Remember: severe tricuspid stenosis
is usually associated with a gradient of 3-10mmHg.
TRICUSPID REGURGITATION AND STENOSIS
469
Table 6.6 Parameters to assess tricuspid regurgitation
Mild
Severe
Jet (Nyquist 50-60cm/s)
<5cm2
>10 cm2
Vena contracta
-
>0.7cm
PISA r (Nyquist 40cm/s)
<0.5cm
>1cm
Hepatic vein flow
Normal
Systolic reversal
Valve structure
Normal
Abnormal
CW trace
Soft & parabolic
Dense & triangular
RV/RA/IVC
Normal size
Usually dilated
Report as moderate if signs of regurgitation are greater than mild but there are few features of
severe regurgitation.
Severe
regurgitation with
0
0
180
dilated right heart
Vena contracta
Fig. 6.31 Severe tricuspid regurgitation in 4-chamber view. See W Video 6.21.
470
CHAPTER 6 Transoesophageal anatomy and pathology
Pulmonary valve
Both transthoracic and transoesophageal imaging tend to have limited
views of the pulmonary valve. There are no consistent views in TOE that
allow Doppler alignment through the valve apart from modified trans-
gastric views in some patients.
Normal findings
Views and findings
The most useful views are based on the short axis 50-80° (right
ventricular inflow/outflow) view. This is a short axis view through
the aortic valve in which the pulmonary valve is seen lying behind and
slightly to the right of the aortic valve. The image may be optimized by
changing the angle slightly from between 50° and 90° until the leaflets
of the pulmonary valve are seen opening and closing. Short axis views
of the pulmonary valve are now possible using X-plane in this view and
aligning the second plane through the valve.
Pulmonary regurgitation and stenosis
Assessment of regurgitation
Colour flow mapping of the pulmonary valve identifies small regurgitant
jets in most people—usually to one edge near the aortic valve. If there
appears to be more regurgitation than normal, comment on size, site, and
severity. Grade severity as mild, moderate, or severe based on colour flow
mapping criteria (b p.172). It may also be possible to use PW Doppler
in the pulmonary artery to look for holodiastolic flow reversal consistent
with severe pulmonary regurgitation. Remember to comment on the right
heart. See Table 6.7.
Assessment of stenosis
Pulmonary stenosis is usually valvular and congenital (e.g. related to rubella,
Noonan’s, or tetralogy of Fallot). Comment on valve appearance and
appearance of related structures (i.e. pulmonary artery, right heart). It is
difficult to align Doppler measures across the pulmonary valve with TOE
but the degree of opening using 2D/3D may be used as an estimate of
severity. See Table 6.8.
PULMONARY REGURGITATION AND STENOSIS
471
Table 6.7 Parameters to assess pulmonary regurgitation
Mild
Severe
Jet size on colour flow <10mm long Large with wide origin
CW density and shape Soft & slow Dense & steep
Pulmonary valve
Normal
Abnormal
Pulmonary artery flow Increased
Greatly increased compared to systemic
Right ventricle size
Normal
Dilated
If features suggest more than mild regurgitation but no features of severe grade as moderate.
Table 6.8 Parameters to assess pulmonary stenosis
Mild
Moderate
Severe
Peak gradient (mmHg)
10-25
25-40
>40
Valve area (cm2)
>1.0
0.5-1.0
<0.5
472
CHAPTER 6 Transoesophageal anatomy and pathology
Endocarditis
TOE has better sensitivity and specificity than TTE for identifying
vegetations. The higher spatial and temporal resolution can identify
smaller vegetations with rapid movement. Image quality is also better to
identify complications of endocarditis: aortic root, fistulae, and valve dys-
function such as leaflet perforation. Remember a normal echocardiogram,
including TOE, never excludes endocarditis.
Assessment
Use a full systematic examination with focus on both left and right-sided
valves. Report on:
Vegetations
Vegetations tend to appear as masses on valves (rarely, septum and
chamber walls (Fig. 6.32). Focus on each valve (aortic, mitral, tricuspid,
and pulmonary valve) and vary position slightly while watching for
‘flicking’ bright objects attached to valve. Record loops and scroll
through frame-by-frame to pick out any abnormal mobile elements.
If one is seen, move probe position and see if you can see it in multiple
planes. Consider possible differential diagnoses, e.g. fibrin strand
(Lambl’s excrescence), chordae (perhaps ruptured).
If vegetation, also look for ‘seeded’ vegetations where the vegetation
(or its associated regurgitant jet) touches other valves or walls
(e.g. outflow tract, septum and aorta).
Report: location, number, size, functional effect.
Abscess
Look particularly at valve rings (but also study leaflets) focus on aortic
root and mitral valve. The aortic root can be seen particularly well so
look for thickening, ‘boggy’ appearances or frank abscesses. If after valve
surgery, remember there may be some normal inflammation associated
with the operation. Report position, size, functional effects (compression)
and whether the abscess has now opened into a cavity (if so, say which).
Fistulae
These can usually be best seen with TOE. Suspect a fistula if there is
a known abscess, a new murmur has been heard or there has been a
sudden haemodynamic change in the patient. Use colour flow mapping
to look for abnormal flow and cavity jets. Fistulae can be between any
adjacent cavities where there has been infection e.g. around valves, aorta
to right heart.
Valve dysfunction
If there is a vegetation give details of functional effect on valve. Even if
you have not seen a vegetation look for suspicious valve dysfunction in a
systematic manner and report.
Pericardial effusion see b p.298.
ENDOCARDITIS
473
LA
0 138 180
CAVITY
LA
LV
THICKENING
AV
Aorta
RA
RV
ENDOCARDITIS AFFECTING AORTIC ROOT
Aortic vegetation seeded to mitral valve
LA
LA
LV
LV
Aorta
Aorta
Fig. 6.32 Examples of aortic root abscess (top) and vegetations of aortic and mitral
valves (bottom). See W Video 6.22 and W Video 6.23.
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475
Chapter 7
Transoesophageal
anatomy and pathology:
chambers and vessels
Left ventricle
476
Left ventricular size and mass
478
Left ventricular function
480
Left ventricular ranges
482
Right ventricle
484
Right ventricular size
486
Right ventricular function
488
Right ventricular ranges
489
Left atrium 490
Left atrial size
490
Left atrial appendage
492
Pulmonary veins 494
Right atrium 496
Right atrial size
496
Right atrial features
498
Coronary sinus 498
Atrial septum 500
Atrial septal defects and patent foramen ovale 502
Contrast study for intracardiac shunts
506
Ventricular septum 508
Pericardium 510
Pericardial effusion
512
Cardiac tamponade 512
Aorta 514
Aortic size
516
Aortic atherosclerosis
518
Aortic dissection
520
Intramural haematoma 524
Aortic transection or traumatic aortic disruption
524
Aortic coarctation 526
Sinus of Valsalva aneurysm 526
Thoracic aortic aneurysm 526
Masses 528
Cardiopulmonary bypass and coronary artery surgery 530
Haemodynamic instability 534
Mechanical cardiac support 538
Pleural space and lungs 542
Pacing wires and other implants 544
476
CHAPTER 7 Transoesophageal chambers and vessels
Left ventricle
TTE usually provides sufficient information to assess the left ventricle and
should be the echocardiographic modality of choice. With TOE the left
ventricle is in the far field and it can be difficult to obtain unforeshortened
views. Transgastric imaging allows accurate measures from stable short
axis views. Nevertheless, during a transoesophageal study assessment
should be made of the left ventricle, even if limited, to gain an impres-
sion of left ventricular size and function and help interpretation of other
findings.
Anatomy is described on b p.192. Briefly, the left ventricle is a muscular
cavity with a septum dividing it from the right ventricle. The ventricle has
anterior, inferior, lateral and inferolateral (or posterior) walls.
Indications for transoesophageal imaging
TOE is indicated when transthoracic windows are poor, in particular situations
such as in Intensive Care Unit or Cardiac Recovery, or when intraopera-
tive evaluation of cardiac function is needed during cardiac surgery.
Normal findings
Views
The key views to assess the left ventricle are the 4-chamber 0°, long axis
135°, 2-chamber 80°, and transgastric 0° short axis view (Fig. 7.1).
Findings
4-chamber 0° view: equivalent to the apical 4-chamber but usually with
marked foreshortening of the left ventricle. The septum is on the left
and lateral wall on the right. To realign the plane through the apex try
probe retroflexion until the apex comes into view. The probe may
lose contact with oesophagus on retroflexion.
Long axis 135° view: equivalent to the parasternal long axis it is often
easier to align through the apex with gentle rotation. The septum
(anterior portion) is seen by the left ventricular outflow and the
posterior (inferolateral) wall is on the left.
2-chamber 70-90° view: equivalent to an apical 2-chamber view. The
inferior wall is on the left and anterior wall on the right. This is a
preferred view for measuring left ventricle size.
Transgastric short axis 0° view: the best view to confidently assess left
ventricle function and obtain systolic and diastolic measures of cavity
size and wall thickness. Equivalent to a parasternal short axis view.
Advancing and withdrawing the probe may make it possible to scan
through the left ventricle in cross section from apex to mitral valve.
The walls of the ventricle are the opposite order to the parasternal
short axis, i.e. inferior wall lies nearest the probe and anterior in the
far field with septum on the left and lateral wall on the right.
LEFT VENTRICLE
477
4 Chamber view—0°
Long axis view—135°
AORTA
RA
LA
LA
RV
INFEROLATERAL
RV
LV
LV
(POSTERIOR)
SEPTUM
LATERAL
SEPTUM
APEX
2 Chamber—90°
APEX
INFERIOR
ANTERIOR
APEX
Transgastric view—90°
Transgastric view—0°
INFERIOR
INFERIOR
LV
SEPTUM
LATERAL
ANTERIOR
ANTERIOR
Fig. 7.1 Key views to assess the left ventricle.
478
CHAPTER 7 Transoesophageal chambers and vessels
Left ventricular size and mass
Report quantitative measures of size (Tables 7.1 and 7.2) if measurements
are possible and include a general summary: normal, mild, moderate, or
severe dilatation; normal, mild, moderate, or severe hypertrophy. Both lin-
ear and volumetric measures are possible with TOE. Use 2D measures
as it is not usually possible to align an M-mode cursor unless transgastric
views are obtained. Start with an overview of the ventricle in all views to
gather an impression of appearance, size, and function.
Linear measures
2D-imaging
Optimize a transgastric 0° view at the mid-papillary level and record a
loop (Fig. 7.3).
Identify the end-diastolic frame (widest ventricle). Measure from
the inferior wall endocardial border to the anterior wall endocardial
border in a line at right angles to each wall. Report the left ventricular
end-diastolic diameter. Scroll through to identify the end-systolic frame
(smallest ventricle) and use the same technique to measure the left
ventricular end-systolic diameter.
M-mode, although not usually done, is technically possible in this view.
The 2-chamber 80° view gives another window to measure left
ventricular diameters from anterior to inferior walls (Fig. 7.2).
Left ventricular hypertrophy can be assessed with measures of wall
thickness from the transgastric 2D images at end-diastole in the
septum and posterior wall.
Volumetric measures
Simpson’s method
Simpsons method of discs can be used if the oesophageal views allow
planes to be set up through the apex. It relies on a good 4-chamber 0°
view that is not foreshortened.
In the 4-chamber 0° view optimize an image of the left ventricle, with
clear endocardial border and enough depth to include the apex.
Record a loop. Trace around the border in diastolic and systolic
frames to obtain left ventricular end-diastolic and end-systolic volumes.
Measure left ventricular length from apex to middle of mitral valve in
the same view to obtain left ventricular long axis.
For biplane measures repeat the process using an optimized
2-chamber 80° view.
Area-length equation
This method (b p.200) can be used based on a transgastric 0° short axis
mid-papillary level view.
Mass
All the equations and models from TTE (b p.210) can be applied. Ideally
use the transgastric 0° view (equivalent to parasternal short axis). For
measurements based on apical 4- and 2-chamber views use the respective
4-chamber 0° and 2-chamber 80° views. Transoesophageal evaluation is
reasonably accurate, but tends to report slightly higher left ventricular
mass.
LEFT VENTRICULAR SIZE AND MASS
479
SYSTOLE
DIASTOLE
0
72
180
0
74
180
LA
LA
LAA
DIAMETERS
LV
LV
0
72
180
0
74
180
LA
LA
VOLUMES
LV
LV
Fig. 7.2 Measures of left ventricle size in 2-chamber view.
0
0
180
SEPTUM
POSTERIOR WALL
LV
Fig. 7.3 Measures of wall thickness in transgastric view.
480
CHAPTER 7 Transoesophageal chambers and vessels
Left ventricular function
Assessment of left ventricular function with TOE is often needed in the
context of Intensive Care or intraoperatively. Assessment has clinical
importance and should be as comprehensive as possible. Minimal re-
quirements are: left ventricular size and shape; systolic function including
regional differences. Diastolic function assessment from transmitral and
pulmonary vein flow is possible.
Global systolic function
As with transthoracic imaging an eyeball assessment of function is often
used and quoted as normal, mild, moderate, or severe impairment. However,
a visual gauge should, when possible, be backed up by quantification. Use
the same equations as for transthoracic imaging (b p.226) based on the
equivalent measures. The transoesophageal views for measurement of left
ventricular diameters are the 4-chamber 0°, 2-chamber 80°, and transgas-
tric views. Left ventricular diameters in transgastric views are measured
from anterior wall to inferior wall in a line perpendicular to the long axis
of the ventricle, at the junction of the basal and middle thirds of the long
axis. Left ventricular volumes are traced as for transthoracic imaging—
with care to avoid using foreshortened images. Doppler-based measures
e.g. dP/dT (b p.232) can be used from the oesophageal views of mitral
regurgitation.
Regional systolic function
The usual requirement for regional assessment is to determine wall move-
ment in coronary artery territories (Fig. 7.4). The standard 16-segment
model can be applied to transoesophageal images and technically wall mo-
tion scores are possible although not normally quoted.
Wall motion
Use 4-chamber 0°, long axis 135°, 2-chamber 80°, and transgastric
0° views. Avoid foreshortening. Endocardial border definition is usually
very good.
Look at the segments and decide whether normal, hypokinetic
(excursion <5mm), akinetic (excursion <2mm), or dyskinetic
(endocardium moves out in systole). If you are unsure look for
thickening >50% between diastole and systole. If present report as
normal or hypokinetic.
Remember, most commonly:
• Left anterior descending artery supplies: mid and apical septum
and lateral wall in 4-chamber 0° view; anterior wall and apex in
2-chamber 80° view, and septum and apex in long axis 135° view.
• Left circumflex artery supplies: basal and mid segments of posterior
(inferolateral) wall in long axis 135° view and basal lateral wall in
four chamber 0° view.
• Right coronary artery supplies: inferior wall in 2-chamber 80° view
and basal septum in 4-chamber 0° view.
• Transgastric short axis view has right coronary territory nearest
the probe, left anterior descending territory in the far field, left
circumflex territory supplying the posterior wall (on the right).
LEFT VENTRICULAR FUNCTION
481
4 Chamber—0°
2 Chamber—75°
RCA
LAD
RCA
LCX (or LAD)
LAD
Transgastric—0°
Long axis—135°
LCX
RCA
(or RCA)
LAD
Left anterior descending artery (LAD)
Left circumflex artery (LCX)
Right coronary artery (RCA)
Boundaries between artery territories will vary slightly
with coronary anatomy
Fig. 7.4 Coronary supply to left and right ventricle.
482
CHAPTER 7 Transoesophageal chambers and vessels
Left ventricular ranges (Table 7.1)
Table 7.1 Left ventricular ranges in women1
Normal
Mild
Moderate
Severe
LV dimension
LV d diameter, cm
3.9-5.3
5.4-5.7
5.8-6.1
>6.1
LV d diameter/BSA, cm/m2 2.4-3.2
3.3-3.4
3.5-3.7
>3.7
LV d diam/height, cm/m
2.5-3.2
3.3-3.4
3.5-3.6
>3.7
LV volume
LV d vol, mL
56-104
105-117
118-130
>130
LV d vol/BSA, mL/m2 35-75
76-86
87-96
>96
LV s vol, mL
19-49
50-59
60-69
>69
LV s vol/BSA, mL/m2
12-30
31-36
37-42
>42
Linear method: fractional shortening
Endocardial, %
27-45
22-26
17-21
<17
Mid-wall, %
15--23
13-14
11-12
<11
2D method: Ejection
>54
45-54
30-44
<30
fraction, %
Linear method
LV mass, g
67-162
163-186
187-210
>210
LV mass/BSA, g/m2
43-95
96-108
109-121
>121
LV mass/height, g/m
41-99
100-115
116-128
>128
LV mass/height2, g/m2
18-44
45-51
52-58
>58
Relative wall
0.22-0.42
0.43-0.47
0.48-0.52
>0.52
thickness, cm
Septal thickness, cm
0.6-0.9
1.0-1.2
1.3-1.5
>1.5
Posterior wall thickness, 0.6-0.9
1.0-1.2
1.3-1.5
>1.5
cm
2D method
LV mass, g
66-150
151-171
172-182
>182
LV mass/BSA, g/m2
44-88
89-100
101-112
>112
BSA, Body surface area; d, diastolic; s, systolic.
Bold rows identify best validated measures.
LEFT VENTRICULAR RANGES
483
Table 7.2 Left ventricular ranges in men1
Normal
Mild
Moderate
Severe
LV dimension
LV d diameter, cm
4.2-5.9
6.0-6.3
6.4-6.8
>6.8
LV d diameter/BSA, cm/m2 2.2-3.1
3.2-3.4
3.5-3.6
>3.6
LV d diam/height, cm/m
2.4-3.3
3.4-3.5
3.6-3.7
>3.7
LV volume
LV d vol, mL
67-155
156-178
179-201
>201
LV d vol/BSA, mL/m2
35-75
76-86
87-96
>96
LV s vol, mL
22-58
59-70
71-82
>82
LV s vol/BSA, mL/m2
12-30
31-36
37-42
>42
Linear method: fractional shortening
Endocardial, %
25-43
20-24
15-19
<15
Mid-wall, %
14-22
12-13
10-11
<10
2D method: Ejection
>54
45-54
30-44
<30
fraction, %
Linear method
LV mass, g
88-224
225-258
259-292
>292
LV mass/BSA, g/m2
49-115
116-131
132-148
>148
LV mass/height, g/m
52-126
127-144
145-162
>163
LV mass/height2, g/m2
20-48
49-55
56-63
>63
Relative wall
0.24-0.42
0.43-0.46
0.47-0.51
>0.51
thickness, cm
Septal thickness, cm
0.6-1.0
1.1-1.3
1.4-1.6
>1.6
Posterior wall
0.6-1.0
1.1-1.3
1.4-1.6
>1.6
thickness, cm
2D method
LV mass, g
96-200
201-227
228-254
>254
LV mass/BSA, g/m2
50-102
103-116
117-130
>130
BSA—Body surface area; d, diastolic; s, systolic.
Bold rows identify best validated measures.
Reference
1 Recommendations for chamber quantification: A report of the American Society of
Echocardiography Guidelines and Standards Committee and the Chamber Quantification
Writing Group, developed in conjunction with the European Association of Echocardiography.
J Am Soc Echocardiogr 2000; 18:1440–63.
484
CHAPTER 7 Transoesophageal chambers and vessels
Right ventricle
The right ventricle is more difficult to see with TOE than transthoracic
imaging because it lies distant to the probe. However with an appropriate
combination of views it is possible to make a reasonable assessment of
right ventricular size and function. Briefly the anatomy consists of a free
wall and the interventricular septum. The cavity is crescent-shaped and
wrapped around the left ventricle. Inflow is through the tricuspid valve and
outflow through the pulmonary valve.
Normal findings
Views
The key views are: 4-chamber 0° view and short axis 50-80° view
(right ventricular inflow/outflow view) (Fig. 7.5). These can be
supplemented by transgastric 90° long axis view with the probe
rotated clockwise away from the left ventricle.
Findings
4-chamber 0° view: rotation to the right focuses on the right atrium
with the right ventricle furthest from the probe. The right ventricular
free wall and septum can be seen. This view permits some assessment
of size although the right ventricle is often foreshortened.
Short axis 50-80° view: this is also known as the right ventricular
inflow/outflow view and allows assessment of the more basal areas
of the right ventricle free wall, as well as, the tricuspid and pulmonary
valves.
Transgastric 0° view: this permits a short axis view through the left
ventricle. The right ventricle will be seen wrapping around the left
ventricle (equivalent to a parasternal short axis). This view can be used
to look for septal motion to assess right ventricle overload.
Transgastric 90° view (right ventricle): rotating the probe away from the
standard left ventricle view may demonstrate the right ventricle. The
tricuspid subvalvular apparatus is visible.
RIGHT VENTRICLE
485
4 Chamber view—0°
Short axis view—50-80°
RA
LA
PULMONARY
ARTERY
LA
RA
RV
LV
RV
Transgastric view—0°
Modified transgastric view—90°
RV
LV
Fig. 7.5 Key views to assess the right ventricle.
486
CHAPTER 7 Transoesophageal chambers and vessels
Right ventricular size
The complex shape of the right ventricle makes assessment complex and
it may be difficult to support a qualitative impression with quantitative
measures. Assessment is similar to transthoracic imaging (b p.264). Use
several views and comment on wall thickness, cavity size, and outflow
tract size (Fig. 7.6).
Wall thickness
Use 4-chamber 0° view and comment on thickness of the free wall
at the level of the tricuspid valve chordae tendinae. Do not include
epicardial fat or coarse trabeculations in the measurement.
Cavity size
Qualitative
Use 4-chamber 0° view and look at mid-cavity diameter. Right
ventricular size is normal if <2/3 left ventricular size, mildly dilated if
slightly smaller than left ventricle, moderately dilated when the same
size, and severely dilated if larger than the left ventricle.
Alternatively, look at the apex and report as mildly dilated if >2/3 of
the way to the left ventricular apex, moderately dilated if it reaches
the left ventricular apex, and severely dilated if it extends past the left
ventricle.
Quantitative
Use the 4-chamber 0° view optimized to avoid foreshortening.
Measure right ventricular length, tricuspid annulus diameter, and mid
cavity diameter (Table 7.3).
Use right ventricular inflow/outflow 80° view to measure right
ventricular outflow diameter, pulmonary valve diameter, and pulmonary
artery diameter.
RIGHT VENTRICULAR SIZE
487
RVD1
LA
RA
LV
RVD2
RVD3
RVOT2
LA
RA
RV
RVOT1
Fig. 7.6 Measures of right ventricular size. These are equivalent to the transthoracic
measures (b p.264). RVD1 = tricuspid annulus diameter, RVD2 = mid cavity
diameter, RVD3 = right ventricle length, RVOT1 = diameter of basal part of
right ventricle, RVOT2 = diameter of outflow tract at pulmonary valve. A further
measure can be made of pulmonary artery diameter.
488
CHAPTER 7 Transoesophageal chambers and vessels
Right ventricular function
The right ventricle contracts in both the long and short axis. The long axis
assessment of the free wall is the easiest way to gauge right ventricular
function.
Assessment
Use a 4-chamber 0° view.
Make a qualitative judgement of global function as mild, moderate, or
severe impairment based on whether there is less than the accepted
25mm movement of the tricuspid annulus towards the apex but not
a major reduction in movement (mild), no movement (severe), or
something in between (moderate).
If you want to quantify the global assessment, measure right ventricular
length in diastole and systole and calculate fractional shortening:
RV diastolic length − RV systolic length
RV length in diastole
(normal is >35% fractional shortening)
For regional assessment look at the basal, mid, and apical segments
of the free wall in the same 4-chamber view and report them as
hypokinetic, akinetic, or dyskinetic. As with the left ventricle you
should be able to see right free wall thickening to corroborate a
statement of normal or hypokinetic motion.
RIGHT VENTRICULAR RANGES
489
Right ventricular ranges (Table 7.3)
Table 7.3 Right ventricular ranges
Normal Mild
Moderate
Severe
RV dimension
Basal RV diameter, cm
2.0-2.8
2.9-3.3 3.4-3.8
>3.8
Mid RV diameter, cm
2.7-3.3
3.4-3.7 3.8-4.1
>4.1
Base-apex length, cm
7.1-7.9
8.0-8.5 8.6-9.1
>9.1
RVOT diameter
Above aortic valve, cm
2.5-2.9
3.0-3.2 3.3-3.5
>3.5
Above pulmonary valve, cm
1.7-2.3
2.4-2.7 2.8-3.1
>3.1
PA diameter
Below pulmonary valve, cm
1.5-2.1
2.2-2.5 2.6-2.9
>2.9
RV area and fractional area change
RV diastolic area, cm2
11-28
29-32 33-37
>37
RV systolic area, cm2
7.5-16
17-19 20-22
>22
Fractional area change, %
32-60
25-31 18-24
<18
In relation to Fig. 7.6 apical 4-chamber view: basal RV = RVD1, mid RV = RVD2, base-apex =
RVD3.
In relation to Fig. 7.6 parasternal short axis view: aortic valve to free wall = RVOT1, level of
pulmonary valve = RVOT2, pulmonary artery = PA1.
490
CHAPTER 7 Transoesophageal chambers and vessels
Left atrium
The transoesophageal probe lies directly behind the left atrium and pro-
vides excellent views of inflow from all pulmonary veins, outflow across
the mitral valve, left atrial appendage, and atrial septum. Any left atrial
masses are therefore seen much better with transoesophageal than trans-
thoracic imaging.
Normal findings
Views
The key views are: 4-chamber 0° view, 2-chamber 75° view, long axis
135° view, and bicaval 110° view.
Further views are needed to look at the pulmonary veins (b p.494).
Findings
4-chamber 0° view: the left atrium lies directly in front of the probe and
may allow measurements of left atrial size.
Long axis 135° view: again the left atrium lies in front of the probe and
can be measured.
2-chamber 75° view: with slight adjustments this is perfect for
assessment of the left atrial appendage.
Bicaval 110° view: the standard view for assessment of the septum.
Left atrial size
Left atrial size is difficult to assess with TOE because the imaging sector
does not normally include the whole of the atrium. Volumes are therefore
unreliable particularly if the atrium is dilated. Linear measures are possible
but may miss longitudinal changes (Fig. 7.7).
Assessment
Give a qualitative judgement of size based on size relative to the left
ventricle. If the left atrium entirely fits into the 4-chamber 0° view it
is likely to be small. If it appears similar in size to the left ventricle it is
probably severely dilated. There may be supportive qualitative changes
of dilatation, such as spontaneous contrast to suggest slow blood
movement in a large cavity.
Use quantitative measures of area in the 4-chamber 0° view if the
boundaries of the left atrium can be seen. Trace around the border to
estimate left atrial size and use equations as for transthoracic imaging
(b p.280).
Simple linear measures are usually sufficient in the long axis 135° view
or short axis 50° view. Measure the distance between the probe and
the left atrial wall by the aortic valve. Remember that quantitative
measures are likely to be unreliable and should be interpreted
taking into account other echocardiographic findings and qualitative
assessment of atrial size.
LEFT ATRIAL SIZE
491
Left atrium
LA
RA
RV
Left atrium
LA
Aorta
LV
Fig. 7.7 Positions to make linear measures of atrial size.
492
CHAPTER 7 Transoesophageal chambers and vessels
Left atrial appendage
The left atrial appendage is the most common site for left atrial thrombi in
at risk patients, e.g. those with atrial fibrillation, and is therefore of great
clinical relevance, for instance when planning cardioversion or looking for
source of emboli.
Normal findings
Views
The key view is the 2-chamber view (Fig. 7.8).
However, the left atrial appendage can have a variable shape so this
key view will need to be adjusted in patients being assessed for cardiac
source of emboli, if the left atrium is enlarged or atrial fibrillation is
found. Once the left atrial appendage is spotted in the 2-chamber
view, adjust the scan angle and move the probe up and down to scan
through the whole appendage.
It can be useful to study the appendage at ~90° to this view to see the
pectinate muscles in more detail. The scan plane can be rotated to
~140° while maintaining the appendage in the centre of the image.
Findings
2-chamber view: the left atrial appendage lies on the right, curving
around the edge of the mitral valve. Parallel to the appendage and
nearer the probe is the left upper pulmonary vein. The appendage and
vein are separated by a bright ridge of tissue known as the warfarin or
coumadin ridge. This can accumulate fat and may appear bulbous.
Assessment
To assess the appendage:
Identify the appendage (in some people it can be absent or have been
removed/tied/stapled during cardiac surgery).
Scan through at different planes to identify shape, orientation and
number of lobes (usually one lobe but bilobed appendages occur in
around 10%). Retroverted appendages (pointing towards the probe)
can occur. Inverted appendages are a rare complication of surgery and
appear as a mobile mass in the left atrium below the pulmonary vein.
Look for evidence of thrombus or rarely tumours. Differentiate
abnormal masses (e.g. thrombus) from pectinate muscles normally
present in the appendage. Thrombus is normally associated with low
flow. If it is not clear whether there is a mass, colour flow mapping can
demonstrate flow down to the apex, or left-sided ultrasound contrast
can opacify the appendage (a mass will remain dark).
X-plane imaging can be very useful to ‘scan’ through the appendage.
Measure filling and emptying velocities (Fig. 7.8). Place PW Doppler
cursor 1cm into the appendage and record a trace. Normal velocities
are >40cm/s. Low velocities are associated with atrial fibrillation or
atrial stunning and should make you suspicious that there may be a
clot. Less than 20cm/s indicates a higher risk of clots. Atrial flutter
is associated with regular velocities, occurring at a faster rate than
the ventricular rate. Look for spontaneous contrast in the atrium or
‘smoking’ out of the appendage if velocities appear low.
LEFT ATRIAL APPENDAGE
493
Spontaneous contrast
Spontaneous contrast in the left atrium appears ‘smoke-like’. It is classified
as mild or severe (based on a qualitative assessment of quantity) and may
be located in the left atrial appendage, or both appendage and atrium.
Usually spontaneous contrast in the left atrium indicates increased risk
of thrombosis. It is due to sludging of the red blood cells and is found
when intracardiac velocities decrease. In particular, a dilated left atrium
and atrial fibrillation cause spontaneous contrast. Anticoagulation does
not affect spontaneous contrast. The higher the frequency of the trans-
ducer the better spontaneous echo contrast is displayed.
Differentiating pectinate muscle from thrombus
Pectinate muscle
Thrombus
Strand-like
Generally rounded
Can span the appendage
May fill the appendage
Adherent
Adherent or pedunculated
Not mobile
Can be mobile
Often associated with spontaneous
contrast
Warfarin
Left upper
ridge
pulmonary vein
LA
LV
Left atrial
appendage
Pulsed wave Doppler in
appendage
Atrial flutter on ECG
Velocities of >40cm/s
Fig. 7.8 2-chamber view (top) demonstrates prominent left atrial appendage,
warfarin ridge and pulmonary vein. PW trace (bottom) demonstrates velocities in
appendage consistent with atrial flutter. See W Video 7.1, W Video 7.2, W Video 7.3.
494
CHAPTER 7 Transoesophageal chambers and vessels
Pulmonary veins
Normal anatomy
There are normally 4 pulmonary veins that drain blood from the pulmo-
nary circulation to the left atrium—2 on the left (lower and upper) and
2 on the right (lower and upper). They all lie at the back of the atrium.
Variations in anatomy include only 1 pulmonary vein on 1 side, usually
because the upper and lower veins have joined proximally, or significant
differences in the size of each vein.
Normal findings
Views
The transoesophageal probe lies behind the atria between the 4 pulmo-
nary veins. To see all 4 pulmonary veins modifications of standard views
are required. The key views are the 4-chamber 0° view, 2-chamber 75°
view, and bicaval 110° view (Fig. 7.9).
Findings
4-chamber 0° view: all 4 veins can usually be tracked down in this
view. Start from the 4-chamber view and rotate to right or left then
advance or withdraw the probe to bring each vein into view. The
upper pulmonary veins on both sides point towards the probe and
are best aligned for Doppler measures. The lower pulmonary veins lie
perpendicular to the probe.
2-chamber 80° view: in this view the the left upper pulmonary vein lies
parallel to the appendage, nearer the probe.
Bicaval 110° view: by rotating the bicaval view the right upper
pulmonary vein can be brought into view as it drains into the left
atrium parallel to the septum and superior vena cava.
How to optimize pulmonary vein views
4-chamber 0° view: if the veins are not obvious, colour flow mapping
placed in the near field on the left or right can be used to highlight
the inflow.
If the veins are seen but not clearly aligned, rotation of probe angle
between 0° and 90° may help to improve the view.
Assessment
Pulmonary veins are often needed for flow assessment relevant to left
atrial pressure, particularly in mitral regurgitation (b p.120). Their anat-
omy may also be relevant to procedures that use the pulmonary veins as
landmarks, such as ablation for atrial fibrillation.
Comment on whether:
• All 4 are seen or whether there are more or less than 4.
• They are in standard locations.
• There is any discrepancy in size.
Report pulmonary vein flow patterns.
PULMONARY VEINS
495
RIGHT PULMONARY VEINS
0
110
180
LA
Septum
RIGHT UPPER
RA
RAA
SVC
0
0
180
RIGHT LOWER
LA
SVC
RIGHT UPPER
LEFT PULMONARY VEINS
0
75
180
Warfarin
ridge
LA
LEFT UPPER
LV
LAA
0
0
180
LEFT LOWER
LA
LEFT UPPER
Fig. 7.9 Diagram highlighting the 3 sectors which can be used to identify all 4
pulmonary veins. LA = left atrium, RA = right atrium, RAA = right atrial appendage,
SVC = superior vena cava, LV = left ventricle.
496
CHAPTER 7 Transoesophageal chambers and vessels
Right atrium
There are good views of the right atrium with TOE because of its relative
proximity to the probe. Right atrial inflow from both superior and inferior
vena cavae as well as coronary sinus are also straightforward to image.
More detailed studies of the right atrial appendage, Eustachian valve and
atrial septum are possible.
Normal findings
Views
Key views are 4-chamber 0° view and bicaval 110° view.
A transgastric view is possible with rotation of the probe from a
standard transgastric 90° long axis view of the left ventricle. This will
normally bring into view the right ventricle and with some withdrawal
of the probe may allow views of the right atrium and tricuspid valve.
Findings
4-chamber 0° view: equivalent to the apical 4-chamber, rotation of
the probe to the right allows focused study of right atrium and a
qualitative assessment of size.
Bicaval 110° view: this is the best view to see the whole of the right
atrium with inferior cava draining on the left and superior vena cava on
the right. The right atrial appendage is invariably present just below the
superior vena cava. The Eustachian valve (if present) will be seen at the
ostium of the inferior superior cava usually directed towards the fossa
ovalis. The atrial septum lies parallel to the probe and the fossa ovalis
is usually seen as a ‘dip’ in the middle of the septum. Use this view to
assess the atrial septum.
Right atrial size
Assess right atrial size qualitatively based on the 4-chamber 0° view
(Fig. 7.10). Judge size relative to the left atrium and right ventricle.
Normally the 2 atria are roughly the same size.
The simplest quantitative assessment is the linear measure of the minor
axis in a 4-chamber 0° view (linear measure from middle of right atrial
lateral wall to mid atrial septum). Volumes have not been validated but
can be attempted as for transthoracic imaging.
RIGHT ATRIAL SIZE
497
0
112
180
LA
IVC
SVC
RA
RAA
Right atrial minor axis
LA
RA
LV
RV
Fig. 7.10 A bicaval view (top) provides excellent depiction of the right atrium.
Thrombus, pacing wires, and lines can be seen in the atrium. The 4-chamber
view (bottom) can be used for limited measures of the right atrium.
498
CHAPTER 7 Transoesophageal chambers and vessels
Right atrial features
These usually do not represent pathological findings, but may be mistaken
for abnormalities:
Eustachian valve
Best seen in the bicaval 110° view (Fig. 7.11). The Eustachian valve is a
membranous structure originating from the junction of the inferior vena
cava and right atrium. It represents a remnant from fetal circulation where
placental oxygenated blood coming from the inferior vena cava has to
be diverted through the foramen secundum into the left heart. Thus the
blood flow coming from the inferior vena cava hits the fossa ovalis. This
has implications for contrast application via injections into the arm veins:
there is usually a wash-out of contrast close to the fossa, which may impair
contrast passage. Size can be highly variable. Rarely thrombosis or endo-
carditis can be attached to the valve.
Chiari network
The Eustachian valve may reach the interatrial septum and have net-like
perforations. This is a Chiari network (Fig. 7.11). The Eustachian valve
forms from the regression of one of the valves of the sinus venosus and
if this is incomplete a Chiari network is formed. Echocardiographically a
network of small strands may be seen—sometimes with a broad base,
which can be attached to different parts of the right atrium.
Thebesian valve
Like the Eustachian valve this does not represent a real valve. It is a muscle
and/or fibrous band at the orifice of the coronary sinus in the right atrium.
It can be seen in views displaying the orifice of the coronary sinus.
Christa terminalis
Separates the smooth part of the right atrium from the pectinated muscle
of the right atrium. In the bicaval view the christa terminalis is displayed as
a ridge at the junction of the right atrium and superior vena cava. When
pulling back from a 4-chamber view the christa terminalis can be seen as a
bright protrusion of the lateral atrial wall. Further pulling back shows how
this structure continues into the superior vena cava.
Coronary sinus
To see the coronary sinus use a 4-chamber 0° view. Advance the probe
slightly and retroflex slightly to look below the mitral valve. The coronary
sinus should appear across the image draining to the right atrium.
The sinus can enlarge if there is anomalous drainage of a persistent left
superior vena cava. Anomalous drainage can be demonstrated by injecting
agitated saline into a left-sided arm vein. Because the left-sided vena cava
drains into the coronary sinus the contrast comes through the coronary
sinus into the right atrium.
CORONARY SINUS
499
0
113 180
LA
ASD
SVC
RAA
Chiari network
Eustachian valve
0
110
180
LA
SVC
RA
Fig. 7.11 Example of Chiari network (top) and Eustachian valve (bottom) in bicaval
views. See W Video 7.4, W Video 7.5, W Video 7.6.
500
CHAPTER 7 Transoesophageal chambers and vessels
Atrial septum
The atrial septum divides the left and right atrium and embryologically has
2 distinct elements—the primum and secundum septum, which fuse after
birth. Abnormal development or closure of the septum is fundamental
to the emergence of septal defects. TOE is uniquely suited to study the
septum because it can be viewed through the left atrium in several planes
suitable for colour flow and continuous wave Doppler, as well as, contrast
studies.
Normal findings
Views
The key views are 4-chamber 0° view, short axis 50° view, bicaval 110°
view (Fig. 7.12).
Findings
4-chamber 0° view: in the 4-chamber view the septum is close to the
probe and rotation to the left can be used for an initial assessment.
Atrial septal defects are usually first evident in this view and colour
flow mapping can identify left to right flow patterns. The atrial septum
normally bows slightly towards the right atrium but in ventilated
patients there is a mild systolic bowing towards the left both during
inspiration and expiration. If right atrial pressure exceeds left atrial
pressure it will bows towards the left.
Short axis 50° view: here the septum extends from the aortic valve ring,
in a line at 10 o’clock. The primum septum is evident closest to the
valve and this view can be used for stable contrast studies.
Bicaval 110° view: the standard view to study the septum as it lies
parallel to the probe. The fossa ovalis is usually easily seen as a
depression. This view should be used for colour flow and contrast
studies.
Assessment
Assess the septum in all views using 2D. Look for:
Lipomatous hypertrophy (bright thickening of the septum that spares
the fossa ovalis).
Septal defects or an appearance of layers in the septum suggestive of a
patent foramen ovale.
Atrial septal aneurysms. The septum should move by >10mm either
towards right or left atrium.
Then use colour flow over the septum in the bicaval view:
A septal defect will be seen as interatrial flow. Also, screen for patent
foramen ovale—a small colour flow jet may be seen in the fossa ovalis
into the atrium during a short part of the cardiac cycle.
ATRIAL SEPTUM
501
0 0 180
LA
ATRIAL SEPTUM
LV
RA
RV
ATRIAL SEPTUM
LA
0
55 180
RA
AoV
RV
ATRIAL SEPTUM
0 112 180
LA
IVC
SVC
RA
RAA
Fig. 7.12 Key views to assess the atrial septum. 4-chamber 0° view (top), short axis
50° view (middle), bicaval 110° view (bottom).
502
CHAPTER 7 Transoesophageal chambers and vessels
Atrial septal defects and patent
foramen ovale
Requests for TOE in people with suspected atrial septal defects and patent
foramen ovale are usually because:
There is a high suspicion from transthoracic imaging of a defect.
The patient is being evaluated for intervention.
The study is to look for an embolic source.
Assessment
As for transthoracic imaging (b p.288) initial assessment should be with
2D imaging to look for obvious defects, followed by colour flow mapping.
If a septal defect is seen, Doppler can be used to quantify the shunt size.
Finally, agitated saline contrast injections should always be used if the septal
defect or foramen ovale has not clearly been seen.
2D and colour flow mapping
Use all 3 views but in particular the bicaval view. Look for gaps and then
overlay the colour flow to look for flow (most likely to be left to right).
Comment on:
Defect position including proximity to aortic valve and likely
classification (primum or secundum) (Figs. 7.13 and 7.14).
Defect size in several directions.
Direction and timing of flow from colour flow mapping.
Associated cardiac defects (particularly relevant for primum defects).
Doppler quantification of shunt
See transthoracic imaging (b p.288). Doppler quantification is not normally
needed for patent foramen ovale. Shunt quantification using measurement
of Qp and Qs is often limited with TOE because alignment of the Doppler
beam to flow through the pulmonary valve is difficult. However measure-
ment of the diameter of the pulmonary artery or right ventricle outflow
tract and of the left ventricle outflow tract is more reliable than on trans-
thoracic images. Pulmonary and aortic vti can be determined separately
with transthoracic imaging.
Agitated saline contrast versus colour flow mapping
In patent foramen ovale or septal defects the left-to-right shunt can be
detected by colour flow mapping. In most patients a right-to-left shunt is
present when right atrial pressure increases, for instance during Valsalva
manoeuvre. However, it may be difficult to display these right-to-left
shunts with colour Doppler. In these cases contrast echocardiography is
indicated (b p.506). Contrast echocardiography is also needed, when
colour flow mapping does not reveal a shunt, since contrast echocardi-
ography appears to be more sensitive.
ATRIAL SEPTAL DEFECTS AND PATENT FORAMEN OVALE
503
0 121 180
Secundum ASD
Primum ASD
Fig. 7.13 Examples of atrial septum abnormalities. See W Video 7.7 and W Video 7.8.
Fig. 7.14 Live 3D acquisition of secundum atrial septal defect (ASD), Image rotated
and cropped so defect is visualized form the left atrium. See W Video 7.9.
504
CHAPTER 7 Transoesophageal chambers and vessels
Secundum atrial septal defect—device closure
TOE is indicated to guide transcatheter closure of secundum defects. 3D
TOE can provide more detailed assessment of the defect during the in-
terventional procedure. The key features to record before the procedure
to plan closure are:
Size in different scan planes (many ASDs are not circular!).
Presence of multiple defects.
Presence of interatrial septal aneurysm.
Size of rim of normal tissue between defect and adjacent structures
for device to fit over. In particular look at rim close to aortic valve.
Assess for thrombus in left atrial appendage.
Other cardiac abnormalities (must assess pulmonary veins and
ensure a structurally normal heart).
During the procedure monitor and advise on:
Guidewire position while crossing the defect.
Defect size for device sizing.
Positioning of closure device during deployment.
Residual shunt after closure.
Development of thrombus.
Any impingement on valves.
After the procedure and during follow-up look for:
Device position.
Residual shunts.
Clots or other abnormalities on the device.
Primum atrial septal defect
Primum septal defects are usually well displayed with TTE. During a
transoesophageal study the beginning of the defect will be seen at the
hinge-points of the mitral and tricuspid valves, which arise from the same
level. A 4-chamber 0° view is usually ideal. TOE (Fig. 7.15) is useful for
a comprehensive assessment of the pathology, which often includes
defects of the proximal interventricular septum, mitral and tricuspid valve
insufficiency (including cleft anterior mitral leaflet).
Sinus venosus defect
Sinus venosus defects are very difficult to display using transthoracic 2D
echocardiography. A superior sinus venosus defect is best displayed in a
modified bicaval view with the probe slightly rotated to the right. There
will often be communication between the pulmonary vein and the supe-
rior vena cava opposite to the sinus venosus defect. The abnormal drain-
age of the right upper pulmonary vein can also be displayed in a 0° view
pulled back from the standard flour chamber image to show a short axis
view of the superior vena cava and ascending aorta.
Inferior sinus venosus defects are less common and may be associated with
abnormal drainage of the right lower pulmonary vein.
Coronary sinus defects are between the coronary sinus and the left atrium.
Coronary sinus views are needed to display the shunt, which may be dif-
ficult to see.
ATRIAL SEPTAL DEFECTS AND PATENT FORAMEN OVALE
505
Fig. 7.15 3D transoesophageal view of atrial septal defect.
506
CHAPTER 7 Transoesophageal chambers and vessels
Contrast study for intracardiac shunts
The 3 elements to ensure a good contrast study looking for an atrial shunt
are identical to those for transthoracic imaging (Fig. 7.16). The sedation
with transoesophageal imaging complicates the Valsalva manoeuvre but
does not make it impossible and the manoeuvre must be used.
1. A stable image
The bicaval 110° view aligns the septum across the image and therefore
provides good views of contrast flow. An alternative view is the short axis
50° view at aortic valve level. The Valsalva manoeuvre causes movement
of the heart up and down. The 50° view tends to be more stable with this
movement as the septum is in line with the image plane.
2. Good quality contrast
The contrast should be 8mL of saline, 1mL of air, and (ideally) 1mL of blood
from the patient mixed in 2 connected syringes until ‘frothy’. Use syringes
with locks to avoid them bursting off. Inject rapidly through a venflon
inserted into the right antecubital vein (if the patient is lying on their left
side this arm will not be compressed and be uppermost). This will ensure
the fastest transit of contrast to the heart (ensure the blood pressure cuff
does not inflate on this arm during the procedure). Good contrast should
completely and rapidly opacify the right atrium. Sometimes rapid flow
from the inferior vena cava causes mixing and partitioning of contrasted
and uncontrasted blood in the right atrium. As the inferior vena cava
directs blood at the foramen ovale the mixing tends to keep contrast away
from the septum. If this persists despite fast boluses then an alternative is
to inject contrast via a femoral vein.
3. A good Valsalva
If further studies are needed after rest injections always do the study with
a Valsalva. The critical time is when the patient relaxes, when right-sided
pressures transiently elevate relative to left. The patient takes a breath and
bears down hard. Inject the contrast and when it fills the right atrium tell
them to relax. If there is a shunt a few bubbles appear in the left atrium
and left ventricle within 5 beats of the patient relaxing. If bubbles appear
later this suggests a pulmonary arteriovenous malformation. This proce-
dure is entirely feasible during transoesophageal imaging with a compliant
patient. To improve compliance lighter sedation can be used and/or the
shunt study can be near the end of the examination (as sedation becomes
lighter). Assistance can be given by asking the patient to press against a
hand placed on the stomach.
Image acquisition
Set the system to capture 10 cardiac cycles and start acquisition on con-
trast injection. Look back through the loop searching for bubbles. Repeat
the study with more contrast until you are happy all 3 elements of the
study are perfect.
CONTRAST STUDY FOR INTRACARDIAC SHUNTS
507
‘Puff’ of contrast enters left atrium through PFO
0
55
180
1. Stable image
2. Good contrast—complete
opacification of right atrium
Set to record 10-15 beats
3. Point of Valsalva release
Fig. 7.16 The 3 key elements of an agitated saline contrast study. See W Video
7.10.
508
CHAPTER 7 Transoesophageal chambers and vessels
Ventricular septum
The ventricular septum can be difficult to see entirely with transoesopha-
geal imaging and therefore it is not indicated for assessment of the septum.
However, it is normal to assess the septum routinely during a study and
comment if abnormalities are identified incidentally. TOE provides reason-
able views of the proximal septum and can be efficient for membranous
septal defects. More apical defects, as often occur post-ischaemia, are dif-
ficult to see.
Normal findings
Views
The key views are the 4-chamber 0° view and the long axis 135° view
(Fig. 7.17). These can be supplemented by the short axis 50° view to look
at septum around the aortic valve. The transgastric short axis 0° view can
also be useful.
Findings
4-chamber 0° view: the septum lies between the left and right ventricle.
With an unforeshortened view it may be possible to see to the apex
but the views are not aligned for colour flow mapping. The view gives
good depiction of the proximal septum. Withdrawal to the 5-chamber
view allows imaging of the septum below the aortic valve.
Short axis 50° view: with a slight advance of the probe the membranous
and outlet septum just below the aortic valve can be seen.
Long axis 135° view: this also demonstrates the septum close to the
aortic valve.
Transgastric view: this gives equivalent information to the parasternal
short axis view and provides information on the muscular (trabecular)
septum in the mid-ventricle.
Assessment
Assess the septum in all views with 2D and then overlay colour flow to
look for defects. If there is evidence of hypertrophy, particularly in the
outflow tract, then colour flow can also be used to look for subaortic
valve flow acceleration.
If comments on the septum are required then report septal thickness
(this can be measured from transgastric views) and comment on any
irregular thickening of the septum.
To identify a ventricular septal defect first look in 2D for evidence of a
‘gap’ then use colour flow to identify definite flow across the septum.
If there is a gap measure the size in two different directions/planes.
Finally, if Doppler alignment is possible consider calculation of a shunt.
However, if a septal defect is sufficient to cause major shunts these
can often be seen most easily with transthoracic imaging.
VENTRICULAR SEPTUM
509
0
109
180
LA
Aorta
LV
Membranous VSD
RV
Fig. 7.17 Example of a large perimembranous ventricular septal defect seen in a
long axis 135° view. A left to right shunt is demonstrated with colour flow mapping.
See W Video 7.11.
510
CHAPTER 7 Transoesophageal chambers and vessels
Pericardium
TTE usually gives all the information needed to assess the pericardium.
However, the pericardium should be assessed routinely during tran-
soesophageal studies. TOE can be useful in perioperative cardiac patients
to assess localized collections or because of poor postoperative windows.
Assessment of the pericardium should follow the same routine as with
transthoracic imaging.
Normal findings
Views
Part of the pericardium can be seen (and should be assessed) in all views.
Findings
Pericardial surfaces
The surfaces are usually a thin white line around the heart (normal 1-2mm
thick). Transoesophageal imaging is more accurate for assessing thickness
than transthoracic but should not be relied upon.
Pericardial space
The space, if it contains fluid, is a black, lucent area associated with the
pericardial surfaces (normally <0.5cm, although small effusions can have
significant effects post surgery).
Transverse and oblique sinuses
TOE is good for studying the transverse and oblique sinuses. The transverse
sinus lies between left atrium and aorta/pulmonary trunk (Fig. 7.18).
Use atrio-ventricular short axis 50° view and then long axis 135° view.
Fluid or haematoma in the sinus appears as space—shaped like a
crescent or triangle—between ascending aorta and left atrium.
Problems with the transverse sinus
To differentiate the space from the left atrium or left atrial appendage
(roof lies in transverse sinus) use colour flow Doppler. There will be no
flow in the sinus. Beware, because of the position of the sinus it can be
mistaken for abscess or cyst or—if containing fat—an atrial mass.
Oblique sinus lies between the pulmonary veins on back of left atrium.
Use 4-chamber 0° view.
Fluid or haematoma in sinus appears as a space between left atrium
and the probe tip in the oesophagus.
PERICARDIUM
511
TRANSVERSE SINUS
AORTA
LEFT
ATRIUM
Fig. 7.18 Mid-oesophageal, ~50° view just above aortic valve. Fluid in transverse
sinus is seen as echolucent area between aorta and left atrium.
512
CHAPTER 7 Transoesophageal chambers and vessels
Pericardial effusion
Assessment
Global effusions
Use all views. Seen well in 4-chamber 0° view or transgastric short axis
90° view (Fig. 7.19).
Report depth in several different sites and report where the
measurements were made.
Gauge global effusion on same parameters as transthoracic imaging
(<0.5cm; 0.5-1cm: mild; 1-2cm: moderate; >2cm: large).
Comment on appearance (fibrin strands, masses, haematoma).
Differentiate between pleural and pericardial fluid by using
descending aorta and left atrium
(as for transthoracic imaging). In
4-chamber view rotate probe to focus on the left ventricle and
descending aorta. Pericardial fluid will pass between aorta and left
atrium (sometimes widening the gap) whereas pleural fluid will extend
to the lateral side of the aorta.
Localized effusions
Common sites are in oblique sinus behind left atrium or a posterolateral
collection against right atrium or right ventricle.
Both can be seen in the 4-chamber 0° view.
Space between probe and left atrium is the oblique sinus collection.
Rotate probe to focus on right heart. Look at right ventricle and
atrium for evidence of localized compression or collapse from a
posterolateral effusion.
Use long axis 135° view to check transverse sinus.
Cardiac tamponade
Features of cardiac tamponade can usually be assessed with transthoracic
imaging. If assessment is required during transoesophageal imaging use
the 2D and Doppler parameters as for transthoracic studies (b p.300).
Remember that tamponade is a clinical diagnosis (hypotension, tachycardia
etc.) and echocardiography will only provide supportive evidence.
Problems in ventilated post-surgery/ITU patients
There will not be the normal respiratory variation in Doppler indices
of mitral and tricuspid inflow and these should not be used. Rely on
2D features.
Look for right or left ventricular or atrial collapse.
Look for localized collection compressing left or right ventricle or
atria reducing chamber function.
With oblique sinus collection look at pulmonary vein flow. Local
compression will reduce flow velocity in vein.
CARDIAC TAMPONADE
513
POSITION OF AN OBLIQUE SINUS
COLLECTION
RIGHT ATRIAL SYSTOLIC
COLLAPSE
POSITION OF A
POSTEROLATERAL
COLLECTION
Fig. 7.19 Mid-oesophageal 4-chamber 0° view showing global pericardial effusion
with exaggerated right atrial collapse during atrial systole. Annotation demonstrates
where an oblique sinus and posterolateral collection would be seen in this view.
514
CHAPTER 7 Transoesophageal chambers and vessels
Aorta
The close proximity of the oesophagous to the aorta makes transoesopha-
geal imaging ideal for assessment of the ascending and descending thoracic
aorta. Parts of the aortic arch including the origin of the brachiocephalic
vessels can also be visualized. The views allow diagnosis and assessment
of aortic dissection and severity of aortic atheroma. The portability of
transoesophageal imaging also permits assessment of traumatic aortic
trans-section.
Normal findings
Views
The key aortic views are the 50° short axis aortic valve view both at aortic
valve level and withdrawn slightly, the 135° long axis view, and dedicated
descending aorta and aortic arch views (Fig. 7.20). Deep transgastric and
110° long axis transgastric views can be used for alignment of Doppler in
the ascending aorta.
Proximal ascending aorta
Proximal ascending aorta is best seen in the 50° short axis view with
slight withdrawal of the probe to scan up the aorta. The 135° long
axis view also allows measures of aortic root size. Transgastric views
sometimes allow Doppler alignment through the proximal ascending
aorta.
Aortic arch
Seen as the last views as the probe is withdrawn in the aortic views
and can be seen in long and short axis.
Descending thoracic aorta
The descending thoracic aorta can be seen in short (0°) and long axis
(90°) with the dedicated posteriorly-directed aortic views. Advancing
and withdrawing the probe allows scanning of the entire length of the
aorta. This view can help demonstrate descending aortic aneurysm and
atheroma,. Rotation will differentiate artefact from true abnormality,
particularly when dissection suspected.
Aortic views can also demonstrate the aortic isthmus, and the ostium,
and proximal part, of the left subclavian artery. This landmark is used
to describe extent of dissection or help assess placement of intra-
aortic balloon pumps.
Emergency evaluation of the aorta
In an emergency where aortic dissection is a major indication proceed
immediately to the 135° long axis view. This view shows the aortic
annulus, aortic valve, and proximal ascending aorta with sinuses of
Valsalva and right and non-coronary leaflets of the aortic valve. A proxi-
mal aortic dissection flap or excessive dilatation of the sinus of Valsalva
is therefore readily diagnosed. Pericardial fluid and aortic regurgitation
can also be detected.
AORTA
515
Short axis view—50°
Long axis view—135°
PULMONARY
ARTERY
AORTA
LA
LA
RA
RV
AORTA
LV
RV
5-chamber view—0°
Aortic view (multiple levels)—0° and 90°
AORTA
RA
LA
AORTA
RV
LV
AORTA
Fig. 7.20 Key views to assess the aorta.
516
CHAPTER 7 Transoesophageal chambers and vessels
Aortic size
Proximal aorta
Make measurements in 2D imaging from mid-oesophageal 135° long
axis view in systole (with valve leaflet tips open to their maximum).
Standard measures are annulus, sinus of Valsalva at aortic leaflet tip
level, sinotubular junction, proximal ascending aorta (Figs. 7.21 and 7.22).
3D TOE to measure aortic annulus
Measurement of the aortic annulus and proximal aorta is of particu-
lar importance in determining suitability of patients for transcutaneous
aortic valve implantation (TAVI) and selecting appropriate prosthesis
size. Use of 3D imaging and the X-plane modality helps ensure true
cross-sectional diameter being measured.
Either obtain short-axis 50° view of aortic valve and then position
X-plane cursor though centre of valve to obtain true long-axis cut,
or preferably, obtain a full volume 3D dataset of the aortic valve and
post process to get a precise cross section at the different levels.
The key level is at the level of the aortic annulus and measurements
should be taken from hinge point to hinge point. Measurements in 2
axes should also be performed as the annulus is often not circular.
It is likely that measurement of true orifice (aortic annulus) from 3D
images will become viewed as the standard. 3D measures are often
slightly larger than 2D measures.
Arch and descending aorta
In aortic short axis 0° view measure aortic diameter at different levels.
Record the distance from incisors (40cm, 35 cm, 30cm) for each
measure. When withdrawn to the aortic arch rotate to 90° to get a
cross-section and measure diameter.
AORTIC SIZE
517
PROXIMAL
ASCENDING
SINUS VALSALVA
AORTA
AORTIC ANNULUS
SINOTUBULAR
JUNCTION
0
139
180
Fig. 7.21 Standard measures of aortic root and proximal aorta in long axis 135° view.
DESCENDING AORTIC DIAMETER
Fig. 7.22 Standard measures of descending aorta diameter from short axis aortic
view.
518
CHAPTER 7 Transoesophageal chambers and vessels
Aortic atherosclerosis
Aortic atherosclerosis is easily seen with TOE. Assessment is important
when hunting for embolic source or before surgery for impression of likely
coronary atherosclerotic disease. Risk of embolic events increases incre-
mentally with extent of atheroma and is dramatically higher once plaque
extends beyond 4mm. Severity is strongly associated with risk factors for
atheroma and, incidence and severity of carotid and coronary disease.
Site of atherosclerosis is not always correlated with stroke localization
and presence of atherosclerosis may simply be a marker of generalized
atherosclerosis.
Assessment
Atherosclerosis is seen as wall thickening, irregular plaque, or as ulcerated,
thrombotic, mobile plaque. Significant atherosclerosis increases the risk
for dissection and aneurysm formation.
In aortic views scan up the descending aorta and aortic arch. Also
assess proximal ascending aorta.
Measure wall thickness at several sites and in particular at any position
where there are irregularities. Aortic thickness is intima-media
thickness. The wall is seen as 2 white lines separated by a black space.
Intima-media thickness is the thickness of the inner white and black
bands added together (Fig. 7.23).
Grade atherosclerosis within the different sections of the aorta as mild,
moderate, or severe (Fig. 7.24).
• Normal wall thickness <2mm.
• Mild atherosclerosis wall thickness 2-4mm moderate
atherosclerosis wall thickness >4mm.
• Severe atherosclerosis irregular protruding plaque (Fig. 7.25).
Comment on specific lesions, such as thrombus or ulcerated plaques,
and comment on location and depth.
AORTA
INTIMA
MEDIA
Fig. 7.23 Measurement of aortic intima media thickness.
AORTIC ATHEROSCLEROSIS
519
NORMAL
MILD (THICKENING 2-4mm)
MODERATE (THICKENING >4mm)
SEVERE (IRREGULAR AND PROTRUDING)
Fig. 7.24 Grades of atheroma within the aorta. See W Video 7.12.
Fig. 7.25 Live 3D acquisition of aorta demonstrating atheroma.
520
CHAPTER 7 Transoesophageal chambers and vessels
Aortic dissection
TOE allows diagnosis and serial monitoring of aortic dissection. Diagnostic
utility with experienced operator is good and comparable to other
modalities (sensitivity and specificity >97%).
Diagnosis
TTE should routinely be performed first as this may be diagnostic and
negate need for TOE.
For transoesophageal imaging adequate sedation and good technique
are essential. Excessive retching can cause acute blood pressure
rise, which could extend dissection and cause acute haemodynamic
deterioration. Therefore, if concerns particularly if haemodynamic
instability consider performing study in theatre with cardiac surgeon
available.
Use all aortic views to scan all of aorta in short and long axes
(Fig. 7.26). In short axis, look for an enlarged aorta with a line across
lumen dividing true and false lumens. True lumen is usually smaller.
Colour flow mapping can be used to demonstrate high velocity flow in
the true lumen and no, or slow flow, in false lumen. In long axis views
dissection flap may be seen as a linear mobile structure with motion
independent of the aortic wall. See Table 7.4.
Limitations—false negative and false positive findings
The distal ascending aorta cannot be assessed by TOE due to
interposition of trachea and left bronchus. Thus pathology in about
5cm in length may be missed. However, isolated dissection in this
location is rare. False negative studies can occur due to localized
root dissection with pericardial haematoma but no false lumen.
Linear artefacts have to be distinguished from real intimal flaps.
Reverberation is the most frequent source of these artefacts. Strong
backscatter from various tissue-fluid interfaces such as the anterior
aortic valve or Swan-Ganz catheters in the pulmonary artery can
cause linear echoes in the aortic lumen. They are typically found at
double the distance from the transducer compared to the source of
the reverberation. Also mirror artefacts showing a reduplication of
the aortic lumen are possible. A real intimal flap should be visible in
at least 2 planes. See Table 7.5.
3D echocardiography is particularly useful in differentiating dissection
flap from artefact: a true flap can be visualized as a sheet, rather than
a linear structure if artefactual.
AORTIC DISSECTION
521
LUMEN DIAMETER AND
DEPTH ANNOTATION
DISSECTION PLANE
40cm
FALSE LUMEN
TRUE LUMEN
TRUE LUMEN
DISSECTION FLAP
0
0
180
FALSE LUMEN
Fig. 7.26 Short axis (top) view of a dissection with measures or false and true
lumen. Long axis view (bottom) of aorta demonstrating dissection flap. See W
Video 7.13 and W Video 7.14.
522
CHAPTER 7 Transoesophageal chambers and vessels
Assessment
If an aortic dissection is diagnosed (Fig. 7.27) or the study is for serial monitor-
ing of a known dissection the objectives of the investigation should be to:
Perform all standard aortic measures and measure diameter of true
and false lumens at different levels.
Try and identify start and end of dissection and record positions.
This allows serial monitoring of size and length of dissection. In the
ascending aorta dissections tend be along the greater curvature and in
the descending aorta may spiral around the true lumen.
Multiple tears may be present and sometimes it is not possible to
locate the entry site with transoesophageal imaging. As you scan
up the aorta use colour flow to identify connections between true
and false lumens (will be seen as colour flow jets). If seen, measure
positions and direction of flow.
Comment on and quantify aortic regurgitation. Aortic valve
insufficiency can occur due to dilatation of the aortic root, impaired
cusp movement by ring haematoma, impaired cusp support and cusp
prolapse, or prolapse of the dissecting flap into outflow tract.
Comment on pericardial fluid and evidence of tamponade.
Assess global and regional left ventricle function in case of coronary
artery involvement. 10% of dissections involve the coronary ostia.
Use 3D assessment to confirm nature and extent of dissection flap.
Orientate the probe in 2D just above aortic valve in cross section
initially. Look for coronary ostia to confirm or exclude involvement:
this may be better visualized and appreciated in 3D. Perform 3D
colour flow study to look for additional tears, the number and extent
of which may be under-appreciated on 2D imaging.
When monitoring dissection, review last study and repeat all measures.
Highlight any changes in appearances or size.
Surgery for aortic dissection
Preoperative
If performing echocardiography before Type A dissection surgery:
Check diagnosis and differentiate between acute dissection, leaking
aneurysm or intramural haematoma. Type and timing of surgery will
vary significantly.
Look at aortic valve cusps and aortic root. If normal cusps, and
aortic annulus and sinotubular junction normal size, then even if
regurgitation is seen, inter-position ascending aortic graft replacement,
rather than total aortic root replacement, can be considered.
Postoperative
Ensure successful repair and no residual evidence of dissection. If native
valve was preserved, ensure normal valve function.
AORTIC DISSECTION
523
Table 7.4 Differentiating true from false lumen
True lumen
False lumen
Diameter
True < false
False > true
Pulsation
Systolic expansion
Systolic compression
Blood flow
Systolic, antegrade
Reduced
Spontaneous contrast Rare
Frequent
Thrombus
Rare
Frequent, depending on flow
communication
Localization
Inner, anterior contour Outer, posterior contour
Table 7.5 Differentiating intimal flap from artefact
Intimal flap
Artefact
Borders
Definite
Indistinct
Movement
Rapid, oscillatory
Parallel to strong reflector
proximal to artefact
Extension
Within aorta
Beyond aortic wall
Colour Doppler
Homogenous colour
Different colour
on both sides
communicating jets
3D
Sheet like appearance
Linear
Fig. 7.27 3D TOE demonstrating dissection flap in the aorta. See WVideo 7.15.
524
CHAPTER 7 Transoesophageal chambers and vessels
Intramural haematoma
There is debate as to whether aortic intramural haematoma is a discrete
pathological entity or precursor of aortic dissection. Haematoma tends to
occur in older patients with hypertension.
Diagnosis and assessment
Intramural haematoma is seen as a generalized thickening of the media
without obvious disruption of the intima and no flow communication.
Wall thickness >7mm suggests haematoma (normal <4mm).
Can affect any area of aorta. Intramural haematoma in ascending aorta
is usually managed similar to type A dissection.
Differential diagnosis of haematoma is atherosclerotic disease with a pen-
etrating aortic ulcer. Penetrating ulcer is always: associated with heavy
atheroma; predominantly affects descending aorta; intima is irregular with
thickening above the intima. Atherosclerosis is also suggested by inward
displacement of any intimal calcification with homogenous mottled thick-
ening of wall either side of the displacement.
Aortic transection or traumatic aortic
disruption
Usually occurs at aortic isthmus following acceleration/deceleration injury
(e.g. restrained passenger or driver in road traffic accident). Usually other
traumatic injuries.
To differentiate from dissection:
Transection is disruption of media rather than intima, resulting in
relatively thick flap, usually very mobile, and perpendicular to aortic
wall (aortic dissection is intimal, with thin flap parallel to wall).
There is usually no thrombus in the false lumen but there may be a
mediastinal haematoma.
Usually asymmetric aortic shape. >4mm difference in anteroposterior
and longitudinal aortic dimensions (dimensions similar with dissection).
Colour flow mapping reveals similar velocities on both sides of any
flap, with turbulence around the point of disruption (turbulence
unusual in dissection and usually slower velocities in false lumen).
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526
CHAPTER 7 Transoesophageal chambers and vessels
Aortic coarctation
Usually diagnosed from transthoracic assessment of Doppler flow in
suprasternal view. Accurate transoesophageal imaging can be difficult but
images are best obtained by examining the descending aorta at 0° in mul-
tiple sections to identify the isthmus. At level of isthmus, rotate to a 90°
longitudinal view to identify the origin of the left subclavian artery. Look
for irregularity of aortic lumen. Morphology of aortic coarctation is often
complex and further imaging is usually necessary.
Assessment
Measure size of aorta proximal, distal, and at the coarctation. For
follow-up, post-repair, compare with previous studies to look for
repair dilatation or persistent gradient.
PW Doppler in long axis aortic views can be used to look for flow
acceleration across a coarctation.
3D volume set acquired at level of maximal narrowing can help
appreciate complexity of coarctation.
Sinus of Valsalva aneurysm
A rare, congenital abnormality (<1:1000 patients). Acquired aneurysms
are even rarer and are predominantly due to endocarditis, trauma, syphilis,
or tuberculosis. Often an incidental finding. When symptomatic, rupture
causes chest pain and breathlessness or, with smaller ruptures, more insidious
onset congestive cardiac failure.
Assessment
Use the 135° long axis view (>95% originate from either right or non-
coronary cusps, both visualized). Aneurysm usually has a wind-sock
appearance blowing in either right atrium or right ventricle.
3D imaging from this view can clarify relationship to cardiac chambers
and aid with planning of interventional approach.
Colour flow mapping will show an aortic to cardiac chamber shunt.
CW Doppler assessment confirms continuous flow.
Use a 50° aortic short axis view with slight probe withdrawal to level
of coronary sinus to identify coronary arteries and exclude coronary
artery fistula as an important differential diagnosis.
Haemodynamic effect of a ruptured coronary sinus is best assessed from
size of atria and left ventricle, reflecting extent of volume overload.
Thoracic aortic aneurysm
Thoracic aortic aneurysm is usually suspected on chest X-ray or TTE.
Confirmation can be by CT, magnetic resonance imaging, or TOE
(Fig.
7.28). CT and magnetic resonance imaging have the advantage of
showing the true extent of the aneurysm and clear identification of the
origin of the head and neck vessels, while TOE more accurately delineates
flow patterns within the aneurysm, the presence of thrombus, and the
presence of atherosclerotic debris.
THORACIC AORTIC ANEURYSM
527
0
111
180
DILATED
ASCENDING
AORTA
Fig. 7.28 Measurements of a dilated ascending aorta.
528
CHAPTER 7 Transoesophageal chambers and vessels
Masses
Masses are usually much clearer on TOE than TTE and therefore TOE is
indicated for definition of masses (Fig. 7.29). Abnormal masses are vegeta-
tions or very rarely thrombi or tumours (see b p.326).
Report position, size, and functional effects. Comment on any suspicions
as to the nature of the mass but remember that echocardiography is
unlikely to give the definitive diagnosis.
Differential diagnosis of masses
Like TTE, transoesophageal imaging does not provide a specific tissue
pattern of the tumours (the exception being lipomas). Therefore it is
not possible to differentiate masses (tumours, thrombi, and vegetations)
according to their structure on echocardiography. However there are
associated features, which help to make a diagnosis.
Myxomas
Myxomas are the most frequent cardiac tumours and usually originate
from the fossa ovalis of the interatrial septum. They also may be found in
other chambers.
Fibroelastoma
Fibroelastoma are mobile tumours on the upstream side of the aortic
valve (rarely mitral valve). In comparison to vegetations there are usually
no other valvular lesions.
Lipomatous interatrial hypertrophy, lipoma in the tricuspid ring
These lipomatous changes have a characteristic high density appearance
but do not result in acoustic shadowing like calcification.
Thrombi
Thrombi are usually associated with reduction in blood flow (atrial fibrilla-
tion, dilated heart chambers, altered or artificial valves or atheroma)
Exceptions to this principle are thrombi associated with coagulopathy and
left ventricular non compaction or on aortic atherosclerosis.
Vegetations
Vegetations are associated with other clinical signs of endocarditis
(e.g. raised inflammatory markers, positive blood cultures).
If the study is for benign or malignant tumours, and there is suspicion of
an extracardiac tumour, consider whether there might be oesophageal
involvement. If this is possible then consider an endoscopy or other
imaging before performing transoesophageal imaging.
MASSES
529
Aorta
THROMBUS
LA
Aorta
LV
FIBROELASTOMA
Fig. 7.29 Examples of aortic thrombus (top) and fibroelastoma (bottom). See W
Video 7.16 for an example of myxoma.
530
CHAPTER 7 Transoesophageal chambers and vessels
Cardiopulmonary bypass and coronary
artery surgery
If cardiopulmonary bypass is used for coronary artery surgery in a patient
with normal left ventricular function and no significant valve disease, it
remains a matter of debate whether intraoperative TOE is used routinely.
However, a comprehensive study performed before establishing cardiop-
ulmonary bypass, provides a comparison for postoperative studies in par-
ticular in patients with suboptimal target vessels and challenging grafting.
Indications
TOE is strongly indicated in coronary artery surgery complicated by:
severe cardiac dysfunction; significant ischaemic mitral regurgitation;
large left ventricular aneurysm; mural thrombus; left ventricular
remodelling (Dor procedure); recent myocardial infarction; ischaemic
ventricular septal defect; requirement for left ventricular assist device
support post surgery.
TOE should be used when a patient preoperatively has mild to
moderate aortic or mitral valve disease to determine whether valve
surgery is also required. Postoperative echocardiography is required to
assess cardiac function and valve performance whether the valve was
operated on or not.
Coming off bypass
Start monitoring with transoesophageal imaging soon after the aortic
cross clamp is removed. Monitor de-airing of the left heart and aorta and
then watch to ensure restoration of cardiac function. After the patient is
weaned off bypass, ensure stable systemic haemodynamics (i.e. systolic
blood pressure >90-100mmHg, adequate left ventricular filling) then assess
effectiveness of surgery. For all surgery, determine global and regional
cardiac function using standard techniques. If global cardiac dysfunction
develops consider:
Was there satisfactory myocardial preservation, in particular with
concomitant coronary artery disease?
Was there a large amount of air emboli into a coronary (particularly
the right as this is uppermost in the supine patient)? Usually causes
severe right, and some left, ventricular failure with significant
tricuspid and mitral regurgitation. Further cardiopulmonary bypass
may be required to wash out air emboli. Monitor recovery with
echocardiography.
Is there insufficient flow in the bypass grafts (kinking, sutures, etc.)
causing regional wall motion abnormality?
CARDIOPULMONARY BYPASS AND CORONARY ARTERY SURGERY
531
Failure to wean off bypass
A possible urgent call for TOE is to evaluate a patient who has failed
to come off bypass following surgery. Ensure you are familiar with what
surgery is being performed and what the preoperative investigations and
transoesophageal findings were i.e. valve disease, left ventricular func-
tion, and degree of coronary disease. Although there could be many
causes look for:
Massive mitral or aortic regurgitation due to prosthesis failure
Acute right ventricular failure due to air emboli (the right coronary
artery is particularly prone to air emboli because of its proximal
position and therefore ‘upper’ position in the supine patient).
Left ventricular failure due to intraoperative myocardial infarction. This
could be due to concomitant coronary disease without sufficient coro-
nary protection or surgical injury (to a coronary ostia in aortic surgery
or the circumflex coronary artery in mitral surgery). Check regional wall
motion abnormalities as a guide to which artery may be affected. Look
at coronary ostia lumen size and flow in short axis views.
532
CHAPTER 7 Transoesophageal chambers and vessels
Off-pump coronary artery bypass
Transoesophageal monitoring can be useful in off-pump coronary artery
bypass graft surgery to monitor cardiac function and potential mitral
regurgitation. Beware of the following aspects of off pump surgery:
Imaging of left ventricular wall motion is limited by the stabilizer
apparatus, which tethers the adjacent myocardium.
During right coronary artery and circumflex grafting major
displacement of the heart does not allow reliable imaging.
Distortion of the heart can also cause transient mitral regurgitation or
increase in right atrial pressure and a shunt via a patent foramen ovale.
It is best to restart imaging after completion of anastomoses and
release of the stabilizer.
For a short period after the anastomosis regional wall motion
abnormalities are seen, representing stunned myocardium. If wall
motion abnormalities are persistent, graft patency should be checked.
Ischaemic mitral regurgitation
Ischaemic mitral regurgitation is regurgitation due to incompetent mitral
valve systolic coaptation with normal valve leaflet structure, in the pres-
ence of ischaemic heart disease. Commonly due to tethered mitral leaflets
after basal posterior myocardial infarction, combined with mild to mod-
erate mitral annulus dilatation. Less frequently due to papillary muscle
dysfunction or detachment.
It is usually present before surgery. In this case imaging has to
assess the severity to decide on the need for mitral valve repair or
replacement. To plan surgery (approach, mitral valve ring size etc.)
measure leaflet tethering distance (distance between posterior
papillary muscle and mitral valve posterior annulus) and mitral valve
annulus diameter.
Ischaemic regurgitation may also evolve during coronary bypass
surgery due to insufficient grafting to the right coronary artery or
diffuse myocardial ischaemia. Ischaemic mitral regurgitation is dynamic
so tends to be less severe during surgery because of the reduced left
ventricular afterload and the general anaesthetic. Moderate to severe
regurgitation on intraoperative echocardiography requires surgical
intervention.
Aneurysm repair
Before and during ventricular aneurysm resection or apex remodelling
(Dor procedure) echocardiography should focus on:
Presence, mobility, and distribution of mural thrombus.
Involvement of mitral valve apparatus and papillary muscle.
Mitral regurgitation caused by surgery.
Amount and function of residual myocardium.
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534
CHAPTER 7 Transoesophageal chambers and vessels
Haemodynamic instability
On the Intensive Care Unit and during intraoperative monitoring TOE
provides a quick and reliable way to investigate the cause of haemodynamic
instability. Haemodynamic instability usually means unexplained hypotension
in some cases associated with unexplained hypoxaemia. TOE provides
information on both intrinsic cardiac causes (e.g. ventricular function,
valve function) and extracardiac factors (e.g. left ventricular preload and
afterload). Assessment should take into account the clinical history and
follow a standard routine to try and exclude common cause (Table 7.6).
Chapter 11 provides information on how to use TTE in this setting.
Hypotension due to hypovolaemia
Hypovolaemia causes reduced left ventricle preload/filling. A simple meas-
ure of preload/filling is the left ventricular end-diastolic area in the short-
axis transgastric view. This view can be used for monitoring during surgery.
It is useful if a baseline area is known (e.g. preoperative or at start of
surgery) in order to judge change from normal filling.
Hypovolaemia causes a reduced end-diastolic left ventricular volume
and, with preserved left ventricular function, an even greater reduction
in end-systolic volume. This results in a very high fractional area
change.
If hypovolaemia is diagnosed, the response to fluid therapy should be
monitored. Optimal filling of the left ventricle is achieved when further
volume supplements do not result in further increases in end-diastolic
left ventricular area. Further volume then merely causes increase in left
ventricular end-diastolic pressure.
Hypotension due to reduced peripheral resistance
Reduced peripheral resistance (e.g. due to sepsis) results in much higher
stroke volumes. End-diastolic volume therefore remains normal but the
end-systolic volume is reduced. This again leads to an increased fractional
area change.
Hypotension due to ischaemia
If there is clinical suspicion of myocardial ischaemia it is useful to compare
any new findings to the preoperative assessment of cardiac function. Look
for:
Left ventricular systolic global and regional function.
Right ventricular systolic dysfunction. Right ventricular dysfunction
is often associated with right ventricular dilatation, tricuspid
regurgitation, paradoxical septal movement and a decrease in left
ventricular chamber size can sometimes occur.
True or pseudo-aneurysm and/or right ventricular rupture in those
known to have had an infarct.
Ischaemic ventricular septal defect or papillary muscle rupture.
Pericardial effusion or tamponade.
HAEMODYNAMIC INSTABILITY
535
Table 7.6 Conditions causing hypotension. Severe aortic stenosis can
also be associated with hypotension and is identified from changes to
the aortic valve and transvalvular gradient. Aortic dissection can cause
hypotension due to associated pericardial effusions and tamponade,
hypovolaemia or aortic regurgitation
Condition
End-diastolic End-systolic Ejection Cardiac
Associated findings
volume*
volume*
fraction** output
Decreased preload
d
dd
i
d
Hypovolaemia
Decreased afterload n
dd
ii
i
Vasodilation/sepsis
LV dysfunction
i
ii
dd
d
Global/regional wall
motion,
rupture
RV dysfunction
d
d
(d)
d
Dilated right heart
thrombus in
pulmonary artery
Tamponade
d
d
d
d
Effusion
*Left ventricle end-diastolic and end-systolic areas in the short axis transgastric views may be
used as markers of left ventricle volume.
**Fractional area change can be substituted for ejection fraction.
536
CHAPTER 7 Transoesophageal chambers and vessels
Unexplained hypoxaemia
Hypoxaemia suggests inadequate lung perfusion. In ventilated patients this
may be a greater than normal need for respiratory support. Cardiac causes
can include right ventricle dysfunction, pulmonary embolism, or right-
to-left shunts. Investigations should also look for primary lung pathology
(e.g. pneumonia with associated sepsis).
Pulmonary embolism
Pulmonary embolism is not easy to diagnose (and can not be excluded)
because large emboli are needed to induce haemodynamic changes or to
be visualized. Helpful features to suggest pulmonary embolism include:
Indirect signs
Dilated right atrium. Dilated and diffusely hypokinetic right ventricle.
Dilated pulmonary artery. (An increased right ventricle wall thickness
suggests a more chronic problem, e.g. pulmonary hypertension.)
An increase in tricuspid regurgitation because of raised pulmonary
artery pressure. Judge pressure from the tricuspid regurgitation.
(However, cardiac shock can lead to a normal gradient.)
Direct signs
Thrombus in the inferior or superior vena cavae, or pulmonary artery.
There are 2 types of thrombi. Type A are highly mobile and
vermiform. They derive from deep veins and can become trapped in a
Chiari network, tricuspid valve chordae or right ventricle trabeculae.
Type B originate from chamber walls, leads, or prostheses.
To see the pulmonary artery withdraw the probe slightly from an
aortic 50° view and angulate the probe forward. The right pulmonary
artery can be seen wrapping around the aorta. The left pulmonary
artery is obscured by the bronchus.
Patent foramen ovale
In suspected pulmonary embolism always assess the inter-atrial septum.
High right atrial pressure opens the foramen and can cause significant
right-to-left shunting. With successful treatment of the embolism the
shunt reduces and then disappears. Paradoxical embolism is possible and
sometimes thrombi can be trapped in the septum.
Right-to-left shunt
Right-to-left shunts can be intracardiac or intrapulmonary. Base initial sur-
vey on colour flow mapping of the atrial and ventricular septa. If no shunt
is displayed by colour flow mapping use agitated saline contrast, injected
through a central line.
If an intracardiac shunt, contrast will pass from right to left atrium, or
from right to left ventricle immediately after arrival in the right atrium.
If an intrapulmonary shunt, contrast will appear in the left atrium via the
pulmonary veins at least 3 beats after the right atrium.
If there is a known pre-existing left-to-right shunt this may be turned
into a right-to-left shunt by the type of surgery, ventilation, or a
super-added pulmonary embolism. Positive end-expiratory pressure
ventilation may open a patent foramen ovale in the presence of severe
pulmonary embolism.
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538
CHAPTER 7 Transoesophageal chambers and vessels
Mechanical cardiac support
Intra-aortic balloon pump
TOE can be used to identify contraindications to a balloon pump and en-
sure the balloon is correctly placed in the thoracic descending aorta, distal
to the subclavian artery (Fig. 7.30).
Complicating factors
Possible contraindications include: descending aortic aneurysm, moderate
to severe aortic regurgitation, severe atheroma.
Placement
To localize the balloon tip start with an aortic arch view. Try and locate
the left subclavian artery origin then advance the probe until the tip of the
balloon pump comes into view. It should be several centimetres below
the left subclavian artery. The tip appears as a bright mark in the centre of
the aorta, with associated artefacts. If the probe is advanced further the
balloon may be seen deflating and inflating in the aorta.
Left ventricular assist devices
Left ventricular assist devices take blood from a cannula placed in the
left atrium or left ventricle, pass it through an extracorporeal pump, and
then pump the blood back into the circulation via a tube inserted into
the ascending aorta. TOE can help in placement, assessment of device
function, and device weaning.
Complicating factors
Before placement, imaging should be used to identify possible contraindi-
cations and complications.
Aortic regurgitation may deteriorate after device placement because
of increased backflow into a relatively decompressed left ventricle. In
moderate aortic regurgitation valvular surgery has to be considered
prior to device placement.
Thrombi within the ventricular cavities may be mobilized by assist
device tubes and should be excluded.
Aortic atheroma may be dislodged during cannula insertion.
Right ventricular dysfunction should be assessed in case right
ventricular assistance is required.
Patent foramen ovale should be identified. Significant right-to-left
shunting can be found after left ventricular assist device placement.
The device significantly offloads the left heart and drops left atrial
pressure, whereas the right atrium remains at a relatively high
pressure.
MECHANICAL CARDIAC SUPPORT
539
LEFT
SUBCLAVIAN
ARTERY
POSITION OF INTRA-
AORTIC BALLOON
PUMP
ASCENDING
AORTA
Fig. 7.30 Position of intra-aortic balloon pump in aorta. The top of the balloon can
be imaged in aortic views.
540
CHAPTER 7 Transoesophageal chambers and vessels
Placement
During placement of a left ventricular assist device use TOE to report to
the surgeon:
Cannulae
Position of the atrial cannula (should be in centre of atrium). It should
not lie against a wall and be away from the subvalvular apparatus.
Flow in the cannulae (can be displayed using colour flow mapping).
Flow pattern in the descending aorta.
De-airing of the system by observing clearing of bubbles through the
ascending or descending aorta.
Changes to valves and septum
Patent foramen ovale, which may have been missed pre-placement.
Presence of tricuspid regurgitation.
Competence of the aortic valve.
Changes to chamber function
Whether adequate left ventricle offload is achieved.
Left atrium filling status and size.
Right ventricle volume status and contraction.
During use
After placement, TOE should monitor for bleeding and pericardial effu-
sion. This is common during the first 24 hours of support and can cause
cardiac tamponade.
Weaning
On removal, TOE should be used to judge weaning of left ventricle
assist support. The emphasis should be on watching the effect of reducing
support on left ventricular function. The left ventricle should gradually
improve and take over haemodynamic function.
Monitor response of the left ventricle to resumed volume loading at
both regional and global levels.
Look at mitral valve competence and systemic haemodynamics.
Check that improvement in left ventricle function is sustained with
minimal support rather than just a shorted-lived improvement of left
ventricle contraction.
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542
CHAPTER 7 Transoesophageal chambers and vessels
Pleural space and lungs
As the probe is rotated during the study the lungs and pleura may come
into view. It is difficult to give accurate information about lung pathology
because they are full of air which does not allow good ultrasound views.
Pleural effusions are easily recognized as crescent or ‘tiger claw’ shaped
areas of fluid. The principle to determine whether it is a right or left effu-
sion is to look at the way the ‘tiger claw’ points. If it points to the right it is
a right-sided effusion and if to the left, a left-sided effusion (Fig. 7.31).
PLEURAL SPACE AND LUNGS
543
RIGHT-SIDED EFFUSION
LEFT-SIDED EFFUSION
AORTA
Fig. 7.31 Pleural effusions.
544
CHAPTER 7 Transoesophageal chambers and vessels
Pacing wires and other implants
As well as prosthetic valves a series of other artificial devices will be seen
during transoesophageal studies. Right-sided implants include pacing and
defibrillator wires in the right atrium and ventricle and central lines in the
superior vena cava and right atrium (Fig. 7.32).
Increasingly, percutaneous closure devices are being implanted. Most
commonly these are seen across the atrial septum but can also be posi-
tioned in the ventricular septum or beside prosthetic valves to close para-
prosthetic leaks. Left atrial appendage occluder devices are also implanted
in some centres. Make sure you check the notes before and during the
procedure if there is an unusual feature identified.
PACING WIRES AND OTHER IMPLANTS
545
LA
ATRIAL PACING WIRE
LA
RA
CENTRAL VENOUS LINE
LEFT ATRIAL OCCLUDER DEVICE
LA
LAA
LV
Fig. 7.32 Examples of pacing wires, central lines, and an atrial occluder.
See W Video 7.17, W Video 7.18, W Video 7.19, W Video 7.20.
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547
Chapter 8
Intracardiac
echocardiography
Background 548
Indications
548
Equipment 550
Procedure 550
Imaging planes 552
Atrial septal interventions
556
Electrophysiological interventions
560
Additional uses 560
548
CHAPTER 8 Intracardiac Echocardiography
Background
Since its initial use over 30 years ago, intracardiac echocardiography
(ICE) has become increasingly available and important as an alternative
to TOE primarily to guide percutaneous interventions and support
electrophysiological procedures.
The limitations of the earliest ICE catheters used (poor tissue
penetration and difficult manipulation) have been overcome with
catheters that use lower frequencies (enabling tissue penetration of up
to 12cm) and have better manoeuvrability (Table 8.1).
ICE provides high-resolution images of cardiac structures which can be
displayed as M- and B-modes, with Doppler (CW, PW, or colour flow
imaging) or reconstructed into 3D (mainly used in research only at the
moment but clinical 3D ICE is not far off now).
Advantages of ICE over TOE during percutaneous interventions
include clearer imaging, shorter procedure times and the use of local
(rather than general) anaesthesia.
ICE catheters are for single-use only and the additional cost that this
incurs is the principal disadvantage although this may be offset by the
shorter procedure times, improved patient turnaround, and reduced
personnel costs.
ICE is ideal for imaging PFO closures as these procedures can now be
performed as a day case under local anaesthetic with total procedure
times of around 30min.
As visualization of the septum is so accurate, ICE has also been
shown to reduce the need for fluoroscopy when compared to
TOE-guided procedures with a reduction in radiation doses used,
shorter procedure times, and shorter hospital stays.
ICE catheters are not inserted ‘over a wire’ and are relatively stiff so
careful intravascular and intracardiac manipulation is required to avoid
perforation.
Indications
Percutaneous ASD/PFO closure.
Percutaneous closure of perimembranous ventricular septal defects.
Balloon mitral commissurotomy.
Left ventricular or atrial septal pacing.
Septal ablation for hypertrophic cardiomyopathy.
Guiding the biopsy of cardiac masses.
Pulmonary valvuloplasty.
Guiding transseptal access during electrophysiological procedures.
Catheter ablation of arrhythmias for defining anatomy.
Paravalvular leak closure.
Left atrial appendage occlusion.
Transcatheter aortic valve implantation.
INDICATIONS
549
Table 8.1 Commercially available ICE catheters
ICE catheter
Company Features
Name
AcuNav®
Biosense
8F or 10F
Webster
5.5-10MHz
64-element phased-array.
PW Doppler, colour Doppler
4-way head articulation for multiple steering
ViewFlex®
St Jude
9F
Medical
4.5-8.5MHz
64-element linear phased-array
Pulsed wave Doppler, tissue Doppler
Bidirectional curved tip
Ultra ICE™
Boston
9F
Scientific
Mechanical catheter
Greyscale imaging
SoundStar™3D Biosense
10F
Webster
5.5-10MHz
64-element linear phased-array
Embedded position sensor allows location
and beam orientation of catheter
550
CHAPTER 8 Intracardiac Echocardiography
Equipment
Mechanical catheters
Mechanical transducers have a rotating element (9MHz) which creates
a 360° imaging plane perpendicular to the long axis of the catheter.
The transducers provide a tissue penetration of around 4cm.
The main limitations of mechanical catheters are the limited imaging
plane (horizontal only), reduced catheter manoeuvrability (versus
more recent phased-array catheters), and the inability to perform
Doppler studies.
Phased-array catheters
Phased-array 64-element transducers are able to scan in a longitudinal
plane, creating a 90° sector image.
Lower range frequencies (5-10MHz) allow better tissue penetration
(up to 12cm).
Improved manoeuvrability is achieved as the head of the catheter has a
multidirection articulation tip and steering locks can maintain catheter
angulation (Fig. 8.1).
Procedure
Patient preparation
Patient preparation relates to the interventional procedure that is to be
undertaken. Normally this will involve:
Pre-procedural fasting for 4 hours. An important aspect for ICE is that
the patient should not be dehydrated so give IV fluids if necessary.
Insertion of a peripheral cannula to allow delivery of sedation if
needed. Both inguinal areas should be prepared and draped.
Catheter preparation
A connector is used to link the ICE catheter to the ultrasound
machine. The connector is covered in a sterile sleeve then connected
to the ICE catheter. Check the catheter steering mechanism before
use.
Vascular access
Venous access is usually obtained via the right femoral vein using a
Seldinger technique although the right jugular vein has also been used.
The catheter is manipulated into the right atrium. Special caution is
needed when manipulating the catheter through the pelvic veins and
fluoroscopy screening is recommended to avoid the catheter catching
on venous branches (Fig. 8.2).
Sometimes gentle AV steering is needed tortuous vessels.
Placement of a guidewire through an adjacent sheath can help guide
the catheter into the right heart, or insertion of a longer sheath
(e.g. 12Fr Mullins sheath) to the IVC or right atrium in particularly
difficult cases.
PROCEDURE
551
Fig. 8.1 AcuNav intracardiac echocardiography catheters. Image courtesy of
Biosense Webster, Inc.
Fig. 8.2 Fluroscopy of the ICE catheter in the right atrium.
552
CHAPTER 8 Intracardiac Echocardiography
Imaging planes
With the use of a phased array catheter, all cardiac anatomical landmarks
can be imaged with the probe positioned either in the right atrium or right
ventricle. A structured system of steering and manipulation of the catheter
is recommended to allow a detailed thorough examination, improving op-
erator orientation and recognition of landmarks.
Standard view
The ‘standard view’ (Fig. 8.3) is achieved with the ICE probe sited in the
mid-right atrium and with the scan plane facing anteriorly.
This provides excellent views of the right atrium, right ventricle, and
tricuspid valve.
Withdrawing the catheter to the inferior right atrium brings the
Eustachian ridge and the tricuspid valve isthmus into view.
What do you see?
Right atrium.
Right ventricle.
Tricuspid valve.
Atrial septum
Slowly advancing the catheter whilst gently retro-flexing and rotating the
catheter tip manipulates the probe towards the intra-atrial septum, high-
lighting the fossa ovalis (Fig. 8.4).
In order to avoid foreshortening some left-to-right manipulation may
be needed.
Detailed interrogation of the atrial septum and fossa ovalis can
be obtained and, if needed, agitated saline bubble contrast studies
(b p.506) can be performed to assess for the presence of a patent
foramen ovale.
This position of the catheter for assessment of the atrial septum is
employed for percutaneous septal procedures as it sits in a neutral
position, without interfering with interventional catheters.
What do you see?
Right atrium.
Atrial septum.
Left atrium.
Aortic valve and root
To view the aortic valve in the short axis the catheter tip is retroflexed
and then rotated clockwise towards the aorta (Fig. 8.5).
What do you see?
Aortic valve.
Ascending aorta.
Left ventricle.
IMAGING PLANES
553
Fig. 8.3 Standard view showing the right atrium (RA), right ventricle (RV), tricuspid
valve (TV), and part of the aortic valve (AV). See W Video 8.1.
Fig. 8.4 Atrial septum view showing the right atrium (RA), atrial septum, and left
atrium (LA). See W Video 8.2.
Fig. 8.5 Aortic valve view. See W Video 8.3. NCC = non-coronary cusp,
LCC = left coronary cusp, RCC = right coronary cusp.
554
CHAPTER 8 Intracardiac Echocardiography
Pulmonary veins
The left superior and inferior pulmonary veins can be viewed by increasing
the depth from the atrial septum view (Fig. 8.6). For finer adjustment inferior
angulation may be needed. The right pulmonary veins can be seen by gen-
tle clockwise rotation and superior advancement of the catheter.
What do you see?
Left and right pulmonary veins.
If needed, Doppler studies can be performed to analyse the venous flow.
Left atrial appendage
Advancing the catheter towards the atrial septum and rotating clockwise
brings the left atrial appendage into view.
What do you see?
Left atrial appendage.
Left ventricle.
Mitral valve.
Mitral valve and left ventricle
Advancing the catheter towards the atrial septum and rotating clockwise
brings the left atrial appendage and mitral valve into view (Fig. 8.7).
What do you see?
Left atrium.
Mitral valve.
Left ventricle.
Right ventricle
From the initial standard view the catheter can be flexed and gently
advanced towards the tricuspid valve. With further careful manipulation
under fluoroscopic control the catheter can be placed in the right ventricle
(Fig. 8.8). Typically the catheter lies against the septum and rotated to scan
either the right ventricular free wall or the left ventricle.
What do you see?
Ventricular septum.
Right ventricular free wall.
Left ventricular lateral wall.
IMAGING PLANES
555
Fig. 8.6 Identifying the pulmonary veins.
Fig. 8.7 Mitral valve and left ventricle (LV) view. The atrial septum and left atrium
(LA) are also seen. See W Video 8.4.
Fig. 8.8 Right ventricle (RV) view. RA = right atrium; TV = tricuspid valve.
See W Video 8.5.
556
CHAPTER 8 Intracardiac Echocardiography
Atrial septal interventions
Visualization of the interatrial septum and fossa ovalis with ICE allows a
detailed assessment of the size and length of the PFO ‘tunnel’ and additional
information gained on the mobility of the atrial septum (Figs. 8.9 and 8.10).
The ICE catheter is usually quite stable for guiding the percutaneous
closure of PFO and atrial septal defects (ASDs).
Key views
The following steps in sequence allow full assessment of the atrial septum
during atrial septal interventions:
After advancing the ICE catheter from the inferior vena cava into the
mid-right atrium rotate the probe clockwise. The aorta and LVOT will
initially be seen. Further clockwise rotation will allow visualization of
the lower atrial septum.
Posterior deflection with continued clockwise (posterior) rotation will
obtain a long axis view of the atrial septum.
Moving the catheter cranially and caudally shows the entire atrial
septum.
If appropriate a bubble contrast study can be performed from this
position to document the presence of a PFO.
From here, the left upper and lower pulmonary veins can be visualized
with the aid of Doppler colour flow.
Clockwise rotation of the catheter allows visualization of the right
upper and lower pulmonary veins.
Gentle anterior flexion and clockwise rotation shows the superior
vena cava.
With anterior and lateral movement of the catheter tip a short axis
view of the atrial septum is obtained.
ATRIAL SEPTAL INTERVENTIONS
557
Fig. 8.9 Atrial septal defect (ASD). LA = left atrium; RA = right atrium.
See W Video 8.6.
Fig. 8.10 Colour flow Doppler showing flow across atrial septal defect (ASD).
See W Video 8.7 and W Video 8.8.
558
CHAPTER 8 Intracardiac Echocardiography
Balloon sizing
The long axis view of the atrial septum usually provides the best
imaging plane for balloon sizing (Fig. 8.11).
Colour flow imaging is used whilst obtaining multiple views of the
inflated balloon to demonstrate complete coverage of the defect.
The balloon size can be obtained from anterior and lateral fluoroscopy
images.
Device deployment
Following sizing, a sheath is positioned over a stiff wire into the left
upper pulmonary vein through which the device is delivered.
After device insertion, prior to and following deployment the adjacent
structures should be interrogated to ensure that there was no
encroachment of the device on the atrioventricular valves, the right
pulmonary vein or the inferior or superior vena cava (Fig. 8.12).
Evaluation of the defect during atrial septal intervention
During atrial septal intervention the key views will allow ASD size
estimation by measurement of the distance between the defect to the:
Aortic valve (superior-anterior rim).
Coronary sinus (posterior rim).
Mitral valve (inferior-anterior rim).
Inferior vena cava (inferior-posterior rim).
Special care should be taken to also evaluate the relationship of the
defect to:
Pulmonary veins.
Atrioventricular valve.
Aortic root.
ATRIAL SEPTAL INTERVENTIONS
559
Fig. 8.11 Fluoroscopy showing balloon crossing atrial septal defect (ASD) (left).
Balloon sizing of ASD (right). See W Video 8.9.
Fig. 8.12 Interventional catheter passed across ASD—device starting to deploy
in image shown (left). ICE imaging during percutaneous ASD closure.
See W Video 8.10, W Video 8.11, W Video 8.12, W Video 8.13, W Video 8.14.
560
CHAPTER 8 Intracardiac Echocardiography
Electrophysiological interventions
The advantage of accurate visualization of anatomical structures means that
ICE can be used to guide interventional physiology. Clinical applications of
ICE during electrophysiology include:
Transseptal puncture guidance
During electrophysiology transseptal puncture is very important to
obtain access into the left atrium for ablation procedures.
Historically fluoroscopy has been used to guide the transseptal
puncture. Here, the anatomical structures are not displayed directly
and the needle puncture is guided by the movement during pullback
from the superior vena cava and position in the cardiac shadow
relative to a catheter in the aortic root.
ICE offers the opportunity to guide the transseptal puncture by
directly visualizing the needle tip within the fossa ovalis region.
By detailing the relevant anatomy, ICE can offer the operator further
information when confronted with anatomical variations (atrial septal
aneurysm or lipomatous hypertrophy of the atrial septum, etc).
Colour flow Doppler can also be helpful to identify the puncture site
should the interventional catheter fall back into the right atrium.
Catheter ablation of arrhythmias
The detailed anatomical orientation provided by ICE has the following
advantages during ablation procedures:
A detailed understanding of the anatomy of the pulmonary veins.
ICE provides the ability to confirm stable, complete catheter-tissue
contact which ensures more complete ablation and reduces the
incidence of clot formation on the catheter.
To identify the presence of thrombus within the left atrial appendage.
To confirm the anatomy of the oesophagus in relation to the left
atrium, to reduce the possibility of atrio-oesophageal fistula.
Assists accurate placement of both mapping and ablation catheters.
Operators are able to prevent tissue overheating (and resultant scar
formation, thrombosis, or stenosis) by delivering ablation therapy until
the onset of microbubble formation, ensuring maximal safety.
Images acquired using ICE have recently been combined with
3D electrophysiological mapping catheters to provide additional
anatomical information during ablation.
Additional uses
ICE has also been used to guide catheter occlusion of the left atrial
appendage by deploying the ICE catheter in the pulmonary artery via
a long sheath, and to guide transcatheter aortic valve implantation
(see b p.464), utilizing both transvenous and transarterial placement.
Radiological interventions such as fenestration of aortic dissection flaps
can also be guided with the use of 8Fr intra-arterial ICE.
561
Chapter 9
Contrast
echocardiography
Introduction 562
Specific contrast agent preparation
564
Administration of contrast agents 568
Contrast safety 570
Right-heart contrast study applications
572
Imaging techniques for left ventricular opacification
576
Left-heart contrast study applications
578
Contrast study in dobutamine stress echocardiography 580
Contrast study for myocardial perfusion 582
562
CHAPTER 9 Contrast echocardiography
Introduction
Contrast imaging relies on the use of an injected agent that is very echo-
genic in order to increase the brightness of the ultrasound image. Broad
types of contrast used are those that are normally only held in the venous
circulation and then absorbed in the lungs (right-heart contrast agents)
and those that are present in both the venous and systemic circulations
(left-heart contrast agents).
Both right and left contrast agents essentially consist of gas bubbles of
varying size. On the right this is air contained in saline and on the left a gas
in a lipid or albumin shell (Figs. 9.1-9.3).
Right-heart contrast agents
Right-heart contrast agents such as agitated saline consist of air
microbubbles (of a relatively large size when compared to left-heart
contrast agents). These are short lived and normally diffuse into
the lungs when crossing the pulmonary circulation. The presence
of agitated saline microbubbles in the left heart indicates either the
presence of a right-to-left intracardiac shunt or an arteriovenous shunt
elsewhere in the body, typically in the pulmonary circulation.
The stability of these bubbles can be improved if the agitation is
performed with blood (<0.5ml in 10ml saline).
Other agents used because they contain bubbles include Gelofusine®
(gelatine) but have the risk of allergic reaction.
Uses
To identify the presence of a right-to-left intracardiac shunt due to an
atrial septal abnormality.
To identify the presence of a right-to-left intrapulmonary shunt.
To enhance the delineation of Doppler signals, e.g. the use of agitated
saline contrast can provide a better Doppler signal assessment of the
tricuspid valve.
Left-heart contrast agents
Left-heart contrast agents must be durable and small enough to be
able to cross the pulmonary circulation and pass into the left atrium
following an intravenous injection.
Left-heart contrast agents comprise a microbubble gas centre with
an outer shell. This makes it durable but also small enough for safe
passage across the pulmonary circulation.
Uses
To improve LV endocardial border definition in order to:
• improve image quality and the percentage of wall segments visualized
• improve the confidence of interpretation of wall motion
abnormalities during stress imaging.
• improve accuracy of ventricular volumes and EF measures.
To improve LV cavity opacification to detect pathology e.g. thrombus,
apical HCM, LV non-compaction.
To enhance the delineation of Doppler signals.
To assess myocardial perfusion.
INTRODUCTION
563
Protective outer shell
Inner microbubble gas
centre
Fig. 9.1 Representation of a left-heart contrast molecule.
Backscattered ultrasound wave
Transmitted ultrasound
back to transducer
wave towards the contrast
molecule
Fig. 9.2 The bubble causes backscatter from the transmitted ultrasound wave
which is picked up by the ultrasound transducer.
High power transmitted
ultrasound wave towards the
Destruction of contrast
contrast molecule
molecule and no ultrasound
waves are able to be
reflected back to the
transducer.
Fig. 9.3 Higher power ultrasound waves will cause the destruction of left-heart
contrast agents by causing them to resonate.
564
CHAPTER 9 Contrast echocardiography
Specific contrast agent preparation
Left-heart contrast agents
SonoVue® (Bracco International BV)
Structure: a phospholipid shell filled with sulphur hexafluoride (SF6).
Preparation and storage: it is reconstituted with sodium chloride
(Fig. 9.4). The authors recommend that the contrast is constituted
within a few minutes of injection and to agitate the vial before each
injection is withdrawn. If given as an infusion it needs to be agitated in
a special agitating pump during delivery.
Bolus: recommended dose is 2.0mL. However, the dose derives from
studies using fundamental imaging, which should be avoided. For
harmonic imaging bolus injections of 0.2-0.4mL are adequate. The
bolus should be followed by a 3-5mL bolus of 0.9% sodium chloride or
5% glucose. Total dose should not exceed 1.6mL.
Infusion: for SonoVue® a special agitation pump is used (Fig. 9.5). For
stress studies 2 vials should be drawn up into the syringe. The rate of
infusion should be initiated at 0.8mL/minute, but titrated as necessary
to achieve optimal image enhancement (the range is 0.6-1.2mL/min).
Optison® (Amersham)
Structure: Optison® (Amersham) an albumin shell containing perflutren
gas.
Preparation and storage: it comes in a vial that requires reconstitution
and manual agitation. It is then drawn up into a 2mL or 1mL syringe.
A second needle is used to vent the vial (this can be removed if
repetitive doses are withdrawn. The authors recommend that the
agent is reconstituted directly before injection and the vial agitated
before each dose is withdrawn. It should be stored in a refrigerator
between 2-8°C.
Dose and administration: the recommended dose is 0.5-3.0mL per
patient injected into a peripheral vein. However, that dosage derives
from studies using fundamental imaging, which should be avoided. For
contrast-specific imaging modalities bolus injections of 0.2-0.4mL are
adequate. Total dose should not exceed 8.7mL. The bolus should be
followed by a 3-5mL bolus of 0.9% sodium chloride or 5% glucose.
SPECIFIC CONTRAST AGENT PREPARATION
565
Fig. 9.4 Preparation of SonoVue®. The agent is packaged as dry powder and
reconstituted using saline. Image courtesy of Bracco International BV.
Fig. 9.5 SonoVue® pump Image courtesy of Bracco International BV. The pump
provides continuous rotation of the syringe in order to prevent accumulation of the
microbubbles in the upper parts of the syringe.
566
CHAPTER 9 Contrast echocardiography
(Bristol Myers Squib)
Structure: Luminity® is composed of lipid-encapsulated perflutren
microspheres. The spheres are between 1-10 micrometres in
diameter.
Preparation and storage: it should be stored in a refrigerator at 2-8°C
until activated. It needs to be activated by a mechanical shaking device
(Vialmix) and then can be used for up to 12 hours (although if left
standing for more than 5min it requires 10sec of shaking by hand
before further use). It can be reactivated once more within 48 hours.
Dose and administration: recommended bolus dose is of 0.1-0.4mL
followed by a bolus of 3-5mL of 0.9% sodium chloride or 5% glucose.
Diluting 0.3mL in 10mL saline (0.9% sodium chloride) and injecting
1-2cc is an alternative and provided good contrast in IE33 scanners.
Total dose should not exceed 1.6mL. The recommended intravenous
infusion is of 1.3mL Luminity® added to 30ml of 0.9% sodium chloride.
The rate of infusion should start at 1mL/min and be titrated to achieve
optimal image enhancement (not to exceed 10mL/min).
Right-heart contrast agents
Agitated saline contrast can be used to demonstrate the presence
of right-to-left shunts across the atrial septum, or to improve the
Doppler envelope when examining the tricuspid valve (Fig. 9.6).
Insert a cannula ideally into the right antecubital fossa.
Attach a 3-way tap to the cannula.
Obtain 2 10mL Luer lock syringe. In one syringe draw up 9mL of saline
and 1mL of air. 0.5mL of the patient’s blood can also be drawn up.
Ensure both Luer lock syringes are firmly attached to the cannula and
force the mixture back and forth between the syringes until frothy.
SPECIFIC CONTRAST AGENT PREPARATION
567
Fig. 9.6 A three-way tap with Luer lock syringes should be used for agitated saline
injections.
568
CHAPTER 9 Contrast echocardiography
Administration of contrast agents
Left-heart contrast agents
Patient preparation requires insertion of an intravenous cannula usually
into an antecubital vein and its connection to a 3-way-tap or small-
bore Y connector. Ultrasound contrast agents can be injected through
this line by bolus injection or an infusion.
The use of smaller diameter cannula should be avoided as the bubbles
from the contrast will be subjected to a large pressure drop as the
fluid exits the tip of the lumen. The faster the injection and the smaller
the diameter of the lumen, the larger the pressure drop and there is
increased chance of damage to the contrast bubbles.
Bolus injection
Slow bolus injections (0.2mL) of all agents (SonoVue®, Luminity®, and
Optison®) can be used followed by a slow 5mL saline flush over 20s.
However, these are not as controllable or reproducible as infusions.
Agitate the contrast immediately before injection slowly and withdraw
the contrast agent from the syringe avoiding high negative pressure.
If giving a bolus injection for left-heart contrast studies, a saline flush
(5mL) may be considered to push the agent into the central blood
stream if there is delayed contrast appearance. Lifting the arm is often
sufficient.
Contrast infusion
Because of microspheres behaviour, continuous agitation of the
contrast is necessary for optimum contrast.
Agitation can be performed manually by slowly rocking the pump to
and fro. A special infusion pump has been developed for SonoVue®.
A constant infusion of SonoVue® 0.8mL/min from the start is usually
satisfactory and need not be changed in the majority of patients.
The pump is particularly useful in stress echocardiography; the infusion
can be stopped at any time and resumed when needed. Between
infusion periods, the contrast agent is gently agitated.
Right-heart contrast agents
Patient preparation also requires insertion of an intravenous cannula,
usually into an antecubital vein.
Need to be given as a bolus injection through a relatively large bore
cannula in a relatively proximal location.
Need to be given as a rapid bolus to ensure complete opacification of
the right atrium. Blood from both the superior and inferior vena cavae
streams into the right atrium and it is possible with slow boluses for
the bubbles not to mix into the flow from the inferior vena cava and
therefore not reach the interatrial septum.
Another way some people use if they are having difficulties with
opacification of the atrium near the interatrial septum is to give an
injection into the femoral vein so that the bubbles travel up the
inferior vena cava.
ADMINISTRATION OF CONTRAST AGENTS
569
Advantages of bolus injections
Easy to perform.
Wash-in period and wash-out is visible.
Agent is quickly used with little stability problems.
Allows the highest peak enhancement.
Disadvantages of bolus injections
Contrast is short-lived.
The contrast effect changes during study.
Timing of injection of bolus can be difficult.
Comparative contrast studies difficult.
Advantages of contrast infusion
Prolongs the period of contrast enhancement.
Provides a steady (constant) effect.
Allows the dose of the agent to be optimized and used efficiently.
Disadvantages of contrast infusion
More complex than bolus injections to perform.
Titration of contrast takes time.
570
CHAPTER 9 Contrast echocardiography
Contrast safety
Left-heart contrast agents
The safety of ultrasound contrast agents has been assessed in cohorts of
several thousand patients. Side effects have been noted but they are usually
mild and transient. Most frequent side effects of SonoVue® in clinical trials
were: headache (2.1%), nausea (1.3%), chest pain (1.3%), taste perversion
(0.9%), hyperglycaemia (0.6%), injection site reaction 0.6%), paraesthesia
(0.6%), vasodilation
(0.6%), injection site pain
(0.5%). Serious adverse
events in particular allergic reactions are very rare
(0.01%) and less
frequent than for X-ray contrast agents.
Allergic reactions: They may happen as acute sensitivity reactions (IgE
mediated type I), but Complement Activation Related Pseudo Allergy
(CARPA) seems to be more typical for the contrast agents with a
phospholipid membrane (SonoVue® and Luminity®). In comparison to
IgE mediated reactions, CARPA reactions need no prior exposure to
the agent, the reaction is milder or absent upon repeated exposures
and spontaneous resolution is possible. Although serious adverse
events are very rare, appropriate allergy and emergency equipment as
well as a physician with knowledge in emergency medicine should be
present or close by.
Acute coronary disease: Only Optison® and Luminity® may be used in
acute coronary syndromes, since their contraindication on the use in
these conditions has been recently withdrawn by FDA, based on the
evidence of their favourable risk:benefit profile and safety. SonoVue®
may be used 7 days after acute coronary syndrome.
Special considerations and precautions with use: mechanical
ventilation, clinically significant pulmonary disease (including diffuse
interstitial pulmonary fibrosis and severe chronic obstructive
pulmonary disease), adult respiratory distress syndrome, severe heart
failure (NYHA IV), endocarditis, acute myocardial infarction with
ongoing angina or unstable angina, hearts with prosthetic valves, acute
states of systemic inflammation or sepsis, known states of hyperactive
coagulation system, recurrent thromboembolism.
Right-heart contrast agents
Reports of serious side effects from the use of agitated saline injection are
rare. There have been a few case reports of agitated saline contrast caus-
ing ischaemic complications such as stroke or transient ischaemic attacks.
Available data is not sufficient to estimate the incidence of these events,
although such complications appear to be extremely rare.
CONTRAST SAFETY
571
Management of allergic reactions1
Recognize signs and symptoms of an allergic reaction: itching,
erythema, urticaria, wheeze, laryngeal obstruction, tachycardia,
hypotension.
Ensure airway is secure and give 100% O2.
If any signs of airway obstruction seek anaesthetic help to maintain
airway patency.
If suspected anaphylaxis give IM adrenaline 0.5mg (i.e. 0.5mL of
1:1000). Repeat every 5min if needed as guided by blood pressure,
pulse, and respiratory function until better.
Secure IV access
Chlorpheniramine 10mg and hydrocortisone 200mg IV.
IV normal saline titrated against blood pressure.
Ensure appropriate monitoring on ward: cardiac monitor, regular blood
pressure review.
Left-heart contrast agents in pregnant or lactating women
No left-heart ultrasound contrast is approved for use in pregnant or
lactating women.
In women of childbearing age the physician has to ask for confirmed
or possible pregnancy.
Ultrasound contrast injections should be avoided unless there is no
alternative imaging method to answer the clinical question and the
clinical need for information is felt to be greater than any potential
risks.
Reference
1 Longmore M et al. (eds) (2010). Oxford Handbook of Clinical Medicine, 8th edn. Oxford: Oxford
University Press.
572
CHAPTER 9 Contrast echocardiography
Right-heart contrast study applications
Contrast study for atrial shunts and patent foramen ovale
Microbubble contrast studies can be used to identify atrial shunts and
confirm the presence of a patent foramen ovale (Fig. 9.7). There are 3
elements to a good contrast study for an atrial shunt:
A stable image
Use apical 4-chamber view (or subcostal view) optimized so that all
4 chambers are seen. Try the view with the patient doing a Valsalva to
ensure you can keep all chambers in view.
Agitated saline injection
Inject rapidly through a Venflon® inserted into an antecubital vein. It
must completely and rapidly opacify the right atrium.
A good Valsalva
Shunting may be evident at rest so the first contrast injection should
be without Valsalva.
If no bubbles appear in the left heart repeat the injection with a
Valsalva manoeuvre.
The critical time of a Valsalva is when the patient relaxes. It is then
that right-sided pressures transiently elevate relative to the left and
contrast shunts.
Get the patient to take a breath and bear down hard. Inject the
contrast and when it has filled the right atrium tell them to relax.
If there is a shunt a few bubbles will appear in the left atrium and left
ventricle within 5 beats of the patient relaxing. If bubbles appear later
this is more consistent with a pulmonary arteriovenous malformation.
Set the system to capture 10-20 beats and start acquisition on
contrast injection. Look back through the loop for bubbles. Repeat
the study with more contrast until all three elements of the study are
perfect.
The appearance of bubbles in the left heart within 5 cardiac cycles
following right chamber opacification and release of Valsalva suggests
an intracardiac shunt.
RIGHT-HEART CONTRAST STUDY APPLICATIONS
573
AT REST
WITH VALSALVA
LV
LV
RV
RV
LA
RA
LA
RA
Right heart opacification with contrast
Contrast evident in LV
Fig. 9.7 Contrast injection: left-sided bubbles with Valsalva (on right) demonstrating
a patent foramen ovale. Also note septal aneurysm. See W Video 9.1.
574
CHAPTER 9 Contrast echocardiography
Contrast study for pulmonary shunts
Intrapulmonary shunts are often the result of pulmonary arteriovenous
malformations. Intravenous agitated saline contrast can be used to aid the
diagnosis of intrapulmonary shunts.
A stable image position and adequate agitated saline injection should
be used as described on b p.572.
The appearance of bubbles in the left heart only after 5 cardiac cycles
suggests an intrapulmonary shunt.
Contrast study for Doppler enhancement
Intravenous injection of agitated saline and other contrast agents can
be used to enhance the tricuspid regurgitation signal (Fig. 9.8). The con-
trast enhancement of a weak TR velocity jet signal allows more accurate
estimation of right heart haemodynamics. Right-heart contrast agents may
also enhance the appearance of hepatic vein flow reversal.
Acquire the TR jet CW signal by placing the CW cursor across the TR
jet as in the normal examination (see b p.162).
Inject the agitated saline or left-heart contrast.
The contrast is likely to generate a lot of noise on the spectral trace so
reduce the gain until the enhanced Doppler envelope is evident.
Diagnosis of persistent left superior vena cava
The diagnosis of a persistent left SVC is usually made incidentally fol-
lowing identification of a dilated coronary sinus or because there are
difficulties with pacemaker lead insertion from the left side. This is be-
cause a persistent left-sided SVC most frequently drains directly into the
coronary sinus.
A good view of the coronary sinus and its insertion into the right
atrium is required. This can often be best done on TOE or with TTE
using a modified apical 4-chamber view tilted down to cut through the
coronary sinus.
Following injection of agitated saline into the left arm the contrast is
seen to appear in the coronary sinus before the right atrium.
In the majority of patients a right (normal) SVC is then also present.
Therefore when agitated saline is injected into the right arm it is
seen to enter the right atrium before any appearing in the coronary
sinus. However, if the right SVC is absent then this injection will also
appear in the coronary sinus first.
RIGHT-HEART CONTRAST STUDY APPLICATIONS
575
Fig. 9.8 Above: TR velocity jet continuous wave Doppler without the use of
contrast. Below: TR velocity jet continuous wave Doppler augmented by contrast.
576
CHAPTER 9 Contrast echocardiography
Imaging techniques for left ventricular
opacification
The durability of the contrast agent within the left ventricle is highly
dependent upon both the bubble composition and also the ultrasound
settings. Optimizing the ultrasound settings is vital to ensure good opacifi-
cation of the LV (Table 9.1).
Imaging presets and analysis
When ultrasound contrast agents are used, contrast-specific imaging
modalities should be employed (Fig. 9.9) based on the use of harmonic
frequencies and low transmit power from the transducer.
There are a range of manufacturer specific presets. The standard is a
real-time, low power mode. The low-power contrast-specific imaging
technology provides excellent ventricular opacification and often
simultaneous myocardial opacification.
In systems without contrast-specific imaging modality use harmonic
imaging but with a mechanical index of <0.6.
Contrast specific imaging
When exposed to ultrasound waves, the contrast bubbles resonate
and emit harmonic frequencies in addition to the frequency that
comes from the transducer, the fundamental frequency. The harmonic
frequencies are two times greater than the fundamental (second
harmonic), three times (third harmonic), and so on. With increasing
frequency the amplitude of the ultrasound waves decreases.
Myocardial tissue shows the same response to ultrasound but only
with high transmit power (MI>1). Microbubbles will resonate at low
powers (MI=2).
Thus, if the transducer is set to low power imaging the harmonic
signals from the contrast in the blood will be significantly stronger than
any signals from the myocardium and therefore excellent blood to
myocardial contrast is obtained.
Image settings to prevent microbubble destruction
The transmitted ultrasound frequency from the ultrasound machine can
destroy the microbubbles. Bubble destruction can be done purposefully
in some forms of imaging such as myocardial flash perfusion imaging but
usually stable micro-bubbles are needed to optimize image quality. To
increase the length of time microbubbles persist in the circulation there
are two imaging aspects that can be varied:
Low mechanical index: The higher the mechanical index, the greater the
transmitted acoustic power and the higher the chance of microbubble
destruction. Using lower mechanical indexes will therefore also reduce
the destruction of micro-bubbles. However, this needs to be balanced
against the need for penetration to achieve adequate depth of imaging,
for which higher mechanical indexes can be used.
Intermittent imaging: Continuous imaging with the transducer on the
chest wall will cause a gradual depletion of microbubbles. Therefore
intermittent imaging is recommended to increase microbubble durability.
IMAGING TECHNIQUES FOR LEFT VENTRICULAR OPACIFICATION
577
Fig. 9.9 Example of contrast-specific imaging. Without contrast agent there are
only faint signals from myocardial tissue. After contrast injection there is bright
opacification of the blood within the left ventricle cavity and excellent delineation
of the endocardium. Opacification of the myocardium is not as intense as the cavity
but provides a good display of left ventricle wall thickness. See W Video 9.2.
578
CHAPTER 9 Contrast echocardiography
Left-heart contrast study applications
Contrast study for left ventricular opacification
European Association of Echocardiography indications for resting left ven-
tricular opacification contrast are as follows:
In patients with suboptimal images:
To enable improved endocardial visualization and assessment of LV
structure and function when 2 or more contiguous segments are not
seen on non-contrast images.
To have accurate and repeatable measurements of LV volumes,
and ejection fraction by 2D/3D echo (e.g. before CRT, follow-up
echocardiograms for assessment of cardiac toxicity) (Fig. 9.10).
To increase the confidence of the interpreting physician in the LV
function, structure, and volume assessments.
To confirm or exclude the echocardiographic diagnosis of the
following LV structural abnormalities, when non-enhanced images are
suboptimal for definitive diagnosis:
• Apical hypertrophic cardiomyopathy, LV non-compaction.
• Ventricular non-compaction.
• Apical thrombus (Fig. 9.11).
• Ventricular pseudoaneurysm.
Contrast study for Doppler enhancement
Intravenous injection of left-heart contrast agents can be used to
enhance Doppler signals. The technique is as for right-heart agents
(see b p.574).
As left-heart contrast agents pass from the right to the left heart,
they can be used to augment Doppler traces from the right heart
(e.g. tricuspid valve) and also the left heart.
In the left heart, contrast can be used to enhance mitral Doppler
traces or pulmonary vein Doppler traces for the assessment of
diastolic dysfunction.
Since only small amounts of contrast are needed for this indication,
Doppler enhancement can be achieved in the wash-out phase after
LV opacification. Usually the Doppler and/or power gain needs to be
reduced to achieve normal intensity spectra.
LEFT-HEART CONTRAST STUDY APPLICATIONS
579
Fig. 9.10 3D LV contrast opacification. See W Video 9.3 and W Video 9.4.
Fig. 9.11 The use of LV opacification to demonstrate the presence of LV apical
thrombus. The LV apical thrombus is not clearly seen without contrast (upper
image) and its presence confirmed following LV contrast opacification (lower
image). See W Video 9.5.
580
CHAPTER 9 Contrast echocardiography
Contrast study in dobutamine stress
echocardiography
Since image quality is crucial for reliable stress echocardiography, review
all baseline images prior to beginning the stress procedure. If endocar-
dial borders are not visible (or barely visible) in 2 or more myocardial
segments consider using an ultrasound contrast agent (Fig. 9.12).
Indications for use of contrast in stress echocardiography
When 2 or more endocardial border contiguous segments of LV are
not well visualized.
To obtain diagnostic assessment of segmental wall motion and
thickening at rest and stress.
To increase the proportion of diagnostic studies.
To increase reader confidence in interpretation.
Contraindications
Known or suspected significant intracardiac shunts.
Known hypersensitivity to the agent.
CONTRAST
STUDY IN DOBUTAMINE STRESS ECHOCARDIOGRAPHY
581
Fig. 9.12 Most contrast agents can be given as a bolus or an infusion. When given
with a dobutamine infusion it can be given via the same cannula using a 3-way tap.
The contrast agent is driven by the dobutamine infusion. No boluses of saline are
necessary. There is no risk of dobutamine boluses since the amount of contrast is
very low.
582
CHAPTER 9 Contrast echocardiography
Contrast study for myocardial
perfusion
The use of left-heart ultrasound contrast agents for the assessment of
myocardial perfusion has the potential to significantly improve myocardial
assessment during stress echocardiography. Myocardial contrast echocar-
diography is quick, easy to perform, and potentially a bedside technique
(as long as facilities for an infusion of contrast are available). Contrast
echocardiography supplements wall motion information with perfusion
judged from the appearance of contrast within the myocardium.
Principle
Myocardial contrast echocardiography (perfusion imaging) describes
echocardiography with intravascular ultrasound contrast agents.
This results in opacification of the cavities and the intramyocardial
blood vessels.
The amount of myocardial opacification depends on the settings of the
ultrasound scanner, the density of the myocardial micro vessels (where
most of the myocardial blood is located), and the myocardial blood
flow.
Differences in the intensity of myocardial opacification and in the
speed of filling the myocardium with contrast can be used to identify
areas of non-viability and/or ischaemia.
Indications
At present most guidelines for echocardiographic assessment of
ischaemia and viability are based on assessment of LV wall motion
alone.
Ultrasound contrast agents are approved for LV opacification
and endocardial definition. At present, assessment of myocardial
perfusion is not an approved indication for ultrasound contrast
agents.
However, using state-of-the-art equipment myocardial opacification
often is inevitable when performing contrast echo for LV
opacification (Table 9.1).
It is worth including these findings when assessing the patient for
myocardial viability and ischaemia as the perfusion data can confirm
sometimes questionable findings on LV wall motion.
Protocols that exclusively make the diagnosis from perfusion images
may be an option in the future.
CONTRAST STUDY FOR MYOCARDIAL PERFUSION
583
Table 9.1 Common pitfalls seen in myocardial contrast
echocardiography and their solutions
Pitfall of myocardial contrast
Solution
echocardiography
Insufficient contrast dosage and/or
Increase contrast dose and/or
setting causing inhomogeneous
correct setting
opacification and swirling
Nearfield destruction artefacts in the
Stepwise reduce transmit power (MI)
apical parts of the left ventricle setting
in 0.1 step and/or change focus to
causing inhomogeneous opacification and
farfield
swirling
Very strong signals in the nearfield and
Increase transmit power or just wait
poor LV contrast in the farfield
several beats, for subsequent
particularly in the basal part of the
injections use a small dosage or a
LV segments
slower bolus
Rib shadows can be found in all segments:
Try modified view
look for the typical band of low
echogenicity
584
CHAPTER 9 Contrast echocardiography
How to set imaging parameters
A balance between having sufficient power of the ultrasound and an
adequate signal-to-noise ratio without significant microbubble destruction
is important to achieving adequate perfusion imaging. Both high power and
low power (MI <0.2) have been used.
High power: High power provides good signal-to-noise ratio although
there is destruction of microbubbles and so assessment of myocardial
perfusion cannot be performed in real time nor can it be performed
simultaneously with assessment of wall motion.
Low power: Low power imaging reduces microbubble destruction
allowing simultaneous assessment of perfusion and wall motion
although has a lower sensitivity for the detection of microbubbles.
How to assess myocardial perfusion
The myocardial contrast distribution can be visually assessed to give
the operator an impression of overall myocardial perfusion (Fig. 9.13).
Continuous infusion of contrast is used and the microbubbles are
destroyed by a high burst of ultrasound at a high mechanical index causing
a ‘flash’. Following this the replenishment of the contrast agent within the
myocardium and its distribution can be visually assessed (Fig. 9.13).
The presence of an intact coronary microvasculature and normal
myocardial blood flow allows an even replenishment of contrast within
the myocardium.
If there is diminished epicardial flow (e.g. following myocardial
infarction) the speed and amount of contrast replenishment will be
Training and accreditation
Basic and stress echocardiography training including BLS/ALS is needed.
As long as there are no approved procedures for accreditation in contrast
echocardiography the following approach appears to be reasonable:
Introduction by a physician with experience in contrast
echocardiography (>50 studies/year).
Participation in a course on contrast echocardiography in order to
learn the performance, interpretation, pitfalls, and adverse effects in
contrast echocardiography.
Perform at least 20 contrast echoes under guidance or supervision.
Experience with contrast agent for left ventricular opacification in at
least 50 cases is a prerequisite for moving on to assess perfusion and
function with contrast agents.
Fig. 9.13 4-Chamber view showing delayed filling in the apicoseptal myocardium after injection of contrast. Top left: LV opacification; top right and bottom
left: early opacification of the myocardium; bottom right: late filling. Note the perfusion defect (arrows) indicating ischaemia in the LAD territory.
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587
Chapter 10
Stress echocardiography
Introduction 588
Indications
590
Contraindications 592
Detection of ischaemia 594
Viability assessment
596
Perfusion assessment 598
Preoperative assessment for non-cardiac surgery 600
Equipment and personnel 602
Patient preparation
604
Performing the study 606
Monitoring and termination criteria 610
Exercise stress protocols 612
Dobutamine stress for ischaemia 614
Dobutamine stress for viability 616
Vasodilator stress
618
Pacing stress
620
Analysis
622
Sample report 624
588
CHAPTER 10 Stress echocardiography
Introduction
Stress echocardiography has become a valuable method for cardiovascular
stress testing. It plays a crucial role in the initial detection of coronary
artery disease, in determining prognosis, and in therapeutic decision-
making. The major use of stress echocardiography is to assess myocar-
dial ischaemia or viability in patients with coronary artery disease. Stress
echocardiography can also be applied to evaluation of valvular disease and
cardiomyopathies.
Stress echocardiography or other non-invasive
imaging tests?
Non-invasive imaging techniques have greatly improved the evalu-
ation of patients with known or suspected coronary artery disease.
Stress echocardiography and myocardial scintigraphy are widely avail-
able and provide similar diagnostic accuracy along with an incremental
value over clinical risk factors for detection of coronary artery disease.
Cardiovascular magnetic resonance (CMR) is the most recent addition
to the functional cardiac imaging armamentarium. It offers a comprehen-
sive assessment of myocardial ischaemia which may include wall-motion
analysis at rest and during dobutamine stress, or rest and stress first-
pass myocardial perfusion during vasodilatory stress. Myocardial viabil-
ity is evaluated with either the late gadolinium enhancement technique
(infarct imaging) or the low-dose dobutamine test. Positron emission
tomography has high diagnostic performance to detect ischaemia and
viability, but continues to have limited clinical use because it is not widely
available. Cardiac computed tomography allows coronary calcium scan-
ning along with non-invasive anatomic assessment of the coronary tree,
but no functional information on ischaemia/hibernation. Therefore, it
should be combined with a functional test (ideally stress echocardiogra-
phy or CMR, and not myocardial scintigraphy which also involves radia-
tion), to provide a complete assessment of the physiological significance
of stenotic lesions in coronary arteries.
There are clinical situations where myocardial scintigraphy is relatively
contraindicated (left bundle branch block, bifascicular block, and ven-
tricular paced rhythms). In these situations dynamic exercise leads to
perfusion abnormalities of the septum and adjacent walls in the absence
of obstructive coronary disease. If there is local expertise, stress echocar-
diography is an option. On the other hand, in patients with known exten-
sive coronary artery disease and regional wall abnormalities at rest, the
diagnostic accuracy of stress echocardiography is somewhat reduced. If
available, CMR with adenosine first-pass perfusion and late gadolinium
enhancement is an attractive option for those patients. No single imag-
ing modality has been proven to be superior overall. Available tests all
have advantages and drawbacks, and none can be considered suitable for
all patients. The choice of the imaging method should be based on the
clinical history and also on local expertise and availability.
INTRODUCTION
589
Pre-test probability
In patients referred for stress echocardiography the likelihood of having
coronary artery disease can usually be estimated from their symptoms
and history. This pre-test probability is useful because the gain by per-
forming a stress test depends on the pre-test probability (Table 10.1).
Based on the accuracy of stress echocardiography to detect coronary
artery disease it is also possible to calculate the probability of coronary
artery disease with a negative or positive result of stress echocardiogra-
phy (post-test probability).
If there is a high pre-test probability (e.g. typical angina and risk factors) the
risk of a cardiac event remains high even if there is a negative test. In patients
with a low pre-test probability (e.g. young patients with atypical chest pain)
a positive test does not predict poor prognosis. Therefore, when used for
diagnosis, stress echocardiography (like nuclear perfusion imaging) is ideal
for patients with intermediate pre-test probability (e.g. women with atypical
chest pain and some risk factors). In this group of patients a negative test
predicts a low risk of further cardiac events, whereas a positive test indicates
a high risk and warrants further invasive diagnostics.
Although stress echocardiography in patients with high pre-test prob-
ability is of limited diagnostic value, it is still of clinical value. In patients
with known coronary artery disease stress echocardiography can help to
define the location and extent of ischaemia.
Table 10.1 Combined Diamond-Forrester and CASS data of pre-test
likelihood of coronary artery disease in symptomatic patients. (Modified
from Committee on the Management of Patients with chronic stable
angina. ACC/AHA 2002 guideline update for the management of
patients with chronic stable angina. J Am Coll Cardiol 2003; 41(1):159-68.)
Age
Atypical angina
Typical angina
Men Women
Men Women
30-39
34
12
76
26
40-49
51
22
87
55
50-59
65
31
93
73
60-69
72
51
94
86
Values represents % with coronary artery disease on angiography
>70%
30-70%
<30%
590
CHAPTER 10 Stress echocardiography
Indications
The main indication for stress echocardiography is the assessment of
coronary artery disease patients (Fig. 10.1). ECG stress testing is the most
frequently used initial stress test to evaluate patients with suspected coro-
nary artery disease. Stress echocardiography is used in addition to stress
ECG or as the initial diagnostic tool. However, stress echocardiography
has been applied to several other pathologies. The key indications are to
aid management of patients with:
Suspected coronary artery disease
As part of an investigational strategy for the diagnosis of patients in
whom stress ECG was inconclusive.
For people for whom treadmill exercise is difficult or impossible
because of poor mobility or inability to perform dynamic exercise.
For people for whom stress ECG poses particular problems of poor
sensitivity or difficulties in interpretation, including women, patients
with cardiac conduction defects (for instance, left bundle branch block
and resting ST segment abnormalities), and diabetes
For people with a lower likelihood of coronary artery disease and
future cardiac events. Likelihood of coronary artery disease depends
on clinical assessment of risk factors including age, gender, ethnic
group, family history, associated comorbidities, clinical presentation,
physical examination, and results from other investigations (e.g. blood
cholesterol levels or resting ECG).
Known coronary artery disease
To determine the likelihood of future coronary events, for
instance after myocardial infarction or risk assessment for proposed
non-cardiac surgery.
To assess myocardial viability and hibernation, particularly with
reference to planned myocardial revascularization.
To guide strategies of myocardial revascularization by determining the
haemodynamic significance of known coronary lesions.
To assess the adequacy of percutaneous and surgical revascularization.
Valvular heart disease
Aortic stenosis with a low gradient and poor left ventricular systolic
function (see Chapter 3).
Aortic stenosis with a high gradient in asymptomatic patients.
Mitral stenosis with discrepancy between haemodynamic and clinical
findings (e.g. dyspnoea despite low gradient at rest, asymptomatic
patient with high-grade stenosis).
Mitral regurgitation (organic, severe) in asymptomatic patients.
To establish evidence of inducible ischaemic mitral regurgitation.
To evaluate aortic regurgitation (severe) in asymptomatic patients.
Hypertrophic cardiomyopathy or subaortic muscular
obstruction
Assessment for dynamic gradient.
INDICATIONS
591
SYMPTOMS
Clearly CARDIAC
DON’T KNOW
Clearly NON-CARDIAC
Classical history
SUITABLE FOR
Reassured
ECG changes
NO
ETT
± ETT
(Normal resting
ECG, mobile)
YES
YES
NO
ETT
Stress Echo
Nuclear study
if previous ETT
+ve
-ve
Equivocal
Equivocal
–ve
+ve
Depending on symptoms
Myocardial
Myocardial
ischaemia
ischaemia
unlikely
unlikely
(coronary
(coronary
artery disease
artery disease
not excluded)
not excluded)
Coronary artery disease -consider coronary angiography
Fig. 10.1 An approach to investigate a patient with suspected coronary artery
disease.
592
CHAPTER 10 Stress echocardiography
Contraindications
Absolute contraindications for all stress modalities
Non-ST-segment elevation acute coronary syndrome. Once stabilized,
exercise stress can be considered 24-72 hours after chest pain, in
low- or intermediate-risk patients. High-dose dobutamine should not
be performed within the first week after a myocardial infarction.
ST-segment elevation myocardial infarction within the previous 4 days.
Left ventricular failure with symptoms at rest.
Recent history of life-threatening arrhythmias.
Severe dynamic or fixed LVOT obstruction (aortic stenosis and
obstructive hypertrophic cardiomyopathy).
Severe systemic hypertension (systolic blood pressure >220mmHg
and/or diastolic blood pressure >120mmHg).
Recent pulmonary embolism or infarction.
Thrombophlebitis or active deep vein thrombosis.
Known hypokalaemia (particularly for dobutamine stress).
Active endocarditis, myocarditis, or pericarditis.
Left main coronary artery stenosis that is likely to be
haemodynamically significant.
Absolute contraindications for vasodilator stress
Suspected or known severe bronchospasm.
2nd- and 3rd-degree atrioventricular block in the absence of a
functioning pacemaker.
Sick sinus syndrome in the absence of a functioning pacemaker.
Hypotension (systolic blood pressure <90mmHg).
Caffeine intake, xanthines, or dipyridamole use in the last 24 hours.
Relative contraindications to vasodilator stress
Bradycardia of <40bpm. Initial dynamic exercise normally increases the
rate sufficiently to start the infusion.
Recent cerebral ischaemia or infarction.
Contraindications to contrast imaging
Known allergy to any of the constituents of contrast agents.
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594
CHAPTER 10 Stress echocardiography
Detection of ischaemia
Principle
The rationale for the diagnosis of myocardial ischaemia with stress
echocardiography is a relative reduction in myocardial blood flow on
stress sufficient to cause a decrease in myocardial contraction. The ischae-
mic changes in left ventricle wall motion appear earlier than ECG changes
and angina (the ischaemic cascade, Fig. 10.2). During stress, in a normal
subject, coronary and myocardial blood flow increases 3-4-fold to comply
with the increased oxygen demand of the myocardium. This can occur
because myocardial arteriolar resistance reduces. If there is a significant
stenosis of an epicardial coronary artery the resistance of the arteriolar
vessels is already reduced at rest. This is known as auto-regulation and
allows preservation of coronary blood flow at rest, and at low levels of
stress, in the territory supplied by the stenosed artery. Therefore, at rest
severe occlusions do not result in wall motion abnormalities. However,
with stress and increased oxygen demand the blood flow cannot be fur-
ther increased and the corresponding myocardial segment cannot con-
tract as well as myocardial segments supplied by patent arteries. The more
severe the epicardial stenosis the smaller the possible increase in coronary
blood flow and the earlier wall motion abnormalities occur.
Limitations
Usually stenosis >50% results in wall motion abnormalities on stress.
However, less severe stenosis in particular with long segments or
vascular remodelling can also cause ab-normalities.
There has to be a significant increase in oxygen demand to disclose
regional wall motion abnormalities—in particular for moderate
stenoses. This is only possible by reaching or exceeding target heart
rates as in exercise ECG stress testing.
Even severe stenosis may be missed if there is a well-developed
collateral circulation.
Worsening of wall motion or an inappropriate loss of contractility in
comparison to other myocardial segments is the hallmark of stress
echocardiography. However, this may be difficult to visualize if resting
function is already reduced.
Abnormal microvascular function, e.g. in arterial hypertension
or diabetes, may reduce the auto-regulation and cause abnormal
responses to stress. However, the changes are usually diffuse and not
segmental as observed in coronary artery disease.
PET
FLOW HETEROGENEITY
Echo-MRI
Stress Echo-MRI
ANAEROBIC METABOLISM
ALTERED DIASTOLIC PROPERTIES
Contrast Echo
MPI
REGIONAL WALL MOTION ABNORMALITIES
MRI
ECG CHANGES
ECG
“THE ISCHAEMIC CASCADE”
ANGINAL PAIN
EXERCISE TIME
Fig. 10.2 The ischaemic cascade.
596
CHAPTER 10 Stress echocardiography
Viability assessment
Viability studies based on left ventricular wall motion are performed
when akinetic (or severely hypokinetic) segments are found and
there is a question as to whether the patient will benefit from
revascularization. If segments are reported as viable this implies the
myocardial function is still preserved even though their blood supply
is limited (Fig. 10.3).
The rationale for the diagnosis of myocardial viability with stress
echocardiography is to demonstrate that the akinetic (or severely
hypokinetic) segments improve contractility when exposed to low
doses of dobutamine. This ability to increase contractility is referred
to as a contractile reserve.
If there is a haemodynamically significant stenosis or an occlusion of
the supplying artery, higher dosages of dobutamine may then result in
ischaemia and the contractility decreases. This improvement and then
deterioration is referred to as a biphasic response.
Limitations
Dobutamine increases oxygen demand and at higher doses induces
ischaemia in hibernating myocardium (biphasic response). This usually
requires doses exceeding 20microgram/kg/min. However, very severe
stenoses may cause ischaemia at the lowest doses of dobutamine and
no improvement of contractility may be seen.
Contractility depends on preservation of the inner layers of the
myocardium. Therefore the lack of contractile reserve does not mean
there is no viable myocardium in the outer layers. Although major
recovery of function after revascularization appears to depend on
preserved contractility, segments with irreversibly damaged inner
layers but preserved outer myocardial layers still may benefit from
improved blood flow and remodelling.
It may be difficult to differentiate passive movement (tethering, i.e.
being pulled with a normally moving segment) of a myocardial segment
from active movement due to contraction. Image processing analysis
tools, such as strain imaging and tissue tracking, may be useful to
differentiate but there is limited experience.
Viability assessment using stress echocardiography relies on good
image quality. Contrast echocardiography is usually needed to improve
border delineation.
VIABILITY ASSESSMENT
597
DOBUTAMINE STRESS
REST
LOW DOSE
HIGH DOSE
SYSTOLE
SYSTOLE
SYSTOLE
NORMAL
*ISCHAEMIA
HIBERNATION
- biphasic
viable
INTRAMURAL SCAR
- viable
SCAR
non-viable
not performed
WALL THICKENING
Fig. 10.3 Changes in wall thickening with dobutamine stress. *Decline in wall thick-
ening with ischaemia can be variable in degree and timing.
Causes of akinetic left ventricle segments
Scar (non-viable)
Irreversible loss of myocardium.
Often reduced diastolic wall thickness <0.6cm.
Stunning (viable)
Transiently reduced contractility after ischaemia.
Usually spontaneous recovery (e.g. transient coronary occlusion in
infarction with early recanalization, or post stress in severe stenosis).
Stunning usually diagnosed by follow-up studies that demonstrate
recovery in function.
If complete occlusion during infarction this can take 4-6 weeks.
Hibernation (viable)
Permanently reduced contractility.
Permanent coronary occlusion or high-grade stenosis with
insufficient collateral blood flow ‘too little to live, too much to die’.
Transient recovery with low-dose dobutamine.
Worsening with high dose ‘biphasic response’.
Intramural scar (viable)
Scar in wall but with no significant stenosis in supplying artery and
remaining viable myocardium in wall.
598
CHAPTER 10 Stress echocardiography
Perfusion assessment
Principle
Normal viable and non-ischaemic myocardium can be recognized
by observing the pattern of myocardial contrast enhancement
(see Chapter 9 and Fig. 10.4).
Usually with normal perfusion the microvessels fill with contrast and
there is homogeneous opacification and prompt refill of contrast
following microbubble destruction.
After myocardial infarction, scar tissue replaces the myocytes and
the density of intramyocardial vessels decreases. Similarly, in acute
myocardial infarction without reperfusion, myocardial blood flow is
absent in the necrotic area. Therefore the myocardial opacification
decreases and ‘dark’ or ‘black’ areas are seen within the myocardium,
usually in the subendocardial region.
Typically infarct and scar tissue do not opacify because the amount
of contrast within the few vessels remaining is not enough to cause
an ultrasound signal. Therefore for viability assessment with contrast
only a resting study is necessary. Nevertheless the echocardiographic
method of choice for viability assessment is still low-dose dobutamine
stress and perfusion imaging is only considered when contrast has
been used for LV opacification or when dobutamine is contraindicated.
If an area of myocardium starts to become ischaemic during a stress
study, again the perfusion with microbubbles decreases and the refill
of contrast reduces. Therefore the area becomes dark.
Myocardial ischaemia is present when 2 or more myocardial segments
show normal opacification at rest and a perfusion defect during stress.
Assessment for inducible ischaemia can be performed with all
approved stress protocols, but appear to be most suitable for
vasodilator protocols.
In the ischaemic cascade, stress-induced myocardial perfusion defects
tend to precede wall motion abnormalities and as a result subtle wall
motion abnormalities can often be identified when a perfusion defect
has also become evident.
It is important to remember that myocardial perfusion defects may be
transient and are often better seen during the replenishment after the
flash.
Limitations of perfusion assessment
Scar tissue sometimes can cause a very echogenic tissue signal. This
makes it very difficult to assess changes in myocardial opacification
after contrast injection.
A perfusion defect at rest is found in an akinetic segment, if not
consider an artefact.
PERFUSION ASSESSMENT
599
Perfusion defect criteria
A relative decrease in contrast enhancement in segment/region
in comparison to another region with comparable image quality/
attenuation.
First appearance in the subendocardial layers rather than
transmurally.
In areas of normal wall motion or reversible wall motion
abnormalities.
Fig. 10.4 4-chamber view showing delayed filling in the apicoseptal myocardium
after injection of contrast. Top left: LV opacification; top right and bot-tom left:
early opacification of the myocardium; bottom right: late filling. Note the perfusion
defect (arrows) indicating ischaemia in the LAD territory. See W Video 10.10 and
W Video 10.12.
600
CHAPTER 10 Stress echocardiography
Preoperative assessment for
non-cardiac surgery
In patients undergoing major vascular surgery a dobutamine stress
echocardiogram allows determination of the perioperative risk for
cardiovascular complications. This is particularly useful if patients have
3 or more of the characteristics: age >70 years; current angina; prior
myocardial infarction; congestive heart failure; prior cerebrovascular
event; diabetes mellitus; or renal failure.
The main method to protect patients with known coronary artery
disease perioperatively is to prescribe effective beta-blockade.
The risk of perioperative cardiac complications has been assessed
in clinical trials and is related to the number of wall segments that
become ischaemic on dobutamine stress echocardiography.
Patients without new wall motion abnormalities have a low risk (<5%).
Patients with 1-4 segments showing new wall motion abnormalities
have a slightly higher perioperative risk but can be protected with
beta-blockers.
If >4 segments exhibit new wall motion abnormalities during stress,
there is a high risk (>30%) of cardiac complications perioperatively.
This risk cannot be reduced by beta-blockers and there is therefore a
potential theoretical benefit from revascularization (although currently
unproven to reduce risk).
The most recent guidelines (Fig. 10.5) were published in 20091. These
take into account the urgency of the surgery, the cardiac risk of the
surgery, the patient’s functional capacity, as well as cardiac risk factors.
In patients with t3 cardiac risk factors then non-invasive testing can
be considered. If this shows dmoderate stress-induced ischaemia
and the patient is stable then the planned surgery can go ahead. If
non-invasive stress testing shows extensive ischaemia then each case
should be considered individually considering the potential benefit of
the proposed surgical procedure with the predicted outcome and the
effect of medical therapy and/or coronary revascularization.
Reference
1 Task Force for Preoperative Cardiac Risk Assessment and Perioperative Cardiac Management
in Non-cardiac Surgery; et al. Guidelines for pre-operative cardiac risk assessment and
perioperative cardiac management in non-cardiac surgery. Eur Heart J 2009; 30:2769–812.
PREOPERATIVE ASSESSMENT FOR NON-CARDIAC SURGERY
601
Cardiac Risk Factors
(angina, previous MI, heart
failure, previous CVA/TIA,
renal dysfunction, diabetes
mellitus requiring insulin)
>3 cardiac risk factors
Yes
No
Consider non invasive
testing prior to surgical
Continue with surgery
procedure
If extensive ischaemia
If non invasive testing
present on non invasive
shows moderate stress-
stress testing then each
induced ischaemia and the
case should be considered
patient is stable then the
individually considering the
planned surgery can go
potential benefit of surgery
ahead
against risks
Fig. 10.5 Flow chart showing preoperative assessment for non-cardiac surgery.
Task Force for Preoperative Cardiac Risk Assessment and Perioperative Cardiac Management in
Non-cardiac Surgery; et al. Guidelines for pre-operative cardiac risk assessment and perioperative
cardiac management in non-cardiac surgery. Eur Heart J 2009; 30:2769–812.
602
CHAPTER 10 Stress echocardiography
Equipment and personnel
Equipment
Because analysis of wall motion abnormalities is difficult and not reliable
in the presence of poor quality images, every effort has to be made to
optimize visualization of the endocardial border and the myocardium.
The scanner should provide tissue harmonic imaging and a contrast-
specific imaging modality in order to be applicable in the majority of
patients.
Use of digital frame grabbers and split or ‘quad-screen’ displays allow
side-by-side comparison of rest and stress images using the same
echocardiographic views and is the current standard for performing
stress echocardiograms.
Tissue Doppler imaging is optional but may add clinical information
(e.g. detection of post-systolic shortening).
3D imaging, which is becoming increasingly available, offers the ability
to eliminate apical foreshortening and shorten the time needed for
acquisition of stress images.
Personnel and experience
Two people are required to record and monitor stress
echocardiography—one of them should have substantial experience in
the evaluation of patients with ischaemic heart disease and in analysis
of wall motion/thickening abnormalities.
Recordings should be performed by a skilled echocardiographer
(technician or physician).
If a physician is not participating in the study, one should be available in
the immediate locality in case of acute problems. One of the personnel
present should be qualified in advanced life support.
Recording and interpretation of stress echocardiograms requires
extensive experience in echocardiography and should be performed
only by technicians and physicians with specific training in the
technique. Most recommendations suggest physicians have performed
and interpreted a minimum of 100 studies under supervision
before they can perform stress echocardiography independently.
Supervised over-reading of at least 100 stress echocardiograms is
required to attain the minimum level of competence for independent
interpretation.
Drugs
Depending on the stress protocol chosen the appropriate drugs
(dobutamine, adenosine, dipyridamole, atropine) and agents to reverse
their effects should be prepared (aminophylline if dipyridamole used,
beta-blockers).
Standard resuscitation drugs and equipment will need to be available in
the room.
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CHAPTER 10 Stress echocardiography
Patient preparation
Patients should be provided with information or have a detailed verbal
explanation. Informed consent is usually considered appropriate especially
for pharmacological stress or with the use of contrast agents.
Safety
A large international study of stress echocardiography reported on
85,997 patients undergoing stress echocardiography.1 The incidence of
life-threatening adverse events in those undergoing stress with exercise
was 1:6574, dobutamine 1:557, and dipyridamole 1:1294. There were
6 deaths (1:14333) related to the procedure (5 with dobutamine, and
1 with dipyridamole). These were mainly due to ventricular arrhythmias.
It was pointed out that the subgroup of patients receiving dobutamine
may have been at higher risk because of viability studies in those with
established coronary disease.
Reference
1 Varga A et al. Safety of Stress Echocardiography (from the International Stress Echo
Complication Registry). Am J Cardiol 2006; 98:541–3.
PATIENT PREPARATION
605
Example information sheet
You have been asked to attend for stress echocardiography. A stress
echocardiogram is an ultrasound scan of your heart, which is performed
after increasing your heart rate. A stress echocardiogram provides in-
formation about the performance of your heart at stress and helps your
doctors to identify symptoms you may have on exertion.
Before the procedure?
Please continue to take all your medications as usual except for your
beta-blocker which should not be taken on the morning of the test.
You will be seen by the doctor who will take a medical history and after
explaining the procedure will ask you to sign a consent form. If you have
any concerns, please do not hesitate to ask, as we would like you to be
as relaxed as possible and are happy to answer questions.
What happens during the procedure?
The doctor will insert a small tube into your arm (cannula) to infuse the
drug (dobutamine), which increases the heart rate. A blood pressure cuff
will be placed on your arm. You will be asked to lie on your left side and
the ultrasound scan will be performed. Dobutamine will be given via the
cannula, which will gradually increase the heart rate. In addition ultra-
sound contrast agents may be given to improve image quality. There will
be a doctor present and also a technician. The procedure takes 20-30min
to examine all areas carefully. When the examination is finished the dob-
utamine is stopped and the heart rate will come down quickly.
Benefits?
The benefits from stress echocardiography are that it can: Define the
nature of cardiac symptoms; Point out the status of the cardiovascular
system; Decide which further therapeutic and diagnostic procedures you
have to undergo following the information derived from this examination.
Risks?
Usually the investigation is tolerated well, some patients could have
some mild symptoms during the test (mostly palpitations, tremor, light
headed sensation). Serious risks are very rare less than 0.3% (1 in every
330 patients) and include heart rhythm problems, myocardial infarction
and low blood pressure. Your doctor would not recommend that you
have a stress echocardiogram unless she/he felt that the benefits of the
procedure outweighed these small risks.
After the procedure?
After the procedure you will be asked to stay for another 30min. This
is the time needed to completely clear the infused drugs. You will be
offered refreshments. The doctor will return and discuss the results of
your procedure. Any relevant advice and literature will then be given.
Your cannula will be removed and you may go home with your relative/
friend. A letter with the results of your procedure will be sent to your
GP and any referring doctor.
606
CHAPTER 10 Stress echocardiography
Performing the study
General
The image acquisition is structured to make it easy to identify changes
from baseline in wall motion and thickening of the left ventricle. The fun-
damental requirement is high-quality 2D echocardiographic recordings
with good endocardial border definition in all segments. These basic im-
ages need to be acquired confidently and quickly during stress. Additional
data can include tissue Doppler profiles (global and regional parameters
of function) and direct assessment of myocardial perfusion by myocardial
contrast enhancement (depending on local licences).
Views
Multiple views are required to ensure all left ventricular segments are
monitored and all 3 major coronary distributions are assessed. The key
4 views are: apical 4- and 2-chamber, parasternal short and long axis (or
apical long axis) (Fig. 10.6). Subcostal or additional short-axis views can be
substituted when necessary or when more appropriate for visualization of
specific anatomy.
Set-up
Spend time ensuring good patient position (they will be in this position
throughout the stress). A clear, stable ECG recording is required.
Study all 4 views and spend time optimizing the images.
Machine settings: select harmonic imaging and adjust focus zone.
Ideally, frame rate should be >25 frames/s (if heart rate >140 then
frame rates >30 frames/s may be better).
Probe position: be very careful not to foreshorten apical views
(Fig. 10.7). The patient may need to do held inspiration or
expiration for clear, stable, unforeshortened images.
Contrast: decide whether there is good endocardial border
definition in each view and whether images can be acquired
confidently and smoothly during the stress in each window. If 2 or
more segments are not seen or the images are difficult use contrast.
PERFORMING THE STUDY
607
FOUR KEY VIEWS
PARASTERNAL LONG AXIS
PARASTERNAL SHORT AXIS
APICAL FOUR CHAMBER
APICAL TWO CHAMBER
Fig. 10.6 There are 4 key views. The parasternal long axis and apical 3-chamber
provide very similar information. See W Video 10.1, W Video 10.2, W Video 10.3,
W Video 10.4, W Video 10.5, W Video 10.6, W Video 10.7, W Video 10.8.
RIB
TRUE APICAL POSITION
FORESHORTENED VENTRICLE
PROBE ROTATION
PROBE ROTATION
Fig. 10.7 It is vital that all apical views are not foreshortened to avoid missing apical
wall motion abnormalities. If the probe is not on the true apex then even though
the apex may be included in the initial plane probe rotation for the next view will
create a foreshortened image.
608
CHAPTER 10 Stress echocardiography
Image acquisition
Record a set of baseline images (use a stress protocol preset if
available). Use a standard acquisition order, e.g. parasternal long
axis, parasternal short axis, apical 4-chamber and apical 2-chamber
(alternatively the apical views can be recorded first).
Start the stress (e.g. pharmacological/physical).
At the preset time-points (depending on stress and clinical response)
record a complete set of images. Some machines have a ‘compare’
mode to ensure your images are in exactly the same position.
Look for changes in wall motion and thickening during image
acquisition so that you interpret the test as you go along.
Once all the images are acquired, review them off-line, ideally with a
second experienced reviewer, to create the final report.
3D stress applications
3D stress echocardiography
Real-time 3D stress echocardiography allows the acquisition of a full
volume image of the left ventricle. This has several advantages: all
segments are imaged quickly and during the same time interval and
accurate comparisons can be made.
The cropping of 3D volumes allows planes to be chosen which are
‘on axis’ which is sometimes difficult to achieve exactly with 2D
stress echocardiography.
The reduced temporal resolution of stress echocardiography means
that LV contrast agents are invariably used.
The presence of stitching artefacts can also hinder image analysis,
particularly if there is quick variability in the heart rate.
However, acquisition of 3D datasets allows for other potential
assement of ischaemia such as changes in strain (Fig. 10.8).
Whilst the advantages of 3D stress echocardiography are clear, the
reduced image quality and problems with stitching has limited its
uptake by cardiology departments.
iRotate
This mode, offered by Phillips allows the 2D image to be rotated to
a different plane whilst maintaining the probe in the same position.
This mode can be of use during stress echocardiography where
for instance following acquisition of the apical 4-chamber view the
ultrasound waves are transmitted in a different direction to obtain
a 2-chamber apical view and then a 3-chamber apical view without
moving the ultrasound probe.
PERFORMING THE STUDY
609
Fig. 10.8 3D strain acquisition and postprocessing on Toshiba Artida system. Top:
from the apical LV window, the LV is displayed in two apical views and three short
axis views. Middle: contouring of the epicardial and endocardial border. Bottom:
normal LV 3D circumferential strain analysis.
610
CHAPTER 10 Stress echocardiography
Monitoring and termination criteria
Monitoring
As with other forms of stress testing, standard ECG and blood pressure
monitoring should be performed. This may provide diagnostic and prog-
nostic information during exercise studies. With pharmacological stress
ECG monitoring has limited diagnostic value but is needed to trigger loop
recording and monitor for arrhythmias. However, if a 12-lead ECG is not
performed during pharmacological stress, a 12-lead ECG recorder should
be readily available in case of problems.
Termination criteria
Treadmill exercise echocardiography should be terminated at traditional
endpoints:
Attainment of target heart rates.
Cardiovascular symptoms.
Significant ECG changes or arrhythmias.
Bicycle exercise and pharmacological stress provide additional echocar-
diographic endpoints because they allow online, continuous visualization
of wall motion and thickening. Stress echocardiography with online moni-
toring should be terminated at:
Traditional endpoints (previously listed).
The development of wall motion abnormalities corresponding to 2 or
more coronary territories.
Wall motion abnormalities associated with ventricular dilation and/or
global reduction of systolic function.
MONITORING AND TERMINATION CRITERIA
611
Target heart rates for stress
Maximum age predicted heart rate = 220 - Age of patient
Target heart rate = 85% x Maximum age predicted
e.g. Age = 67
Maximum age predicted = 220 - 67 = 153bpm
Target heart rate = 0.85 × 153 = 130
Target heart rate according to age
Age
100%
85%
85
135
115
80
140
119
75
145
123
70
150
128
65
155
132
60
160
136
55
165
140
50
170
145
45
175
149
40
180
153
35
185
157
30
190
162
25
195
166
20
200
170
612
CHAPTER 10 Stress echocardiography
Exercise stress protocols
Exercise is the most physiological stressor for assessment of myocardial
ischaemia in patients able to exercise.
Stress protocol
The protocols are the same as for exercise stress ECG testing.
A Bruce treadmill protocol with 3-min stages of graded increases
in speed and gradient, or an ergometer with 3-min stages of graded
cycling resistance at a fixed cycling rate (Fig. 10.9).
Treadmill exercise should be terminated at traditional endpoints such
as attainment of target heart rates, cardiovascular symptoms, and/or
significant ECG changes suggestive of ischaemia.
Supine and upright bicycle exercise appear to have equivalent degrees
of accuracy. Supine bicycle ergometry on a special bed, which can be
rotated, provides additional echocardiographic endpoints because it
allows continuous visualization of wall motion at incremental levels of
stress, including peak exercise. Bicycle exercise should be terminated
at traditional endpoints and, if a supine bicycle is used, when wall
motion abnormalities develop that correspond with 2 or more
coronary territories, or wall motion abnormalities associated with
ventricular dilation and/or global reduction of systolic function.
Image acquisition
Imaging should be performed at:
Baseline.
Post treadmill exercise (because ischaemia-induced wall motion
abnormalities may resolve quickly, post-exercise imaging should be
accomplished within 60-90sec of termination of exercise). If the
patient is asymptomatic and there are no ECG changes then extending
the exercise up to 100% of target heart rate provides more time
post-exercise to acquire images.
If supine bicycle ergometry is used imaging should also be performed
during exercise and an intermediate stage can be recorded.
Exercise or dobutamine?
For the diagnosis of myocardial ischaemia, there appears to be no dif-
ference in the accuracy and prognostic information obtained with dob-
utamine compared to exercise stress. It is possible that for milder forms
of coronary artery disease, treadmill may be advantageous. Exercise
stress echocardiography presents a challenge to obtain good quality
images. For patients unable to exercise, dobutamine is indicated. An
advantage of dobutamine is that it has a rapid onset and cessation of
action, and its effects can be reversed by beta-blocker administration. If
there is a contraindication to dobutamine then dipyridamole, adenosine
or pacing may be used. For risk assessment prior to non-cardiac sur-
gery the accuracy of dobutamine stress echocardiography is proven. For
assessment of myocardial viability use of low- and high-dose dobutamine
seems to be the best stress method for echocardiography.
EXERCISE STRESS PROTOCOLS
613
BRUCE EXERCISE PROTOCOL
5.0mph
4.2mph
18% slope
3.4mph
16% slope
2.5mph
14% slope
1.7mph
12% slope
10% slope
STAGE 5
STAGE 4
STAGE 3
STAGE 2
STAGE 1
3 mins
3 mins
3 mins
3 mins
3 mins
Modified Bruce has 2 extra 3 minute stages at start
(1.7mph/0% slope and 1.7mph/5% slope)
then continues as above
ERGOMETER PROTOCOL
125 WATTS
100 WATTS
75 WATTS
50 WATTS
25 WATTS
STAGE 5
STAGE 4
STAGE 3
STAGE 2
STAGE 1
3 mins
3 mins
3 mins
3 mins
3 mins
AT CONSTANT PEDAL RATE OF 50 CYCLES PER MINUTE
Fig. 10.9 Standard protocols for exercise testing.
614
CHAPTER 10 Stress echocardiography
Dobutamine stress for ischaemia
Myocardial ischaemia is assessed by graded dobutamine infusion. This increases
myocardial oxygen demand in a fashion analogous to staged exercise.
Contractility, heart rate, and systolic blood pressure are all increased.
Dobutamine infusion
Start the infusion at 5 or 10microgram/kg/min dobutamine.
At 3-min intervals increase the infusion to 20, 30, and then 40microgram/
kg/min.
If the rise in heart rate is minimal by 30microgram/kg/min dobutamine
then consider using atropine (Fig. 10.10). Check for contraindications
to atropine, in particular glaucoma, before administration.
Atropine should be used at the minimum effective dose. Administer
0.3mg doses at 60sec intervals until the desired heart rate response is
seen. Maximum dose should be 1.2mg. The effect on accuracy is not
fully established but appears beneficial.
Dobutamine stress and beta-blockers
In patients with ongoing beta-blocker treatment a reduced sensitivity
for reversible ischaemia has been found. This is seen even if target heart
rate is reached with additional atropine injections due to the negative
inotropic effect of beta-blockers. Therefore, it is recommended to stop
beta-blockers ideally 48 hours prior to the test to increase sensitivity
(avoid false negatives). However, if not possible, patients can still be
accepted for exercise or dobutamine stress with atropine accepting that
sensitivity is lower.
Image acquisition
See W Video 10.9, W Video 10.10, and W Video 10.11 for examples of wall motion
abnormalities. Images should be recorded at:
Baseline.
Intermediate stage (70% of the age-predicted heart rate).
Peak stress (>85% of the age-predicted heart rate).
Recovery.
The minimal images are baseline and peak. More than 4 stages can be
recorded as felt clinically needed.
Termination of test
Diagnostic endpoints of stress echocardiographic testing are: maximum
dose (for pharmacological) or maximum workload (for exercise testing):
achievement of target heart rate; obvious echocardiographic positiv-
ity (with akinesis of t2LV segments); severe chest pain; or obvious ECG
positivity
(with >2mV ST-segment shift). Submaximal non-diagnostic
endpoints of stress echo testing are non-tolerable symptoms or limiting
asymptomatic side effects such as hypertension, with systolic blood pres-
sure >220mmHg or diastolic blood pressure >120mmHg, symptomatic
hypotension, with >40mmHg drop in blood pressure; supraventricular
arrhythmias, such as supraventricular tachycardia or atrial fibrillation;
and complex ventricular arrhythmias, such as ventricular tachycardia or
frequent, polymorphic premature ventricular beats.
DOBUTAMINE ISCHAEMIA PROTOCOL
40 microgram/kg/min
30 microgram/kg/min
20 microgram/kg/min
10 microgram/kg/min
STAGE 4
STAGE 3
STAGE 2
STAGE 1
3 mins
3 mins
3 mins
3 mins
ATROPINE (0.3mg boluses up to 1.2mg)
Fig. 10.10 Standard protocol for dobutamine ischaemia stress testing.
616
CHAPTER 10 Stress echocardiography
Dobutamine stress for viability
The basis for the diagnosis of myocardial viability is contraction of the
myocardium either spontaneously or after inotropic stimulation by acti-
vating contractile reserve. The principle of low-dose dobutamine stress is
to assess contractile reserve, i.e. look for evidence of improvement in wall
motion abnormalities or clear inotropic response in areas that are thought
to have coronary stenoses (Fig. 10.11). The need for viability assessment is
usually to determine the value of performing revascularization.
Dobutamine infusion
Start the infusion at 5microgram/kg/min dobutamine.
Continue the infusion for up to 5min and then increase to 10microgram/
kg/min. This can be increased to 20microgram/kg/min (Fig. 10.12).
A 10% increase in heart rate marks the end of the low-dose protocol.
After completing the low-dose protocol higher doses of dobutamine
(30 and then 40microgram/kg/min for 5-min periods) may be given
to look for a biphasic response (improved contraction at low dose
followed by reduced contraction at peak).
The presence of a biphasic response indicates inducible myocardial
ischaemia and is perhaps the strongest predictor for recovery of
myocardial dysfunction following revascularization. It will indicate a
viable but jeopardized myocardial region.
Image acquisition
A full set of images should be recorded at:
Baseline.
Low stress (10% increase in heart rate).
High stress (if performed).
LOW DOSE DOBUTAMINE
SCAR or LIMITED VIABILITY
SIGNIFICANT VIABILITY
1. No improved wall motion
1. Improved wall motion in
or <4 segments improve*
>4 segments improve*
2. Diastolic wall thickness <0.6cm
2. Diastolic wall thickness >0.6cm
3. End-systolic volume >140mL**
3. End-systolic volume <140mL**
HIGH DOSE DOBUTAMINE
INTRAMURAL SCAR
HIBERNATION
1. No change in wall motion
1. Ischaemic response
2. Worsening wall motion
*Improvement in 4 segments is a good predictor for recovery of left ventricle
function after coronary revascularization in patients with hibernating myocardium.
** End systolic volume >140mL indicates an advanced stage of remodelling.
Revascularization may not result in reverse remodelling.
Fig. 10.11 Viable or non-viable?
DOBUTAMINE VIABILITY PROTOCOL
40 microgram/kg/min
30 microgram/kg/min
20 microgram/kg/min
10 microgram/kg/min
5 microgram/kg/min
STAGE 5
STAGE 4
STAGE 3
STAGE 2
STAGE 1
5 mins
5 mins
5 mins
3 mins
3 mins
VIABILITY
ISCHAEMIA
Fig. 10.12 Standard protocol for dobutamine viability stress testing.
618
CHAPTER 10 Stress echocardiography
Vasodilator stress
Vasodilator stress echocardiography should only be considered when
physical stress is not possible and there are contraindications to dob-
utamine. It is less sensitive for identification of mild to moderate coronary
artery disease. Vasodilator stress, however, may become more important
as perfusion imaging becomes more widely clinically applicable.
Vasodilators are effective because they induce regional variation in cor-
onary blood flow. Dipyridamole or adenosine cause a 2- or more fold
increase in myocardial blood flow in segments supplied by normal coro-
nary arteries whereas in segments supplied by stenotic arteries flow is
unchanged or decreased. If oxygen demand increases with flow changes,
regional abnormalities in wall motion and thickening appear.
Because vasodilator stress acts via change in perfusion, theoretically, it
should be more suitable for direct assessment of myocardial perfusion
using contrast echocardiography.
Dipyridamole protocol for myocardial ischaemia
The protocol for dipyridamole is based on continuous ECG and echocar-
diographic monitoring during a 2-stage infusion.
Infusion
Check for contraindications to dipyridamole.
Initially infuse 0.56mg/kg of dipyridamole over 4min.
Monitor for 4min. If there are no adverse effects and no clinical or
echocardiographic endpoints occur (significant anginal symptoms, wall
motion abnormalities) infuse 0.28mg/kg over 2min.
As with dobutamine (b p.614 and Fig. 10.13), atropine (doses of
0.25mg up to a maximum of 1mg) can be used after the second stage
to increase heart rate and improve sensitivity.
Aminophylline (240mg; IV) should be available for immediate use in
case of an adverse dipyridamole-related event.
Imaging
Imaging should be performed continuously, and images captured at base-
line, end of phase 1, end of phase 2 (if performed), and during recovery.
The minimal images are baseline and hyperaemia. When ultrasound con-
trast is used during the stress test (indicated for improved endocardial
definition) myocardial opacification can be assessed in addition to LV wall
motion (see b p.582).
Adenosine protocol for myocardial ischaemia
Adenosine works on a 6-min protocol with ECG and echocardiographic
monitoring.
Infusion
Check for contraindication to adenosine.
Infuse at a maximum dose of 140microgram/kg/min over 6min.
Stop the infusion if clinical or echocardiographic endpoints are reached
(limiting symptoms or wall motion abnormalities).
VASODILATOR STRESS
619
Imaging
Image continuously and record at baseline, 3min, 6min, and during recov-
ery. Adenosine is less sensitive than other stress modalities for detecting
coronary disease by ischaemic wall motion abnormalities compared to
other stress modalities.
DIPYRIDAMOLE PROTOCOL
IMAGING
BASELINE
INTERMEDIATE
PEAK
RECOVERY
0.56 mg/kg
0.28 mg/kg
STAGE 1
MONITOR
STAGE 2
4 mins
4 mins
2 mins
ATROPINE
0.3mg boluses up to 1.2mg
(if required)
ADENOSINE PROTOCOL
IMAGING
BASELINE
INTERMEDIATE
PEAK
RECOVERY
140 microgram/kg/min
STAGE 1
3 mins
3 mins
Fig. 10.13 Standard protocols for vasodilator stress testing.
620
CHAPTER 10 Stress echocardiography
Pacing stress
This may be considered in patients with a permanent or temporary
pacemaker.
Pacing by temporary intravascular or oesophageal leads is usually not
needed for clinically-indicated stress echocardiography.
In most paced patients exercise, dobutamine, and vasodilator
protocols are applicable.
Pacing stress can be considered when an increase in heart rate cannot
be achieved by exercise or dobutamine. Since pacing alone only
produces chronotropic stress, it is usually considered to have lower
sensitivity than the inotropic and chronotropic stress achieved by
pharmacological stress.
Dobutamine can be given at the same time as increasing the pacing
rate to create both chronotropic and inotropic stress.
Pacing protocol
Pacing stress should preferably be performed with atrial pacing to
ensure natural ventricular contraction and to avoid pacing-induced wall
motion abnormalities.
In patients with permanent pacemakers, ensure the assistance of a
pacemaker programmer and experienced operator.
Record baseline images.
Start pacing at 100bpm.
Increase every 2min by 10bpm until the target heart rate (85% of
age-predicted maximal heart rate) is achieved or until other standard
endpoints are reached.
After reaching target heart rate, reduce heart rate every minute by
20bpm till baseline heart rate is reached.
Image acquisition
Record baseline images and then at every stage and in recovery.
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622
CHAPTER 10 Stress echocardiography
Analysis
Echocardiographic recordings have to be evaluated during image acquisi-
tion in order to assess for echocardiographic endpoints. This should be
followed by a comprehensive assessment after the stress test with side-
by-side comparisons of recordings captured at baseline and stress.
Stress echocardiograms can be analysed on several planes of complexity,
which range from a qualitative assessment of segmental wall motion in
response to stress, to highly detailed schemes for quantitative analysis.
For image interpretation, multiple cine loop display allows up to 4 differ-
ent stress levels for each imaging plane to be displayed simultaneously.
Standard review
Start with assessment of image quality. Endocardial border definition
can be used as an indicator of image quality. If endocardial border
is not seen or is barely visible, wall motion and thickening cannot
be reliably assessed in this segment. Grade image quality as good,
acceptable, or poor and identify non-diagnostic segments.
On resting images assess global function by LV ejection fraction using
a visual estimate or from measuring end-diastolic or end-systolic
volumes in 2 apical views.
Compare rest and stress images for the development of global LV
dysfunction (left ventricular enlargement and shape changes) and
remeasure global function at stress if there appears to be a change.
Then evaluate segmental wall motion at rest and at each level of stress
using a 16- or 17-segment model. Use a 4-step visual score for each
segment: 1—normal, 2—hypokinetic, 3—akinetic; 4—dyskinetic.
Calculate a wall motion score at each stage, if required, to facilitate
serial comparison. Divide the sum of the points by the number of
segments analysed. Normal contraction has a wall motion score of 1;
a higher score indicates wall motion abnormalities.
For assessment of myocardial viability wall thickness is useful. Diastolic
wall thickness <5mm at rest indicates non-viability and increases
diagnostic confidence in combination with absent contractile response
to dobutamine.
If using contrast during stress echocardiography, it may be useful to
assess the myocardial contrast enhancement. With current knowledge
the results of perfusion imaging should be used in conjunction with the
findings of visual left ventricular wall motion analysis.
The adequacy of stress should be noted and records kept of the
exercise time, symptoms, haemodynamic observations, and ECG
changes.
ANALYSIS
623
Stress echo training
EAE recommends performing at least 100 exams under the supervision
of an expert reader in a high-volume laboratory, and ideally with the
possibility of angiographic verification, before starting stress echocardi-
ography on a routine basis. Maintenance of competence requires at least
100 stress echo exams per year.
Audit and quality control
It is usually accepted that operators should interpret a minimum of 10
stress echocardiograms per month to maintain interpretational skills and
sonographers should perform a minimum of 10 stress echocardiograms
per month to maintain an appropriate level of skill.
Regular audits are useful to review the quality and accuracy of the stress
echocardiograms. The audit should include the total number of stress
echocardiograms performed per month for the time period audited: the
number of procedures per sonographer and reads per physician; indica-
tions; imaging technology; use of contrast; stress protocols; quality of the
studies; termination criteria; results (negative or positive for assessment
of ischaemia, viable or non-viable for viability studies); and complica-
tions. For those patients undergoing coronary angiography, it would be
ideal to have the results of coronary angiography for quality control with
routine review of false positive and negative findings.
Future technologies
Echocardiography technology is progressing rapidly and has been devel-
oped to ensure assessment of left ventricular wall motion is more objec-
tive. Automatic wall tracking software, tissue Doppler imaging, and strain
imaging are becoming clinically viable. The use of tissue Doppler velocity
measurements during stress echocardiography allows the identification
of post-systolic shortening—a known sign of regional ischaemia—which
can be used in order to increase the sensitivity of the test. However, no
data currently demonstrate the superiority of quantitative techniques
over conventional wall motion analysis for the assessment of viable and
ischaemic myocardium. 3D echocardiography has introduced a further
exciting option for stress echocardiography with rapid acquisition of 3D
volume datasets and reconstruction of 3D motion. The lower spatial
and temporal resolutions of 3D imaging are limitations of the current 3D
technique. However, 3D imaging eliminates apical foreshortening, which
is common with 2D imaging, and may improve the detection of apical
wall motion abnormalities. Moreover, 3D imaging generally shortens the
time required for acquisition of stress images.
624
CHAPTER 10 Stress echocardiography
Sample report
Section 1. Demographic and other information
All the standard demographic details should be included. Stress echocar-
diography should also include:
The clinical indication, including relevant clinical history and
medications. This provides justification for the study and summarizes
clinical information from a number of sources to focus the final
conclusion.
The stress protocol and imaging technique used with justification,
including the name and dosage of contrast agents.
Changes of blood pressure and heart rate should be described briefly.
Reporting resting and peak stress blood pressure is usually sufficient.
For exercise and dobutamine stress echocardiography the age, sex,
and specific target heart rate should be included.
Further measurements or details of ECG changes can be included if
relevant.
Section 2. Description of observations and diagnostic
statements
Start with a statement about the completeness of the study and image
quality, since diagnostic confidence heavily depends on high-quality
recordings.
Next report the baseline analysis. If global and/or regional left
ventricular function is abnormal, the segments involved and the
degree of abnormality (hypokinetic, akinetic, dyskinetic) should be
demonstrated or listed. Schematics of the single views help to illustrate
the distribution of wall motion abnormalities. Non-diagnostic segments
can be marked (Fig. 10.14).
Then report each of the stress recordings in the same way describing
whether there was a normal response to stress or abnormal response
with worsening wall motion. Segments that deteriorate should be
listed or marked on the schematic and degree of abnormality noted.
In viability studies it is important to evaluate whether the akinetic
segments show improvement during stress.
Section 3. M-mode, 2D, and Doppler measurements
In stress echocardiography this section will include quantitative measures
of LV function (e.g. ejection fraction) at baseline and on stress. There may
also be information on left ventricular outflow velocities in patients with
suspected stress-induced gradients or changes in mitral valve function. If
tissue Doppler imaging or other analysis methods were used these can
be documented.
Section 4. Conclusions
The conclusion should comment on any suboptimal aspect of the study
(e.g. image quality, target heart rate reached, etc.) and any complica-
tions or adverse events. It should then address the clinical question and
detail the main abnormalities that occurred during stress, or summarize the
response as normal.
Long axis
Short axis
4 chamber
2 chamber
Rest
Wall motion
1.0
score index
% Normal
100
Intermediate
Wall motion
1.0
score index
% Normal
100
Peak
Wall motion
1.25
score index
% Normal
81
Recovery
Wall motion
1.0
score index
% Normal
100
X - Cannot interpret
1 - Normal
2 - Hypokinetic
3 - Akinetic
4 - Dyskinetic
5 - Aneurysmal
Fig. 10.14 Example of an annotated report demonstrating segmental abnormalities.
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627
Chapter 11
Acute echocardiography
‘Front door’ echocardiography 628
Safeguarding patient care
630
Cardiopulmonary resuscitation 632
Acute diagnostics 634
Critically ill: volume status
636
Critically ill: fluid responsiveness
640
Critically ill: advanced haemodynamics
642
Critically ill: weaning from a ventilator
646
628
CHAPTER 11 Acute echocardiography
‘Front door’ echocardiography
Practice development
The last decade has seen the rapid development and refinement of port-
able echo technology. A simultaneous growth in interest in non-invasive
diagnostic tools has driven a worldwide development of transthoracic
echocardiography. As a result it has become a vital skill for those involved
in acute patient care.
‘Acute echocardiography’ refers to the use of echocardiography at the
bedside in the acute management of patients receiving urgent care in
ward-based, high-dependency and critical care settings.
The majority of this patient population do not have artificial airways
and may have limited, established, invasive monitoring, particularly
if they have become acutely unwell. Transthoracic echo therefore
becomes an invaluable and powerful tool for rapid non-invasive
haemodynamic assessment.
This chapter focuses on the use of transthoracic echocardiography in
the acute setting. This ‘front door’ echocardiography often operates in
time critical situations and relies on more limited types of equipment
with more focused data acquisition than might be expected in full
echocardiographic studies. Local practice, and acceptability, may
therefore vary and therefore local guidelines for use should be
established.
A unique role for echocardiography
The unique value of this tool comes from the fact it provides direct
assessment of acute cardiac function combined with diagnostic
echocardiographic information.
Acute echocardiography is most powerful when viewed as part of
a global patient assessment allowing full integration of clinical and
echocardiographic findings.
Acute echocardiography supports and augments:
Peri-arrest and resuscitation care.
Acute medical and trauma diagnostics.
Stabilization and management of the critically ill.
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630
CHAPTER 11 Acute echocardiography
Safeguarding patient care
Practice safety framework
Where a new practice is being established to provide acute
echocardiography it is essential that the practitioners delivering the
service have a level of echocardiographic expertise that allows them
to make independent, and correct, clinical decisions based on their
images.
Therefore the service needs to develop approaches for appropriate
operator training and accreditation.
The individual arrangements for experience and training in an acute
echocardiography service will vary between institutions, but, for many,
this may be best achieved with a service that has some devolved
autonomy from the parent cardiology echocardiography department.
Governance pathways
As with any investigation that is routinely performed within a
department effective clinical governance pathways must be established.
This should include:
• Systems for reporting and storing studies whilst maintaining patient
confidentiality.
• A forum for reviewing images with the parent cardiology
department.
• Established pathways to obtain urgent expert help.
• Identification of a service lead to coordinate clinical governance.
Technology
A primary requirement for the establishment of an acute
echocardiography service will be acquisition of appropriate echo
equipment.
A good starting point is to align equipment with the parent cardiology
department. This reduces operator errors and improves technological
compatibility, for example, where sharing image storage systems.
SAFEGUARDING PATIENT CARE
631
Echocardiography training in the UK
Resuscitation echocardiography
There are a number of courses available in the UK; for example Focused
Echocardiographic Evaluation in Life Support (FEEL) and Focus Assessed
Transthoracic Echo (FATE). Prior to attending a course we recom-
mend that a mentor is identified who will review and sign off the studies
required to complete the log-book to the expected standard. Time
investment from the mentor should be between 1-2 hours per 10 stud-
ies performed by the candidate. A time frame of 6 months is expected
to complete the accreditation process. Certification entitles the opera-
tor to perform transthoracic studies in the arrest setting provided that
they maintain reasonable competence. Practice must remain within the
resuscitation framework.
Accreditation with the British Society of Echocardiography
Full transthoracic accreditation allows the operator to function as
an independent practitioner and to perform comprehensive studies.
Accreditation requires completion of a log-book of 250 specific cases,
a written examination, and submission of 5 selected recorded studies
illustrating specific pathologies. Completion of the accreditation process
requires a significant time commitment from the operator over a 2-year
period and provision of departmental supervision and training. Following
achievement of accreditation, re-certification is required 5-yearly with
demonstration of continued echo practice and learning.
Contemporary training issues
The qualifications described were not designed to address the spe-
cific practice requirements of clinicians working in acute care areas.
At the time of writing in the UK the representative societies of
Emergency Medicine, Acute medicine and Critical Care, in partnership
with the British Society of Echocardiography, are individually considering
certification processes to address clinicians’ requirements and support
the practice of acute echocardiography. It is likely that these certification
processes will become available in the next 2 years. For more informa-
tion please see the website of the relevant society:
Acute Medicine: M http://www.acutemedicine.org.uk
Emergency Medicine: M http://www.collemergencymed.ac.uk
Critical Care Medicine: M http://www.ics.ac.uk
632
CHAPTER 11 Acute echocardiography
Cardiopulmonary resuscitation
Introduction
Although there are a number of courses providing training in peri-
resuscitation echocardiography Focused Echocardiographic Evaluation
in Life Support has been developed as a consensus approach for the
UK and is endorsed by both the British Society of Echocardiography
and the Resuscitation Council.
The FEEL algorithm guides the operator through rapid
echocardiographic assessment during resuscitation using the Advanced
Life Support protocol.
The aim of the protocol is to identify reversible causes of cardiac
arrest:
• Cardiac tamponade.
• Gross left ventricular overload and failure.
• Gross hypovolaemia.
• Massive pulmonary embolus.
No measurements, colour imaging, or Doppler are used during the
protocol; diagnosis relies solely on the operator’s ability to observe
pathology accurately.
Echocardiographic assessment must be performed during the 10-s
pulse check after 5 cycles of CPR and repeated only after completion
of a further 5 cycles.
Echocardiography must not delay the return of chest compressions.
The FEEL protocol
The FEEL protocol is based on 4 views:
• Parasternal long axis.
• Parasternal short axis.
• Apical 4-chamber.
• Subcostal.
It may be unnecessary to obtain all views: a single view may be
adequate if diagnostic.
The flow diagram in Fig. 11.1 can be used as a guide to asking pertinent
clinical questions in a logical order during the resuscitation, the
implications of key findings and urgent management.
Tips for success
Clarity of communication is key to obtaining a useful echo study in
this situation.
Ensure the machine is set up and ready to go before approaching the
patient.
Negotiate the correct time to perform echocardiography with the
team leader.
Ask the time-keeper to count 10sec out loud while you perform the
study.
Communicate your findings to the team aloud.
Do not compromise patient care: if you cannot locate adequate
images obtain senior help.
Step 1: Is there evidence
If pericardial fluid is present:
of pericardial fluid?
drain immediately.
If the ventricle is still: this
Step 2: Is the left ventricle
If the ventricle is mobile: a
indicates true pulseless
If hypovolaemia is suspected give
mobile or still?
small left ventricular cavity
electrical activity and
aggressive fluid therapy.
indicates hypovolaemia.
ventricular standstill.
If the ventricle is minimally mobile:
Step 3: If the ventricle is
ventricular dilatation indicates left
mobile and not
ventricular failure.
underfilled: is the right
ventricle severely dilated?
If the right ventricle is severely dilated:
If the right ventricle is not dilated:
is there paradoxical motion of the left
consider needle thoracocentesis for
ventricular septum?
the treatment of tension
pneumothorax.
Either or both of these findings should
prompt consideration of thrombolytic
therapy for massive pulmonary
embolus.
Fig. 11.1 Flowchart for FEEL algorithm.
634
CHAPTER 11 Acute echocardiography
Acute diagnostics
Diagnostic transthoracic echocardiography in the acute setting plays a par-
ticular role in the diagnosis and management of the patient presenting
with:
Acute shortness of breath.
Suspected cardiac tamponade.
Suspected sub-massive pulmonary embolus.
Low cardiac output states.
Clinical acute coronary syndromes.
Blunt and penetrating thoracic trauma.
Transthoracic echocardiography is urgently indicated to assist in management
decisions relating to:
Thrombolysis in sub-massive pulmonary embolism.
Urgent percutaneous coronary intervention in acute coronary
syndromes.
Drainage of pericardial fluid in cardiac tamponade.
Management of acute cardiac failure.
Transfer to cardiothoracic theatre for operative management of
mechanical problems.
A full BSE minimum dataset should be the aim of all transthoracic studies
in this setting. However, given the need for urgent management triggered
by some echocardiographic findings, completion of a full study should not
delay patient management. Fig. 11.2 outlines a practical guide to echocar-
diology in the acutely unwell patient.
It is good practice to repeat the echo study following patient stabilization to
ensure a full dataset is achieved whenever possible and to record echocar-
diographic correlation with signs of improvement in the patient’s clinical
state.
Tips for success
Optimize patient comfort and safety prior to attempting a study: for
example, ensure they have adequate oxygen to maintain saturations
and they are not in pain.
Optimize patient position prior to commencing the study wherever
possible: for example, left lateral position can be maintained with
pillows, ask for help in turning the patient into a suitable position
to optimize views, ask for assistance in maintaining the left arm in a
suitable position.
Be prepared: time available to perform a study may be limited. Think
about what you need to look for and exclude in a systematic fashion
using the protocol given in Fig. 11.2.
Minimize time wasted: prepare the machine before optimizing patient
position.
Utilize all available acoustic windows to achieve answers to clinical
questions: diagnostic acoustic windows can be achieved in 90-95% of
acute cases.
ACUTE DIAGNOSTICS
635
Step 1: Exclude
In a trauma situation:
pericardial fluid.
Notes: Ensure depth
In a non-trauma
The presence of fluid in
is adequate.
situation:
the pericardium in blunt
or penetrating chest
Assess for signs of
trauma should prompt
cardiac tamponade
IMMEDIATE assessment
Step 2: Categorise
by the cardiothoracic
global LV function.
If absent return to
team.
Notes: Use qualitative
step 2 & complete study.
or quantitative methods.
Following urgent referral
If present stop study
return to the patient: if
and contact cardiology
appropriate to continue the
Step 3: Assess each
and appropriate
study examine the aorta
wall region.
supportive teams urgently.
for signs of dissection and
then continue from step 2.
Septal dyskinesia
Other wall
Step 3a: Consider management as
motion
ACS if appropriate clinical context.
abnormality
Contact cardiology team and
appropriate supportive teams urgently.
Step 4: Assess the RV
free wall size and function.
Image the pulmonary
Notes: RV dilatation and
failure should prompt:
Step 3b: Make as specific search for:
arteries to exclude
Assessment of TR jet
VSD
visible thrombus.
Estimation of PAP
Papillary muscle dysfunction/rupture.
Categorise RA as dilated
Continue from step 4.
or non-dilated
Evidence of acute RV
Red arrows indicate pathological
pressure and volume
findings and specific relevant
overload supports
Step 5: Assess AV
pathway.
the decision to
opening and regurgitation.
thrombolyse a
pulmonary embolus
in the context of a
compatible clinical
Step 6: Assess MV
presentation and
opening and regurgitation.
evidence of
cardiovascular
compromise.
Step 7: Assess TV
forward flow &
regurgitation.
Step 8: Assess PV
forward flow &
regurgitation.
If no abnormality is found
assess fluid balance using
the flow diagram shown
overleaf.
Fig. 11.2 Transthoracic echocardiogarphy thought process in the acutely unwell
patient.
636
CHAPTER 11 Acute echocardiography
Critically ill: volume status
Dynamic fluid balance can be effectively assessed using transthoracic
echocardiography. The more profound the hypovolaemia or hypervolae-
mia the easier it is to demonstrate with echocardiography and the more
parameters assessed the more accurate the evaluation.
Fig. 11.3 and Table 11.2 provide details of the key parameters and
imaging process that can help differentiate between hypovolaemia,
normal volume status and volume overload. The key parameters to
assess are:
• IVC diameter and response, and right atrial size.
• Parameters of left and right ventricular size.
Change in measurements is of particular value. Therefore compare
with previous images whenever possible and repeat assessments
after therapy (diuresis or fluid) to determine whether fluid status is
changing.
Beware of:
• Pre-existing regional wall motion abnormalities and chronic
chamber dilatation: these will alter the measurements and reduce
their value for assessment of volume status.
• Body size: dimensions should be adjusted for body surface area
(BSA) where possible:
BSA (m2) =([Height(cm) × Weight(kg)]/3600)
Assessment of the inferior vena cava and right atrium
In spontaneously breathing patients the degree of collapse with inspiration
correlates well with right atrial pressure. However, right atrial pressure
itself only becomes an accurate assessment of volume status when signifi-
cantly high or low (Table 11.1).
Measuring the IVC
Use the subcostal view and get the vessel in its long axis (though a
cross-section can be used).
Measurement of IVC size should be taken 1-2cm below the entrance
to the right atrium if possible, just above or below the hepatic vein.
Accurate measurement in 2D requires the vessel to be followed
throughout the respiratory cycle, keeping the junction of IVC and
hepatic vein in view. If using 2D then you may need to capture 5 or
more beats depending on the respiratory rate.
M-mode gives better resolution and allows easy visualization of several
cycles but keeping the vessel in view can be more difficult.
Measuring the right atrium
Area measures are acquired from apical 4-chamber views.
Beware of long-standing right atrial dilatation that will make
correlations between size and right atrial pressure inaccurate.
CRITICALLY ILL: VOLUME STATUS
637
Volume Status
Assess the Inferior
Subcostal view
Vena Cava
Measure maximum diameter.
Gauge diameter change with respiration.
Check for hepatic vein dilatation.
In any view
Visually assess the LV - small and hyperdynamic suggests hypovolaemia.
Assess the Left
Papillary apposition suggests severe hypovolaemia.
Ventricle
Parasternal view
Look for causes of dynamic outflow obstruction: severe LVH, HOCM,
subaortic bulge.
Separation of the Anterior Mitral Valve leaflet tip
(End-Point Septal Separation) from the septum in diastole.
Measure the end diastolic internal dimension and calculate LVIDd/BSA
In PSAX measure end diastolic area index by plamimetry and calculate
Assess the Right
LVEDAI.
Atrium
Apical view
Where there is suspicion of dynamic outflow tract obstruction use
Continuous-Wave Doppler to assess LVOT gradient.
Measure LVEDAI if not done already or, if time allows, measure
End-Diastolic Volume using Simpson’s biplane method.
Look for dilatation - measure at least 2 RV dimensions from any of the
standard views.
Assess the Right
Parasternal view
Ventricle
In PSAX, look for septal flattening causing a ‘D’-shaped LV, suggesting
RV volume overload.
If flattening present, does it extend into systole? Is there clinical
suspicion of pulmonary embolism?
Apical view
Visually assess the RV and estimate RV/LV ratio.
Estimate RV systolic function using lateral Tricuspid annulus longitudinal
excursion (normal TAPSE is more than 1.8cm) or using tissue Doppler
at the same point (normal is more than 10 m/s).
Fig. 11.3 Emergency assessment of inferior vena cava, left ventricle, right atrium,
and right ventricle to guide volume status.
Table 11.1 Assessment of right atrial pressure
RAP (mmHg)
0-5
5-10
10-15 15-20 >20
IVC size (cm)
<1.5
1.5-2.5
1.5-2.5 >2.5
>2.5
Respiratory variation Collapses >50% collapse <50%
<50% No
change
638
CHAPTER 11 Acute echocardiography
Assessment of the left ventricle
A very under-filled
(small, cavity obliteration in systole) or severely
dilated (large) left ventricle is easy to spot, but for more subtle states the
measurement of dimensions and incorporation with other measures is
imperative (Fig. 11.3).
A significant amount of information can be derived from measurements of
left ventricular cavity size. The key measures that reflect cavity size are:
Left ventricular internal diameter in diastole (LVIDd) (see b p.196).
Left ventricular end-diastolic area index (LVDAI) (See Table 11.)—this
is left ventricular area in the short axis normalized for BSA.
End-point septal separation—this is measured from the M-mode trace
at the level of the mitral valve and represents the distance between
the top of the first peak (E wave) of the mitral valve opening to the
interventricular septum. It increases with both ventricular dilatation
and reduced function (normal 6mm).
Left ventricular end-systolic diameter (see b p.196).
Hypovolaemia can convert lesser degrees of left ventricular hypertrophy
into effective outflow obstruction because of the reduction in size of the
end systolic left ventricular cavity.
Assessment of the right ventricle
Right ventricular dimensions can be measured in several different views so
it is usually possible to get at least one accurate measurement. Standard
measures should ideally be used (Table 4.6) or simplified ‘rules of thumb’
can be found in Table 11.3.
Acute dilatation implies pressure or volume overload. The common
causes for this in the critically ill include pulmonary embolus and acute
lung injury or acute respiratory distress syndrome; less common are
right ventricular infarction or acute tricuspid valve disease.
In RV dilatation the right ventricular output is unlikely to be preload
dependent, making detailed fluid balance decisions difficult.
Diastolic flattening of the interventricular septum occurs with acute
RV volume overload.
Diastolic and systolic flattening suggests more severe volume overload
or the existence of RV pressure overload. (see b p.276).
Severe dilatation is usually accompanied by systolic dysfunction and at
least moderate TR.
Beware of long-standing RV dilatation that makes inferences
concerning size difficult in the acute setting.
CRITICALLY ILL: VOLUME STATUS
639
Table 11.2 Parameters to help identify fluid status
Suggests
Normal range
Suggests volume
hypovolaemia
overload
IVC diameter
<1cm and
1-2.5cm, collapsing >2.5cm, no response
and response
collapsing
25-75%
to respiration
LVIDd/BSA
<2.4 women
2.4-3.2
>3.2
(cm/m2)
<2.2 men
2.2-3.1
>3.1
LVEDAI
<5.5
5.5-10
>10
(short axis)
End point septal
<0.5m
>0.5cm
-
separation
LVESD
Papillary
2.0-4.0cm
-
apposition
RV internal
-
See below
RVIDd >LVIDd
dimensions
Interventricular
-
No flattening
Diastolic flattening
septum
Right atrium
-
<20cm2
>30cm2
Table 11.3 Right ventricular dimensions
Normal range (cm)
PLAX
AP dimension: 1.8-3.0
PSAX
RVOT: 2.0-3.2
A4C
TV annulus: 1.6-3.1
Mid RVIDd: 2.4-3.7
RV length (diastole): 6.9-8.9
640
CHAPTER 11 Acute echocardiography
Critically ill: fluid responsiveness
Any method of measuring change in stroke volume or cardiac output can
be used to assess whether a patient responds to a given volume of fluid.
Being able to predict whether a patient is likely to respond to that fluid
(‘fluid responsive’) is even more useful as it can avoid the potential detri-
mental effect of excessive fluid administration.
The term ‘fluid responsive’ implies that stroke volume will increase by
10-15% when a fluid load is delivered (usually 500mL, or 70-80mL/kg,
of crystalloid or colloid given rapidly).
Dynamic indicators of fluid responsiveness (such as parameters that
change with respiration or patient position) are significantly more
accurate than static (such as end-diastolic volumes).
Mechanical ventilation allows more reliable assessment of the
likelihood of fluid responsiveness.
IVC
Assessment of fluid responsiveness using the IVC is only reliable during
mechanical ventilation. In this situation if the IVC collapses by >20% then
the patient should respond to fluids (Fig. 11.4). In spontaneous ventilation
complete collapse during inspiration is consistent with fluid responsive-
ness but may be confounded by respiratory effort and state of the right
heart.
Left ventricle
A simple way to assess fluid responsiveness is to assess for variation in
flow across the aortic valve or LVOT with different manoeuvres:
Variation with respiration: variation with respiration in the vti across
any valve or outflow tract can be used. However, the best validated
method is flow variation across the aortic valve or LVOT. A change
in left heart flow of >10% suggests the patient is likely to be ‘fluid
responsive’.
Passive leg raising: Change in the vti (and therefore stroke volume)
after passive leg raising is another method of fluid responsiveness
assessment. This works because raising the legs effectively redistributes
blood from the legs to the thorax which mimics a fluid challenge.
To do a ‘passive leg raise’ raise both of the patient’s legs to 45° for
1-2min. A change in SV of 720% suggests fluid responsiveness.
Dysrhythmias reduce the utility of these measurements, but if present,
then at least 3 or more representative waveforms should be recorded and
the results then averaged.
CRITICALLY ILL: FLUID RESPONSIVENESS
641
<1.5cm - fluid response likely
Spontaneous ventilation:
Measure diameter in
expiration.
>1.5cm - uncertain significance
Assess
IVC
No spontaneous ventilation:
Measure minimum and
>18% - fluid response likely
maximum diameter during
ventilation.
<15% - fluid response unlikely
Calculate distensibility using:
100 x (Dmax Dmin)/Dmin.
If a passive leg raise is
possible:
In A4C, A5C or angled sub-
costal view sample the LVOT
with PWD and measure vti
>15% - fluid response likely
(ideally average the smallest
and largest).
<10% - fluid response unlikely
Assess
Repeat after raising the legs
LV
45* (or by reclining the
patient).
Calculate increase in integral.
Fig. 11.4 Assessing fluid responsiveness.
642
CHAPTER 11 Acute echocardiography
Critically ill: advanced haemodynamics
A number of measurements may be of use in the critically ill both for
diagnosis and to guide fluid, inotrope or vasopressor therapy (Fig. 11.5).
Serial focused assessments can eliminate the need for invasive monitoring
in some instances.
Stroke volume (SV) and cardiac output (CO)
Stroke volume can be measured using PW Doppler of the LVOT (or
the RVOT) combined with measurement of the outflow tract diameter
(b p.230). Alternatively, it can be determined measuring change in area of
the ventricle. CO is then derived from multiplying SV by heart rate. When
assessing these parameters with echo beware:
An accurate measurement of the outflow tract diameter is required as
any error will be squared in the calculation.
A clear Doppler trace, properly aligned through the aortic valve and
LVOT is required, as a suboptimal trace may underestimate true
velocities.
Significant MR or TR will lead to inaccuracies in measurement of
stroke volume based on PW Doppler in the outflow tract as it will not
take account of the volume of blood that regurgitates into the atria.
Systemic vascular resistance (SVR)
SVR measurements can be used in diagnosis of underlying causes for
haemodynamic problems, e.g. sepsis will lower systemic vascular resist-
ance. Changes in systemic vascular resistance can be used as a guide to
effectiveness of vasopressor therapy or changes in clinical status.
To calculate SVR measure cardiac output, the mean arterial pressure,
and the right atrial pressure. Then use the equation
SVR = 80 × (MAP − RAP)/CO
5).
Left atrial pressures (LAP)
Approximate LAP is most accurately confirmed by Doppler assessment
of the MV inflow and annular tissue velocity, or by pulmonary vein
flow pattern. The measure closely reflects LVEDP (see b p.644). The
two measures are therefore often discussed interchangeably but are
presented in this chapter under both ‘titles’. E/E’ (septal) >15 suggests
severely elevated LAP. A predominant and increased D wave in the
pulmonary vein flow also suggests elevated pressures (a pre-dominant
D wave is also seen in patients with severe mitral regurgitation although
this is also, in part, due to a reduction in size of the S wave).
CRITICALLY ILL: ADVANCED HAEMODYNAMICS
643
Using Doppler
In A4C, A5C or angled sub-costal view sample
the LVOT using Pulsed Wave Doppler.
Trace a representative waveform to measure the
velocity-time integral in cm.
Measure the LVOT diameter in cm.
Stroke Volume in mL = VTI x 3.14 x (LVOT
diameter/2)2
Stroke Volume
If the LVOT view is poor use the RVOT in the
and
PSAX or sub-costal view.
Cardiac Output
Cardiac output is the product of heart rate and
stroke volume.
Using volumetric method
Simpson’s biplane method gives a an end-
systolic and end-diastolic volume from which
SV can be calculated.
Assess using Cardiac output, blood pressure and
CVP:
Measure the Cardiac output as detailed above.
If RAP is not known then estimate it using the
dimension and degree of collapse of the IVC.
Use the equation SVR = (MAP-RAP)/CO (in
Systemic
mmHg and L/min respectively)
Vascular
Normal SVR = 800-1200 dyne.sec/cm5
Resistance
A qualitative assessment can be made using
CWD assessment of the maximum velocity of an
MR jet, if present:
MR Vmax/VTI1
A result of more than 0.27 suggests high
resistance, <0.2 normal.
Fig. 11.5 Advanced haemodynamics.
644
CHAPTER 11 Acute echocardiography
Estimated LV end-diastolic pressure (LVEDP)
LVEDP is useful in both the differentiation of pulmonary oedema from
acute lung injury and estimating adequacy of preload. In pulmonary oede-
ma LVEDP will increase whereas in acute lung injury it will decrease or not
change. In estimation of preload, LVEDP will decrease as preload reduces.
In the acute setting measures based on aortic or mitral regurgitation have
been used. In the non-acute setting measures based on tissue Doppler
imaging and pulmonary vein flow are routinely used to evaluate LVEDP
to aid diagnosis of diastolic dysfunction and HFNEF (see Chapter 3).
Estimated LV end-diastolic pressure also closely reflects left atrial pres-
sure (see b p.642).
To measure LVEDP based on valvular regurgitation obtain a Doppler
trace of the aortic regurgitation and measure the velocity at the end of
the regurgitation trace. Get a measure of diastolic blood pressure at
the same time as your measurement and then use the equation:
LVEDP = DBP - end aortic regurgitation gradient
If the patient does not have aortic regurgitation but has some mitral
regurgitation this can also be used to estimate LVEDP based on the
initial slope of the regurgitation Doppler profile (see b p.232).
To measure LVEDP with tissue Doppler imaging, obtain a TDI trace
based on movement of the mitral annulus in the 4-chamber view and
get a Doppler spectral trace of mitral valve inflow. E/E’ (septal)
<8 suggests a normal LVEDP. E/E’>15 suggests LVEDP is elevated.
Corrected aortic flow time (FTc) and assessment of preload
Corrected aortic flow time can be used to assess preload. An increment
caused by volume loading is a useful marker of fluid responsiveness (see
b p.642). It is however also affected by changes in inotropy and after-
load, and also by the existence of bundle branch block. Normal FTc is
330-360ms. To measure corrected aortic flow time:
Obtain an apical 5-chamber view (or suprasternal view) and align CW
Doppler across the aortic valve and LVOT.
On the Doppler tracing measure the duration (in ms) of forward flow
across the aortic valve.
Then correct this value for heart rate using the equation:
FTc = FT/Square root of R-R interval or
(simplified) FTc = FT + [1.29 x (HR − 60)]
Pulmonary arterial occlusion pressure (PAOP)
PAOP is useful in the assessment of acute lung injury, respira-tory distress
syndrome, and pulmonary oedema. PAOP can be assessed using a visual
analysis of the interatrial septum, or by Doppler echocardiography. In any
appropriate view:
Watch the movement of the interatrial septum relative to the right
atrium. If:
• Septum persistently bows towards the right atrium PAOP = ~18mmHg.
• Only bows in mid-systole but fully PAOP = ~13mmHg.
• Only bows in mid-systole and only partially PAOP = ~10mmHg.
CRITICALLY ILL: ADVANCED HAEMODYNAMICS
645
Doppler indices suggesting PAOP <18mmHg are: E/A<1.4;
E deceleration time >100ms; pulmonary vein S/D >0.65; pulmonary
vein Doppler systolic fraction >44%; E/E’(lateral) <8. Also, E/Vp <1.7
(where V = propagation velocity, measured by calculating the velocity
of the first aliasing time of the mitral inflow E wave using colour
M-mode) predicts PAOP <18mmHg.
646
CHAPTER 11 Acute echocardiography
Critically ill: weaning from a ventilator
Difficulty in weaning a patient who has been critically ill from ventilatory
support may occur whenever there is a mismatch between metabolic supply
to the respiratory muscles and demand on those muscles.
The three most common factors affecting this balance are:
Muscular weakness.
Poor respiratory drive.
Inadequate cardiac reserve.
The algorithm in Fig. 11.6 describes the thought processes and actions
through which transthoracic echocardiography can assist in the manage-
ment of the difficult to wean patient.
Tips for success
Image quality should be maximized by taking time to optimize patient
positioning.
If previous echo images are available from the acute stages of the
patient’s illness it is important to comment on the comparative
behaviour of the left ventricle in particular. The concept of the ‘acute
ventricle’ is very relevant here. Systolic and diastolic dysfunction in
acute illness from a range of causes including sepsis and polytrauma
may take a variable time to resolve: optimization of the ventricle in
the recovery phase of illness with interval monitoring thereafter is
therefore optimal.
Assessment of diastolic dysfunction should be based upon transmitral
velocity assessment, tissue Doppler imaging of the mitral annulus,
and PW Doppler assessment of the pulmonary venous inflow.
Valsalva manoeuvre in this patient group will be either impossible or
inadequate.
This patient group is prone to the development of pulmonary emboli:
clinician-echocardiographers should make a thorough assessment
of pulmonary artery pressure and have a low threshold for further
investigation of this potentially reversible cause of failure to wean.
The pathway shown should be undertaken in conjunction with a
full assessment of fluid balance as shown in the flow diagram on
b p.639. This assessment should be made alongside clinical enquiry
into fluid balance over the total length of the patient’s illness: acute
assessment of echocardiographic indicators of fluid balance may not
reflect the need for fluid off-loading to facilitate weaning.
When assessing valve
Step 1: Assess LV structure
Significant LVH may suggest diastolic dysfunction.
LV dilatation may correlate with LV systolic
structure and function in the
dysfunction or fluid overload.
critically ill always search for
Where a RWMA is seen
unsuspected vegetations.
Step 2: Assess LV systolic function
Global systolic dysfunction should prompt calculation
RWMA should prompt referral for
of EF and optimisation with rate control and ACEI.
consideration of coronary assessment
exclude VSD and acute MV
or medical therapy.
dysfunction.
Step 3: Assess LV diastolic function
Evidence of diastolic dysfunction should prompt
MS will require cardiology
scrupulous rate control, and ACE inhibition.
referral.
MR should be treated with
Step 4: Assess MV opening
diuretic therapy and rate
and incompetence
control where the patient
is in AF.
Step 5: Assess AV opening and
incompetence
AVG > 40mmHg or valve area < 1.0 cm2 should
AR graded as >mild should
Ensure the CE is included in this
prompt cardiology referral.
prompt cardiology referral.
The finding of significant
assessment since
pulmonary hypertension:
LV function may be abnormal
PAP>35 mmHg should
following critical illness
prompt exclusion
pulmonary emboli and
Step 6: Assess RV dilatation
RV dilatation and reduced annular function should
prompt a search for pulmonary emboli where
Image the pulmonary trunk for
management of the PAP
and function
right sided coronary disease is not suspected.
evidence of thrombus:
with medical therapy.
Where TR is present
Step 7: Assess TV forward flow
measure the RVSP from
and incompetence
several views and
calculate the PAP as a
product of the RVSP and
the RAP estimated from
Step 8: Assess PV forward flow
the behaviour of the IVC
and incompetence
The presence of pericardial fluid in a patient with
Step 10: Assess the IVC
Step 9: Examine the pericardium
previous or current sepsis should prompt
to exclude volume overload
from multiple views
consideration of a pyopericardium.
Fig. 11.6 Thought processes and actions through which transthoracic echocardiography can assist in the management of the difficult to wean patient.
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649
Chapter 12
Reporting and normal
ranges
Reporting 650
Left ventricle
652
Left ventricular size, mass, and function
654
Right ventricle
656
Right ventricular size and function
657
Ventricular septum 658
Atrial septum 659
Left atrium 660
Right atrium 660
Atrial size
661
Aortic valve
662
Aortic stenosis
662
Aortic regurgitation
662
Mitral valve
664
Mitral stenosis
666
Mitral regurgitation
666
Tricuspid valve
668
Tricuspid regurgitation
669
Right atrial pressure
669
Pulmonary valve 670
Pulmonary artery 670
Pulmonary regurgitation 671
Pulmonary stenosis 671
Prosthetic valves
672
Prosthetic valve velocities
673
Aorta 674
Aortic size
675
Masses 676
Endocarditis 677
Pericardium 678
Pericardial fluid
678
650
CHAPTER 12 Reporting and normal ranges
Reporting
A standard approach to reporting ensures complete studies, and improves
comprehension for other readers during interpretation or follow-up. Here
we describe a suggested structure for a report and anatomical structures
are listed with examples of appropriate descriptions (b ‘Section 2’, p.650).
The calculations (b ‘Section 3’, p.650) will have been collected as part of
the minimal dataset (described in Chapter 2) and can be interpreted based
on tables of expected values for different anatomy and pathology (these
tables have been replicated in this chapter).
Section 1. Demographic and other information
Patient’s name, date of birth, gender, hospital number.
Date on which study was performed.
Location (inpatient, outpatient) and urgency.
Indications for test.
Referring physician.
Sonographer/physician performing and interpreting the study.
Height, weight, blood pressure (if available).
Ultrasound machine and data storage.
Image quality and any suboptimal views (if applicable).
Section 2. Description of observations and diagnostic
statements
A brief description should be given of each anatomical feature. The descrip-
tion should summarize findings from all views (comments should be able
to be supported from measurements later in report). It is unpractical to
include all statements if everything is normal and usually it is sufficient just
to call them normal in structure and function. However, there should be a
protocol or check list to ensure all comments are based on facts (visual and
quantitative assessment). For each anatomical detail, when appropriate,
there should also be a diagnostic statement, such as, appearances sugges-
tive of rheumatic mitral disease.
Section 3. M-mode, 2D, and Doppler measurements
This section is based on a minimal dataset that should be included in every
report (b p.85), supplemented with additional measures as required to
describe any pathology. Ideally the report should include normal values for
particular measurements.
Section 4. Conclusions
This section is often read first by the referring physicians, who may not
be cardiologists. It has to be easily understood and should summarize
the whole study. Identify any abnormality, its cause (if identifiable) and
any secondary effect. This may involve repeating some of the information
from Sections 2 and 3. The questions of the referring physicians should
be answered. If not possible, then the reasons should be included and
alternative methods suggested (e.g. transoesophageal echocardiography
or contrast echocardiography). Medical advice should be separated from
the report of the study.
REPORTING
651
Sample report: normal
John Smith
DoB: 10:07:1935
Inpatient: Ward A
Height: 182 cm
Weight: 74kg
BP: 120/70
Indication:?LV function
Referring Physician: Dr Smith
Sonographer: John Brown
Interpreting Physician: Dr Jones
Machine: Ultrasound Machine A Images saved: Server
Image Quality: Good
Descriptions
1. Left ventricle: normal cavity size, normal wall thickness, normal
systolic and diastolic funtion
2. Right ventricle: normal size, normal wall thickness, normal systolic
function
3. Ventricular septum: normal
4. Left atrium: normal size
5. Right atrium: normal size
6. Atrial septum: normal
7. Inferior vena cava: normal diameter, normal response during
respiration
8. Aortic valve: normal structure and function
9. Mitral valve: normal structure and function
10. Tricuspid valve: normal structure and function
11. Pulmonary valve: normal structure and function
12. Pulmonary artery: normal diameter
13. Pericardium: no thickening, no effusion
14. Aorta: normal diameter of root and ascending aorta
Measurements
1. Left ventricle
LVED-5.0cm, LVES-3.5cm, FS - 30% IVS-
1.0cm, LVPW-0.9cm normal diastolic LV
function, E' (Medial) 6.9 cm/s, E' (lateral)
10.9, E/E' 12.0
2. Right ventricle
RVED - 2.0cm
3. Left atrium
LA diameter - 3.2cm
4. Right atrium
5. Inferior vena cava
6. Aortic valve
peak velocity - 1.2m/s
7. Mitral valve
E: A ratio - 1.1
8. Tricuspid valve
TR maximum velocity - 1m/s
9. Pulmonary valve
PW peak velocity - 1m/s
10. Pulmonary artery
Root diameter - 2.6cm
11. Pericardium
12. Aorta
Root diameter - 2.7cm
Conclusions
Normal echocardiogram. Normal left ventricle size. Normal left ventricle
systolic and diastolic function.
Dr. Jones
652
CHAPTER 12 Reporting and normal ranges
Left ventricle
Descriptive terms
Cavity size
Normal, dilated (mild/moderate/severe), decreased.
Wall thickness
Normal, hypertrophy (mild/moderate/severe).
Pattern (concentric, eccentric, asymmetric + location)
Decreased.
LV Mass
Normal, mild, moderate, severe increase.
Shape
Normal, aneurysm, pseudoaneurysm (+ location).
Global systolic function
Normal, borderline, low normal.
Decreased (mild, mild to moderate, moderate, moderate to severe,
severe).
Increased (hyperdynamic).
Estimated ejection fraction.
Regional systolic function
Normal, hypokinetic, akinetic, dyskinetic, scar.
Asynchronous, not seen. Describe for each segment of the walls:
• Anterior (basal, mid, apical).
• Anteroseptal (basal, mid).
• Inferoseptal (basal, mid, apical).
• Inferior wall (basal, mid, apical).
• Posterior (inferolateral) wall (basal, mid, apical).
• Lateral wall (basal, mid, apical).
Diastolic filling
Normal, abnormal (Impaired relaxation, pseudonormal, restrictive).
Elevated left atrial pressure (E/E’ >15, normal <18).
Left ventricle outflow tract
No obstruction, obstruction (mild/moderate/severe).
Septal hypertrophy, subaortic membrane.
Associated with mitral valve systolic anterior motion.
Thrombus
Absent, present (+ location and description).
Mass
Absent, present (+ location and description).
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654
CHAPTER 12 Reporting and normal ranges
Left ventricular size, mass, and
function (Tables 12.1 and 12.2)
Table 12.1 Ranges for measurements of LV size and mass
Women
Normal
Mild
Moderate
Severe
LV dimension
LVED diameter, cm
3.9-5.3
5.4-5.7
5.8-6.1
>6.1
LVED diameter/BSA, cm/m2
2.4-3.2
3.3-3.4
3.5-3.7
>3.7
LV volume
LVED vol, mL
56-104
105-117
118-130
>130
LVED vol/BSA, mL/m2
35-75
76-86
87-96
>96
LVES vol, mL
19-49
50-59
60-69
>69
LVES vol/BSA, mL/m2
12-30
31-36
37-42
>42
Linear method: fractional shortening
Endocardial, %
27-45
22-26
17-21
<17
2D method
Ejection fraction, %
>54
45-54
30-44
<30
Linear method: wall thickness
Relative wall thickness, cm
0.22-0.42
0.43-0.47
0.48-0.52
>0.52
Septal thickness, cm
0.6-0.9
1.0-1.2
1.3-1.5
>1.5
Posterior wall thickness, cm 0.6-0.9
1.0-1.2
1.3-1.5
>1.5
2D method
LV mass, g
66-150
151-171
172-182
>182
LV mass/BSA, g/m2
44-88
89-100
101-112
>112
BSA, body surface area; d, diastolic; s, systolic. Bold rows identify best validated measures.
3D LV volume and ejection fraction
Upper normal values (mean + 2 standard deviations [SD])
LV end-diastolic volume index (LVEDVI)
82mL/m2
LV end-systolic volume index (LVESVI)
38mL/m2
Lower limit (mean − 2 SD)
LVEF
49%
EF, ejection fraction; LVEDVI, LV end-diastolic volume index; LVESVI, LV end-systolic volume
index.
LEFT VENTRICULAR SIZE, MASS, AND FUNCTION
655
Table 12.2 Ranges for measurements of LV size and mass
Men
Normal
Mild
Moderate Severe
LV dimension
LVED diameter, cm
4.2-5.9
6.0-6.3
6.4-6.8
>6.8
LVED diameter/BSA, cm/m2 2.2-3.1
3.2-3.4
3.5-3.6
>3.6
LV volume
LVED vol, mL
67-155
156-178
179-201
>201
LVED vol/BSA, mL/m2 35-75
76-86
87-96
>96
LVES vol, mL
22-58
59-70
71-82
>82
LVES vol/BSA, mL/m2
12-30
31-36
37-42
>42
Linear method: fractional shortening
Endocardial, %
25-43
20-24
15-19
<15
2D method
Ejection fraction, %
>54
45-54
30-44
<30
Linear method: wall thickness
Relative wall thickness, cm 0.24-0.42
0.43-0.46
0.47-0.51
>0.51
Septal thickness, cm
0.6-1.0
1.1-1.3
1.4-1.6
>1.6
Posterior wall
0.6-1.0
1.1-1.3
1.4-1.6
>1.6
thickness, cm
2D method
LV mass, g
96-200
201-227
228-254
>254
LV mass/BSA, g/m2
50-102
103-116
117-130
>130
BSA, body surface area; d, diastolic; s, systolic. Bold rows identify best validated measures.
3D LV volume and ejection fraction
Upper normal values (mean + 2 standard deviations [SD])
LV end-diastolic volume index (LVEDVI)
82mL/m2
LV end-systolic volume index (LVESVI)
38mL/m2
Lower limit (mean − 2 SD)
LVEF
49%
EF, ejection fraction; LVEDVI, LV end-diastolic volume index; LVESVI, LV end-systolic volume
index.
656
CHAPTER 12 Reporting and normal ranges
Right ventricle
Descriptive terms
Cavity size
Normal.
Dilated (mild/moderate/severe).
Decreased.
Wall thickness
Normal.
Hypertrophy.
Decreased.
Global systolic function
Normal.
Decreased (mild, moderate, severe).
Increased (hyperdynamic).
Regional systolic function
Normal.
Hypokinetic.
Akinetic.
Not seen.
Describe for free wall/apex/outflow tract.
Thrombus
Absent, present (+ location and description).
Mass
Absent, present (+ location and description).
RIGHT VENTRICULAR SIZE AND FUNCTION
657
Right ventricular size and function
(Tables 12.3 and 12.4)
Table 12.3 2D parameters to assess right ventricle size and function
(ASE guidelines)
Measure
Abnormal
Chamber dimensions
RV basal diameter (RVD1)
>4.2cm
RV subcostal wall thickness
>0.5cm
RVOT PSAX distal diameter (RVOT2)
>2.7cm
RVOT PSAX proximal diameter (RVOT1)
>3.3cm
Systolic function
TAPSE
<1.6cm
Tissue Doppler peak velocity at the annulus
<10cm/s
Pulsed Doppler myocardial performance index
>0.40
Tissue Doppler myocardial performance index
>0.55
Fractional area change (%)
>35%
Table 12.4 3D RV volumes and ejection fraction
LRV (95% CI) Mean (95% CI) URV (95% CI)
3D RV EF (%)
44 (39-49)
57 (53-61)
69 (65-74)
3D RV EDV indexed (mL/m2) 40 (28-52) 65 (54-76)
89 (77-101)
3D RV ESV indexed (mL/m2)
12 (1-23)
28 (18-38)
45 (34-56)
CI, confidence interval; EF, ejection fraction; EDV, endiastolic volume; ESV, endsystolic volume;
LRV, lower reference value; URV, upper reference value.
658
CHAPTER 12 Reporting and normal ranges
Ventricular septum
Descriptive terms
Abnormal septal motion
Abnormal (paradoxical) motion consistent with right ventricle volume
overload.
Abnormal (paradoxical) motion consistent with postoperative status.
Abnormal (paradoxical) motion consistent with left bundle branch
block.
Abnormal (paradoxical) motion consistent with right ventricle
pacemaker.
Abnormal (paradoxical) motion due to pre-excitation.
Flattened in diastole (‘D’-shaped left ventricle) consistent with right
ventricle volume overload.
Flattened in systole consistent with right ventricle pressure overload.
Flattened in systole and diastole consistent with right ventricle
pressure and volume overload.
Septal ‘bounce’ consistent with constrictive physiology.
Excessive respiratory change consistent with tamponade, constriction,
ventilation-related.
Other (specify).
Ventricular septal defect
Absent, present.
Location (perimembranous, subpulmonary/doubly committed, inlet,
muscular, multiple.
Size (small/moderate/large).
Shunt (left-to-right/right-to-left/bidirectional).
ATRIAL SEPTUM
659
Atrial septum
Descriptive terms
Atrial septal defect
Absent, present.
Location (primum, secundum, sinus venosus).
Size (dimensions in 2 planes and area from 3D study).
Shunt (left-to-right, right-to-left, bidirectional).
Qp/Qs.
Patent foramen ovale
Absent, present.
Contrast study
Normal, shunt present (small <5 bubbles/moderate 5-20 bubbles/large
>20 bubbles).
660
CHAPTER 12 Reporting and normal ranges
Left atrium
Descriptive terms
Cavity size
Normal, dilated (mild/moderate/severe), decreased.
Thrombus
Absent, present (+ location and description).
Mass
Absent, present (+ location and description).
Spontaneous contrast
Absent, present.
Other
Cor triatriatum, hypoplastic left atrium, consistent with cardiac
transplantation.
Right atrium
Descriptive terms
Cavity size
Normal, dilated (mild/moderate/severe), decreased.
Thrombus
Absent, present (+ location and description).
Mass
Absent, present (+ location and description).
Catheter/pacing wire
Absent, present.
Right atrial pressure
Septum bowed to left consistent with elevated right atrial pressure.
Dilated coronary sinus consistent with elevated right atrial pressure or
left superior vena cava.
Persistent left superior vena cava.
Normal inferior vena cava size/respiratory variation—right atrial
pressure normal.
Normal inferior vena cava size/reduced variation—right atrial pressure
mildly increased (10mmHg).
Dilated inferior vena cava size/reduced variation—right atrial pressure
moderately increased (15mmHg).
Dilated inferior vena cava/absent variation/dilated hepatic veins—right
atrial pressure severely increased (20mmHg).
Other
Prominent Eustachian valve, Chiari network.
ATRIAL SIZE
661
Atrial size (Table 12.5)
Table 12.5 Parameters to assess left and right atria
Women
Normal
Mild
Moderate Severe
Atrial dimension
LA diameter, cm
2.7-3.8
3.9-4.2
4.3-4.6
>4.6
LA diameter, BSA, cm/m2
1.5-2.3
2.4-2.6
2.7-2.9
>2.9
RA minor axis, cm
2.9-4.5
4.6-4.9
5.0-5.4
>5.4
RA minor axis/BSA, cm/m2
1.7-2.5
2.6-2.8
2.9-3.1
>3.1
Atrial area
LA area, cm2
<20
20-30
31-40
>40
Atrial volume
LA vol, mL
22-52
53-62
63-72
>72
*LA vol/BSA, mL/m2
<29
29-33
34-39
>39
Men
Normal
Mild
Moderate Severe
Atrial dimension
LA diameter, cm
3.0-4.8
4.1-4.6
4.7-5.2
>5.2
LA diameter, BSA, cm/m2
1.5-2.3
2.4-2.6
2.7-2.9
>2.9
RA minor axis, cm
2.9-4.5
4.6-4.9
5.0-5.4
>5.4
RA minor axis/BSA, cm/m2
1.7-2.5
2.6-2.8
2.9-3.1
>3.1
Atrial area
LA area, cm2
<20
20-30
31-40
>40
Atrial volume
LA vol, mL
18-58
59-68
69-78
>78
*LA vol/BSA, mL/m2
<29
29-33
34-39
>39
BSA, Body surface area. *Bold rows identify best validated measures.
662
CHAPTER 12 Reporting and normal ranges
Aortic valve
Descriptive terms
Structure
Normal, degenerative, rheumatic.
Bicuspid, fused (RCC-LCC/RCC-NCC/NCC-LCC).
Unicuspid, quadricuspid.
Leaflet thickness
Focal thickening (RCC/LCC/NCC), diffuse thickening.
Severity (mild/moderate/severe).
Calcification
Present (mild/moderate/severe).
Focal calcification (RCC/LCC/NCC).
Diffuse calcification.
Leaflet mobility
Normal, reduced (mild/moderate/severe), doming.
Other
Leaflet perforation (RCC/LCC/NCC).
Leaflet prolapse/flail (RCC/LCC/NCC).
Vegetation
Location (RCC/LCC/NCC).
Mobility (non-mobile/mobile), pedunculated.
Size (small/moderate/large) + dimensions.
Abscess
Location (RCC-annulus/LCC-annulus/NCC-annulus).
Size (small/moderate/large) + dimensions.
Mass
Location (RCC/LCC/NCC), description (see b p.530).
Aortic stenosis (Table 12.6)
None, present (mild/moderate/severe).
Quantification:
• Peak and mean transaortic velocity/gradient.
• Aortic valve area.
Aortic regurgitation (Table 12.7)
None, present (trace, mild, moderate, severe).
AORTIC REGURGITATION
663
Table 12.6 Parameters to assess severity of aortic stenosis
Mild
Moderate
Severe
Peak velocity (m/s)
2.5-2.9
3.0-4.0
>4.0
Peak gradient (mmHg)
<35
35-65
>65
Mean gradient (mmHg)
<20
20-40
>40
Valve area (cm2)
>1.5
1.0-1.5
<1.0
Table 12.7 Parameters to determine severity of aortic regurgitation
Specific signs of severity
Mild
Severe
Vena contracta
<0.3cm
>0.6cm
Jet (Nyquist
Central, <25% of LVOT Central, >65% of LVOT
50-60cm/s)
Descending aorta
No or brief early
diastolic flow reversal
Supportive signs of severity
Mild
Severe
Pressure half time
>500ms
<200ms
Descending aorta
-
Holodiastolic flow reversal
Left ventricle (only for Normal LV
Moderate or greater LV
chronic lesions)
enlargement (no other cause)
Report as moderate if signs of regurgitation are greater than mild but there are no features of
severe regurgitation.
664
CHAPTER 12 Reporting and normal ranges
Mitral valve
Descriptive terms
Structure
Normal, rheumatic, myxomatous, degenerative.
Annulus
Normal, dilated, calcified (mild/moderate/severe).
Leaflet thickness
Normal, thickened (mild/moderate/severe).
Leaflet tips, Leaflet body (aMVL/pMVL).
Commissures
Antero-lateral fusion, posteromedial fusion.
Calcification
Focal calcification (aMVL/pMVL), diffuse calcification.
Commissural calcification (anterolateral/posteromedial).
Cleft
Anterior leaflet, posterior leaflet.
Chordal disease
Shortening, fusion/thickening, elongation.
Rupture, calcification.
Papillary muscle
Rupture, partial rupture (anterolateral/posteromedial).
Calcification/fibrosis (anterolateral/posteromedial).
Leaflet mobility
Normal, reduced (mild/moderate/severe).
Doming, prolapse, bowing.
Systolic anterior motion (mild/moderate/severe—based on outflow
tract gradient).
Chordal systolic anterior motion.
Prolapse
Anterior, posterior leaflet (mild/mod/severe/flail).
A1, A2, A3, P1, P2, P3 (mild/mod/severe/flail).
Vegetation
Location (aMVL/pMVL).
Mobility (non-mobile/mobile), pedunculated.
Size (small/moderate/large), dimensions.
Abscess
Location (aorto-mitral/pMVL/annulus).
Size (small/moderate/large), dimensions.
Mass
Location (aMVL/pMVL), description (see b p.530).
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666
CHAPTER 12 Reporting and normal ranges
Mitral stenosis (Table 12.8)
None, present (mild/moderate/severe).
Quantitative measurements:
• Peak and mean transmitral velocity/gradient.
• Pressure half-time, mitral valve area.
Suitable for commissurotomy.
Mitral regurgitation (Table 12.9)
None, present (trace, mild, moderate, severe).
Jet direction:
• Anteriorly-, posteriorly-, centrally-directed.
• Wall-impinging jet, directed down pulmonary veins.
Diastolic mitral regurgitation (present/absent).
Quantitative measurements:
• MR: LA area ratio, regurgitant volume.
• Vena contracta width, EROA.
Pulmonary venous flow (normal, blunted systolic flow, systolic flow
reversal).
MITRAL REGURGITATION
667
Table 12.8 Parameters to determine severity of mitral stenosis
Mild
Moderate
Severe
MV area (cm2)
2.2-1.5
1.5-1.0
<1.0
MV pressure half-time (ms)
100-150 150-220
>220
Mean pressure gradient (mmHg)
<5
Variable
>10
TR velocity (m/s)
<2.7
Variable
>3
PA pressure (mmHg)
<30
Variable
>50
Table 12.9 Parameters to assess severity of mitral regurgitation
Specific signs of severity
Mild
Severe
Jet (Nyquist
<4cm2 or <20% left
>40% left atrium
50-60cm/s)
atrium
Small & central
Large & central or wall
impinging and swirling
Vena contracta
<0.3cm
>0.7cm
PISA r (Nyquist
None/minimal
Large (>1cm)
40cm/s)
(<0.4cm)
Pulmonary vein flow
-
Systolic reversal
Valve structure
-
Flail or rupture
Supportive signs of severity
Mild
Severe
Pulmonary vein flow
Systolic dominant
Mitral inflow
A-wave dominant
E-wave dominant (>1.2m/s)
CW trace
Soft & parabolic
Dense & triangular
LV and LA
Normal size LV if
Enlarged LV & LA if no
chronic MR
other cause
Report as moderate if signs of regurgitation are greater than mild but there are no features
of severe regurgitation.
668
CHAPTER 12 Reporting and normal ranges
Tricuspid valve
Descriptive terms
Structure
Normal, rheumatic, myxomatous (redundant).
Ebstein.
Annulus
Normal, dilated.
Calcified.
Leaflet thickness
Normal, increased.
Leaflet tips, leaflet body (anterior/posterior/septal).
Calcification
Focal calcification (anterior/posterior/septal).
Diffuse calcification.
Papillary muscle
Rupture.
Leaflet mobility
Normal, reduced (mild/moderate/severe).
Doming, prolapse, bowing.
Prolapse
Anterior leaflet (mild/mod/severe/flail).
Posterior leaflet (mild/mod/severe/flail).
Septal leaflet (mild/mod/severe/flail).
Vegetation
Location (anterior/posterior/septal).
Mobility (non-mobile/mobile), pedunculated.
Size (small/moderate/large) + dimensions.
Abscess
Location (anterior-annulus/posterior-annulus/septal).
Size (small/moderate/large) + dimensions.
Mass
Location (anterior/posterior/septal).
Description (see b p.530).
Tricuspid stenosis
None, present.
Quantitative measurements.
• Peak and mean transtricuspid gradient.
• Tricuspid valve area.
Tricuspid regurgitation
None, present (trace, mild, moderate, severe).
Jet direction: free wall-directed, septal-directed, centrally-directed.
Hepatic vein flow:
• Normal, blunted systolic flow.
• Systolic flow reversal.
RIGHT ATRIAL PRESSURE
669
Tricuspid regurgitation (Table 12.10)
Table 12.10 Parameters to assess severity of tricuspid regurgitation
Mild
Severe
Qualitative
Valve structure
Normal
Abnormal
Jet (Nyquist 50-60cm/s)
<5cm2
>10cm2
CW trace
Soft & parabolic Dense & triangular
Semi-quantitative
Vena contracta
-
>0.7cm
PISA r (Nyquist 40cm/s)
>0.9cm
<0.5cm
Tricuspid inflow
Normal
E wave dominant >1m/s
Hepatic vein flow
Normal
Systolic reversal
Quantitative
EROA
Not defined
>/40mm2
R vol
Not defined
>45mL
RV/RA/IVC
Normal size
Usually dilated
Report as moderate if signs of regurgitation are greater than mild but there are few features
of severe regurgitation.
Right atrial pressure (Table 12.11)
Table 12.11 Assessment of right atrial pressure
RAP (mmHg)
0-5
5-10
10-15 15-20 >20
IVC size (cm)
<1.5
1.5-2.5
1.5-2.5 >2.5
>2.5
Respiratory variation Collapses >50% collapse <50%
<50% No
change
670
CHAPTER 12 Reporting and normal ranges
Pulmonary valve
Descriptive terms
Structure
Normal, dysplastic, bicuspid.
Mobility
Normal, reduced.
Doming.
Vegetation
Location.
Mobility (non-mobile/mobile), pedunculated.
Size (small/moderate/large) + dimensions.
Mass
Location, description (see b p.530).
Stenosis
None, present (mild/moderate/severe).
Location (valvular, infundibular, valvular +infundibular supravalvular,
branch).
Left or right main pulmonary artery.
Quantitative measurements: peak and mean transpulmonary gradient.
Regurgitation
None, present (trace, mild, moderate, severe).
Pulmonary pressure
Normal.
Elevated systolic pressure (mild/moderate/severe).
Elevated diastolic pressure (mild/moderate/severe).
Estimated pulmonary artery.
Pulmonary artery
Descriptive terms
Appearance
Normal, abnormal.
Dilatation
Absent, present (mild/moderate/severe).
Thrombus
Main/right/left pulmonary artery.
Pulmonary artery stenosis
Main/right/left pulmonary artery (mild/moderate/severe).
Patent ductus arteriosus
Absent, present.
PULMONARY STENOSIS
671
Pulmonary regurgitation (Table 12.12)
Table 12.12 Parameters to assess pulmonary regurgitation
Mild
Severe
Pulmonary valve anatomy
Normal
Abnormal
Jet size on colour flow
<10mm long
Large with wide origin
CW density and shape
Soft and slow
Dense and steep
PR index
<0.77
Jet width of RVOT
>65%
PA flow
Increased
Greatly increased
compared to systemic
Right ventricle size
Normal
Dilated
If features suggest more than mild regurgitation but no features of severe grade as moderate.
Pulmonary stenosis (Table 12.13)
Table 12.13 Parameters to determine severity of pulmonary stenosis
Mild
Moderate
Severe
Peak velocity (m/s)
<3
3-4
>4
Peak gradient (mmHg)
<36
36-64
>64
Valve area (cm2)
>1.0
0.5-1.0
<0.5
672
CHAPTER 12 Reporting and normal ranges
Prosthetic valves
Descriptive terms
Type
Mechanical (tilting disk/bileaflet/ball and cage/other).
Bioprosthesis (stented xenograft/homograft/stentless.
Autograft (Ross)/other).
Manufacturer & size.
Annuloplasty ring, valve repair.
Sewing ring
Well seated, rocking, dehisced.
Occluder mechanism
Normal, thickened leaflets (bioprosthesis).
Normal mobility, restricted mobility, flail.
Abnormal masses
Strand(s), micro-cavitations, pannus, thrombus.
Vegetation (+description), abscess (+description).
Fistula.
Stenosis
Present, severity (as for native valve).
Regurgitation
Physiologic, prosthetic, paraprosthetic.
Severity (as for native valve).
PROSTHETIC VALVE VELOCITIES
673
Prosthetic valve velocities
Table 12.14 provides a guide to maximal expected velocities for different
valve types. Refer to manufacturer guidelines for definitive measures and
take into account clinical scenario. Velocities depend on left ventricle func-
tion, volume, and ionotropic status. Therefore minimal gradients are not
presented. In individual cases the threshold may be exceeded with a func-
tionally normal prosthesis—in particular if there is a hyperdynamic state.
Table 12.14 Maximum prosthetic velocities
Aortic prosthetic valves:
Bileaflet valve (e.g. St Jude)
Size (mm)
19
21
23
25
27
29
Vmax (m/s)
4.5
3.5
3.5
3.5
3.1
2.5
Tilting disc (e.g. Medtronic Hall, BS)
Size (mm)
— 21 23
25
27
29
Vmax (m/s)
— 3.7 3.0
2.4
2.1
2.1
Ball and cage (e.g. Starr-Edwards)
Vmax (m/s)
3.6
Bioprostheses (e.g. Hancock, Carpentier Edwards)
Size (mm)
19
21
23
25
27
29
Vmax (m/s)
3.5
3.0
3.0
2.9
2.9
2.5
Mitral prosthetic valves:
Bileaflet valve (e.g. St Jude)
Size (mm)
19
21
23
25
27
29
Vmax (m/s)
4.5
3.5
3.5
3.5
3.1
2.5
Tilting disc (e.g. Medtronic Hall, BS)
Size (mm)
— 21 23
25
27
29
Vmax (m/s)
— 3.7 3.0
2.4
2.1
2.1
Ball and cage (e.g. Starr-Edwards)
Vmax (m/s)
3.6
Bioprostheses (e.g. Hancock, Carpentier Edwards)
Size (mm)
19
21
23
25
27
29
Vmax (m/s)
3.5
3.0
3.0
2.9
2.9
2.5
674
CHAPTER 12 Reporting and normal ranges
Aorta
Descriptive terms
Appearance
Normal, abnormal.
Dilatation
Absent, present (mild/moderate/severe).
Location and dimensions:
• Dilated atrioventricular annulus.
• Dilated aortic root/sinuses.
• Dilated sinotubular ridge.
• Dilated ascending aorta.
• Dilated transverse aorta.
• Dilated descending thoracic aorta.
• Dilated abdominal aorta.
Aneurysm
Absent, sinuses of Valsalva (left/right/non-coronary).
Aortic root, ascending aorta, transverse aorta.
Descending thoracic aorta, abdominal aorta.
Dimensions, type (fusiform, saccular).
Ruptured sinus of Valsalva (to right atrium, right ventricle, left atrium,
left ventricle).
Atheroma/thrombus
Absent, present.
Location (aortic root, ascending aorta, transverse aorta, descending
thoracic aorta, abdominal aorta).
Appearance (layered/mural, protruding, ulcer).
Severity (mild/moderate/severe).
Mobility (immobile/mobile).
Graft (prosthetic/homograft) + location.
Dissection
Location, entry point, exit point(s).
False lumen thrombus (absent/partial/present).
Stanford type A or B.
Intramural haematoma and location.
Transection and location.
Coarctation
Absent, repaired/residual, present.
Severity (mild/moderate/severe).
Measurements (minimum diameter, gradient).
AORTIC SIZE
675
Aortic size (Fig. 12.1)
AGED 20-39 years
4.2
4.0
3.8
3.6
3.4
3.2
3.0
2.8
2.6
2.4
2.2
2.0
1.2
1.4
1.6
1.8
2.0
2.2
Body surface area (m2)
AGED >40 years
4.4
4.2
4.0
3.8
3.6
3.4
3.2
3.0
2.8
2.6
2.4
2.2
1.2
1.4
1.6
1.8
2.0
2.2
2.4
Body surface area (m2)
Fig. 12.1 Ranges of normal sinus of Valsalva size according to age.
676
CHAPTER 12 Reporting and normal ranges
Masses
Descriptive terms
Thrombus
Absent, present.
Size (small/moderate/large).
Location.
Description:
• Shape (flat or mural/protruding/spherical/other).
• Surface (regular/irregular).
• Texture (layered/solid/part solid/calcified).
• Mobility (mobile/fixed).
Dimensions.
Tumour
Absent, present.
Size (small/moderate/large).
Location.
Description:
• Shape (flat or mural/pedunculated/papillary/spherical/other).
• Surface (regular/irregular/multilobular/other).
• Texture (solid/layered/cystic/calcified/heterogeneous).
• Mobility (mobile/fixed).
Dimensions.
Type (suggestive of myxoma/fibroelastoma/etc.).
ENDOCARDITIS
677
Endocarditis
Descriptive terms
Vegetation
Valvular/mural mass consistent with a vegetation.
Location (atrial or ventricular side of valves, ventricular . . .).
Mobility (non-mobile, mobile, pedunculated).
Size (small, moderate, large).
Dimensions.
Abscess
Perivalvular or valvular cavity suggesting abscess.
Location (annulus right coronary cusp etc.)
Size (small, moderate, large).
Dimensions.
Fistula
From . . . to . . . .
Size/haemodynamically relevant.
Severity of valvular lesion
See native valves, Chapter 3.
Pericardial effusion
See b p.306.
678
CHAPTER 12 Reporting and normal ranges
Pericardium
Descriptive terms
Appearance
Normal, abnormal.
Effusion
Absent, present.
Size (small/moderate/large).
Location:
• Circumferential.
• Localized (near . . . left ventricle, right ventricle, left atrium, right
atrium).
Appearance/content (clear fluid, fibrinous, focal strands/masses,
effusive-constrictive.
Thickening/calcification
Absent, present.
Mass
Absent, present.
Haemodynamic effects
Septal bounce.
Chamber collapse (absent/present + chamber).
Increased respiratory variation (absent, present + location).
Compatible with tamponade or constrictive.
Pericardial fluid (Table 12.15)
Table 12.15 Assessment of pericardial effusion based on thickness and
volume
Trace
Mild
Moderate
Severe
Thickness (cm)
<0.5
0.5-1
1-2
>2
Volume (mL)
50-100
100-250
250-500
>500
679
Index
false lumen 318, 522, 525
planimetry 454
A
hypotension 537
pulmonary
A’ 248
Stanford classification 318
hypertension 138
abdominal aorta 308, 310
surgery 524
septal hypertrophy 138
abdominal aorta view 90-1
TOE 522-3
subaortic
abdominal aortic
true lumen 522, 525
membrane 110
aneurysm 324-5
TTE 318-19
3D assessment 138-9
abnormal relaxation 246,
aortic regurgitation
TOE 454
249, 251
acute/chronic 150
TTE 134-5
abscess 188-9, 472-3
age 142
valve area 50
accreditation 584, 631
aortic stenosis 138
aortic transection 526
AcuNav® 549, 551
causes 143
aortic valve
acute
colour M-mode 148-9,
anatomy 132
echocardiography 628
456
bicuspid 134, 138, 152-3,
cardiopulmonary
deceleration slope 146
460
resuscitation 631-2
descending aorta
five cusps 152
diagnostic 634
flow 144, 147, 458-9
mitral valve repair 447
FEEL algorithm 632-3
grading severity 144-5,
normal TOE
safety issues 630
147, 456-8, 663
findings 452-3
acute pericarditis 306
holodiastolic aortic flow
normal TTE findings
acute ventricle 646
reversal 144, 147,
132-3
adenosine protocol 618-19
458-9
preoperative assessment
agitated saline 562, 566-7,
jet area 148
using TOE 460
570
jet length 148-9
quadricuspid 152-3
akinetic left ventricle
jet width 144
reporting 662
segments 597
left ventricle 146
vti and passive leg
ALARA principle 54
PISA 150
raising 640
aliasing 28-30
pressure half-time 146-7,
aortic valve and root
allergic reaction
150
view 552-3
management 571
regurgitant volume 150
aortic valve replacement,
A-mode 8-9
3D assessment 148, 456
postoperative
analgesia, TOE 358
TOE 456
assessment 462-3
anomalous pulmonary
TTE 142-3
aortic views 400-1
drainage 671
vena contracta 144-5,
apex forming 264
antibiotic prophylaxis,
148
apex remodelling 534
TOE 349
aortic remodelling 460
apical five chamber
aorta
aortic root 310
view 80-1, 102
anatomy 308
aortic root dilatation 143,
apical four chamber
emergency evaluation 514
310-11
view 78-9, 100-1
isthmus 309
aortic root
apical three chamber
normal TOE
replacement 314
view 84-5, 103
findings 514-15
aortic sclerosis 134
apical 3D views 86-7
normal TTE findings
aortic size 310-11, 675
apical two chamber
308-9
aortic stenosis
view 82-3, 103
reporting 674
aortic regurgitation 138
apical window 60-3
traumatic injury 526
dobutamine stress
area length equation 200-1,
aortic annulus 310
echo 140-1
212, 280, 478
aortic arch 308, 514, 516
effective orifice area/valve
artefacts
aortic atherosclerosis
area 136-7
beam-width 318
324-5, 520-1
grading severity 134-6,
drop out 38
aortic coarctation 320-1,
137, 454-5, 663
reverberation 16-17, 32,
528
hypotension 537
318
aortic dilatation 314-15
left ventricle 138, 140-1
stitch 38-9
aortic dissection
mean pressure
ascending aorta 308
differentiating intimal flaps
gradient 136
atrial chamber
from artefacts 522, 525
peak pressure
arrangement 334
dissection flap 318-19,
gradient 136
atrial septal aneurysm
522, 525
peak velocity 134, 137
290-1
680
INDEX
atrial septal defects
cardiovascular magnetic
lactation 571
ICE 556, 557-8, 559
resonance 588
left-sided contrast
TOE 502-3, 505
CARPA reactions 570
agents 562, 564-5, 570
TTE 288-9
Carpentier
left ventricular
atrial septal view 552-3
classification 424
opacification 576,
atrial septum
catheter ablation of
577-8, 579
anatomy 286
arrhythmias 560
low mechanical index
normal TOE
catheter occlusion of left
imaging 576
findings 500-1
atrial appendage 560
myocardial
normal TTE findings
central venous line 546
perfusion 582-3, 585
286-7
Chiari network 284, 498-9
patent foramen
reporting 661
christa terminalis 498
ovale 572-3
atrial septum (bicaval)
circumferential strain 44-5,
persistent left superior
view 380-1
239, 241
vena cava 574
attenuation 14-15, 38
cleft mitral valve leaflet 289
pregnancy 571
audit 623
closing jets 178, 448
pulmonary shunts 574
autografts 180
coaption 132
right-sided contrast
auto-regulation 594
coarctation of the
agents 562, 566-7, 570
AV delay 260-1
aorta 320-1, 528
right-sided contrast
axial resolution 20
colour flow mapping
studies 572-3, 575
30-1, 96
safety issues 54, 570-1
colour inversion 30
second harmonics 48, 576
B
commissures 132
shunts 502, 506-7, 562,
ball and cage valves 176-7,
complete atrio-ventricular
572, 574
179, 463, 672
canal defect 289
training 584
BART principle 30-1
compress 18, 42
tricuspid
beam-width artefact 318
concentric left ventricular
regurgitation 574-5
benign cardiac
hypertrophy 218
CoreValve® 465
tumours 326-7
concentric remodelling 140,
coronary artery disease,
Bernoulli equation 52-3
218
stress echo 590-1
Beutel display 269
congenital heart
coronary artery supply to
bicuspid valves 134, 138,
disease 330-1, 333,
ventricles 235, 481
152-3, 460
335-6
coronary artery surgery,
bicycle protocol 612-13
surgical correction 340-1
TOE 532
bileaflet valves 177-9, 672
congenital pericardial
coronary sinus 498
bioprosthetic valves 180-2,
disease 306
coronary sinus
672
constrictive
defect 504
biphasic response 596
pericarditis 302-3, 305
coronary sinus
biplane imaging 64
continuity equation 50-1
view 386-7
Blalock-Taussig shunt 340
continuous wave
corrected aortic flow
blunted systolic pulmonary
Doppler 26-7
time 644
vein flow 120
contractile reserve 596, 616
cor triatum 278
B-mode 8-9
critical illness
contrast echocardiography
body surface area 636
561
advanced haemodynamics
bowing 128-9
accreditation 584
642-3
Bruce protocol 612-13
acute coronary
fluid responsiveness
syndromes 570
640-1
administration of contrast
volume status 636-9
C
agents 568-9
weaning from
carcinoid syndrome 166
adverse events 570
ventilator 646-7
cardiac computed
agitated saline 562, 566-7,
cropping 40-1
tomography 588
570
cardiac index 230
allergic reaction
cardiac output 230, 642-3
management 571
D
cardiac tamponade
bolus injection 568-9
de-airing 447, 462
TOE 512
contrast infusion 568-9
deceleration slope 146
TTE 300-1
dobutamine stress
deceleration time 246
cardiac tumours 326-7, 329
echo 580-1
deep transgastric
cardiac twisting 44
Doppler enhancement
view 396-7
cardiopulmonary
574-5, 578
depth compensation 14, 18
bypass 532-3
gas microspheres 48, 562
descending aorta 308
cardiopulmonary
intermittent imaging 576
descending aortic flow 144,
resuscitation 631-2
intravenous injection 568
147, 458-9
INDEX
681
descending thoracic
Ebstein’s anomaly 166, 337
G
aorta 308, 310, 514,
eccentric left ventricular
516, 518
hypertrophy 218
gain 18-19
diastolic function 246-7,
echoes 12
gas microspheres 48, 562
249-50
Edwards Sapien® 465
Gerbode defects 294
diastolic tail 320-1
E/E’ 248, 252
Glenn shunt 340
DICOM 66
effective orifice area 136-7
global strain 238
digital image storage 66
prosthetic valves 184
global systolic function
dilated cardiomyopathy 222
effective regurgitant orifice
228-9, 231, 233, 480
dipyridamole
area 126
glutaraldehyde 354
protocol 618-19
ejection fraction 228-9,
governance 590
dissection flap 318-19,
266, 274
grey scale 18
522, 525
elbowing appearance 110
dobutamine stress echo
electrophysiology,
aortic stenosis 140-1
ICE 560
H
atropine use 614
ellipsoid formula 212, 280
haemodynamic
beta-blockers 614
endocardial cushion
instability 536-7
compared to exercise 612
defect 289
harmonic imaging 22-3,
contrast echo 580-1
endocarditis
48, 576
myocardial
reporting 677
harmonics 22
ischaemia 614-15
TOE 472-3
heart failure with normal
myocardial viability 616-17
TTE 166-7, 188-9
ejection fraction
preoperative assessment
Eustachian valve 284,
(HFNEF) 252-3
for non-cardiac
498-9
high pulse repetition
surgery 600-1
exercise stress
frequency pulsed wave
wall thickening 597
protocols 612-13
Doppler 29
Doppler echocardiography
excursion 132
hockey stick
aortic stenosis 454
extra-cardiac tumours 328,
appearance 110
cardiac tamponade 300-1
333
holodiastolic aortic flow
constrictive
reversal 144, 147, 458-9
pericarditis 304-5
homografts 180
continuous wave
F
hypertrophic
Doppler 26-7
failure to wean off
cardiomyopathy 220-1,
contrast studies 574-5,
bypass 533
225, 590
578
false lumen 318, 522, 525
hypoplastic left
global systolic
FEEL algorithm 632-3
ventricle 338
function 230-1, 233
fentanyl 358
hypotension 536-7
high pulse repetition
fibrin strands 182, 298-9
hypovolaemic
frequency pulsed wave
fibroelastoma 326-7, 530-1
hypotension 536-7
Doppler 29
fibroma 326
hypoxaemia 536, 538
image quality 96
fibrous pericardium 296
pulsed wave Doppler
fistula 188, 472
28-9
five chamber view 370-1
I
shunt quantification 288,
five cusps 152
idiopathic dilated
502
flail leaflets 129-31
cardiomyopathy 222
theory behind 24-5
flow convergence
image resolution 20-1
3D colour Doppler 36-7
zone 126-7
infective endocarditis, see
tissue Doppler, see tissue
fluid dynamics 50-1, 53
endocarditis
Doppler imaging
fluid responsiveness 640-1
inferior sinus venosus
Doppler effect 24-5
fluid status 636-7
defect 504
Doppler frequency 26
focusing 20
inferior vena cava
Doppler shift 24, 26
Fontan procedure 340
fluid responsiveness
Dor procedure 534
foramen ovale 286
640-1
double outlet right
foreshortening 200
volume status 636, 639
ventricle 338
fossa ovalis 286
inferior vena cava
dP/dt 232-3
four chamber view 368-9
view 90-1
drop out artefacts 38
fractional area change
information for patients 56,
dynamic range 18-19
228-9, 274-5
350, 604
fractional shortening 228-9,
inlet septum 292
488
intensive care units,
E
‘front door’
TOE 345
E’ 248
echocardiography 628
interatrial septum, see atrial
E/A ratio 246
fundamental frequency 22
septum
682
INDEX
interventricular
left ventricular function
J
dyssynchrony 254-5
diastolic function 246-7,
interventricular septum, see
jet area 118-19, 148,
249-50
ventricular septum
158, 422
global systolic
intima-media thickness 520
jet length 148-9
function 228-9, 231,
intra-aortic balloon
jet width 144
233, 480
pump 540-1
mitral valve repair 447
intracardiac
mitral valve
echocardiography (ICE)
L
replacement 450
aortic valve and root
Lambl’s excresences 152
normal ranges 654-5
view 552-3
Langranian strain 46
regional systolic
atrial septal
lateral resolution 20
function 234-7, 480
interventions 556,
left atrial appendage
TOE 480-1
557-8, 559
catheter ablation 560
TTE 226-7
atrial septal view 552-3
ICE 554
left ventricular hypertrophy
catheter ablation of
TOE 492-3
aortic stenosis 140
arrhythmias 560
left atrial function 282
physiological 218
catheter occlusion of left
left atrial occluder 546
TTE 218-19
atrial appendage 560
left atrial pressure 642
left ventricular mass
catheter preparation 550
left atrial size
normal ranges 216, 482-3,
commercially available
normal ranges 283, 660
654-5
catheters 549
TOE 490-1
TOE 478
electrophysiological
TTE 248, 280-1
TTE 210-11, 213, 215
interventions 560
left atrium
left ventricular non-
fluoroscopy
anatomy 278
compaction 222-3
screening 550-1
normal TOE findings 490
left ventricular
imaging planes 552-3, 555
normal TTE findings
opacification 576,
indications 548
278-9
577-8, 579
left atrial appendage 554
reporting 659
left ventricular outflow
left ventricle view 554-5
spontaneous
tract 132
mechanical catheters 550
contrast 493
obstruction 220, 448
mitral valve view 554-5
left lower pulmonary vein
vti 232
patient preparation 550
view 384-5
left ventricular size
phased-array
left upper pulmonary vein
area length equation
catheters 550
view 384-5
200-1, 478
pulmonary vein view
left ventricle
foreshortening 200
554-5
anatomy 192
linear measures 196-7,
radiological
aortic regurgitation 146
478
interventions 560
aortic stenosis 138,
normal ranges 198, 206,
right ventricle view 554-5
140-1
208, 482-3, 654-5
standard view 552-3
assessment 194
Simpson’s method 198-9,
TAVI 560
concentric
478
transducers 6-7, 549-50
remodelling 140, 218
3D volumetric
transseptal puncture
fluid responsiveness
measures 196, 202-3,
guidance 560
640-1
205-6, 207
vascular access 550-1
hypoplastic 338
TOE 478-9
intracardiac shunt 538
normal TOE
TTE 196, 208
intramural haematoma 526
findings 476-7
2D volumetric
intraoperative TOE 345,
normal TTE findings
measures 196,
438
192-3
198-201, 478
intrapulmonary shunt 538
reporting 652
left ventricular strain 238
intravascular probes 6, 21
volume status 638-9
advantages and
intravenous drug users 166
left ventricle view 554-5
disadvantages of strain
intraventricular
left ventricular assist
imaging 240
dyssynchrony 254-5
devices 540
normal values 239
intubation 362-3
left ventricular ejection
speckle tracking 238,
iRotate imaging 64, 608
fraction 228-9
242-4, 245
ischaemic cascade 594-5
left ventricular end-diastolic
left ventricular
ischaemic mitral
pressure 644
synchrony 254-7, 258-9
regurgitation 534
left ventricular fractional
left ventricular thickness
isovolumetric relaxation
area change 228-9
normal ranges 216
time 246
left ventricular fractional
TTE 210-11, 213, 215
isthmus 309
shortening 228-9
lipoma 326, 530
INDEX
683
lipomatous interatrial
TTE 116
modes 8-9
hypertrophy 530
vena contracta 120, 422
multiplane image
local anaesthetic, TOE 358
mitral stenosis
acquisition 64-5
long axis (aortic valve)
differentiating rheumatic
myocardial ischaemia
view 376-7
stenosis from
adenosine protocol
long axis (mitral valve)
calcification 110
618-19
view 378
elbowing appearance 110
detection using stress
longitudinal strain 44-5,
grading severity 112-13,
echo 594-5
239
114-15, 432-3, 435, 666
dipyridamole
lossless image
hockey stick
protocol 618-19
compression 67
appearance 110
dobutamine stress
lossy image compression 67
new stenosis
echo 614-15
Luminity® 566
postoperative 446
hypotension 536-7
lungs 544
percutaneous valvotomy
Myocardial Performance
suitability
Index (MPI) 272-3
assessment 444-5
myocardial perfusion
M
planimetry 112-13, 434-5
contrast echo 582-3, 585
malignant cardiac
preoperative assessment
stress echo 598-9
tumours 326-7
using TOE 438
myocardial scintigraphy 588
Marfan syndrome 316-17
pressure gradient 114-15,
myocardial viability, stress
432
echo 596, 616-17
masses 326-7, 329, 530-1,
676
pressure half-time
myocarditis 224
matrix array transducers
114-15, 432-3
myxoma 326-7, 530
4-5
3D assessment 112-13,
mechanical cardiac
434-5
support 540-1
TOE 432
N
mechanical index 18, 54
TTE 110-11
natural strain 46
mechanical prosthetic
mitral valve
nodule of Arantius 132
valves 176-7
anatomy 106
non-cardiac surgery,
metastases 328
identifying leaflets and
preoperative stress
midazolam 358
segments 418
echo 600-1
MitraClip® 440-1, 443
normal TOE
Nyquist limit 28
mitral regurgitation
findings 418-19
Carpentier
normal TTE findings
classification 424
106-7, 109
O
continuous wave Doppler
postoperative assessment
oblique sinus 296, 510
intensity/shape 122
of repair 446
obstructive congenital
effective regurgitant
postoperative systolic
disorders 673
orifice area 126
anterior motion 439,
oesophageal varices 348
grading severity 118,
446
off-pump coronary artery
119-20, 121, 123, 422,
preoperative assessment
bypass 534
423-5, 666
using TOE 436-8, 439
optimization 260-1
intraoperative TOE 438
reporting 664
Optison® 564
ischaemic 534
suitability for repair 130
outlet septum 292
jet area 118-19, 422
mitral valve balloon
mild/trivial 117
valvotomy, TOE
MitraClip® 440-1, 443
assessment for
P
mitral inflow 122-3
suitability 444-5
physiological 116-17
mitral valve inflow 246-7,
pacing stress 620
PISA 126-7
249, 251
pacing wires 546
postoperative residual
mitral valve prolapse
pannus 182
regurgitation 446
bowing 128-9
papillary
preoperative assessment
flail leaflets 129-31
fibroelastoma 326-7
using TOE 436
3D assessment 128-9,
parasternal long axis
pulmonary venous
428, 429-30, 431
view 68-9, 97
flow 120-1, 422-3
TOE 426-7
parasternal right ventricle
regurgitant flow 126
TTE 128
inflow view 70-1
regurgitant fraction 122
mitral valve replacement,
parasternal right ventricle
regurgitant jet
postoperative
outflow view 70-1
appearance 116-17
assessment 448-9, 451
parasternal short axis
regurgitant volume 122
mitral valve view 554-5
(aortic) view 72-3, 99
3D assessment 124-5
M-mode 8-10
parasternal short axis
TOE 420-1
moderator band 262
(mitral) view 74-5, 98
684
INDEX
parasternal short axis
post processing 40-1
pulmonary artery diastolic
(ventricle) view
power mode (amplitude)
pressure 172
74-5, 98
imaging 48
pulmonary artery systolic
parasternal 3D views 76-7
pregnancy
pressure 162
parasternal window 60-3
aortic dilatation 314
pulmonary artery
paravalvular
contrast echo 571
view 398-9
regurgitation 186-7
pressure gradient 26,
pulmonary embolism 538
partial atrio-ventricular
114-15, 184, 432
pulmonary hypertension,
canal defect 289
pressure half-time 114-15,
aortic stenosis
passive leg raising 640
146-7, 150, 432-3
grading 138
patent ductus
pressure overload 276-7
pulmonary regurgitation
arteriosus 336
primum atrial septal
grading severity 172-3,
patent foramen ovale 286,
defect 288-9, 504
670
290, 502, 538, 572-3
probes
TOE 470-1
patient information 56,
frequency and
TTE 170-1, 173
350, 604
resolution 20-1
pulmonary regurgitation
peak systolic right
intracardiac 6-7, 549-50
index 172
ventricular basal free
intravascular 6, 21
pulmonary shunts 562, 574
wall TDI 274
transoesophageal
pulmonary stenosis
peak systolic strain 32
6-7, 21
grading severity 174-5, 670
peak systolic strain rate 32
transthoracic 4-5, 21
TOE 470-1
pectinate muscle 493
prolate ellipse of
TTE 174
penetrating aortic ulcer 526
revolution 210
pulmonary valve
perfusion imaging
prosthetic valves
anatomy 168
contrast echo 582-3, 585
degeneration 182
normal TOE findings 470
stress echo 598-9
dehiscence 182-3
normal TTE findings 168-9
pericardial cysts 306, 328
fibrin strands 182
reporting 669
pericardial effusion
orifice area 184
pulmonary veins, TOE 384,
thickness and volume 673
pannus 182
494-5
TOE 512-13
physiological
pulmonary vein view 384-5,
TTE 298-9
regurgitation 178
554-5
pericardial space 296, 510
postoperative
pulmonary venous
pericardial surfaces 296,
assessment 448-9,
flow 120-1, 248, 251,
510
451, 462-3
422-3
pericardial thickness 296
pressure gradients 184
pulmonary wedge
pericardial tumours 306
prolapse 182
pressure 644
pericardiocentesis 306-7
pseudo-microbubbles 182-3
pulsed wave Doppler 28-9
pericarditis
regurgitation 142, 186-7,
pulse repetition
acute 306
448, 462
frequency 28
constrictive 302-3, 305
reporting 671
pulsus paradoxus 301
pericardium
rocking valve 182-3
anatomy 296
stenosis 184
congenital disease 306
structural damage 182
Q
reporting 673
sutures 182
Qp/Qs 288
TOE 510-11
thrombus 182
quadricuspid valves 152-3
TTE 296-7
TOE 177
quality control 623
persistent left superior vena
TTE 176-80, 181
cava 574, 671
vegetations 182
persistent truncus
velocities 184, 672
R
arteriosus 338
proximal aorta 310, 516,
pethidine 358
518
radial strain 44-5, 239
phased-array catheters 550
proximal ascending
reflection 12-14
piezoelectric crystals 4
aorta 308, 310, 514
refraction 12-13
PISA 126-7, 150
proximal isovelocity surface
regional strain 240
planimetry 112-13, 434-5,
area (PISA) 126-7, 150
regional systolic
454
pseudo-microbubbles
function 234-7, 480
pleural effusions 544-5
182-3
regurgitant flow 126
pleural fluid 296, 512
pseudonormal filling 246,
regurgitant fraction 122
pleural space 544
249, 251
regurgitant volume 122,
positron emission
pulmonary arterial occlusion
150
tomography 588
pressure 644
relative wall thickness 218
posterior wall
pulmonary artery,
reporting, standard
thickness 210-11
reporting 669
approach 650-1
INDEX
685
restrictive
TOE 488
situs inversus 334-5
cardiomyopathy 222,
TTE 272-3, 275
situs solitus 334-5
303
right ventricular outflow
slice modes 40-1
restrictive filling 246,
tract 264
SonoVue® 564-5, 570
249, 251
right ventricular
SoundStar™3D 549
reverberation artefacts
overload 276-7
sound waves 2-3
16-17, 32, 318
right ventricular size
spatial resolution 20
reversed systolic pulmonary
normal ranges 489, 657
speckle pattern 44
vein flow 120
TOE 486-7
speckle tracking
rhabdomyoma 326
TTE 264-5, 267, 269
echocardiography
right atrial pressure 162-3,
right ventricular systolic
44-5, 46-7, 238,
636-7, 668
pressures 162-3
242-4, 245
right atrial size
right ventricular wall
specular echoes 12
normal ranges 283, 660
thickness 270-1, 486
specular reflection 12
TOE 496
Ritter method 260
stand-alone probes 4-5
TTE 284-5
rocking valve 182-3
Stanford classification 318
right atrium
Ross procedure 180
stented bioprostheses 177,
anatomy 284
180-1, 463
normal TOE
stentless bioprostheses 180
findings 496-7
S
stitch artefacts 38-9
normal TTE findings
S’ 274
strain 32, 238
284-5
safety issues
advantages and
reporting 659
acute echo 630
disadvantages of strain
volume status 636, 639
contrast echo 54, 570-1
imaging 240
right heart
stress echo 605
circumferential 44-5, 239,
haemodynamics 162-3
ultrasound 54
241
right lower pulmonary vein
scattering 12-13
global 238
view 384-5
screenwiper principle
Langranian 46
right parasternal view 94-5
364-6
longitudinal 44-5, 239
right parasternal
second harmonic
natural 46
window 60-1
imaging 22-3, 48, 576
normal values 239
right-to-left shunts 538,
secundum atrial septal
radial 44-5, 239
540, 562
defect 288
regional 240
right upper pulmonary vein
device closure 504-5
speckle tracking 44-6, 47,
view 384-5
sedation, TOE 358-60
238, 242-4, 245
right ventricle
segment models 234, 237
strain rate 32
anatomy 262
sepsis, hypotension 536-7
stress echocardiography
double outlet 338
septal hypertrophy 138
587
normal TOE
serous membranes 296
adenosine protocol
findings 484-5
sheathed probes 354
618-19
normal TTE findings
short axis (aortic valve)
analysis 622
262-3
view 372-3
aortic stenosis 140-1
reporting 656
short axis (right ventricle)
audit 623
volume status 638-9
view 374-5
bicycle protocol 612-13
right ventricle inflow-
shunts
Bruce protocol 612-13
outflow view 374-5
contrast echo 502, 506-7,
contraindications 592
right ventricle view 554-5
562, 572, 574
contrast echo 580-1
right ventricular cavity
hypoxaemia 538
dipyridamole
size 264, 486
left ventricular assist
protocol 618-19
right ventricular
devices 540
dobutamine stress, see
contouring 268-9
quantification 288, 502
dobutamine stress
right ventricular ejection
surgical correction of
echo
fraction 266, 274
congenital heart
drugs 602
right ventricular end-
defects 340
equipment 602
diastolic volume 266
Simpson’s biplane
exercise stress
right ventricular end-systolic
method 198-9, 212, 478
protocols 612-13
volume 266
single ventricle 337-8
hypertrophic
right ventricular fractional
sinotubular junction 132
cardiomyopathy 590
area change 274-5
sinus of Valsalva 132,
image acquisition 608
right ventricular fractional
310-11, 313, 517
indications 590-1
shortening 488
sinus of Valsalva
information for
right ventricular function
aneurysm 322-3, 528
patients 605
normal ranges 657
sinus venosus defect 288, 504
iRotate 608
686
INDEX
stress echocardiography
tetralogy of Fallot 673
stress echo 608, 623
(Cont.)
Thebesian valve 498
3D vision 42
known coronary artery
thermal index 54
thresholding 42
disease 590
thoracic aortic
transducers 4-5
monitoring 610
aneurysm 324, 528
tricuspid
myocardial
3D echocardiography 34
regurgitation 160-1
ischaemia 594-5,
aorta view 406
tricuspid stenosis 164
614-15
aortic regurgitation 148, 456
tricuspid valve view 408-9
myocardial
aortic stenosis 138-9
windows 62-3
perfusion 598-9
aortic valve views 406-7
3D-mode 8-9
myocardial viability 596,
apical views 86-7
thrombus 326, 493, 530-1,
616-17
applications 36
538
pacing stress 620
artefacts 38-9
prosthetic valves 182
patient preparation 604
atrial septum view 412-13
tilting disc valves 176-7,
personnel 602
balloon valvotomy 445
463, 672
preoperative assessment
cardiomyopathies 225
time-gain compensation
for non-cardiac
colour Doppler 36-7
14, 18
surgery 600-1
colour maps 42
tissue Doppler imaging 32-3
pre-test probability of
cropping 40-1
diastolic function 248, 251
coronary artery
full volume 3D data
left ventricular
disease 589
sets 34-5
synchrony 256-7
quality control 623
gain adjustment 42-3
stress echo 623
safety issues 605
global systolic
trabecular septum 292
sample report 624-5
function 230
training 584, 623, 631
set-up 606-7
image acquisition 62-3
transcatheter aortic
subaortic muscular
image display 40-1
valve implantation
obstruction 590
image optimization 62
(TAVI) 464-7, 560
suspected coronary artery
image quality 96
transducers
disease 590-1
image rendering 42
frequency and
target heart rates 611
left ventricle view 410-11
resolution 20-1
termination criteria 610,
left ventricular
intracardiac 6-7, 549-50
614
dyssynchrony 258
intravascular 6, 21
3D imaging 608, 623
left ventricular mass
transoesophageal 6-7, 21
tissue Doppler 623
214-15
transthoracic 4-5, 21
training 623
left ventricular size 196,
transgastric long axis
treadmill protocol 612-13
202-3, 205-6, 207
(aortic) view 392-3
valvular heart disease 590
limitations 36
transgastric long axis
vasodilator stress 618-19
live images 34
view 390-1
views 606-7
live 3D 36-7
transgastric right ventricle
stroke volume 230-1,
live 3D zoom 36
view 394-5
642-3
magnification 42
transgastric short axis
subaortic membrane 138
mitral regurgitation 124-5
view 388-9
subcostal views 88-9, 104
mitral stenosis 112-13,
transmit power 18
subcostal window 60-1
434-5
transoesophageal
supraclavicular window 60
mitral valve, preoperative
echocardiography (TOE)
suprasternal view 92-3, 104
assessment 436-7
advantages over TTE 344
suprasternal window 60-1
mitral valve
analgesia 358
swinging right atrium and
prolapse 128-9, 428-9
antibiotic prophylaxis 349
ventricle 300
mitral valve views 404-5
aortic views 400-1
systemic vascular
near real-time (full
atrial septum (bicaval)
resistance 642-3
volume) images 34-5
view 380-1
systolic anterior (leaflet)
oesophageal views 402-3
cleaning the probe 354-5
motion, mitral
opacification/
complications 348
valve 439, 446
compression 42
contraindications 348
systolic dyssynchrony
parasternal views 76-7
coronary sinus view 386-7
index 258
post processing 40-1
deep transgastric
pulmonary valve view 408
view 396-7
right ventricular size
five chamber view 370-1
T
266-7
four chamber view 368-9
TAPSE 273-4
slice modes 40-1
heating/thermal cutout 54
Teichholz method 210
smoothness 42
history of
TEI index 272-3
speckle tracking 46-7,
development 344
temporal resolution 20
244-5
ICU 345
INDEX
687
image acquisition 364-6
transgastric short axis
transducers (probes)
indications 346
view 388-9
4-5, 21
information for
two chamber (atrial
triplane imaging 64-5
patients 350
appendage) view 382-3
2D image acquisition
intraoperative 345, 438
X-plane 414-15
60-1
intubation 362-3
transseptal puncture
2D image optimization 59
left lower pulmonary vein
guidance 560
windows 60-1
view 384-5
transthoracic
xPlane imaging 64-5
left upper pulmonary vein
echocardiography (TTE)
transvalvular
view 384-5
abdominal aorta view 90-1
regurgitation 186-7
local anaesthetic 358
apical five chamber
transverse sinus 296, 510
long axis (aortic valve)
view 80-1, 102
traumatic aortic
view 376-7
apical four chamber
disruption 526
long axis (mitral valve)
view 78-9, 100-1
treadmill protocol 612-13
view 378
apical three chamber
tricuspid annular plane
oesophageal varices 348
view 84-5, 103
systolic excursion
oversedation in older
apical two chamber
(TAPSE) 273-4
patients 358
view 82-3, 103
tricuspid regurgitation
perforation risk 348
biplane imaging 64
carcinoid syndrome 166
post-procedure care 360
data acquisition 66-7
causes 157
preparation 352-3
digital storage 66
continuous wave
probe movements 356-7
ECG electrodes 56
Doppler 158-9
probe preparation 354-5
gel 58
contrast echo 574-5
pulmonary artery
image compression 67
grading severity 157-8,
view 398-9
image formats 66
159, 668
pulmonary vein
image quality 96
hepatic vein outflow 158
views 384-5
image storage 66
jet area 158
right lower pulmonary
inferior vena cava
pacemakers 156
vein view 384-5
view 90-1
physiological 156
right upper pulmonary
iRotate imaging 64
right ventricular
vein view 384-5
machine and probe
inflow 158
right ventricle inflow-
preparation 58
right ventricular systolic
outflow view 374-5
minimal data set 96-104
pressure 162-3
screenwiper
multiplane image
3D assessment 160-1
principle 364-6
acquisition 64-5
TOE 468-9
sedation 358-60
operator positioning 58
TTE 156
short axis (aortic valve)
parasternal long axis
vena contracta 158-9
view 372-3
view 68-9, 97
tricuspid stenosis
short axis (right ventricle)
parasternal right ventricle
3D assessment 164
view 374-5
inflow view 70-1
TOE 468
3D aorta view 406
parasternal right ventricle
TTE 164-5
3D aortic valve
outflow view 70-1
tricuspid valve
views 406-7
parasternal short axis
anatomy 154
3D atrial septum
(aortic) view 72-3, 99
area 164
view 412-13
parasternal short axis
normal TOE
3D left ventricle
(mitral) view 74-5, 98
findings 468
view 410-11
parasternal short axis
normal TTE findings
3D mitral valve
(ventricle) view 74-5, 98
154-5
views 404-5
parasternal 3D views 76-7
reporting 667
3D oesophageal
patient information 56
surgery 166
views 402-3
patient positioning 56
vegetations 166-7
3D pulmonary valve
patient preparation 56
tricuspid velocity 162-3
view 408
probe handling and
triplane imaging 64-5
3D tricuspid valve
movements 58
Tristel sporicidal wipe 355
view 408-9
quality of recordings 96
truncated ellipsoid
transducers (probes)
right parasternal view 94-5
model 212
6-7, 21
standard examination
tumours 306, 326-7, 329
transgastric long axis
96-104
tunica adventitia 308
(aortic) view 392-3
standard sequence of
tunica intima 308
transgastric long axis
views 61
two chamber (atrial
view 390-1
subcostal views 88-9, 104
appendage) view
transgastric right ventricle
suprasternal view 92-3,
382-3
view 394-5
104
2D-mode 8-9
688
INDEX
apical two chamber 82-3,
3D oesophageal 402-3
U
103
3D parasternal 76-7
Ultra ICE™ 549
atrial septal 552-3
3D pulmonary
ultrasound 2-3, 12-13
atrial septum
valve 408
ultrasound-triggered drug
(bicaval) 380-1
3D tricuspid valve
and gene delivery 577
coronary sinus 386-7
408-9
deep transgastric 396-7
transgastric long
five chamber 370-1
axis 390-1
V
four chamber 368-9
transgastric long axis
Valsalva manoeuvre
inferior vena cava 90-1
(aortic) 392-3
mitral inflow 246
left atrial appendage 554
transgastric right
shunt studies 506, 572
left ventricle 554-5
ventricle 394-5
valve cysts 328-9
long axis (aortic
transgastric short
variance mapping 30
valve) 376-7
axis 388-9
vascular access, ICE 550-1
long axis (mitral
two chamber (atrial
vascular transducers 4, 21
valve) 378
appendage) 382-3
vasodilator stress
mitral valve 554-5
X-plane 414-15
echocardiography
parasternal long axis
volume overload 276-7
618-19
68-9, 97
volume status 636-9
vegetations 166-7, 188-9,
parasternal right ventricle
volumetric flow 50
472-3, 530
inflow 70-1
VV delay 260-1
prosthetic valves 182
parasternal right ventricle
velocity time integral 50
outflow 70-1
vena contracta 120, 144-5,
parasternal short axis
W
148, 158-9, 422
(aortic) 72-3, 99
wall motion 234, 480
ventricle, single 337-8
parasternal short axis
wall motion score 234
ventricle outflow
(mitral) 74-5, 98
wall motion score
obstruction, post mitral
parasternal short axis
index 234
valve repair 446
(ventricle) 74-5, 98
wall thickness 210-11, 218,
ventricular aneurysm
pulmonary artery 398-9
270-1, 486, 597
resection 534
pulmonary vein 384-5,
washing jets 178, 448
ventricular reserve 140
554-5
weaning
ventricular septal
right parasternal 94-5
failure to wean off
defects 294-5, 508-9
right ventricle 554-5
bypass 533
ventricular septum 210-11,
right ventricle inflow-
from ventilator 646-7
292-3, 508, 658
outflow 374-5
left ventricular assist
ViewFlex® 549
short axis (aortic
devices 542
views
valve) 372-3
Wilkin’s score 444
abdominal aorta 90-1
short axis (right
windows 60, 61-2, 63
aortic 400-1
ventricle) 374-5
aortic valve and
subcostal 88-9, 104
root 552-3
suprasternal 92-3, 104
X
apical five chamber 80-1,
3D aorta 406
3D aortic valve 406-7
X-plane 64-5, 414-15
102
apical four chamber 78-9,
3D apical 86-7
100-1
3D atrial septum 412-13
Z
apical three chamber
3D left ventricle 410-11
84-5, 103
3D mitral valve 404-5
z-score 312