Critical Care Ultrasound: Comprehensive

Comprehensive
Critical Care Ultrasound

Editors:
Samuel M. Brown , MD, MS, FASE, FCCM
Michael Blaivas, MD, FAIUM
Eliotte L. Hirshberg, MD, MS
Jan Kasal, MD, FCCM
Aliaksei Pustavoitau, MD, MHS
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Editors
Samuel M. Brown, MD, MS, FASE, FCCM

Assistant Professor of Medicine
University of Utah School of Medicine
Intermountain Medical Center
Shock Trauma ICU
Murray, Utah, USA
Research Grants: National Institutes of Health, Moore Foundation, Intermountain Research and Medical
Foundation; Committee Service: American Thoracic Society; Lectures: academic continuing medical
education activities
Michael M. Blaivas, MD, FAIUM

University of South Carolina School of Medicine
Department of Emergency Medicine
St. Francis Hospital
Columbus, Georgia, USA
Consultant: GE, Analogic, Sonosim, Inc.; Third Vice President: American Institute of Ultrasound in
Medicine; President: Society of Ultrasound in Medical Education; Task Force: American College of
Emergency Physicians (U.S. section); Alternate Delegate: American Medical Association

Associate Professor
Department of Internal Medicine and Department of Pediatrics
University of Utah
Attending, Shock Trauma ICU Intermountain Medical Center
Attending, Pediatric ICU Primary Children’s Hospital
Murray, Utah, USA
No disclosures
Jan Kasal, MD, FCCM

Clinical Assistant Professor
Mercy Hospital
Division of Pulmonary and Critical Care Medicine
Saint Louis University
Saint Louis, Missouri, USA
No disclosures

Assistant Professor
Department of Anesthesiology and Critical Care Medicine
Johns Hopkins University School of Medicine
Johns Hopkins Hospital
Baltimore, Maryland, USA
Presenter, Instructor: Society of Critical Care Anesthesiologists (ultrasound courses)
Authors
Srikar Adhikari, MD, MS

Chief, Section of Emergency Ultrasound
Associate Professor
University of Arizona
Tucson, Arizona, USA
No disclosures
Sasikanth Adigopula, MD
Division of Cardiology
Stanford University Medical Center
Palo Alto, California, USA
No disclosures
Myriam Amsallem, MD
Department of Cardiology
No disclosures
Cameron M. Bass, MD
Chief Resident
Department of Internal Medicine
University of Washington
Seattle, Washington, USA
No disclosures
Rachel E. Beard, MD
Department of Surgery
Beth Israel Deaconess Medical Center
Boston, Massachusetts, USA
No disclosures
S. Patrick Bender, MD
University of Vermont College of Medicine
Associate Professor
Department of Anesthesiology and Department of Surgery
University of Vermont Medical Center
Attending – Anesthesiology and Critical Care
Burlington, Vermont, USA
Lecturer: Society of Critical Care Medicine, American Thoracic Society, World Interactive Network
Focused on Critical Ultrasound; Junior Editor on Written Examinations; Oral Board Examiner: American
Board of Anesthesiology
Anne-Sophie Beraud, MD
Stanford Hospital
Stanford University
Service de Cardiologie
Clinique Pasteur
Toulouse, France
No disclosures
Keith S. Boniface, MD
Associate Professor
George Washington University
Washington, DC, USA
Committee Member: American College of Emergency
Physicians; Speaker: American College of Physicians, Society of Critical Care Medicine, World
Interactive
Network Focused on Critical Ultrasound
Justin Bosley, MD
Alameda Health System
Highland General Hospital
Oakland, California, USA
Instructor: American College of Emergency Physicians (procedural training sessions)
Samantha K. Brenner, MD, MPH

Fellow in Critical Care Medicine
Stanford, California, USA
Reviewer: American Medical Informatics Association, American Journal of Public Health
Jeff Burzynski, MD, FRCPC

Sections of Critical Care and Emergency Medicine
University of Manitoba
Winnipeg, Manitoba, Canada
No disclosures
Ryan D. Clouser, DO
Associate Director of MICU
Pulmonary/Critical Care Division
UVM College of Medicine
No disclosures
Thomas W. Conlon, MD
Children’s Hospital of Philadelphia
Philadelphia, Pennsylvania, USA
No disclosures
Ranjit Deshpande, MD
Assistant Professor of Anesthesiology
Department of Anesthesiology
Yale School of Medicine
New Haven, Connecticut, USA
No disclosures
R. Eliot Fagley, MD
Anesthesiologist and Intensivist
Virginia Mason Medical Center
Committee Member: Society of Critical Care Anesthesiologists (Mentorship Committee), Society of
Critical Care Anesthesiologists Ultrasound Interest Group
James Fair, MD
University of Utah Medical Center
Salt Lake City, Utah, USA
No disclosures
David Feller-Kopman, MD
Director
Bronchoscopy and Interventional Pulmonology
Associate Professor of Medicine
Otolaryngology – Head and Neck Surgery
President: American Association of Bronchology and Interventional Pulmonology; Chair: American
College of Chest Physicians Interventional Chest/Diagnostic Procedures NetWork
Michelle L. Freeman, MD
Pulmonary and Critical Care
Mayo Clinic
Jacksonville, Florida, USA
Speaker: Mayo Clinic, American Thoracic Society
Colin K. Grissom, MD, FASE, FCCM

Shock Trauma ICU
Professor of Medicine
University of Utah
Murray, Utah, USA
No disclosures
Mark P. Hamlin, MD, MS

Associate Professor of Anesthesiology and Surgery
University of Vermont College of Medicine
Director of General and Subspecialty Surgery
Critical Care
Medical Director of Respiratory Care
No disclosures
John Hardin, MD
Emergency Ultrasound Fellow
No disclosures
Thomas Heflin, MD
No disclosures
Brooke Hensley, MD, RDMS

Massachusetts General Hospital
No disclosures
Robert Hieronimus, MD
The University of Vermont Medical Center
No disclosures
Beatrice Hoffmann, MD, PhD

Emergency Ultrasound and Fellowship Director
Harvard Medical School
Committee Chair: American College of Emergency Physicians, Academy of Emergency Ultrasound;
European Society for Emergency Medicine
Dave Kirschner, MD, FRCPC
Emergency Room Physician, Grace General Hospital &
Children’s Hospital
Lecturer, Department of Emergency Medicine
College of Medicine, Faculty of Health Sciences
University of Manitoba
Winnipeg, Manitoba, Canada
No disclosures
Michael J. Lanspa, MD, MS

Shock Trauma ICU
Research Grant: Intermountain Research and Medical Foundation (critical care echocardiography)
Michael Mallin, MD
Ultrasound Director
Emergency Medicine
University of Utah
No disclosures
Paul K. Mohabir, MD
Clinical Associate Professor
Stanford, California, USA
No disclosures
Xavier Monnet, MD, PhD

Professor
Medical Intensive Care Unit
Bicêtre Hospital
Paris-Sud University Hospitals
Paris-Sud University
Paris, France
Advisory Board: Pulsion Maquet
Mark Munoz, MD
No disclosures
Arun Nagdev, MD
Director, Emergency Ultrasound
Assistant Clinical Professor
University of California San Francisco School of Medicine
San Francisco, California, USA
Chair: American College of Emergency Physicians Subcommittee
Akira Nishisaki, MD, MSCE

Children’s Hospital of Philadelphia
Philadelphia, Pennsylvania, USA
No disclosures
Vicki E. Noble, MD
Director, Division of Emergency Ultrasound
Massachusetts General Hospital
Associate Professor
Harvard Medical School
Speakers Bureau: Sonosite, Inc.; Board Member: American Institute of Ultrasound in Medicine, World
Interactive Network Focused on Critical Ultrasound
Stephen R. Odom, MD
Assistant Professor
Acute Care Surgery Division
Department of Surgery
No disclosures
Susanna Price, MD, PhD

Consultant Cardiologist and Intensivist
Royal Brompton Hospital
London, United Kingdom
Board Member: Acute Cardiovascular Care Association; Committee Member: European Society of
Cardiology; Subcommittee Member: Resuscitation Council, UK (ALS)
Todd W. Sarge, MD
Assistant Professor in Anesthesia, Critical Care and Pain Medicine
Department of Anesthesia and Critical Care
Speaker: World Interactive Network Focused on
Critical Ultrasound
Habib Srour, MD
Critical Care Fellow
Washington University in Saint Louis
No disclosures
Julie St-Cyr Bourque, MD, FRCPC

No disclosures
Lori Stolz, MD
Assistant Professor
University of Arizona
Tucson, Arizona, USA
No disclosures
Erik Su, MD
Assistant Professor
Director of Critical Care Ultrasound
Division of Anesthesiology and Critical Care Medicine
Johns Hopkins University School of Medicine
No disclosures
Jean-Louis Teboul, MD, PhD

Professor
Medical ICU
Bicêtre University Hospital
Paris-Sud University
Paris, France
Chair: European Society of Intensive Care Medicine Cardiovascular-Dynamics Section
Daniel Theodoro, MD
Assistant Professor, Emergency Medicine
Washington University School of Medicine in Saint Louis
Research Support: Siemens, Garfield
Alfredo E. Urdaneta, MD
University of Washington
No disclosures
Eric Ursprung, MD
Department of Anesthesia, Critical Care and Pain Medicine
No disclosures
Chakradhar Venkata, MD
Critical Care Medicine
Mercy Hospital
Saint Louis University
No disclosures
CONTENTS
Introduction
SECT ION 1: T HE BASICS
CHAPT ER 1 Ultrasound Basics: Physics, Modalities, and Image Acquisition

CHAPT ER 2 Ultrasound Basics: Safety, Ergonomics, and Knobology
Eric Ursprung, MD; Todd W. Sarge, MD
SECT ION 2: T HE HEART
CHAPT ER 3 Basic Windows and Views

CHAPT ER 4 Basic Evaluation of Left Ventricular Systolic Function and Cardiac Output
CHAPT ER 5 Basic Evaluation of Right Ventricular Systolic Function
Samantha K. Brenner, MD, MPH; Paul K. Mohabir, MD
CHAPT ER 6 Volume Expansion and Fluid Responsiveness
Xavier Monnet, MD, PhD; Jean-Louis Teboul, MD, PhD
CHAPT ER 7 Advanced Cardiac Ultrasound Evaluation
Sasikanth Adigopula, MD; Myriam Amsallam, MD; Anne-Sophie Beraud, MD
CHAPT ER 8 Assessment and Implications of Diastolic Dysfunction in Critical Illness
SECT ION 3: T HE LUNGS
CHAPT ER 9 T horacic Ultrasound: Pleural Effusion and Pneumothorax

Mark P. Hamlin, MD, MS; Ryan D. Clouser, DO
CHAPT ER 10 Pulmonary Edema and Consolidation
SECT ION 4: T HE ABDOMEN
CHAPT ER 11 General Diagnostic Abdominal Sonography

Brooke Hensley, MD; Julie St-Cyr Bourque, MD; Vicki E. Noble, MD
CHAPT ER 12 Focused Assessment with Sonography in T rauma (FAST )
Rachel E. Beard, MD; Stephen R. Odom, MD
SECT ION 5: PROCEDURAL GUIDANCE
CHAPT ER 13 Ultrasound-Guided Vascular Cannulation

Arun Nagdev, MD; Justin Bosley, MD; T homas Heflin, MD
CHAPT ER 14 Chest T ubes and T horacentesis
Mark Munoz, MD; David Feller-Kopman, MD
CHAPT ER 15 Paracentesis and Abscess Drainage
Lori A. Stolz, MD; Srikar Adhikari, MD, MS
SECT ION 6: CLINICAL PROBLEM SOLVING
CHAPT ER 16 Tamponade
CHAPT ER 17 T he Use of Ultrasound in the Diagnosis of Shock
Cameron Bass, MD; Habib Srour, MD; Alfredo E. Urdaneta, MD; R. Eliot Fagley, MD
CHAPT ER 18 Respiratory Failure
Jan Kasal, MD, FCCM; Chakradhar, Venkata, MD
CHAPT ER 19 T hromboembolism
John Hardin, MD; Beatrice Hoffmann, MD, PhD
CHAPT ER 20 Cardiac Arrest: Focused Echocardiographic Evaluation in Life Support (FEEL)
James Fair, MD; Michael Mallin, MD
CHAPT ER 21 Infection: Septic Shock
Patrick Bender, MD; Robert Hieronimus, MD
CHAPT ER 22 Vascular Injuries
Daniel T heodoro, MD, MSCI
SECT ION 7: LOGIST ICS
CHAPT ER 23 Ultrasound Quality Improvement, Documentation, and Billing

CHAPT ER 24 Credentialing in Ultrasound for Critical Care Medicine Providers
Aliaksei Pustavoitau, MD, MHS; Ranjit Deshpande, MD
SECT ION 8: PEDIAT RICS

CHAPT ER 25 Basic Evaluation of the Pediatric Patient
T homas Conlon, MD; Eric Su, MD; Akira Nishisaki, MD, MSCE
CHAPT ER 26 Pediatric Ultrasound Procedures: Central Venous Access and Arterial Access
Jeff Burzynski, MD, FRCPC; David Kirschner, MD, FRCPC; Eliotte L. Hirshberg, MD,
MS
INDEX
INTRODUCTION
With this textbook, we hope to provide a useful, concise introduction to the burgeoning field of bedside
ultrasound in critical care environments, including intensive care units, emergency departments, and
similar settings. Building on years of experience with the Society of Critical Care Medicine’s highly
successful Critical Care Ultrasound and Advanced Critical Care Ultrasound courses, we brought together
the best of the faculty and other content experts to write these chapters, which are intended to provide
crisp, authoritative introductions to their topics.
After much discussion, we felt that it was best to allow some repetition of material between chapters, so
that the user could go to a relevant chapter, read that chapter in its entirety, and not be required to chase
down relevant information in other chapters. While we believe that reading Comprehensive Critical Care
Ultrasound cover to cover would be a fruitful and pleasurable investment of several hours, we expect that
most users will be reading specific chapters to clarify a particular set of questions.
We hope this textbook will encourage more critical care providers to take up ultrasound and incorporate
it into their practice. Bedside ultrasound has already improved the safety of many intensive care
procedures. While we acknowledge that the evidence for the impact of ultrasound on patient outcomes is
still evolving and that more research is necessary, we believe that ultrasound skills are highly relevant to
patient care in contemporary critical care environments.
In Comprehensive Critical Care Ultrasound, we sought to balance practical advice and guidance for the
new user with brief reviews of the relevant literature. Recognizing the centrality of video to contemporary
ultrasound, we have tied video clips to the relevant chapters. These are located at
www.sccm.me/ultcomp, and indicated with this icon throughout the text. We welcome feedback about
errors of content or interpretation, perceived strengths or shortcomings, and topics that readers wish we
would engage in greater detail.
We wish you all successes in your clinical and research endeavors, and humbly hope that this textbook
will assist you in them. Happy scanning!

Michael Blaivas, MD, FAIUM
Jan Kasal, MD, FCCM
Chapter 1
Ultrasound Basics: Physics, Modalities, and Image Acquisition
Chapter 2
Ultrasound Basics: Safety, Ergonomics, and Knobology
Chapter 1
Ultrasound Basics: Physics, Modalities, and
Image Acquisition
OBJECTIVES
Review basic ultrasound wave physics
Describe different ultrasound modalities
Understand continuous, pulsed-wave, and color and tissue Doppler
Describe common ultrasound artifacts
INTRODUCTION
An understanding of the physics of basic ultrasound is fundamental to the ability to adequately acquire and
interpret ultrasound images. Factors such as choice of ultrasound transducer, depth of the structure of
interest, and gain have a complex relationship that determines the highest quality image. By understanding
the fundamental physics of ultrasound, clinician users can feel comfortable manipulating the controls on
different ultrasound machines, and thus maximize their user experience.
CASE STUDY 1
A morbidly obese 71-year-old woman with a history of breast cancer presents with dyspnea and
hypotension. She receives an initial crystalloid bolus, but remains hypotensive. Bedside
echocardiography is performed using a phased-array probe. The technically difficult apical view is
optimized by adjusting depth, overall gain, and time gain compensation (TGC). Right ventricular
dilatation is identified, and color Doppler at the tricuspid valve demonstrates regurgitant flow.
Continuous-wave Doppler of the regurgitant jet allows a calculation of the elevated pulmonary arterial
pressure, raising concern for pulmonary embolism. Subsequently, to identify whether further fluid
administration would improve her hemodynamics, a straight leg-raising test is performed with pulsed-
wave Doppler interrogation of the left ventricular outflow tract to determine if stroke volume increases
with the increased venous return.
CASE STUDY 2
A cachectic 41-year-old man with end-stage renal disease, emphysema, and hypertension presents with
shortness of breath and hypotension. His chest radiograph demonstrates an enlarged cardiac silhouette,
and bedside echocardiography is performed using a phased-array probe to fit between the ribs. The
parasternal long-axis view is optimized by adjusting depth, overall gain, and TGC, and a pericardial
effusion is demonstrated. Because of his deteriorating hemodynamics, pericardiocentesis is performed
using ultrasound guidance. The transducer is switched to a linear, high-frequency transducer covered in a
sterile probe cover, and a view of the anterior portion of the pericardial effusion is again acquired using a
parasternal long-axis view. Adjusting the depth so that the most anterior portion of the right ventricle is
visible, as well as the pericardium and pericardial effusion, the pericardial effusion is drained under
ultrasound guidance, and a pigtail catheter is placed.
Both cases illustrate the importance of understanding basic ultrasound physics and manipulation of
machine controls. Mastery of critical care ultrasound concepts and basic physics facilitates rapid
treatment and enhances patient safety.
ULTRASOUND PHYSICS
Ultrasound acts as a mechanical longitudinal wave, traveling through and interacting with tissue as it
penetrates. The ultrasound wave is formed in the ultrasound transducer using the piezoelectric effect of
crystals. The piezoelectric effect refers to the elastic property of crystals that leads to deformation of
those crystals when an electrical current is applied, causing vibration and generation of the ultrasound
wave. Similarly, the reverse piezoelectric effect is achieved when the returning sound wave strikes the
crystals in the transducer, leading to a mechanical deformation, thereby generating electrical current. Most
ultrasound transducers use what is known as pulsed echo mode, in which the crystals spend a small
fraction of the time generating bursts of ultrasound, and the majority of the time “listening” for returning
impulses. In most diagnostic ultrasound scans, the transducer spends around 1% of the time sending
impulses and 99% of the time listening for returning echoes, resulting in a duty factor of 1%. The number
of pulses of send/listen cycles that are sent each second is referred to as the pulse repetition frequency
(PRF). PRF is dependent on the depth of tissue being evaluated, because echoes from deeper tissue
require a longer time to return to the transducer; therefore, increasing depth leads to lower PRF.
Wave Characteristics
Human hearing typically ranges from 20 to 20,000 cycles/s, or hertz (Hz), and anything above the range of
human hearing is considered ultrasound. Diagnostic ultrasound uses a much higher frequency, ranging
from 1 to 15 MHz (1,000,000 to 15,000,000 Hz) in common usage. The frequency of the ultrasound is a
function of the transducer, and is a major factor in determining how deep the ultrasound beam can
penetrate into the tissues, as well as the resolution of the image. A higher frequency translates to
decreased penetration into tissues but better resolution. Conversely, a lower frequency enables
penetration to deeper tissues at a sacrifice of some degree of resolution. For example, an ultrasound used
to guide a needle through the superficial tissues of the neck to the internal jugular vein would ideally have
high resolution, and would only need to penetrate a few centimeters into the neck, so a higher-frequency
transducer can be used (on the order of 10 MHz). On the other hand, an ultrasound used to assess the
abdominal aorta in a 200-kg patient would need to penetrate deeply into the tissues, requiring the
sacrifice of resolution, making a lower -frequency probe necessary (on the order of 2 to 4 MHz).
E X P E RT T I P
Frequency of the ultrasound is a function of the transducer. This is a major factor in determining
how deep the ultrasound beam can penetrate into the tissues.
Resolution is the ability to distinguish between 2 adjacent objects. Lower resolution results in these
objects blurring together, while higher resolution allows differentiation. Resolution can be considered in
2 planes—axial (2 objects lying atop one another, parallel to the ultrasound beam) and lateral (2 objects
lying side by side perpendicular to the ultrasound beam). Axial resolution improves with increasing
frequency. Lateral resolution is maximized at the depth on the screen designated by the focal zone,
adjustable on most ultrasound equipment, where the ultrasound beam width is at its narrowest.
Although the ultrasound wave frequency is determined by the transducer, the velocity of the sound wave is
a function of the medium through which the wave is traveling. As the ultrasound wave passes from one
tissue to another, the velocity changes. At interfaces between tissues where there is a marked change in
velocity, a significant amount of sound energy is lost. For example, the velocity of sound is 1,430 m/s
through water, and 1,540 m/s through soft tissue. These velocities are very close, and subsequently no
significant amount of ultrasound energy is lost between the two. However, the velocity of sound through
air is 331 m/s and through bone is 4,080 m/s. This partially explains the significant loss of ultrasound
signal when attempting to scan soft tissue through a layer of air or bone, making these tissues a poor
acoustic window.
Although ultrasound has no known bioeffects at the levels typically used in the absence of contrast agents,
it is recommended that the total scan time and intensity be kept “as low as reasonably achievable,” also
known as the ALARA principle.1 In addition to limiting the number and duration of scans, ALARA also
means scanning with the lowest intensity possible. Amplitude and intensity of the ultrasound wave are
functions of the transducer and are the major determinants of power output of the ultrasound machine.
Although there are no known bioeffects of diagnostic ultrasound at typical usage levels, the theoretical
concerns about bioeffects are mediated by the amplitude and power. Ultrasound manufacturers typically
take this into account when creating preset examination types; when examining potentially sensitive
tissues, such as the retina and the developing fetus, selecting the appropriate preset automatically
decreases amplitude.
E X P E RT T I P
ALARA (as low as reasonably achievable) means scanning with the lowest intensity possible.
Amplitude and intensity of the ultrasound wave are the major determinants of intensity.
Wave Propagation Phenomena

Once the ultrasound wave is generated and transmitted into the tissues, the wave either can bounce off
tissues and return to the probe to be displayed as a returning echo (reflection), or it can be lost and not
return (attenuation). Reflection is generated at interfaces between tissues with differing acoustic
impedance. It is maximized by maintaining a perpendicular incidence of the ultrasound probe/beam to the
tissue being imaged. The intensity of the reflected returning echo determines the brightness of the
corresponding point on the ultrasound machine display—an area generating an intense reflection is
displayed as a bright signal (hyperechoic), whereas an area that does not reflect as much of the ultrasound
beam is darker (hypoechoic). An area that reflects no sound waves is completely black (anechoic)(
Figure 1-1).
Attenuation is the sum of all lost ultrasound energy that does not reflect back to the probe. It is composed
of refraction, scatter, and absorption. Refraction of ultrasound occurs at interfaces with differing
propagation speeds. It is inversely proportional to the angle of incidence of the ultrasound wave to the
interface—maximal when the beam and the tissue plane are nearly parallel, and minimal when
perpendicular. This is analogous to the refraction of light that occurs when looking at a coin at the bottom
of a pool. If you stand directly over the coin, it lies exactly where you see it, as the light waves strike the
interface between water and air at a 90° angle, and no refraction takes place. If you look at the coin from
the side, the smaller angle of incidence leads to a degree of refraction and the light waves bend at the
interface; thus, the coin appears to shift in position. This principle is applied when trying to get the best
image with ultrasound. Sound waves refracted away into the tissues do not return to the probe, minimizing
the returning echo of information that is used to generate the image on the screen. A second cause of
attenuation is scatter, a random reflection of sound waves in multiple directions. The third cause of
attenuation is absorption, or the conversion of sound energy into heat. Total attenuation is equal to an
attenuation coefficient multiplied by the depth—for each unit of depth, more ultrasound signal strength is
lost. The attenuation coefficient is proportional to frequency, so as frequency increases, so does the
amount of attenuation per unit of depth.
Figure 1-1. Image of Gallbladder with Gallstone

Abbreviation: GB, gallbladder.
The inside of the bile-filled gallbladder is black, or anechoic, except for the hyperechoic gallstone, which casts an anechoic acoustic shadow.
The liver is relatively hypoechoic compared with the gallstone.
Tissue harmonic imaging is a feature of modern ultrasound equipment that can lead to images with less
“noise.” Harmonic frequencies are integer multiples of the frequency of the transmitted ultrasound pulse
(also known as the fundamental frequency or first harmonic). As the fundamental frequency passes into the
tissue, echoes of several different frequencies are generated and can lead to indistinct tissue interfaces.
The use of harmonic imaging eliminates some of these artifactual reflections, increases the signal-to-noise
ratio, focuses on the fundamental and second harmonic frequency, and leads to better imaging in patients
who are otherwise technically difficult to examine via ultrasound.2
E X P E RT T I P S
Reflections are generated at the interface between 2 tissues with differing acoustic impedance.
As frequency increases, the attenuation for each additional unit of depth increases.
Attenuation is the sum of all lost ultrasound energy that does not reflect back to the ultrasound probe. It is
composed of refraction, scatter, and absorption.
Ultrasound Transducer
Most ultrasound machines have various transducers that can be selected depending on the clinical
indication. These transducers have intrinsic characteristics—such as size, form factor, and frequency—
that make them suited for a specific task. Linear transducers are often referred to as “vascular” or “high-
frequency” probes; these have a long, narrow rectangular probe face, have a frequency range of 5 to 13
MHz, and are used in superficial structures (such as the pleura), procedural guidance, and vascular and
soft tissue. Phased-array transducers have a small, nearly square probe face, have a frequency range of 1
to 5 MHz, and are used for imaging the heart as well as the abdomen, where its small footprint allows it
to get between rib spaces. Curvilinear transducers can be small (microconvex) or large, have a frequency
range of 1 to 5 MHz, and are used for abdominal imaging. Endocavitary transducers are essentially
microconvex curvilinear transducers on the end of a probe; these have a frequency range of 4 to 10 MHz
and are used for transvaginal, transrectal, and pharyngeal ultrasound.
ULTRASOUND MODALITIES
The earliest ultrasound was known as A-mode or amplitude mode ultrasound. This mode displays depth
on the x-axis and amplitude on the y-axis. A-mode ultrasound now is used mainly in ophthalmology
practice.
B-mode, or brightness mode, is what we commonly think of as ultrasound. This mode uses an array of
imaging crystals to generate a series of scan lines through a tissue plane, generating a 2-dimensional
image (B-mode ultrasound is also known as 2-dimensional ultrasound for that reason). The image
refreshes multiple times each second, with the exact frame rate dependent on multiple factors, such as
depth and width of the sector of ultrasound image displayed.
M-mode, or motion mode, is a form of ultrasound that narrows down to a single line of a B-mode display
to markedly increase the frame rate to orders of magnitude higher than B-mode (Figure 1-2). The intensity
of reflection is displayed as brightness, with depth on the y-axis and time on the x-axis. This permits a
still image to demonstrate motion, and is useful in cardiology to measure dimensions of rapidly moving
structures.
Doppler
The Doppler effect is an important feature of ultrasound that allows the velocity to be calculated. This
effect, which can be experienced standing on a train platform as a train approaches, is caused by the
relative compression of sound waves generated by an approaching object, and a relative rare faction of
sound waves after the object passes. This leads to a higher pitch as an object travels toward the listener,
and a lower pitch as the object travels away. The most common modes of Doppler ultrasound used
clinically are color Doppler, pulsed-wave Doppler, continuous-wave Doppler, and tissue Doppler.
Color Doppler is the easiest mode to conceptualize. Activating the color Doppler causes a box to appear
on the screen, which can be moved to overlie the area of interest. Any movement inside the box is
depicted by shades of red or blue demonstrating its velocity and direction relative to the probe face,
superimposed on the B-mode image (Figure 1-3). Color power Doppler is a form of color Doppler that
uses the same principles, but disregards the direction of flow and displays motion as an orange signal.
This direction-independent mode is very useful for identifying flow in low-flow states, such as ovarian or
testicular ultrasound.
Figure 1-2. M-Mode Ultrasound Across Mitral Valve Leaflet Tips

Time is depicted on the x-axis and depth is on the y-axis.
Figure 1-3. Color Doppler Image of Severe Tricuspid Regurgitation
Flow moving away from the probe face is displayed in blue.
Spectral Doppler uses the same frequency shift as color Doppler, but displays the information as a tracing
of velocity on the y-axis versus time on the x-axis. This is also demonstrated with audio in real time.
Spectral Doppler images are usually displayed with a small B-mode image above the velocity tracing.
Three different modes of spectral Doppler are commonly encountered in critical care: pulsed-wave,
continuous-wave, and tissue Doppler.
Pulsed-wave Doppler is commonly used in echocardiography and vascular ultrasound. This form of
spectral Doppler has a vertical cursor that can be manipulated across the image, and a small gate can shift
location and size (Figure 1-4). The velocity measurement is made only along this line, inside the gate—all
other velocities will be ignored. This Doppler modality is formed by pulses of ultrasound energy, and the
machine is able to “listen” for echoes that return only from the area inside the gate. This gives the pulsed-
wave Doppler range specificity, which is ideal for determining the velocity of blood at a particular point.
The main limitation of pulsed-wave Doppler is its inability to measure very high velocities because of
aliasing, whereby the velocity tracing will cut off at a specific velocity and then wrap around to the other
side of the baseline (Figure 1-5).4 Aliasing is a result of the Nyquist limit, the upper limit of velocity of
the Doppler shift that can be displayed. The Nyquist limit is equal to the PRF divided by 2. Aliasing can
be minimized by a few techniques, as described in Table 1-1, but limits the ability of pulsed-wave
Doppler to measure the high velocities commonly found in valvular disease. Uses of pulsed-wave
Doppler include assessing velocities in the aortic outflow tract to estimate stroke volume, as well as in
mitral valve inflow to evaluate diastolic function.
Figure 1-4. Pulsed-Wave Doppler Image of Mitral Valve Inflow

Flow moving toward the probe face is displayed above the baseline. Laminar flow via pulsed-wave Doppler is demonstrated by a sharp white
“envelope” and a dark center to the Doppler profile.
Continuous-wave Doppler uses 2 piezoelectric crystals, one sending ultrasound waves continuously and
the other receiving continuously. The velocities displayed represent all of the motion detected along the
entire Doppler cursor (Figure 1-6). Thus, the continuous stream of ultrasound energy limits the ability of
the machine to distinguish the origin of a particular velocity, resulting in range ambiguity. Continuous-
wave Doppler is not subject to the same Nyquist limitations of velocity measurement as pulsed-wave
Doppler, making it ideal for measuring very fast velocities when it is not necessary to know where it is
found (typically the narrowest point). Common uses are in finding the fastest jet of tricuspid regurgitation
to estimate pulmonary pressures and in assessing a stenotic valve.
E X P E RT T I P S
In pulsed-wave Doppler, a signal is sent and received from a particular depth at the exact
placement of the gate. This is used for measuring velocities at a particular point as when
calculating cardiac output or measuring mitral inflow.
With continuous wave, a signal is sent and received continuously. Depth cannot be determined. This is
used for valve areas and peak gradients.
Figure 1-5. Pulsed-Wave Doppler Image of Carotid Artery Flow

A) Aliasing, whereby the top of the Doppler profile is truncated and displayed underneath the baseline. B) Flow is seen through the same
vessel after the baseline and pulse repetition frequency have been adjusted to eliminate aliasing.
Table 1-1. Tuning the Doppler
1. Start with the best possible B-mode acoustic window.

2. Adjust 2-dimensional gain appropriately.
3. Minimize depth and sector width as much as feasible to increase frame rate.
4. Position color Doppler box or spectral Doppler cursor over area of interest.
5. Size the box/gate to appropriate size—as small as possible, but large enough to answer the clinical
question, to increase frame rate.
6. Steer: If performing vascular ultrasound, steer the color Doppler box so that the vessel traverses the
long axis of the parallelogram.
7. Angle correction: For arterial ultrasound, the sample volume should be as close to parallel to the
flow as possible, and an acceptable angle correction is 60°. In cardiac ultrasound, the sample
volume is not typically angle corrected or steered.
8. Gain: Turn up the color gain until the artifactual signal appears from tissues without flow, then
decrease the gain until artifact disappears.
9. Baseline: Adjust the baseline up or down, depending on the direction of the waveform of interest, to
minimize aliasing.
10. Pulse repetition frequency (PRF): Adjust PRF (velocity scale) to minimize aliasing.
Figure 1-6. Continuous-wave Doppler Image of Tricuspid Valve
A regurgitant jet is displayed below the baseline as it moves away from the probe face.
Figure 1-7. Tissue Doppler Image of the Lateral Mitral Valve Annulus
Direction and velocity of travel of the myocardium is displayed relative to the probe face.
Tissue Doppler is essentially pulsed-wave Doppler that is filtered differently to evaluate for the typically
slower velocities of tissue compared with intracardiac blood flow. Tissue Doppler is used to assess
myocardial motion during the evaluation of diastolic dysfunction as well as other clinical questions
(Figure 1-7).
ULTRASOUND ARTIFACTS
Before discussing a few ultrasound artifacts,5 it would be helpful to discuss the concept of acoustic
window. An acoustic window is a path that allows sound waves to penetrate the body to the structure of
interest, reflect off that structure, and then return to the probe at the surface. Good acoustic windows
include the liver and the spleen, as well as the urine-filled bladder. Poor acoustic windows are gas
(intestines, lung) and bone. A similar concept is that of posterior acoustic enhancement, in which a
structure (typically fluid-filled, such as the bladder or a cyst cavity) will attenuate fewer sound waves
than the neighboring soft tissue, and the area posterior to that structure will have more ultrasound energy
affecting it, generating correspondingly brighter reflections and appearing more hyperechoic on the
ultrasound display.
Acoustic shadowing is essentially the opposite of acoustic window—a structure that reflects a large
component of the ultrasound beam (such as bones and gallstones) will reflect most of the ultrasound
energy, resulting in a bright image on the ultrasound display. The underlying area is left in relative
darkness because of the markedly attenuated ultrasound beam (Figure 1-8).
Edge artifact occurs at the lateral border of a circular structure, such as a vessel or gallbladder, as the
beam approaches nearly at a tangent to the structure. The increased refraction at this interface results in a
dark artifact deep to this edge, which is not to be confused with an acoustic shadow (Figure 1-9).
Side lobe artifact typically appears in anechoic or hypoechoic structures, such as the bladder, and results
from strong reflectors outside the main ultrasound beam. These reflect back off-axis low-energy beams
and are displayed overlying the main image (Figure 1-10).
Figure 1-8. Acoustic Shadowing

Acoustic shadowing demonstrated as black band below bright white hyperechoic gallstone.
Figure 1-9. Edge Artifact
Arrows point out the dark lines of the edge artifact arising from the edge of the curved artery.
Reverberation is an artifact generated between 2 parallel highly reflective surfaces, often the skin and a
deeper structure (such as the pleural line), a metallic structure (such as a needle or wire), or from air in
the soft tissues. This is displayed as parallel hyperechoic lines parallel to, and deep to, the structure
generating the deep reflection (Figure 1-11).
Figure 1-10. Side Lobe Artifact
Arrow indicates the artifact arising in the center of the vessel at the same depth as the brightly echogenic structure to the left, which is
responsible for the artifact.
Figure 1-11. Reverberation Artifact
In this axial view of the anterior neck, the arrow indicates a ring-down reverberation artifact arising from air tracking through the fascial planes
of the neck from a pneumomediastinum.
ULTRASOUND MACHINE CONTROLS AND IMAGE ACQUISITION

The “knobology” of the ultrasound machine can be overwhelming with more complicated machines,
though some equipment designed for point-of-care use simplifies the control panel. Regardless of the
make or complexity of the equipment, it is important to be able to identify certain key controls, such as
depth, gain, frequency, focus, sector width, and freeze/cine.6
E X P E RT T I P
Remember to choose the transducer with the best resolution and footprint for the depth and
anatomic location of the structure of interest.
Once the machine is powered on, the transducer that is most appropriate for the clinical question at hand
is selected, based on frequency required and the trade-off between resolution and depth of penetration, as
well as the shape and form of the ultrasound probe. After grasping the transducer in a tripod grip, gel is
placed generously across the region to be scanned, and the probe is applied to the patient according to the
external landmarks and orientation conventions, which are described in the following chapters. If no
structures can be visualized, sliding the probe in a small circle or spiral will often reveal the acoustic
window. At that point, the probe can be stabilized by the tripod grip and the view improved by smaller,
slower movements in other planes.
As the acoustic window is located and an image is generated, the first control to adjust is the depth.
Sufficient depth should be used to display the necessary structures, but not so much that screen space deep
to the structures of interest is wasted. This optimum depth enables the field to be displayed at the maximal
size, without cutting off any areas of interest.
Gain is an important adjustment to make as well. There are 2 ways to control the gain: total gain and
TGC. Total gain controls the overall brightness of the screen by amplifying the brightness of all returning
echoes equally, similar to the brightness control of a computer screen. Ideal adjustment results in a screen
that is neither too bright nor too dark, enabling the distinction between tissues of varying acoustic
impedance. TGC is typically controlled by a series of sliders, with each slider controlling the brightness
of a separate depth on the screen; these should be adjusted such that similar tissues display the same
brightness from superficial to deep tissues.
After depth and gain (both overall and TGC) are adjusted to optimize the image, frequency and focus can
be manipulated to fine tune it (Table 1-2). The structure is then typically scanned in 2 orthogonal planes to
understand the structure in 3 dimensions.
Table 1-2. Tuning the B-Mode Image
1. Choose the correct transducer type.

2. Choose the applicable preset.
3. Adjust depth to center area of interest.
4. Optimize gain (overall and time gain compensation).
5. If necessary, adjust frequency: for deeper penetration and higher resolution, use lower frequency;
for shallower imaging and better resolution, use higher frequency.
6. Adjust focal zone to the depth of, or slightly deeper to, the area of interest.
7. If necessary, make sector width smaller to increase frame rate of area of interest.
One of the more challenging aspects of ultrasound for the beginner is acquiring a diagnostically usable
image. Some tips can increase the chance of success, beginning with how one holds the ultrasound probe.
Grasp the transducer as if it were a pen, between the thumb on one side and index and long finger on the
other, close to the probe face. The fourth and fifth fingers and the side of the hand serve as a base for the
tripod grip. This will allow the sonographer to scan using the small muscles of the hand and wrist and not
the large muscles of the upper arm and shoulder, increasing control and decreasing fatigue. It also enables
the sonographer to stay anchored to a very small acoustic window without sliding away.
As one becomes more comfortable performing ultrasound, significant improvements in skills can be made
by scanning patients at every opportunity. In a busy critical care environment, this can be challenging.
However, by having the machine available when evaluating patients, time is not lost “hunting” for it,
which often can result in the ultrasound scan not being performed. Any patient with a known abnormality
represents an opportunity to learn the ultrasound characteristics of that abnormality, which enables the
detection of the pathology in the as-yet-undiagnosed patient.
E X P E RT T I P
Grasp the transducer as if it were a pen, between the thumb on one side and index and long
finger on the other, close to the probe face. The fourth and fifth fingers and the side of the hand
serve as a base for the tripod grip.
KEY POINTS
Ultrasound frequency is the single most important determinant of image resolution and depth of
penetration. Low frequency provides lower resolution but deeper penetration, while high frequency
gives higher resolution but shallow depth of penetration.
Doppler ultrasound is a mode of ultrasound useful for characterizing velocity and direction of
motion of blood and tissue. Color Doppler uses color to depict motion of blood, while continuous-
wave and pulsed-wave Doppler show velocity in waveform. Tissue Doppler depicts velocity and
direction of myocardial movement in waveform.
A good ultrasound window is able to conduct sound waves from the ultrasound probe toward a
target and then back to the probe. Fluid and soft-tissue densities (such as bladder and liver/spleen)
are good acoustic windows. Bone and air (such as found in ribs and lungs/intestines) are poor
acoustic windows.
REFERENCES
1. Prudent Use and Clinical Safety. Official statement of the American Institute of Ultrasound in Medicine. Approved April 1,
2012.http://www.aium.org/officialStatements/34. Accessed March 29, 2014.
2. Choudhry S, Gorman B, Charboneau JW, et al. Comparison of tissue harmonic imaging with conventional ultrasound in abdominal disease.
Radiographics. 2000;20:1127-1135.
3. Feigenbaum H. Role of M-mode technique in today’s echocardiography. J Am Soc Echocardiogr. 2010;23:240-257.
4. Lawrence JP. Physics and instrumentation of ultrasound. Crit Care Med. 2007;35(Suppl):S314-S322.
5. Feldman M, Katyal S, Blackwood MS. US artifacts. Radiographics. 2009;29:1179-1189.
6. Enriquez JL, Wu TS. An introduction to ultrasound instrumentation and knobology. Crit Care Clin. 2014;30:25-45.
Chapter 2
Ultrasound Basics: Safety, Ergonomics, and
Knobology
Eric Ursprung, MD; Todd Sarge, MD
OBJECTIVES
Understand safe practices and how to minimize potential hazards to the patient in the practice of ultrasonography
Appreciate how proper ergonomics can enhance sonography technique, image acquisition, and daily workflow, and
reduce ultrasound scanning-related injury
Learn the practical art of “knobology” and put the more abstract principles of ultrasound physics to work
INTRODUCTION
With the advanced processing power of modern ultrasound machines, capturing clinically useful images is
becoming easier every day. A basic understanding of the technical details of the ultrasound system
controls—their capabilities and limitations—will help to optimize image acquisition markedly. The use
of ultrasound system controls is known somewhat pejoratively as “knobology.” Perhaps because of its
somewhat pedestrian nature, it is often given short shrift, but knobology is in actuality applied ultrasound
physics. Practicing the optimization of ultrasound image acquisition techniques in day-to-day care of
patients is surely the best way to cement the more abstract concepts learned in ultrasound physics.
SAFETY
The primary reason ultrasound has become so popular in recent years is that the technology allows for
safe, fast, and reliable imaging. There are no concerns regarding ionizing radiation, damage to
implantable hardware, or side effects related to invasive imaging procedures. Although generally
believed to be relatively free of side effects, ultrasound does have a number of safety considerations that
are important for both the patient and sonographer.
Ultrasound equipment is used on multiple patients every day, with exposure to bodily fluids, bacteria, and
viruses. It is of utmost importance that personnel using the ultrasound equipment disinfect the equipment
after every use. Although time consuming, ultrasound machines have been demonstrated to be vectors of
disease transmission in the hospital setting. A recent study examined 5 ICUs and 5 emergency departments
in Australia. The authors demonstrated that 68% of the transducers were contaminated with blood, and
48% were contaminated with bacteria. Ultrasound can be an enormously helpful diagnostic aid, but it
should be recognized that improperly sterilized transducers can facilitate disease transmission.1
There are few known biological effects of ultrasound, and as a whole, ultrasound is regarded as safe.
However, the sonographer should attempt to limit the exposure of the patient to ultrasound to the extent
that is possible. Ultrasound waves are capable of generating cavitation and heat, and correspondingly may
do damage to tissues. Ultrasound sound waves impart shear forces as well as cavitation, which have been
shown in animal models to cause significant damage in vulnerable tissues, notably the developing fetal
chicken brain.2 It should be noted that 2-dimensional (2D) imaging generates far less energy and heat than
Doppler imaging modalities. The spatial peak temporal average (ISPTA) is a commonly used measure of
ultrasound energy output. The ISPTA of 2D imaging is 34 mW/cm2, whereas 1,180 mW/cm2 is the ISPTA for
pulsed-wave Doppler.3 For this reason, the ultrasound power should be adjusted as low as possible for
good-quality images. This concept is referred to as the “ALARA” principle, which stands for “As Low as
Reasonably Achievable.” Ultrasound power and exposure should be limited as much as possible to
minimize the inherent risks. The American Institute of Ultrasound in Medicine has issued the following
statement on ultrasound safety:
“Diagnostic ultrasound has been in use since the late 1950s. Given its known benefits and
recognized efficacy for medical diagnosis, including use during human pregnancy, the American
Institute of Ultrasound in Medicine herein addresses the clinical safety of such use: No
independently confirmed adverse effects caused by exposure from present diagnostic ultrasound
instruments have been reported in human patients in the absence of contrast agents. Biological
effects (such as localized pulmonary bleeding) have been reported in mammalian systems at
diagnostically relevant exposures but the clinical significance of such effects is not yet known.
Ultrasound should be used by qualified health professionals to provide medical benefit to the
patient. Ultrasound exposures during examinations should be as low as reasonably achievable
(ALARA).”4
It should be noted as well that after prolonged use, the transducer itself can become hot. Probes that are
left in patients for long periods, such as transesophageal transducers, should be either unplugged or
placed in standby mode when not being used to let them cool down. As a safety measure, modern
transesophageal echocardiography probes will automatically shut off if they reach a user-defined
temperature threshold. However, this is not a substitute for operator vigilance.
ERGONOMICS
A survey of professional sonographers revealed that 80% had developed new-onset arm, leg, or neck
pain, with almost half requiring physical therapy to resolve the problem.5 Attention to ergonomics is
critical, because it not only helps the clinician avoid pain and discomfort, but also allows for better
conditions to obtain the best images possible. Before starting an examination, take pains to orient the
ultrasound machine in the room such that the operation of the transducer and system controls will be
comfortable. The height of the bed should be raised or lowered so that the clinician performing the
examination does not need to bend or crouch awkwardly. The patient should be positioned to facilitate
optimal imaging. For the cardiac examination, this means either supine and level, or left lateral decubitus.
In the patient receiving mechanical ventilation, the positioning may be significantly more challenging;
however, the time and effort put into this are well worth the improved imaging output.
It is up to the individual to decide with which hand it is best to scan and with which to operate the system
controls. However, some feel that the most comfortable way to obtain transthoracic echocardiography
images is through a left-handed grip of the transducer. When the patient is in the left lateral decubitus
position, the sonographer can sit next to the patient’s bedside, rest the left arm on the bedrail, and use the
right hand to operate the system controls. When using the right-handed approach, the sonographer must
stand to the patient’s right, drape his or her right arm over the patient, and turn slightly to use the
ultrasound controls. The right-handed approach is ergonomically more challenging but may be easier for
right-handed clinicians to obtain images, particularly when first starting to learn the scanning technique.
Practically, clinicians in critical care practice should learn to operate the machine and transducer with
both left and right hands, because it can be challenging to position the machine optimally in a room filled
with machines and monitoring equipment. Figures 2-1 and 2-2 demonstrate inappropriate and corrected
ergonomic positions.
ULTRASOUND SYSTEM CONTROLS: KNOBOLOGY AS APPLIED PHYSICS

Every ultrasound machine is slightly different in terms of layout, but there exist distinct commonalities
among different manufacturers and machines. Figure 2-3 depicts commonly used ultrasound systems in
critical care practice. Note that despite their differences, they retain the same basic set of functions. The
critical care sonographer should take time to study and explore the ultrasound machine before putting it to
use at the bedside. Knowledge of the system controls increases efficiency and speed in clinical imaging
and separates the novice from the expert.
Gain
Perhaps the most commonly accessed system control is that of overall gain. Gain simply amplifies the
signal that the ultrasound transducer receives, increasing the amplitude of the incoming sound waves.
Gain does not increase the output of the transducer and is purely a control of the received signals. It is
commonly confused with power, which will be discussed shortly.
Figure 2-1. Incorrect Ergonomic Position

Note how the clinician is reaching uncomfortably over the patient, and is forced to reach back and hyperextend his neck to operate the
ultrasound system controls.
Figure 2-2. Proper Ergonomic Positioning
The clinician is facing the ultrasound machine, resting the scanning arm on a pillow, and appears comfortable. This will allow for a much more
successful examination.
Figure 2-3. Ultrasound System Controls

Three common portable ultrasound machines used in critical care are shown. In general, platforms vary but knobs and concepts do not.
C AVE AT
Gain amplifies the signal received from the transducer. It does not increase the output of the
transducer.
The human eye can detect between 700 and 900 shades of gray. A 10-bit ultrasound machine is capable of
producing 1,024 shades of gray, more than any that humans can differentiate. 6 If the gain is too high or too
low, the system will not render the full gray scale on the display, and thus important information will be
lost. Proper gain adjustment can make an enormous difference when attempting to distinguish fine details
such as endocardial borders or valvular pathology. The gain is dialed up high, and then back down until
the blood appears black in the image. Figure 2-4 shows an example of how gain affects image quality.
Time Gain Compensation

As sound waves travel through soft tissue, they are dampened—or attenuated—by the medium through
which they travel. Therefore, when placing an ultrasound transducer on a patient, the sound waves that
travel the shortest distance through tissue will have the largest amplitude and will thus appear brighter
than sound waves that traveled to further depths.
To produce an image of equal brightness throughout, it is important to optimize the time gain
compensation (TGC). TGC is present on every ultrasound machine, and is typically represented as a
vertically stacked series of buttons that slide horizontally. An example of this control can be seen in
Figure 2-5. Typically, these sliders are set to lower the near-field gain and progressively boost the far-
field gain. The degrees to which these adjustments are necessary are heavily dependent on the individual
ultrasound machine, frequency of the transducer, and use of harmonic imaging. Therefore there are no hard
and fast rules regarding the TGC adjustment, except that the sonographer should take pains to ensure equal
brightness in the near and far fields.
Figure 2-4. Demonstrating the Importance of Gain on Evaluating Pleural Effusion

A) Undergained image, without appreciation of the lung within the black region representing the effusion. B) Properly gained image, which
allows better differentiation of the effusion and lung.
Figure 2-5. Time Gain Compensation Controls on Common Portable Ultrasound Platform
Compression
The range of signals acquired by the transducer and ultrasound machine are outside the range of human
discernment. To produce a meaningful image, the machine must squeeze or compress the wide spectrum of
signals into a narrow range of visible shades of gray. This more limited range of signals retains the
characteristics of the original; the highest amplitude waves are still high and the low amplitude waves are
still low. This system function is termed compression or dynamic range, and is adjustable on most
machines.
Power
One of the most frequently confused concepts in ultrasound is the difference between output power and
gain. Although increasing the power has similar results on the ultrasound display screen as increasing the
gain, it works in a wholly different way. Gain amplifies the received signals. Power increases the
amplitude of the ultrasound pulse from the transducer, and as a result, the received signals are stronger.
Increasing power will thus increase the ultrasound output and has the effect of increasing transducer
temperature and patient exposure to ultrasound. As a result, power is usually adjusted to the lowest
possible level that yields clinically useful images. Most ultrasound machines come with preset power
levels that conform to the ALARA principle and Food and Drug Administration guidelines regarding the
exposure of tissue to ultrasound. Power must be dialed down in the use of contrast agents to avoid
excessive cavitation and rupture of the microspheres found in the agent. Each contrast agent is different,
and the exact power setting necessary for the agent is specified by the manufacturer.7
Frequency
Ultrasound systems allow users to optimize the ultrasound frequency to account for variable imaging
circumstances. In general, higher frequency results in better axial resolution of the image. However, these
higher frequencies are attenuated more as they travel through soft tissue. Lower frequency waves are
much better at imaging deep structures because of their lower rate of attenuation. A balance must therefore
be struck between imaging depth and resolution. Most ultrasound machines allow the user to control the
transducer frequency, and on some, it is accomplished through the use of preset ultrasound modes for
Penetration, Resolution, or General. In this case, the penetration mode uses lower frequencies to image
deep structures at the expense of axial resolution. Resolution mode uses higher frequencies and should
only be used on superficial structures. General mode is a compromise between the 2 extremes and is used
for most imaging sessions. Other machines allow the user to select 1 of several available frequencies,
requiring slightly more understanding from the operator regarding the best frequency for the particular
application and patient.
E X P E RT T I P
Higher transducer frequency results in a better image at shallow depths.
Reject
Reject allows the sonographer to filter out noise from the returning signal, eliminating the incoming data
below a certain frequency threshold. This threshold is adjustable, though not commonly used after initial
setup of the ultrasound machine.
Focal Zone
The ultrasound beam can be divided into 3 parts: the near field, focal zone, and far field. The near field is
as wide as the transducer. The beam converges into a width one-half of the transducer size at the focal
zone. This is important to the sonographer because the consequence of the narrow beam size at the focal
zone means that this area has the best lateral resolution in the entire imaging field. Modern ultrasound
transducers are capable of adjusting this focal zone, and therefore the sonographer should make certain to
place the focal zone on the area of interest to optimize the imaging. Newer machines may be particularly
sensitive to focus position, as the refinement of electronic beam formation technology has led to better
resolution at this focal zone at the cost of decreased performance outside of it. In addition, it should be
noted that certain machines may allow for multiple focal zones. This technology relies on sending out
alternating pulses with different shaped beams, which improves lateral resolution at the cost of frame rate
and temporal resolution.
Depth
The ultrasound machine is capable of adjusting the imaging depth. The depth should be adjusted to the
shallowest level at which the entire structure of interest can be visualized The minimization of imaging
depth is important because there are serious consequences to image acquisition with increased depth.
Depth should be optimized such that the entire structure of interest is visible in the top two-thirds of the
screen to balance image resolution with imagery of the surrounding anatomy, which will provide context
to the shot.
The deeper the ultrasound waves have to travel, the longer it takes for the waves to return to the
transducer. Therefore, the temporal resolution is degraded with increased depth. Furthermore, ultrasound
waves are attenuated as they travel through tissue, making deeper structures appear dimmer. This can be
partially addressed with the judicious use of TGC, but because the TGC only amplifies the signal, it
means that the signal-to-noise ratio is greater with increased depth. Most modern ultrasound machines
will automatically adjust for this signal attenuation, leaving the TGC controls for fine tuning.
Imaging deep structures requires intelligent use of the focus control. The focal length refers to the distance
from the transducer to the focus point. At a length of twice the focal length, the beam width equals the
width of the transducer, and will increase to be wider than the transducer as the length of the ultrasound
beam increases past this point. Therefore, if the focus is placed superficially and the imaging depth is
increased, the deep structures will have poor lateral resolution. It should be noted that some machines
may change the focal point when the depth is changed. Care should be taken to note the position of the
focal zone, particularly when imaging deep structures.
Sector Size
The width of the image is adjustable with the sector size control. This control is usually left at the widest
possible image size, but it should be noted that decreasing the sector size decreases the amount of signal
that must be processed. This allows for higher frame rates and increased temporal resolution with
decreased sector size (Figure 2-6). As a result, this can be a useful strategy while imaging deep
structures. When the sector size is decreased, a control becomes available which allows the sector
position to be adjusted. This allows the sonographer to steer the ultrasound beam without moving the
transducer.
I M A G E O P T I M I ZAT I O N T I P
When imaging deep structures, a quick way to increase resolution and image quality is to decrease the
sector size.
Figure 2-6. Sector Width
Sector size can be decreased as shown going from image A to B, which in turn increases the frame rate and temporal resolution of the image.
Zoom
The zoom control allows the sonographer to select and zoom into an area of interest. Typically the zoom
is used to magnify areas of interest to take measurements of valves and vessels. It is important
aesthetically to capture the zoomed-out shot first, before acquiring the magnified image to show the
ultrasound reader the surrounding structures and provide context for the shot, and to ensure that no
significant pathology is missed in the vicinity of the scanning area. In addition, it should be noted that the
width and depth of the zoom will affect the frame rate of the image. The use of zoom does not improve
image resolution, because this is a function of sector width and imaging depth. This concept is important
and warrants further emphasis, as it is a common misconception and is frequently seen on board
examinations: resolution is a function of depth and width, zoom merely makes the image bigger.
Freeze
The freeze button allows the sonographer to stop acquiring the ultrasound image and, using the trackball,
rewind to a clinically useful image. A common application of this control is to acquire images of the heart
in end diastole, to obtain measurements of the myocardial thickness and internal chamber dimensions.
PULSED-WAVE DOPPLER CONTROLS

Pulsed-wave Doppler is used to determine the velocity profile of a specific region of blood flow.
Commonly, pulsed-wave Doppler is used to determine blood flow through the left and right ventricular
outflow tract, descending thoracic aorta, mitral valve inflow in diastole, and hepatic and pulmonary vein
flow.
In this mode, the transducer will first send a burst (or pulse) of sound wave toward the sampling volume
at a specific frequency known as the pulse repetition frequency (PRF). Depending on the depth, the system
will wait for a determined period to listen only to signals returning from the site of the sampling volume.
Doppler signal is ignored above and below the sampling volume, allowing the sonographer the ability to
distinguish regional flow variation as well as target-specific areas of interest. The shift in frequency
between the transmitted sound waves and returning sound waves is a function of the velocity of blood
moving through the area of interest. This velocity is then plotted by the ultrasound machine on the y-axis
as a function of time on the x-axis (Figure 2-7).
To use pulsed-wave Doppler, the sonographer first obtains a 2D view of the area of interest. The cursor
is then selected, which is then controlled with the trackball. The plane through which the pulsed wave is
determined with horizontal movements, the sample volume, is controlled with vertical movements.
Sample volume is the term used to describe the target of the pulsed-wave signal. Depending on the make
and model of the ultrasound machine, it is represented as either horizontal lines along the dotted cursor
line, or as a large, bold dot on the cursor line. Care should be taken to position this sample volume
precisely on the area of interest. Once this sample volume is targeted properly, the pulsed-wave button is
activated and the ultrasound machine will begin pulsed-wave mode.
C AVE AT
Resolution is a function of depth and width, zoom merely makes the image bigger.
Figure 2-7. Pulsed-Wave Doppler Used to Detect Flow Through Left Ventricular Outflow Tract
This, in turn, can be used to calculate the cardiac output. The spectral tracing of the pulsed wave appears as a line because the probe is
alternately transmitting and listening.
The methods by which pulsed-wave Doppler renders a signal introduce an important discussion point
regarding aliasing artifact (Figure 2-8). The transducer samples the incoming signal at a determined rate.
If the received signal is moving fast in comparison to the sampling frequency or PRF, it may appear to the
machine that it is moving in the opposite direction, which is referred to as aliasing. The Nyquist limit is
the speed at which this aliasing occurs and is defined as the PRF/2.
When the sample volume is close to the transducer, the signal is able to travel to and from the area of
interest relatively quickly. Therefore, at shallow depths aliasing is much less of a concern. As the depth of
the sampling volume increases, the system requires more time to receive the returning sample of the
signal, and the likelihood of aliasing increases. Thus, pulsed-wave Doppler has limitations on the
maximal velocity of blood flow that it can measure and is determined by the depth of the sample volume
and PRF.
Once the pulsed-wave display appears on the monitor, dials become available to control for scale, sweep
speed, gain, and baseline. The scale simply determines the y-axis scale, which is represented in either
centimeters per second or meters per second, depending on the make and model of the ultrasound
machine. The scale should be adjusted such that the entire Doppler envelope is seen, but large enough to
make accurate measurements. Likewise, sweep speed is adjusted so that the envelopes are wide enough to
comfortably trace. Usually adjusting this control to include 4 to 5 envelopes per screen is ideal. The
baseline control is responsible for the zero position on the y-axis. If the interrogated signal is moving
away from the probe, setting the baseline high on the display will allow the scale to be optimized and
maximize the envelope. The larger the envelope, the easier it will be to take the subsequent
measurements.
In certain instances, it may be necessary to determine the spectral velocity changes with other
hemodynamic events such as breathing or valsalva maneuvers. In these instances, adjusting the sweep
speed to a slower setting may be desirable.
Gain may be adjusted in the pulsed-wave mode, in much the same way it is used in 2D imaging. Over- or
underadjustment of gain may lead to errors in measurement, therefore pains should be taken to adjust the
gain so that the blood in the 2D image appears black in order to optimize the gain setting.
Figure 2-8. Examples of Aliasing

A) Note how the Doppler signal indicated by the blue arrow exceeds the limits of the spectral display and wraps around to the bottom of the
display, as indicated by the green arrow. Aliasing can be observed in color Doppler imaging as well. B) Blood is demonstrated exiting the left
ventricular outflow tract in systole. As the blood exits through the orifice, it accelerates. As it picks up speed, it exceeds the Nyquist limit, and
the color changes from blue to red, a transition highlighted by the red arrow.
CONTINUOUS-WAVE CONTROLS
Continuous-wave Doppler allows the sonographer to identify high-velocity jets, as seen in cases of
valvular or subvalvular stenosis. The machine is able to avoid the errors inherent to sampling and
aliasing as seen in pulsed-wave Doppler through continuous beam transmission and reception. Because
the system does not keep track of time with regard to the returning signals, range ambiguity is introduced.
That is, with pulsed-wave Doppler, the system is able to measure high velocities of blood along the
direction of the cursor; however, it is unable to determine at what depth these velocities occur.
To use continuous-wave Doppler, the cursor is selected, and using the trackball, the direction of the
continuous-wave beam is determined. Because of range ambiguity, the placement of the sample volume is
irrelevant. Figure 2-9 demonstrates the typical shaded envelope characteristic of continuous-wave
Doppler for measuring blood velocity.
Figure 2-9. Continuous-Wave Doppler

This can be used to evaluate extremely fast-moving jets seen in valvular regurgitation. Continuous-wave tracings appear as filled-in envelopes
because the probe is continuously transmitting and receiving velocity data along the entire path of the cursor.
E X P E RT T I P
Continuous-wave Doppler can measure very high velocities and does not alias. However, it is
impossible to know where the signals are coming from along the path of the ultrasound beam.
This uncertainty is called “range ambiguity.”
E X P E RT T I P
Decrease the Nyquist limit to examine slow movement, such as flow across a patent foramen
ovale.
COLOR DOPPLER
The “color” button toggles on and off the color Doppler mode. Color Doppler allows the sonographer to
generate a graphic representation of blood flow based on velocity and direction (Figure 2-8B). Color
Doppler allows the clinician to diagnose and grade the severity of valvular regurgitation as well as map
the location of atrial and ventricular septal defects. Color Doppler works in much the same fashion as
pulsed-wave Doppler. However, instead of mapping velocities on an x-y axis at a predetermined depth, it
scans through a user-defined area and codes the pixels with a color that corresponds to its movement
either toward or away from the probe.
Most ultrasound machines allow the user to define a color map. Conventionally, this is a color scale
ranging from red to blue, with red indicating movement toward the probe and blue moving away. Variance
mapping is also available on ultrasound machines equipped for cardiac imaging, which uses a 4-color
map and is used to detect lateral movement. Variance mapping is superior to the traditional 2-color setup
in detecting turbulent flow.
Color Doppler is subject to the same restrictions and limitations as pulsed-wave, and is subject to
aliasing as a function of the Nyquist limit. A fast-moving, incoming jet may change from red to blue and
back to red again. As discussed earlier, this aliasing is determined by the PRF or Nyquist limit. The
Nyquist limit is adjustable in color Doppler mode; this control is often labeled “baseline,” but regardless
of the label, this controls the PRF. Lower-velocity jets seen in atrial septal defects and patent foramen
ovale may be better characterized by a lower Nyquist limit. As such, the limit is usually set at 20 cm/sec.
Faster-moving jets, seen in valvular regurgitation, require a higher limit and are usually set in the range of
55 to 65 cm/sec.
It should be noted that an important side effect of color Doppler is the degradation of frame rate.
Typically, ultrasound machines alternate in the imaging of color Doppler and the 2D image. The color
image is superimposed onto the 2D background. This drops the frame rate immediately to about half the
rate of the 2D frame. Color sector width affects frame rate in the same way as discussed with 2D sector
width—the wider the sector, the lower the resulting frame rate. The color sector should therefore be
widened at the outset to scan for possible jets of interest and then immediately narrowed in the following
images to increase the temporal resolution.
M-MODE
Ultrasound technology has progressed markedly since its inception. In the beginning, there was amplitude
mode, also known as “A-mode.” A-mode displayed the transducer output as a graph of signal intensity
and distance. The qualitative demonstration of these data was known as “Brightness Mode,” or “B-
mode.” This was a 1-dimensional display with pixel brightness representing signal intensity. Motion
mode, which is known as “M-mode” captures B-mode output at a very fast frame rate. In the early days of
ultrasound, before 2D imaging became widespread, M-mode allowed for the evaluation of fast-moving
structures in the heart.
In the days of 3-dimensional imaging, one might be forgiven for thinking M-mode is largely a historic
relic. M-mode has retained its prominence in the formal ultrasound examination because of its extremely
fast frame rate. As discussed earlier, in 2D echocardiography, the sector width is decreased to limit the
amount of signal processing performed. This allows for greater temporal resolution because of the
increased frame rate. M-mode is the ultimate extension of this principle. Narrowing the ultrasound beam
to 1 dimension allows the sonographer to examine extremely fast-moving structures, such as valve leaflets
and their behavior timed throughout the cardiac cycle. For example, M-mode allows the sonographer to
examine the fluttering of aortic valve leaflets and early closure, which can help make the diagnosis of a
dynamic left ventricular outflow obstruction.
To use M-mode, the sonographer first locates the structure of interest using 2D ultrasound. Using the
trackball to place the cursor through the targeted area, M-mode is selected and the machine begins
recording 1-dimensional data. By convention, the data are acquired only after selecting “Freeze,” which
arrests data collection.
In this mode, sweep speed, depth, and color are available as display options. Sweep speed controls the
time scale, and more practically, how many beats of the heart are displayed on the screen. Depth functions
in the same manner as 2D echocardiography, with the same caveats regarding image brightness and signal
intensity. Figure 2-10 shows examples of M-mode and how sweep speed is used to affect image
acquisition.
The high resolution of M-mode makes it ideal for making measurements such as wall thickness, chamber
dimensions, and movement of the tricuspid annulus.
E X P E RT T I P
The high resolution of M-mode makes it ideal for making measurements such as wall thickness,
chamber dimensions, and movement of the tricuspid annulus.
Figure 2-10. M-Mode Images

A) Inferior vena cava (IVC) and (B) left ventricular outflow tract (LVOT) demonstrating the movement of the aortic valve. Note that the
sweep speed has been adjusted on the image of the IVC to accommodate the respiratory cycle and thus demonstrate the changes in IVC
diameter. The LVOT image is at a faster sweep speed because the intent is to demonstrate 2 to 3 cardiac cycles in the image for the purposes
of measurement and visualization of valvular movement.
Tissue Doppler
To the ultrasound transducer, the walls of the heart carry loud, slow-moving signals, at least in
comparison to the relatively quiet and fast movement of blood. Tissue Doppler, usually labeled TDI on
the ultrasound control panel, applies a filter that allows only the high-amplitude and low-velocity signals
to pass through. Therefore, TDI is useful in the examination of myocardial function. The TDI mode is
useful in determining the diastolic function of the left heart through the examination of the E′ velocity, as
well as systolic function of the right heart through the measurement of S′.
KEY POINTS
Although safe compared with other imaging techniques, the patient’s exposure to ultrasound should
be limited as much as possible.
The ultrasound machine can act as a disease vector, so careful decontamination is necessary
between patients.
The judicious use of ultrasound system controls is necessary to optimize imaging.
A working knowledge of ultrasound physics is the key to mastering system controls.
Ultrasound system controls have minor differences across platforms, but the fundamentals remain
the same.
REFERENCES
1. Keys M, Sim BZ, Thom O, et al. Efforts to attenuate the spread of infection (EASI): a prospective, observational multicentre survey of
ultrasound equipment in Australian emergency departments and intensive care units. Crit Care Resusc. 2015;17:43-46.
2. Schneider-Kolsky ME, Ayobi Z, Lombardo P, et al. Ultrasound exposure of the foetal chick brain: effects on learning and memory. Int J
Dev Neurosci. 2009;27:677-683.
3. Abramowicz JS. Benefits and risks of ultrasound in pregnancy. Semin Perinatol. 2013;37:295-300.
4. American Institute for Ultrasound in Medicine. Prudent use and clinical safety. Available at http://www.aium.org/officialStatements/34.
5. Smith AC, Wolf JG, Xie GY, et al. Musculoskeletal pain in cardiac ultrasonographers: results of a random survey. J Am Soc Echocardiogr.
1997;10:357-362.
6. Kimpe T, Tuytschaever T. Increasing the number of gray shades in medical display systems—how much is enough? J Digit Imaging.
2007;20:422-432.
7. Calliada F, Campani R, Bottinelli O, et al. Ultrasound contrast agents: basic principles. Eur J Radiol. 1998;27: S157-S160.
Chapter 3
Basic Windows and Views
Chapter 4
Basic Evaluation of Left Ventricular Systolic Function and Cardiac Output
Chapter 5
Basic Evaluation of Right Ventricular Systolic Function
Chapter 6
Volume Expansion and Fluid Responsiveness
Chapter 7
Advanced Cardiac Ultrasound Evaluation
Chapter 8
Assessment and Implications of Diastolic Dysfunction in Critical Illness
Chapter 3
Basic Windows and Views
True navigation begins in the human heart. It’s the most important map of all.
—Elizabeth Kapu’uwailani Lindsey, explorer and anthropologist
OBJECTIVES
Discuss how to configure the ultrasound machine for imaging the adult heart
Demonstrate how to acquire and optimize basic windows and views of the heart
Distinguish cardiac anatomy from the basic windows and views
INTRODUCTION
The goal of echocardiography is to identify and evaluate the heart and surrounding structures. Because of
the complexity of blood and valve movement within the heart, echocardiography allows for many
sophisticated measurements that are absent in other types of ultrasound. This chapter addresses the
practical aspects of properly obtaining echocardiographic images and how to correctly identify cardiac
anatomy from standard echocardiographic views. Throughout this chapter, images will conform to
standards established by the American Society of Echocardiography.1,2
SELECTING THE CORRECT TRANSDUCER AND CONFIGURING THE ULTRASOUND

For adult echocardiography, select a cardiac transducer (Figure 3-1). A cardiac transducer is typically a
phased-array transducer with frequencies of 1 to 5 MHz. Phased-array probes, by token of their
electronically steerable beams, have small, flat footprints, allowing them to scan well between the ribs.
Most medical ultrasound devices will have preconfigured echocardiography settings. For the novice
echocardiographer, 3 recommendations are helpful for starting echocardiography:
Use the default settings established by the manufacturer for most imaging.
Most ultrasound machines now include automatic image optimization algorithms that adjust gain and
contrast. These generally work better than manual adjustments.
When imaging has become distorted, most ultrasound machines will allow return to default settings.
This is an excellent way to start over.
E X P E RT T I P
Much like driving a car, there is no substitute for practice. Practice image acquisition on
yourself, your colleagues, your patients.
The default image position for adult echocardiography in most of the United States is with the indicator on
the right side of the screen and the narrow part of the scanning sector at the top of the screen (Figure 3-2).
Intensivists and emergency medicine physicians familiar with abdominal ultrasonography or focused
assessment with sonography in trauma (FAST) may be accustomed to placing the indicator on the left, as
per general radiology conventions. Inconsistent placement of the indicator can lead to errors of
interpretation, especially from the apical 4-chamber view, in which it may be difficult to otherwise
differentiate the right and left ventricles, especially for novice sonographers. In the default image
position, superficial structures are on top, and deep structures are on bottom. Harmonic imaging, which
decreases artifacts and provides generally clearer images, is now routinely used in most
echocardiography, and should be a default in most manufacturer preconfigured settings. For most critical
care echocardiography, there is no need to switch from harmonic to fundamental imaging.
Figure 3-1. Cardiac Transducer

Figure 3-2. Ultrasound Screen with Indicator (Blue Dot) on Right
This orientation is standard for echocardiography, whereas in many other types of ultrasonography, the indicator is oriented to the left.
When you are first starting, using the manufacturer preset and the auto-optimize button is often
sufficient for image optimization. The only thing you will need to adjust is depth. With more
experience, you can adjust some of the other settings to improve your image quality.
The frequency of the ultrasound is important because it determines resolution and penetration. Often
machines will have preset frequencies for improved penetration (harmonic 1.5 MHz/3 MHz), general
imaging (1.7 Mhz/3.4 Mhz), or improved resolution (2.3 MHz/4.6 Mhz). When imaging deeper structures
or obese patients, a lower frequency is often preferred. A good rule of thumb is that the worse the
acoustic window, the lower the frequency to be used, though one can typically acquire acceptable images
without ever adjusting the frequency from default settings. Some ultrasound systems may automatically
switch from harmonic to fundamental imaging when the frequency is increased to improve spatial
resolution. Many ultrasound machines allow the operator to adjust the focal zone, which optimizes lateral
resolution at a given depth. In such a system, simply place the focal position at the depth at which the
highest resolution is desired.
Because the heart is a moving object and some objects of interest, such as valves, move very quickly,
there may be times when the echocardiographer selects temporal resolution over image quality. Temporal
resolution is determined by frame rate, the number of images displayed per second. The frame rate is
often displayed on the screen in hertz. Frame rate is affected less by the frequency of a modern ultrasound
transducer than by the sector width, depth, and scan line density. It takes 0.1 msec for an ultrasound beam
to go through 7.7 cm of tissue and return. Because the phased array has to sweep through the entire image
sector, the wider or deeper the sector, the more time it takes to create an image, which decreases the
frame rate. This limitation is even more noticeable when performing color Doppler imaging. Therefore,
one should optimize the image according to the clinical context. If one needs to scrutinize the mitral valve
carefully, for example, narrowing the sector width to include only the mitral valve can improve frame
rate. The best temporal resolution typically occurs with M-mode imaging. In M-mode imaging, the
ultrasound transducer transmits and receives in 1 direction only. Because the transducer does not have to
sweep through a large sector, the frame rate is extremely high. For this reason, M-mode imaging is often
useful for imaging quickly moving objects such as valves.
PATIENT AND ECHOCARDIOGRAPHER POSITIONING

The most ergonomic way to image the heart is to stand at the patient’s left side and hold the transducer
with your left hand. The right hand manages the ultrasound controls. This position is routine among
echocardiographers. However, many intensivists have learned ultrasound imaging from various
disciplines other than echocardiography, and many are accustomed to different positioning. An intensivist
who is familiar with abdominal ultrasonography in trauma may feel more comfortable standing at the
patient’s right side holding the transducer with his or her right hand.
Ideally, the patient should be positioned in the left lateral decubitus position with the left arm raised.
However, in the critical care setting, this is often not feasible, and the imaging is often done with the
patient supine. It is a good idea to practice imaging the supine patient, because an intensivist should be
competent at imaging in such a position. If image quality is of utmost importance, and if it is feasible, one
can place pillows under the patient’s right shoulder and hip to bring the patient closer to a left lateral
decubitus position. Interpretation of echocardiography often requires timing to phases of the cardiac
cycle, so electrocardiograph leads should be attached. Many ultrasound machines will allow for
placement of electrocardiograph leads or will allow the user to obtain the data from a standard bedside
monitor. The patient should be draped to preserve modesty and patient dignity; positions should also
optimize the comfort of the patient and the examiner. One method is to use 2 towels over the left chest,
which allows the echocardiographer to minimize exposure of the patient (Figure 3-3).
Figure 3-3. Patient Draped with 2 Towels
HOW TO HOLD AND MOVE THE TRANSDUCER

For most echocardiographic imaging, hold the transducer as you would a pencil. This allows for greater
precision with fine movements, and also allows you to brace your hand with your 4th or 5th finger or
pisiform bone to avoid sliding and to isolate fine motor activity. In some instances, it may be easier to
hold the transducer with an overhand grip, similar to holding a microphone. Such instances include
imaging when the transducer is tilted down or when pressure needs to be applied, for example, against
abdominal muscles. The subcostal window commonly requires an overhand grip.
The field of ultrasound is plagued by inconsistent terminology describing movements of the probe used to
improve visualization. In this book we have used the most common, standardized terminology. Alternative
terms are included here in parentheses. Figure 3-4 demonstrates these movements.
Slide (Pan, Translate)

Sliding the transducer means to move it along the surface of the chest while keeping the same probe
orientation. The axis and rotation of the transducer remain unchanged. Sliding changes the acoustic
window used – the point of contact between the probe and the skin. By way of example, sliding is often
required to obtain an apical window. For the novice echocardiographer, this is often an unintentional and
undesired movement that occurs when his or her attention is on the screen rather than on the transducer.
Bracing the 5th finger on the patient’s skin can help to minimize sliding.
Figure 3-4. Transducer Movements
Tilting the transducer changes the ultrasound plane, whereas rocking occurs in the same plane.
Tilt (Fan)
Tilting the transducer is to keep the transducer in the same position on the body, while changing the plane
of insonation. If you imagine the ultrasound sector as a handheld fan, this movement is the same one that
occurs with fanning. In nautical terms, tilting is similar to changing the pitch of the boat, assuming the
plane of the ultrasound beam is the horizon. Directions of tilting generally refer to the tail of the
transducer. Tilting up means to tilt the tail of the ultrasound transducer cephalad. As a consequence of
such an upward tilt, the probe scans a more caudal position within the body. The acoustic window does
not change during tilting. By way of example, tilting is the movement within the parasternal short-axis
(PSAX) view by which the different levels of the left ventricle are imaged.
E X P E RT T I P
It’s easy to get lost with all these directions. Try to visualize where the heart is in the patient’s
chest, and think of holding your transducer like a flashlight. Shine the beam at the part of the
heart you would like to view.
Rock (Scan)
Rocking the transducer is to maintain the transducer in the same position on the body and in the same
plane of insonation, while moving the tail laterally within the same plane. This movement is
perpendicular to tilting. The movement of the ultrasound sector is much like the rocker on a rocking chair.
Continuing the nautical example, this is similar to changing the yaw of the boat. To rock left is to move the
tail of the transducer to the left. This movement is perhaps the most intuitive for the novice
echocardiographer when attempting to optimize the image, as the image stays in the same plane. Rocking
will move objects just outside the sector into view. Rocking allows you to look to either side of the
image. If a structure is just off the right side of the image on the screen, then rocking the tail away from the
probe indicator will bring it into view.
Rotate
Rotating the transducer is to keep the transducer in the same position on the body and orientation while
rotating, in place, clockwise or counterclockwise. This movement is commonly used to obtain different
views from within the same echocardiographic window. It moves from the parasternal long-axis (PLAX)
to PSAX view, for example.
With the combination of these movements, all degrees of freedom for the probe are described and,
assuming there is no interposed structure such as the lung, allows imaging of all windows and views.
When attempting to optimize an image by probe manipulation, it helps to imagine the structure of interest
in the body and visualize aiming the ultrasound transducer like a flashlight at the object of interest.
Typically, once the heart is identified, small movements are all that is required to optimize the image.
BASIC WINDOWS AND VIEWS

An echocardiographic window is a location on the body through which the transducer sends sound waves,
much like a keyhole through which a flashlight is shone. Comprehensive echocardiography uses 4
standard windows: parasternal, apical, subcostal, and suprasternal. For critical care echocardiography,
we limit ourselves to the first 3 windows. From these windows, one can obtain several views. Some
views can be obtained from multiple windows, such as the PLAX and the apical long-axis views.
Proficiency at obtaining all the views is necessary for comprehensive echocardiography, but for critical
care echocardiography, the priorities are: PLAX, PSAX, apical 4-chamber (A4C), apical 5-chamber
(A5C), apical 2-chamber (A2C), subcostal 4-chamber, and subcostal inferior vena cava/cavoatrial.
Parasternal Window, Long-Axis View (PLAX)

Place the transducer between the 3rd and 4th ribs, just left of the sternum. In a subset of patients with
inadequate imaging, sliding the transducer down 1 or 2 intercostal spaces may improve the image (Figure
3-5). For almost all imaging from the parasternal window, the transducer is held with a pencil grip.
The parasternal window is often one of the easier windows to obtain for the novice. It is also one of the
easiest windows with which to obtain off-axis images. This text will focus on the PLAX and PSAX
views, and illustrate some other views that are part of a comprehensive examination but not necessarily
included in a focused echocardiogram.
For the PLAX view, the indicator is pointed toward the patient’s right shoulder, aligned along the heart’s
longitudinal axis (Figure 3-5). Ideally, one should see the right ventricle, left ventricle, left atrium, mitral
valve, aortic valve, and aortic root (Figure 3-6). The descending aorta is adjacent and deep to the left
atrium. The apex of the left ventricle is typically off the left side of the image. The PLAX view shows the
right ventricular anterior wall, the left ventricular anteroseptal and inferolateral walls, the anterior and
posterior mitral leaflets, and the right and noncoronary (or sometimes left coronary, depending on the
imaging plane) cusps of the aortic valve. From the PLAX view, one can perform color imaging of the
mitral or aortic valves (Figure 3-7). One can also perform M-mode over the aortic valve, mitral valve, or
midchamber of the left ventricle (Figure 3-8).
If the PLAX view looks like that shown in Figure 3-9, the transducer is likely either too lateral or too
low. Remember, the top of the screen is the part of the body that is closest to the transducer. Therefore, the
transducer is too close to the apex. The transducer should be over the midventricle or base of the
ventricle, so either slide it up a rib space or slide it medially.
Figure 3-5. Transducer Position for Parasternal Long-Axis View

The indicator is pointed to the patient’s right shoulder.
Figure 3-6. Parasternal Long-Axis View

Abbreviations: LV, left ventricle; RV, right ventricle; LA, left atrium; Ao, aorta.
Figure 3-7. Mitral Valve from Parasternal Long-Axis View
Figure 3-8. M-Mode of Midventricle from Parasternal Long-Axis View

This view allows for measurement of ventricular shortening, interventricular septal wall, and inferolateral wall thickness.
Figure 3-9. Off-Axis Parasternal Long-Axis View with Too Much Apex
Abbreviations: LV, left ventricle; RV, right ventricle; LA, left atrium; Ao, aorta; MV, mitral valve.
This occurs from positioning the transducer either too laterally or too inferiorly.
If the image looks like that shown in Figure 3-10, the echocardiographer may have inadvertently
performed a right ventricular inflow view. This view is part of comprehensive echocardiography, but not
part of the focused critical care examination. This view occurs when the tail is tilted up from a standard
PLAX view. Correct the image by tilting the tail down slightly. Conversely, if the tail is tilted down from
a standard PLAX view, one may see an image similar to Figure 3-11; which is the right ventricular
outflow view. Correct the image by tilting the tail of the transducer up.
Parasternal Window, Short-Axis View (PSAX)

To obtain the PSAX view, simply obtain a PLAX view and rotate the transducer 90 degrees clockwise.
The indicator should now be pointing toward the patient’s left shoulder. Take care to maintain the
transducer axis while rotating. It may take some practice to get accustomed to rotating the transducer
without sliding, tilting, or rocking. If inadvertent movement results in an improper image, it is sometimes
easier to go back and obtain a standard PLAX view, and then rotate back to a PSAX view. If done
perfectly, the image should be of the PSAX view at the level of the midventricle (Figure 3-12).
Midventricle (also called “midpapillary”) view is identified by the presence of the anterolateral and
posteromedial papillary muscles. To obtain all the PSAX views, start by imaging the apex and then work
toward the base, where the valves lie. Tilt the tail toward the patient’s right shoulder so the transducer is
pointing toward the apex of the heart. The apex is readily identified by the absence of papillary muscles
(Figure 3-13 ). Slowly tilt the tail of the transducer caudad and toward the patient’s left (move the tail
from approximately the 10 o’clock to the 4 o’clock position) to visualize the midventricle, and then
continue toward the ventricular base. The ventricular base is identified by the presence of the anterior and
posterior leaflets of the mitral valve in short axis (Figure 3-14); some call this the “fish mouth view.”
Tilting the tail even further in the same direction will display the aortic valve in short axis, with all 3
cusps (Figure 3-15). This view is also called the “right ventricular basal view,” or the “right ventricular
inflow-outflow view.” In addition to displaying the right ventricle, this view includes both atria,
interatrial septum, the proximal pulmonary artery, and the tricuspid and pulmonic valves. Tilting through
the PSAX from apex to base displays all segments of the left ventricular walls, which is useful for
assessing wall motion abnormality, identifying hypertrophy, and septal flattening. Assessment of septal
flattening requires an on-axis view of the heart in the PSAX midventricle. An on-axis PSAX will
demonstrate a normal circular left ventricle, or a D-shaped ventricle in the setting of right ventricular
pressure or volume overload. An off-axis view may have a teardrop-shaped left ventricle, which may be
mistaken for septal flattening (Figure 3-16). Correcting a teardrop-shaped left ventricle is not always
straightforward, because many transducer movements from a PSAX view can yield this image. Often the
problem may be fixed by sliding up or down an intercostal space, or by tilting or rocking the transducer.
Occasionally, the rotation may be incorrect. If the PSAX appears elongated and the image looks like a
cross between a PSAX and an apical 4-chamber view (Figure 3-17), the transducer has slid too close to
the apex. Slide the transducer medially.
Figure 3-10. Right Ventricular Inflow View

Abbreviations: RV, right ventricle; RA, right atrium; TV, tricuspid valve.
Figure 3-11. Right Ventricular Outflow View
Abbreviations: RVOT, right ventricular outflow tract; PV, pulmonic valve; PA, pulmonary artery; LV, left ventricle.
Figure 3-12. Parasternal Short-Axis View of Midventricle

Abbreviations: RV, right ventricle; LV, left ventricle.
The midventricular parasternal short-axis view is defined by the presence of the anterolateral (3 o’clock position) and posteromedial (7 o’clock
position) papillary muscles.
Figure 13-13. Parasternal Short-Axis View of Apex

This view should depict the left ventricle without papillary muscles or mitral valve.
Figure 3-14. Parasternal Short-Axis View of Base
In the basal parasternal short-axis view, the anterior and posterior leaflets of the mitral valve are seen in the LV.
Apical Window, 4-Chamber View (A4C)

For the apical window, the transducer traditionally is placed at the point of apical pulse in a patient lying
in the left lateral decubitus position. The apical pulse is identified by following the nipple line to the left
lateral side of the body. This is often between the 5th and 6th ribs (Figure 3-18). The apex may be slightly
more medial in a supine patient than in a patient in left lateral decubitus position. In the supine patient,
placing the transducer within the breast crease below the nipple is a good starting spot. Lung and air do
not insonate well, and they often can interfere with acquiring images in the apical window.
Figure 3-15. Parasternal Short-Axis View at Level of Aortic Valve and Basal Right Ventricle
Abbreviations: RV, right ventricle; RA, right atrium; LA, left atrium; TV, tricuspid valve; PV, pulmonic valve; AV, aortic valve.
This is also called the RV inflow-outflow view.
Figure 3-16. Parasternal Short-Axis View, Midchamber

The image on the left has a flattened septum from pulmonary hypertension. The image on the right is a normal heart, but the image is off-axis,
which can also give an incorrect impression of a flattened septum. When examining the interventricular septum, it is important to obtain
multiple views and to obtain the images correctly. An appropriate parasternal short-axis view with flattening will show a D-shaped left
ventricle, while an off-axis left ventricle may look like a teardrop, oval, or pear.
E X P E RT T I P
Some beginners have problems getting good apical views. One tip that helps when tilting the
transducer down is to thrust and lift the transducer gently up between the ribs, almost as if you
are trying to lift the breast or pectoralis with the transducer. This movement allows the
transducer to maintain better contact with the skin, and allows for better image quality.
This problem is often more prevalent in the critical care setting, where patients commonly undergo
positive pressure ventilation. It may also be difficult to obtain an apical image in a patient with
chronically hyperinflated lungs. In such patients, the image is sometimes improved by sliding the
transducer medially or inferiorly. For the apical window, depending on one’s positioning, either a pencil
grip or overhand grip may be appropriate.
Figure 3-17. Parasternal Short-Axis View, Off-Axis

This is a parasternal short-axis (PSAX) view, off-axis, in which the transducer is too close to apex. This view is a hybrid between a PSAX and
an apical 4-chamber (A4C) view. You can recognize this error because the left ventricle is elongated rather than a circle. The transducer is
either too lateral or too inferior. If you see this when attempting an A4C, the transducer is likely too close to the base, either too medial or too
superior.
For the A4C view, the indicator is pointed straight toward the patient’s left (3 o’clock position). An
appropriate image contains all 4 chambers of the heart, with the apex at the top of the screen (Figure 3-
19). The left ventricle is on the right side of the screen, and the right ventricle is on the left side of the
screen. A standard view will show the anterolateral and inferoseptal walls of the left ventricle and the
lateral wall of the right ventricle. The aortic valve should be out of view. The A4C is perhaps the view
most familiar to the novice echocardiographer. This view is ideal for calculation of ejection fraction. It
also allows for recognition of segmental wall motion abnormality, though the PSAX view may be better
for this. Many advanced echocardiographic measures that use spectral Doppler are obtained from this
view, because the flows of blood in the mitral and tricuspid valves are aligned with the ultrasound beam.
If the heart looks like it is leaning to the left, with the right ventricle near the top of the screen (Figure 3-
20), the transducer is too medial. In such a case, the image can be optimized by sliding the transducer
laterally and rocking the tail to the left until the apex is near the top and the septum is vertical. Sometimes
an off-axis view is the best one can achieve in a critically ill patient. Although not perfect, it is still
sufficient for most critical care echocardiography.
If the image looks like Figure 3-21, the transducer is insonating the caudal aspect of the heart. The left
atrium is foreshortened or absent, and the coronary sinus is visible between the ventricles and atria. To
correct this, tilt the tail caudad. It is possible that by tilting the tail caudad, the image is occluded by lung.
When this occurs, sliding down an intercostal space may achieve a superior window.
Figure 3-18. Transducer Position for Apical Window

The indicator is pointed to the patient’s left.
Figure 3-19. Apical 4-Chamber View

Abbreviations: LV, left ventricle; RV, right ventricle; LA, left atrium; RA, right atrium.
Figure 3-20. Apical 4-Chamber View, Off-Axis
Abbreviations: LV, left ventricle; RV, right ventricle; LA, left atrium; RA, right atrium.
In this image, the heart looks like it is leaning to the side, and the right ventricle is near the top of the screen. This occurs when the transducer
is placed too medially.

This view is obtained by starting from the A4C and tilting the tail caudad slightly to insonate the cephalad
aspect of the heart. This tilting is the same movement used to correct an off-axis view of an A4C that
displays the caudal aspect of the heart. By convention, the left ventricular outflow tract/proximal aorta is
considered the 5th chamber. In addition to the chambers seen in the A4C view, the image includes the
aortic valve and aorta positioned between the atria (Figure 3-22). The left ventricular walls are not
identical to those visible in the A4C. Because the transducer tail is tilted caudad, the basal walls of the
A5C are more anterior than the A4C. The principal advantage of this window is assessment of the blood
flow through the aortic valve and left ventricular outflow tract. This view allows calculation of cardiac
output and assessment for aortic stenosis.
Figure 3-21. Apical 4-Chamber View, Off-Axis
Abbreviations: LV, left ventricle; RV, right ventricle; RA, right atrium.
In this image, the transducer is aimed at the inferior aspect of the heart. The left atrium is foreshortened or absent. Occasionally, the coronary
sinus is visible. To correct this image, tilt the tail down.

This view is obtained by starting from the A4C and rotating counterclockwise by 60 degrees. The image
will show the left ventricle, with the anterior and inferior walls, and the left atrium (Figure 3-23).
Occasionally, the left atrial appendage is visualized. The right ventricle is absent in this view. If the
transducer were rotated another 60 degrees counterclockwise, the indicator would be pointing toward the
right shoulder, demonstrating an apical long-axis view (ALAX, Figure 3-24). Although this view is part
of comprehensive echocardiography, it is generally unnecessary for critical care echocardiography. One
way to visualize the different apical views is to think of the left ventricle in short axis, and picture the
ultrasound beam slicing up the ventricle in different planes (Figure 3-25). The advantage of using the
long-axis, 4-chamber, and 2-chamber views is that together they show all wall segments of the left
ventricle. Good images of the PLAX, A4C, and A2C, combined with a scan of all of the PSAX images
will result in imaging every left ventricular wall segment from at least 2 angles.
Abbreviations: LV, left ventricle; RV, right ventricle; LA, left atrium; RA, right atrium; Ao, aorta.

Abbreviations: LV, left ventricle; LA, left atrium.
Figure 3-24. Apical Long-Axis View

Abbreviations: LV, left ventricle; RV, right ventricle; LA, left atrium; Ao, aorta.
Figure 3-25. Different Apical Views
The apical 4-chamber view, with the transducer indicator on the left, shows the anterolateral and inferoseptal walls of the left ventricle. The
apical 2-chamber view is imaged by rotating the transducer 60 degrees counterclockwise, showing the anterior and inferior walls of the left
ventricle. The apical long axis is imaged by rotating the transducer another 60 degrees counterclockwise, showing the anteroseptal and the
inferolateral walls of the left ventricle.
Subcostal Window, 4-Chamber View

The patient is preferentially positioned supine. If possible, it may help to flex the hips and knees to relax
the rectus abdominis muscles to allow for better transducer position. Place the transducer 2 cm below the
xiphoid, and tilt the tail down until it is nearly flat (Figure 3-26). Overhand grip is necessary, because it
allows for increased application of pressure on the abdomen and placing the probe down flatter against
the skin. The indicator should be pointed straight to the patient’s left (3 o’clock position). Rock the tail of
the transducer slightly until the transducer is pointing directly at the patient’s left shoulder. The resulting
image should look similar to the A4C, except that the heart is leaning to the right, and the liver is at the top
of the screen (Figure 3-27). This view is an ideal image with which to assess right ventricular wall
thickness, and to assess inferior pericardial effusions. However, because it is similar to the A4C, the
subcostal 4-chamber view does not offer much new information. If there is difficulty obtaining an A4C
view because of the patient’s body habitus, mechanical ventilation, or chest dressings, the subcostal 4-
chamber view is a nice substitute. Although not covered in this text, one can replicate many of the apical
or parasternal views from the subcostal window. By tilting the transducer tail up, one can follow the
inferior vena cava (IVC) in short axis as it enters the right atrium (Figure 3-28). It may be difficult or
impossible in some patients to image the subcostal window, because abdominal gas or surgical bandages
may sometimes interfere with the image. Imaging may be difficult in patients with extreme morbid obesity
because of the increased image depth. Conversely, imaging may sometimes be difficult in an extremely
gaunt patient or a patient with a prominent xiphoid process, because the xiphoid may interfere with
imaging. Some awake patients may experience discomfort with subcostal imaging if too much pressure is
applied to the abdomen or xiphoid.
Figure 3-26. Transducer Position for Subcostal 4-Chamber View
The indicator is pointed to the patient’s left.
Figure 3-27. Subcostal 4-Chamber View

Abbreviations: LA, right atrium; RV, right ventricle; LV, left ventricle; LA, left atrium.
Figure 3-28. Subcostal Inferior Vena Cava in Short Axis with M-Mode
M-mode allows for measurement of vena cava collapsibility.
Subcostal Window, IVC in Long Axis

Keep the transducer in the same window as the subcostal 4-chamber view. Tilt the tail up, and rotate the
transducer counterclockwise until the indicator is pointing at the patient’s head. The transducer should be
nearly vertical, but still pointing at the patient’s heart (Figure 3-29). The transducer tail may need to be
tilted slightly to the left to see the IVC in long axis (Figure 3-30). When imaging the IVC in long axis, it is
important to record the IVC entering the right atrium. This method will ensure that the visualized vessel is
not the aorta (Figure 3-31), and will ensure that the IVC measurements are accurate, as the measurements
have been standardized near the cavoatrial junction. Often, the hepatic vein is seen. This view is ideal for
measuring the IVC diameter, a measurement that is important in critical care echocardiography, especially
for the evaluation of fluid responsiveness. Although nearly every other structure in the heart can be
imaged from multiple windows, the IVC is not visible from the parasternal or apical windows.
C AVE AT
By tilting the transducer tail only slightly to the left, you can end up imaging the aorta (Figure 3-
31). Therefore, make sure you see the IVC enter the right atrium to ensure you actually are
imaging the IVC. When measuring the IVC diameter while the patient is breathing, be aware that
lateral movement of the IVC could move the vessel out of the imaging plane. Therefore, be sure to
acquire images of the IVC in both short and long axis.
PUTTING IT ALL TOGETHER

The object of critical care echocardiography is goal-directed rather than comprehensive imaging. The
task is to answer a limited number of questions, such as recognizing ventricular failure, significant
valvulopathy, or pericardial tamponade. These assessments are typically qualitative, not quantitative. One
does not need to know how to calculate ejection fraction to recognize a severely dysfunctional ventricle.
Unlike traditional echocardiography, the goal of critical care echocardiography is to provide a snapshot
of a patient’s heart and central hemodynamics. The examination is therefore often repeated. An example
would be repeating an echocardiographic examination after adding an inotrope. Last, when performing
critical care echocardiography, one should favor specificity over sensitivity, meaning that a definite
finding should result in a change in management, whereas an uncertain finding will require either
consultation or additional evidence.
Multiple protocols exist for focused critical care echocardiography. The focused assessment of
transthoracic echocardiography (FATE) protocol is perhaps most popular.3 This assessment can obtain at
least 1 usable window in critically ill patients about 98% of the time. The protocol offered decisive
clinical information in 25% of patients, and offered new information in 62% of critically ill patients who
underwent conventional monitoring.3 The basic FATE protocol, in order, is listed below. The sequence of
image acquisition differs from the sequence of standard comprehensive echocardiography performed in
the United States.
Basic and Extended FATE Examination
Subcostal 4-chamber
Subcostal IVC in long axis*
A4C
A2C*
ALAX*
A5C*
PLAX
M-Mode of PLAX through midventricle, mitral valve, aorta*
PSAX at the midventricle
PSAX at the mitral valve*
PSAX at the aortic valve*
Pleural (see Chapter 9)
* Views from the extended FATE protocol.
Regardless of what protocol one adopts, it is important to use the same method every time to avoid
missing crucial information. I adopt the protocol on the next page for focused critical care
echocardiography. This protocol is similar to the FATE protocol, but acquires images in the same order
as standard comprehensive echocardiography performed in the United States. By imaging in the same
order as standard comprehensive echocardiography, the intensivist will recognize echocardiographic
images acquired by trained cardiac sonographers, and the intensivist’s echocardiogram is more
recognizable to a cardiologist, should a consultation be necessary. Once familiar with acquiring these
images in 2-dimensional mode, you can later add advanced measurements where appropriate, such as
color or spectral Doppler assessments of valvular flow in the A4C or A5C views.
Figure 3-29. Subcostal Inferior Vena Cava, Long-Axis Transducer Position
Figure 3-30. Subcostal Inferior Vena Cava, Long Axis

Abbreviations: IVC, inferior vena cava; HV, hepatic vein; RA, right atrium.
Figure 3-31. Subcostal Aorta
Alternate Examination
PLAX, with increased depth, to assess for pericardial effusion

PLAX, normal depth
PSAX at the apex
PSAX at the midventricle
PSAX at the mitral valve
PSAX at the aortic valve
A4C
A5C
A2C
Subcostal 4-chamber
Subcostal IVC in short axis
Subcostal IVC in long axis
Throughout this protocol, the intensivist should look for obvious pathology, such as effusions, aortic
dissection, severe valvular regurgitation, severe ventricular hypertrophy or dysfunction, or severe atrial
enlargement. Examinations must be thorough and complete: one must not stop the examination at the first
abnormal findings. For example, when assessing the subcostal view, one may see a pericardial effusion
and tamponade. By terminating the examination prematurely without doing a PLAX, one may miss an
aortic root dissection that communicates with the pericardial space.
When performing critical care echocardiography, one should always record the images. Recording images
is necessary for billing and legal reasons, and the recording of images decreases the chance of missing a
subtle finding at the time the image is acquired. Recording of images is especially important when
performing echocardiography in an emergent setting, or a cardiac arrest situation, where one may have
only seconds between chest compressions to acquire an image.
When in doubt, correlate findings to the clinical context. With more knowledge of ultrasonography and
echocardiography comes greater confidence in one’s interpretation. However, one should not anchor on to
a finding that does not make sense. For example, when performing echocardiography on a patient with
massive hemorrhage who has been receiving transfusions, the presence of right ventricular enlargement
and an underfilled left ventricle does not always indicate pulmonary embolism. Perhaps the patient may
have transfusion-related acute lung injury. Stop and ask whether the proposed echocardiographic
diagnosis makes sense within the clinical context.
Finally, never be afraid to seek consultation. Transthoracic echocardiography poses 2 risks. The first is
when echocardiography interrupts chest compressions during resuscitation. This risk is easily avoided.
The second risk is that of misdiagnosis. This risk is extremely common among novice
echocardiographers, and is present even among experts. Any uncertainty about interpretation of
echocardiographic findings should prompt consultation with a local expert.
KEY POINTS
When first learning, practice image acquisition frequently, on a variety of patients or volunteers.
Try to visualize the heart in the chest when positioning the transducer.
Acquire images in a consistent manner, according to a protocol.
Complete the examination; do not stop when you encounter an abnormal finding.
Record images for later review and/or archiving.
Correlate findings to the clinical context.
When in doubt, consult a local expert.
REFERENCES
1. Spencer KT, Kimura BJ, Korcarz CE, et al. Focused cardiac ultrasound: recommendations from the American Society of
Echocardiography. J Am Soc Echocardiogr. 2013;26:567- 581.
2. Lang RM, Badano LP, Mor-Avi V, et al. Recommendations for cardiac chamber quantification by echocardiography in adults: an update
from the American Society of Echocardiography and the European Association of Cardiovascular Imaging. J Am Soc Echocardiogr.
2015;28:1-39.e14.
3. Jensen MB, Sloth E, Larsen KM, et al. Transthoracic echocardiography for cardiopulmonary monitoring in intensive care. Eur J
Anaesthesiol. 2004;21:700-707.
Chapter 4
Basic Evaluation of Left Ventricular Systolic
Function and Cardiac Output
OBJECTIVES
Recognize the normal dimensions of the left ventricle (LV)
Describe the principles of quantitative assessment of LV systolic function
Understand the validity of making a qualitative assessment of LV function
Be able to describe the qualitative abnormalities of LV systolic function
Detail the distribution of coronary artery flow with respect to LV anatomy
Describe the steps in the estimation of cardiac output using echocardiography
INTRODUCTION
In the outpatient setting, the echocardiographic assessment of left ventricular (LV) systolic function plays
a pivotal role in diagnosis, risk stratification, and guidance of therapeutic interventions in patients with
suspected or known cardiac disease. In critical care, assessment of LV systolic function and cardiac
output (CO) form part of the echocardiographic evaluation. More importantly, in situations in which CO is
inadequate and LV function is abnormal, echocardiography can be used to recognize the underlying cause
of inadequate CO and/or LV dysfunction, with potentially life-saving consequences1 and to help evaluate
response to therapy.
CASE STUDY
A 74-year-old man was admitted to the ICU with fever (38.5°C [101.3°F]), bilateral pulmonary
infiltrates, and hypotension (blood pressure 74/40 mm Hg). He had a history of coronary artery disease
that had been treated with percutaneous coronary intervention and stenting to the left anterior descending
(LAD) coronary artery. His chest radiograph showed bilateral pulmonary infiltrates with a right-sided air
bronchogram. A presumptive diagnosis of community-acquired pneumonia was made, and he was given
volume expansion. Antimicrobial therapy was commenced as well as vasopressors, with which he
initially improved. He developed progressive hypotension 24 hours later and was unresponsive to
escalating vasopressor support. His serum troponin was significantly elevated (>100 times the upper limit
of normal); however, the cardiologists did not feel that the electrocardiogram (Figure 4-1A) was
suggestive of acute coronary occlusion. They diagnosed the patient as having “demand ischemia” (type 2
infarction). Echocardiography was technically challenging, and LV systolic function appeared globally
impaired, perhaps consistent with septic shock. However, reduced long-axis function with marked
postejection shortening was seen in the septal and lateral walls (Figure 4-1B), suggesting significant
ischemia in the LAD and circumflex territories. The patient was taken urgently to cardiac catheterization,
where fresh thrombus was aspirated from both the LAD and the circumflex. His electrocardiographic and
echocardiographic changes resolved, and he made a full recovery.
ASSESSMENT OF LV SYSTOLIC FUNCTION

Assessment of LV systolic function, although seemingly one of the more simple echocardiographic
measurements, is one of the most complex because it comprises a number of motion vectors (radial,
longitudinal, circumferential, and torsional) related to the sum effects of myocyte contraction and their
orientation within the layers of the myocardium (Figure 4-2). Echocardiography has only recently been
able to interrogate true contractility of the myocardium using advanced techniques, such as strain/strain-
rate imaging, velocity of circumferential fiber shortening, or 3-dimensional (3D) echocardiography, the
majority of which remain research rather than clinical techniques.2 In clinical practice, echocardiographic
assessment of LV systolic function evaluates changes in LV cavity dimension as a substitute for LV
systolic function assessment using multiple techniques, including M-mode and Doppler imaging.3
Assessment of contractility requires consideration of the following aspects of the LV:
Cavity size
Wall thickness
Changes in cavity dimensions between systole and diastole
Changes in wall thickness between systole and diastole
Wall movement in the different regions
All measurements (except where stated otherwise) are timed according to the electrocardiogram, with
end-diastole considered at the onset of the Q wave, and end-systole near the end of the T wave.
Figure 4-1.
Electrocardiographic (A) and echocardiographic (B) findings in 74-year-old patient suggestive of significant ischemia.
Figure 4-2.
Motion vectors related to the sum effects of myocyte contraction and their orientation within myocardial layers.
Global LV Systolic Function: Cavity Size

LV dimensions are measured in the parasternal long-axis view, with measurements taken at end-diastole
either using the cursor from the 2-dimensional (2D) image (having scrolled to the appropriate part of the
cardiac cycle, Figure 4-3A) or from the corresponding M-mode (Figure 4-3B).3 Pitfalls in taking this
measurement include using an off-axis image (tending to overestimate LV dimensions), failure to identify
and measure the actual myocardial border (should determine the fastest moving line on the M-mode), and
poor endocardial border definition. Where visualization of the endocardial border is suboptimal, contrast
echocardiography is occasionally used. LV dimensions vary with gender, body habitus, filling status, and
presence of disease. The internal dimensions of the LV stratified by severity of LV impairment are shown
in Table 4-1.
Figure 4-3.
Abbreviations: LV, left ventricle; RV, right ventricle; Ao, aorta; LA, left atrium.
Left ventricle dimensions are measured in the parasternal long-axis view, with measurements taken at end-diastole either using the cursor from
the 2-dimensional image (A) or from the corresponding M-mode (B).
Global LV Systolic Function: Wall Thickness

In a healthy adult, LV wall thickness is usually 6 to 12 mm in diastole. Disease may cause the walls to
become hypertrophied or thickened (eg, hypertensive disease, hypertrophic cardiomyopathy, and aortic
stenosis).3 A wall thickness greater than 20 mm is consistent with severe hypertrophy. The LV may
additionally become dilated, with or without wall thinning less than 6 mm (eg, in dilated cardiomyopathy,
previous myocardial infarction, severe aortic, and/or mitral regurgitation). In ischemic heart disease, LV
wall thickness less than 2 mm is consistent with a nonviable myocardium.4 In trauma, where cardiac
contusion is suspected, the ventricular wall should be carefully scanned to exclude areas of thinning,
which are therefore at risk of rupture.
Table 4-1. Normal Values for Basic LV Systolic Function Assessment of Radial Function LV dimension Normal Mild Moderate Severe
LV dimension Normal Mild Moderate Severe
LVIDd (cm)
Male 4.2-5.9 6.0–6.3 6.4–6.8 ≥6.9
Female 3.9-5.3 5.4–5.7 5.8–6.1 ≥6.2
Fractional Shortening (%)
Male 25-43 20-24 15-19 ≤14
Female 27-45 22-26 17-21 ≤16
Teichholz Ejection Fraction (%)
Male >55 45-54 30-44 <30
Female >55 45-54 30-44 <30
Simpson’s Ejection Fraction (%)
Mean ± SD 2-SD range
Male 62 ± 5 52-72
Female 64 ± 5 54-74
Abbreviations: LV, left ventricle; LVIDd, left ventricular internal dimension in diastole.
Global LV Systolic Function: Change in Cavity Dimensions

The change in LV dimensions/volumes between systole and diastole can be used as a measure of
contractility. The most common ways to measure LV contractility in this manner are measurement of
fractional shortening (FS), which indicates changes in 1 dimension, and ejection fraction (EF), which
indicates changes in 2 dimensions.
Fractional Shortening
Fractional shortening uses the change in a single dimension to estimate the change in LV volume that
results from contraction, measuring along a line in the parasternal long-axis view, just below the mitral
valve leaflet tips (Figure 4-3). It is ideally measured using M-mode (when the LV is on the axis, with a
horizontally positioned septum; Figure 4-3A).3 These dimensions are then used to calculate FS as
follows:
FS = [(a–b)/a] × 100%
Most ultrasound machines make this calculation automatically once the values are entered. Reference
ranges for FS stratified by the degree of LV impairment are shown in Table 4-1.
Teichholz Ejection Fraction

Ejection fraction measurements add a second dimension to estimate volume from area. The simplest (but
often inaccurate) way of measuring EF is the Teichholz method, which is halfway between the FS and
disc summation methods. The Teichholz method takes linear dimensions and then, using generic models of
the shape of the LV, estimates volumes. The linear measurements are also taken from a 2D parasternal
long-axis view, with the M-mode cursor in a position similar to that used when measuring FS, just below
the mitral valve leaflet tips at end-diastole and end-systole (Figure 4-3).3 These dimensions are then used
to estimate volumes, based on which the Teichholz EF is calculated as follows:
EF = [LVEDV – LVESV] × 100/LVEDV)
where left ventricular end-diastolic volume (LVEDV) = [7/(2.4 + a)] × a and left ventricular end-systolic
volume (LVESV) = [7/(2.4 + b)]/b
Most ultrasound machines make this calculation automatically once the values are entered. The reference
ranges of EF stratified by degree of LV dysfunction are shown in Table 4-1.
A number of caveats must be considered when evaluating FS and EF that are measured using these
methods:
They rely on linear measurements at the base of the LV, and thus are unreliable in the presence of
regional wall motion abnormalities (RWMAs).
Minor degrees of off-axis measurement result in significant errors in estimates.
They are highly dependent on inotropy, activation, and load.
Neither has been validated in critically ill patients.
The inherent inaccuracy of these methods has led to the development of more sophisticated
echocardiographic techniques to assess LV systolic function.
C AVE AT
For all measures of LV systolic function, remember that positive inotropic agents will alter the
echocardiographic findings significantly by increasing the EF. Thus, the finding of a “normal” EF
measured in a patient receiving inotropic support may be very misleading, and changes in the
level of support may result in different values measured, which may not necessarily reflect
changes in intrinsic LV function.
Simpson Biplane Ejection Fraction

The biplane disc summation method (Simpson) uses 2D measurements taken in perpendicular planes to
estimate volumes – a substantial improvement over 1-dimensional measurements. The disc summation
method requires acquisition of high-quality apical 4-chamber and 2-chamber views, tracing the
endocardium on the 2D image (excluding the papillary muscles, which contribute trivially to the overall
LV volume along its length), and then measuring the long axis of the LV cavity from the apex to the
midpoint of the mitral plane in both views (Figure 4-4). Image optimization (depth and focus) is crucial to
minimize error, and in cases of suboptimal 2D images, LV contrast may be required to improve
endocardial border definition. Using these values, one can approximate the actual LV volume by
“stacking” short cylinders over the length of the LV. (Most ultrasound machines make this calculation
automatically once the values are entered.) The normal reference ranges for EF measured using the
Simpson biplane method are shown in Table 4-1. Compared with simpler estimations, the Simpson
method decreases the effect of LV shape distortion and minimizes (but does not abolish) mathematical
assumptions regarding LV geometry. The Simpson method is limited because (1) the apex is frequently
foreshortened (it should always appear slightly thinner than the neighboring myocardium); (2) endocardial
dropout is common because of poor image quality (mitigated by harmonic imaging and/or the use of
contrast); and (3) it is time consuming. The single-plane Simpson method, in which only apical 4-chamber
views are measured, is sometimes used and correlates reasonably with the biplane method.3
Figure 4-4.
The biplane disc summation method requires acquisition of high-quality apical 4-chamber (A) and 2-chamber (B) views, tracing the
endocardium on the 2D image and then measuring the long axis of the left ventricular cavity from the apex to the midpoint of the mitral plane
in both views.
Visual Estimation
Visual estimation (“eyeballing”) of global LV function has been shown to correlate well with quantitative
measures of EF.5 In the emergency and pericardiac arrest situation, eyeballing is probably most useful
because it can be performed faster and is relatively easier, even in the context of relatively poor image
quality.6 In its simplest form, 4 grades of LV systolic function are described according to the subjective
radial change of the LV size in the parasternal short-axis view between systole and diastole:
Normal FS (>30%)
Moderate dysfunction (10% to 30%)
Severe dysfunction (<10%)
Hyperdynamic
In a more comprehensive visual estimation of LV systolic function, a number of features are taken into
account when estimating LV systolic function in all views and all regions of myocardium. These include
inward movement of the endocardium, myocardial thickening, movement of the mitral valve toward the
LV apex (longitudinal mitral annular excursion) and LV size and geometry. A number of studies have
shown that, with appropriate training, visual estimation of LV EF correlates reasonably with more
complex quantitative analyses.7 Advantages of comprehensive visual estimation of EF include its
independence of endocardial border tracing (frequently challenging in ventilated patients) and the
assessment and integration of both global and regional contractility, though this method does require
training to perform accurately.
Regional LV Systolic Function

The various regions of the myocardium are supplied by different coronary arteries: the LAD, left
circumflex, and right arteries. Although there are minor variations among patients, in general, the regions
supplied by each coronary artery are consistent. The American Society of Echocardiography (ASE)
criteria define a widely used score for wall motion abnormalities3:
Normal wall motion (LV wall thickness increases >50% from diastole to systole)
Hypokinesia (increased thickness in systole, <40% thickness in diastole)
Akinesia (increased thickness in systole, <10% thickness in diastole)
Dyskinesia (wall thinning and outward motion in systole)
Although ASE criteria do not specify this condition, ventricular hyperkinesis is common in the ICU, often
reflecting high adrenergic tone and/or low afterload (Figure 4-5).
The areas supplied by each coronary artery are well described in the literature, according to each of the
echocardiographic views used (Figure 4-6).3 Only one view consistently shows all coronary territories
simultaneously— the parasternal short-axis. In every view that shows the LV, each region should be
examined for the movement and thickening of the myocardium, both alone and in comparison with the
other regions of the LV visible in the same view. For each view, the best way to assess wall motion is to
regard the endocardial border and the epicardium as distinct surfaces whose movement is tracked over
time. In normal contraction, the endocardium moves inward (endocardial excursion), the distance
between the endocardium and epicardium increases (wall thickening), and the LV cavity decreases in
size. In ischemia, both endocardial excursion and wall thickening decrease. Adjacent areas of the
myocardium should be compared, taking care to consider translatory and torsional motion of the LV walls
that may give a false impression of preserved wall motion. When an RWMA corresponds to 1 (or more)
coronary artery territory(ies), obstructive coronary artery disease is the most likely (but not the only)
cause.1 Interpretation of RWMAs is challenging, in particular in the context of preexisting myocardial
disease and inotropic support. Although the patient in the case study had coronary occlusion, some
patients with similar presentations do not.
Figure 4-5. American Society of Echocardiography Criteria for Wall Motion Abnormalities
LONGITUDINAL LV FUNCTION
All methods described thus far (FS, EF, and RWMA) primarily assess radial LV function. However, it is
also possible to assess longitudinal LV function using standard echocardiography techniques, either M-
mode or tissue Doppler imaging.
Mitral Annular Plane Systolic Excursion

In the apical views, M-mode is recorded across the point where the mitral annulus joins the LV,
demonstrating the basal longitudinal excursion toward the apex in systole and away in diastole (Figure 4-
7). Normal values correspond relatively well with EF and are shown in Table 4-2.8 Abnormalities in
mitral annular plane systolic excursion (MAPSE) relate to its onset (bundle-branch block, dyssynchrony),
magnitude (ischemia, reduced EF), velocity (ischemia, reduced EF), and duration (ischemia). The
advantages of MAPSE in critically ill patients are that it does not rely on high-quality images or
sophisticated machine software for measurement, and it is impossible to overestimate. An additional
advantage is that as the longitudinal fibers are endocardial and coronary arteries are epicardial,
abnormalities related to myocardial ischemia occur earlier than those seen using 2D imaging, and can be
mapped to the corresponding coronary artery that is the likely culprit (Figure 4-1B; also see the case
study earlier in this chapter).9
Figure 4-6.
Abbreviations: A4Ch, apical 4-chamber; PSAX, parasternal short-axis; PLAX, parasternal long-axis. Areas supplied by each coronary artery,
according to each of the echocardiographic views used.
Figure 4-7.
In the apical views, M-mode is recorded across the point where the mitral annulus joins the left ventricle, demonstrating the basal longitudinal
excursion toward the apex in systole and away in diastole.
Table 4-2. Normal Values for Basic LV Systolic Function Assessment of Longitudinal Function
Parameter Range
MAPSE amplitude (mm)
Lateral 15-20
Septal 12-17
Posterior 15-20
T iming (msec)
q-OS 80-90
Abbreviations: MAPSE, mitral annular plane systolic excursion; q-OS, timing of Q wave from the electrocardiogram to opening snap of the
mitral valve.
C AVE AT
In practice, the absolute numbers related to LV function are not particularly helpful in undertaking
serial LV assessment in the critically ill because of the significant confounding factors relating to
cardiorespiratory support and volume resuscitation. Note the potentially reversible pathology (ie,
RWMA suggesting coronary ischemia, hyperdynamic LV with structurally abnormal mitral valve
suggesting significant MR) and determine whether the CO from the left heart is adequate and
corresponds to the clinical gestalt of the patient.
C AVE AT
All measures of systolic function are highly load dependent, with MAPSE possibly marginally
less so than FS and EF.
CARDIAC OUTPUT
Echocardiography can be used to estimate the stroke volume from the left and right heart by measuring the
relevant outflow tract cross-sectional area (calculated from the outflow tract diameter) and multiplying
this by the velocity time integral (VTI) or stroke distance, measured using pulsed-wave Doppler.10 The
principles of estimating stroke volume using echocardiography are relatively simple, namely that at any
given time, flow through a vessel (including the LV outflow tract [LVOT] as a “vessel”) represents the
average velocity of all cells, multiplied by the cross-sectional area of the vessel. A number of
assumptions are made:
Flow is laminar.
The LVOT is circular.
The dimensions of the LVOT do not change during systole.
The sample volume is at the same position at which the LVOT diameter is measured.
The stroke volume does not change significantly from beat to beat.
The average velocity of cells is measured from the apical 5-chamber view, with the pulsed-wave sample
volume placed in the LVOT, 5 mm proximal to the aortic valve annulus. To avoid error, the Doppler
should be well-aligned with the LVOT, a clean Doppler envelope (white outline, black center) should be
obtained, and the opening click of the aortic valve should not be seen, because that would suggest that the
sample volume is placed too distally—though the closing click is often seen (Figure 4-9A). The brightest
portion of the spectral tracing represents the velocity of most blood cells (modal velocity), and tracing
this (avoiding overshoot at the maximal velocity) will provide the VTI (or average velocity of cells) in
the LVOT. The cross-sectional area is measured from a zoomed parasternal long-axis view, taken at the
level where the aortic cusps insert onto the annulus, 1 or 2 frames after maximal leaflet separation,
measuring from leading edge to leading edge (Figure 4-9B). The LVOT area is then calculated from the
measured diameter (D2 × 0.785) or using the machine software. Since stroke volume is VTI multiplied by
the LVOT area, multiplying this value by the heart rate will give the CO. If serial measurements of stroke
volume are made, the LVOT area calculated can be reused, but care must be taken to obtain equivalent
apical 5-chamber images for the pulsed-wave Doppler sample position each time and ideally to measure
at end expiration with a stable interbeat interval.
Figure 4-9.
Abbreviation: VTI, velocity time integral; LVOT, left ventricular outflow tract.
When evaluating cardiac output, the opening click of the aortic valve should not be seen, because that would suggest that the sample volume is
placed too distally—though the closing click is often seen (A). The brightest portion of the spectral tracing represents the modal velocity, and
will provide the VTI in the LVOT. The cross-sectional area is measured from a zoomed parasternal long-axis view, taken at the level where
the aortic cusps insert onto the annulus (B).
Suboptimal images present challenges, because any error in measurement of LVOT will result in a
squared error in stroke volume calculation. Irregular rhythm (ie, atrial fibrillation) will result in very
different values; an average of 10 to 13 beats with similar interbeat intervals has been suggested.1 Finally,
in cases of high subaortic velocities (LVOT obstruction/very high CO states), this technique cannot be
used.
A number of parameters can be used for the basic echocardiographic assessment of LV function. These
techniques for measuring systolic LV function all depend on the load and activation, and all measurements
depend on the inotropy and operator. Normal ranges among the critically ill are unknown, because little is
known about the effects of critical care interventions on measures of LV function or on the true nature of
LV dysfunction in critical illness.
KEY POINTS
Although a number of echocardiographic techniques are used to evaluate LV function, few are true
measures of myocardial contractility.
Positive inotropic agents may profoundly affect measures of LV function; the normal ranges in
critically ill patients have not been defined.
Any assessment of LV function and CO must be made in the context of the patient’s
cardiorespiratory support.
When right ventricular dysfunction supervenes, LV dysfunction can easily be underestimated
because the LV will be relatively unloaded.
The strength of echocardiography is not in measuring LV function or CO per se, but in diagnosing
underlying cardiac pathology, determining how to optimize CO, and recognizing when increased
support is required.
REFERENCES
1. Lancellotti P, Price S, Edvardsen T, et al. The use of echocardiography in acute cardiovascular care: recommendations of the European
Association of Cardiovascular Imaging and the Acute Cardiovascular Care Association. Eur Heart J Acute Cardiovasc Care. 2015;4:3-5.
2. Mor-Avi V, Lang RM, Badano LP, et al. Current and evolving echocardiographic techniques for the quantitative evaluation of cardiac
mechanics: ASE/EAE consensus statement on methodology and indications endorsed by the Japanese Society of Echocardiography. Eur J
Echocardiogr. 2011;12:167-205.
2015;28:1-39.
4. Armstrong WF, Ryan T. Feigenbaum’s Echocardiography. 7th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2009.
5. Shahgaldi K, Gudmundsson P, Manouras A, Brodin LA, Winter R. Visually estimated ejection fraction by two dimensional and triplane
echocardiography is closely correlated with quantitative ejection fraction by real-time three dimensional echocardiography. Cardiovasc
Ultrasound. 2009;7:41.
6. Labovitz AJ, Noble VE, Bierig M, et al. Focused cardiac ultrasound in the emergent setting: a consensus statement of the American
Society of Echocardiography and American College of Emergency Physicians. J Am Soc Echocardiogr. 2010;23:1225-1230.
7. Unluer EE, Karagoz A, Akoglu H, Bayata S. Visual estimation of bedside echocardiographic ejection fraction by emergency physicians.
West J Emerg Med. 2014;15:221- 226.
8. Matos J, Kronzon I, Panagopoulos G, Perk G. Mitral annular plane systolic excursion as a surrogate for left ventricular ejection fraction. J
Am Soc Echocardiogr. 2012;25:969- 974.
9. Duncan AM, Francis DP, Gibson DG, Henein MY. Differentiation of ischemic from nonischemic cardiomyopathy during dobutamine stress
by left ventricular long-axis function additional effect of left bundle-branch block. Circulation. 2003;108:1214-1220.
10. de Backer D, Cholley BP, Slama M, Vieillard-Baron A, Vignon P, eds. Hemodynamic Monitoring Using Echocardiography in the Critically
Ill [e-book]. New York, NY: Springer-Verlag; 2011.
11. Kern KB, Hilwig RW, Berg RA, et al. Postresuscitation left ventricular systolic and diastolic dysfunction: treatment with dobutamine.
Circulation. 1997;95:2610-2613.
Chapter 5
Basic Evaluation of Right Ventricular Systolic
Function
Samantha K. Brenner, MD, MPH; Paul K. Mohabir,
MD
Videos referred to in this chapter may be accessed by visiting www.sccm.me/ultcomp.
OBJECTIVES
Understand basic right ventricular (RV) anatomy and physiology
Learn to conduct a bedside evaluation of RV morphology including: RV wall thickness, RV dimensional analysis, and
RV:LV ratio
Describe the basics of assessing RV functionality including fractional area change, tricuspid annular plane systolic
excursion, and RV systolic pressure techniques for measurement
Identify the conditions that are associated with RV dysfunction
INTRODUCTION
The earliest description of the right ventricle (RV) dates back to the 16th century, when it was considered
a conduit for blood flow to the lungs with no significant physiologic consequence.1 This understanding led
to experiments throughout the early 20th century, which focused on creating animal models in which
perfusion was maintained in the absence of the RV.2 Although these models have shown that replacement
or ablation of the RV free wall can be tolerated in instances of good functional reserve, the RV has more
recently been shown to have prognostic and diagnostic significance across an array of conditions
commonly diagnosed and treated in the ICU. Some of these morbidities include myocardial infarction,
septic cardiomyopathy, pulmonary embolism, and pulmonary hypertension.3-6The understanding that
ventricular interdependence governs much of the function of both ventricles has also come to the forefront,
leading to a better appreciation of the functionality of the RV in patient care. Bedside echocardiography is
a powerful tool that clinicians can use to evaluate the RV in real time to obtain volume measurements,
function estimates, and wall thickness. With these bedside tools, ICU clinicians are better equipped to
diagnose and treat critically ill patients.
CASE STUDY
A 24-year-old woman (gravida 2, para 2) delivered a healthy infant 14 hours ago. The ICU team is
consulted regarding hypotension and tachycardia that persisted despite administration of 4 L of
crystalloid. In speaking to the obstetrics team, you are informed that her delivery was complicated by
failure to progress, thereby requiring a cesarean delivery. During the procedure, she required a
transfusion of 2 U of packed red blood cells, 1 U of fresh frozen plasma, and 1 U of platelets. This
morning, she got up for the first time and walked around. She has reported a bloody vaginal discharge, but
the nursing staff threw away the pads, and the obstetrics team cannot identify any external sites of vaginal
bleeding.
Her heart rate is 130 beats/min; blood pressure is 80/60 mm Hg with fluids running; oxygen saturation is
95% on 4 L via nasal cannula; and temperature is 38.5°C (101.3°F). Laboratory results on her morning
blood sample will not be available for another half hour. The electrocardiography and chest radiography
technicians are en route. On examination, the patient appears to be cold and diaphoretic but is able to talk
in full sentences. Her lungs are clear, she has some mildly elevated jugular vein distension, and her heart
sounds are normal with the exception of her tachycardia.
Using a portable echocardiogram probe to help you distinguish among hemorrhagic shock, septic shock,
transfusion-associated cardiac overload, transfusion-associated lung injury, pulmonary embolism, and
amniotic fluid embolism, you perform a basic ICU echocardiographic examination. The results are seen in
Video 5-1 . You conclude that this is most likely a case of pulmonary embolism or amniotic fluid
embolism.
ANATOMY
The RV is the most anterior structure of the heart, usually sitting immediately posterior to the sternum. The
RV wraps around the left ventricle (LV), forming the inferior border of the heart. In the absence of
pathology, during both systole and diastole, the septum remains concave to the LV. The shape of the RV
varies when viewed from different angles. From the side, the RV is triangular; in cross-section, it is
viewed as crescentic.
The RV is divided into the 3 segments: the inlet, the trabeculated apical myocardium, and the
infundibulum or conus. The inlet is composed of the tricuspid valve, chordae tendineae, and papillary
muscles. The apex of the RV is composed of trabeculae. The infundibulum is the smooth myocardial RV
outflow tract (Figure 5-1).1 The RV receives its blood supply from the right coronary artery in right-
dominant hearts, which make up 80% of the population.
With a thickness of only 3 to 5 mm, the RV has significantly thinner walls than the LV. The RV is shaped
such that its size or volume is greater than that of the LV, but the RV mass is a fraction of the LV mass.
However, unlike the LV, the RV lacks a middle layer. This absence reduces the extent to which the RV can
contract by torsion. Instead, the RV relies primarily on longitudinal shortening. The interventricular
septum is shared by both ventricles, and its fibers are intertwined and contributed by both. The RV’s
contributory fibers run longitudinally in the interventricular septum.7
PHYSIOLOGY
The RV pumps systemic venous deoxygenated blood into the pulmonary system for oxygenation. The LV
and RV are connected in series and thus pump the same volume. The RV function is dependent on RV
contractility, preload, and afterload.
Figure 5-1. Right Ventricular Segmental Anatomy
Abbreviations: MB, moderator band; RV, right ventricle; RA, right atrium; LV, left ventricle; LA, left atrium; Ao, aortic artery; PT, pulmonary
trunk.
The RV segmental anatomy is composed of the inlet, the apex, and the infundibulum or conus. The trabeculum is the apex of the RV. The
infundibulum is the smooth myocardial RV outflow tract.
Reproduced with permission Haddad F, Hunt SA, Rosenthal DN, Murphy D. Right ventricular function in cardiovascular disease: I, anatomy,
physiology, aging, and functional assessment of the right ventricle. Circulation. 2008;117:1436-1448. Copyright © 2008 American Heart
Association, Inc.
The RV fibers have a faster twitch velocity than the LV fibers. RV contraction occurs sequentially over the
course of 25 to 50 msec, starting with the inlet and ending with the infundibulum, its action similar to that
of a bellow. In systole, the ventricle narrows by the contraction of the free wall fibers with the LV
contraction at the attachment points causing the RV free wall to move inward. The longitudinal fibers of
the RV shorten the long axis and bring the tricuspid annulus closer to the apex. Tricuspid valve opening
and closure is primarily a function of atrial and ventricular pressure gradients. The RV shortens to a
greater extent longitudinally than radially.2 When electrically isolated from the LV, RV function can
diminish by as much as 70% because of loss of transseptal pressure generation.8 In contrast to the LV, the
RV has very minimal twisting and rotational movement in systole.
Stroke volume in the RV is similar to that in the LV because of the low-impedance system of the normal
pulmonary vasculature bed. The pulmonary circulation has not only a lower resistance, but also a greater
arterial dispensability compared with the systemic vasculature. As a result, right-sided cardiovascular
pressures are far below those in the left side of the heart. Consequently, the RV isovolumetric contraction
time (ie, time it takes to overcome the pulmonary artery diastolic pressure) is shorter than that in the LV.9
Increasing afterload significantly affects RV function. The RV response to afterload is significantly

different and less robust with acute dilatation of the free wall. The slope of end-systolic pressure volume
relationship, commonly referred to as ventricular elastance, is considered to be the most reliable index of
contractility because of its relative load independence. In contrast to the LV, the RV maximal time-varying
elastance reflects RV contractility, not end-systolic elastance.
Although the RV and LV are connected in a series, recent studies have demonstrated that even under
normal physiologic conditions, the ventricles function as if they were in parallel. Interventricular
dependence is created by the shared myofibers of the septum as well as the pericardial sac. With an intact
pericardium, RV dilatation impedes normal LV function both through shared myofibers and morphologic
constraints on the LV. Another consequence of ventricular interdependence is that the RV is more sensitive
to the extracardiac pressures governing respiration and the thoracic cavity.10
Morphologic Assessment of the RV

The RV can be visualized in multiple views on bedside echocardiographic imaging. It can been seen in
the left parasternal long-axis, parasternal short-axis, left parasternal RV inflow, apical 4-chamber,
modified apical 4-chamber, and subcostal views. When obtaining RV measurements, it may be helpful to
narrow the sector width to focus specifically on RV structures and obtain images of the RV during quiet
respirations—apnea, if possible—to minimize variation.
RV Wall Thickness
RV wall thickness greater than 5 mm indicates RV hypertrophy. The differential for RV hypertrophy is
broad, and includes infiltrative and hypertrophic cardiomyopathies and chronically increased RV systolic
pressure (RVSP). Relatively short exposures to elevated RV afterload can induce RV hypertrophy.11,12
The RV wall thickness should be measured in diastole using either 2-dimensional (2D) or M-mode at the
level of the tip of the anterior tricuspid leaflet in the subcostal view. The ultrasound beam should be lined
up perpendicular to the RV free wall. The RV trabeculations and papillary muscles should be excluded
from the measurement, as well as any epicardial fat, thickened pericardium, or liver in view, which
should all appear hyperechoic relative to the RV wall. The zoom function can be used to focus on the RV
wall. If the machine does not have a zoom function, decreasing the depth to focus on the RV wall is
another option to increase the accuracy of measurement (Figure 5-2).10
Figure 5-2. Right Ventricular Wall Thickness Measurement Technique

A) From the subxiphoid view, the RV free wall can be identified in zoom (B). C) Using M-mode, the image can be frozen, end-diastole can be
identified, and the RV free wall thickness can be measured (D).
Reprinted from Rudski LG, Lai WW, Afilalo J, et al. Guidelines for the echocardiographic assessment of the right heart in adults: a report from
the American Society of Echocardiography endorsed by the European Association of Echocardiography, a registered branch of the European
Society of Cardiology, and the Canadian Society of Echocardiography. J Am Soc Echocardiogr. 2010;23:685-713. Copyright (2010), with
permission from Elsevier.
RV Dimensions
In the apical 4-chamber view, the RV can be seen clearly, and morphologic measurements of ventricular
dimension can be taken during end-diastole. An attempt should be made to obtain 2 measurements in the
minor plane of the RV and 1 in the major (longitudinal) plane (Figure 5-3). To obtain RV measurements,
an RV-focused apical 4-chamber view must be obtained. To ensure that the operator is in an RV-focused
view, the transducer must be rotated to find the plane in which the largest visible minor diameter distance
is in view. To avoid overestimation of the RV diameter, the RV must not be foreshortened and the LV
outflow tract should not be in view. Therefore, a 4-chamber and not a 5-chamber view should be
obtained.
Figure 5-3. Quantitative Right Ventricular Dimensional Analysis
Abbreviations: RV, right ventricle; LV, left ventricle; RA, right atrium; LA, left atrium; RVLD, RV longitudinal diameter; RVMCD, RV
midcavity diameter; RVBD, RV basal diameter.
As a qualitative evaluation, the normal RV is two-thirds the size of the LV. The RV diameter measures are obtained in end-diastole. The
RVLD should be less than 8.6 cm, RVMCD less than 3.5 cm, and the RVBD less than 4.2 cm.
Table 5-1. Right Ventricle Reference Measurements

Measurement Abnormal Value Echocardiography View
RVEDA/LVEDA ratio >0.6 Subcostal, apical 4C
RV wall thickness >0.5 cm Subcostal, PLAX
RV basal dimension >4.2 cm RV-focused apical 4C
RV midlevel dimension >3.5 cm RV-focused apical 4C
RV longitudinal dimension >8.6 cm RV-focused apical 4C
RV FAC >35% Apical 4C
TAPSE <17 mm Apical 4C
Abbreviations: RV, right ventricle; RVEDA, RV end-diastolic area; LVEDA, left ventricular end-diastolic area; PLAX, left parasternal long
axis; 4C, 4 chamber; FAC, fractional area change; TAPSE, tricuspid annular plane systolic excursion.
The basal diameter is defined as the maximal short-axis (minor) dimension in the basal one-third of the
RV. The upper limit of normal for the basal diameter is 4.2 cm. The midcavity diameter should be
measured at the level of the LV papillary muscles and should be less than 3.5 cm. The longitudinal
dimension should be measured from the plane of the tricuspid annulus to the RV apex. The longitudinal
dimension of the RV should be no more than 8.6 cm (Table 5-1). These measurements have been
recommended by the American Society of Echocardiography.11 In the ICU setting, these measurements are
challenging to obtain during bedside echocardiography, making the next set of measurements more
valuable to bedside clinicians.
RV Size Relative to LV Size

Qualitative measurements of RV size relative to LV size should be obtained at end-diastole. The cardiac
monitor tracing helps to identify end-diastole. If cardiac monitoring is not possible, the freeze function
can be used to scroll back to the moment before systole begins. In the standard apical 4-chamber view,
with visualization of both ventricular free walls (Figure 5-3), the RV end-diastolic area should be no
more than two-thirds the size of the LV end-diastolic area. The LV should also be the apex-forming
ventricle. If the RV displaces the LV and is the apical ventricle, this may suggest RV enlargement. When
seen in the subcostal view, the same relationship applies; however, the subcostal view tends to
underestimate the size of the RV. Thus, an enlarged RV from this view should strongly suggest RV
enlargement. In a left parasternal long-axis view that is not foreshortened, the RV, aortic outflow tract, and
left atrium should each stack on top of one another (Figure 5-4) and each take up roughly one-third of the
screen. If the RV is significantly larger than the others, this may also suggest RV enlargement.
Functional Assessment of the RV

There are 2 main echocardiographic methods that critical care providers should use to determine RV
function: the fractional area change (FAC) and the tricuspid annular plane systolic excursion (TAPSE),
also called tricuspid annual motion (TAM).
RV FAC
The RV FAC has been shown to correlate with the gold standard RV ejection fraction (EF) measurement
by means of cardiac magnetic resonance imaging. The RV FAC approach assumes that the change in area
during systole and diastole is a valid proxy for the RV percentage change in volume (EF).13 RV FAC is
determined using following equation:
The FAC should be obtained in the apical 4-chamber view and can be found by tracing the RV
endocardium both in end-systole and end-diastole from the free annulus, along the free wall to the apex,
and then back to the annulus following the line of the interventricular septum. All tracings must be made
beneath the numerous and coarse trabeculations of the RV (Figure 5-5). A normal RV systolic function is
defined as an RV EF greater than 35%.11
Figure 5-4. Visual Right Ventricular Dimensional Analysis
Abbreviations: RV, right ventricle; Ao, aorta; LV, left ventricle; LA, left atrium.
In the parasternal long-axis view, the RV, Ao tract, and LA should be stacked on top of one another, each taking up roughly one-third of the
screen.
TAPSE or TAM
TAPSE, also known as TAM, is a regional measurement that allows for the estimation of RV systolic
function. The measurement is obtained from an apical 4-chamber view and requires a good view of the
RV free wall. This method is the direct correlate of the mitral annular plane systolic excursion by Doppler
tissue imaging in the LV. It is based on the assumption that the greater the excursion of the RV free wall
during systole, the greater is the RV systolic function. This method is inherently invalid in cases of RV
regional wall motion abnormalities, such as acute RV infarction or RV strain from acute cor pulmonale,
because regional RV motions will no longer be a valid estimate of the overall function.10,11
TAPSE measurements are best obtained with the Doppler M-beam passing through the lateral annulus
in the 4-chamber view. Ensure that the image is not foreshortened by fanning anteriorly and
posteriorly and getting the true apex in view. You may also need to rotate the probe to make sure that both
valves are properly transected and not rotated off axis.
Figure 5-5. Calculation of Fractional Area Change

The fractional area change (FAC) is calculated by measuring the change in area of the right ventricle (RV) between end-diastole and end-
systole. The top images demonstrate a normal FAC greater than 35%, and the bottom images show reduced FAC of 22%, consistent with
reduced RV function.
The TAPSE measurements can be obtained by placing an M-mode cursor through the tricuspid annulus
and measuring the longitudinal motion of the annulus. This measurement should be obtained at peak
systole.14 TAPSE can be obtained even with less-than-optimal imaging because it remains a regional
measurement without a lot of tracing or image manipulation, which makes it an excellent and powerful
bedside tool. Although no large-scale validation studies exist, compilation of many studies has yielded a
robust enough sample for the method to be endorsed by the American Society of Echocardiography. Any
excursion less than 17 mm is highly specific, but not necessarily sensitive, for depressed RV EF (Figure
5-6).11
Pathologic RV Morphology
The morphology of the interventricular septum, particularly in the parasternal short-axis view, is critical
in determining the presence of RV overload.1 Furthermore, the pattern of movement of the septum
throughout the cardiac cycle can help distinguish RV volume overload from RV pressure overload (with
or without concomitant RV volume overload).15,16 When the RV is overloaded, RV morphology changes
such that the septum becomes flat, resulting in a loss of the RV crescent shape and in the LV contour
resembling the letter D. Functionally, this causes an impediment to LV filling and a resultant decrease in
cardiac output.12 When patients have RV volume overload (eg, an atrial septal defect), the flattening of the
septum is seen only in diastole, with normal septal and RV morphology in systole. When patients have RV
pressure overload (eg, pulmonary hypertension), the septum will initially flatten in systole, but as the
condition becomes worse, the septum will be flattened or even collapsed throughout the entire cardiac
cycle (Figure 5-7).12,17 RV volume overload is frequently coupled with RV diastolic dysfunction and
elevated filling pressures (Video 5-1 ).12,17,18
Pulmonary Arterial Vasculature

Estimating pulmonary arterial pressures on bedside echocardiography may be useful to clinicians in
determining the origins of RV dysfunction. Using the apical 4-chamber view, elevations in RV pressure
may be indicated by tricuspid regurgitation (TR). Color flow Doppler can be used to identify the TR jet
and find its point of maximal flow, while continuous-wave Doppler can be used to find the point of
maximal velocity. Using TR jet velocity, RVSP can be estimated. RVSP is considered a good surrogate of
systolic pulmonary artery pressure, assuming no gradient across the pulmonic valve or RV outflow tract.
Many bedside machines will do the calculation once the measurement has been taken, using the modified
Bernoulli equation:
Figure 5-6. Tricuspid Annular Plane Systolic Excursion Measuring 20 mm
Abbreviations: RV, right ventricle; LV, left ventricle; TA, tricuspid annulus; LA, left atrium; RA, right atrium.
To obtain this view, M-mode is applied across the tricuspid annulus, allowing for accurate measurements. Point A marks the greatest amplitude
of annular excursion during systole; point B is the location of the annulus during diastole. The solid and dashed orthogonal lines demonstrate
how the measurement is calculated, and the solid line represents the extent of excursion.
Figure 5-7. Interventricular Septum During RV Pressure Overload

The interventricular septum has a bowed appearance, creating a characteristic D shape. This bowing is seen only in diastole for right
ventricular (RV) volume overload, but is seen in both mid- to end-systole and diastole early in the course of RV pressure overload. Eventually,
if the patient’s condition continues to worsen, bowing will be seen throughout the cardiac cycle.
RVSP = 4 * V2 + RAP
where V is TR peak velocity and RAP is right atrial pressure, which can be estimated using the inferior
vena cava (see Chapter 6). If the right atrial pressure measurements are too difficult to obtain, most
clinicians use 3 to 5 mm Hg as an approximation, which may cause the RVSP to be underestimated. At
rest, the peak TR gradient should be less than or equal to 2.8 to 2.9 m/s. The RVSP or systolic pulmonary
artery pressure estimation should not exceed 35 to 40 mm Hg, otherwise it can be considered abnormal,
and clinical correlation is warranted to consider pulmonary hypertension.11
DISEASES THAT COMMONLY AFFECT RV FUNCTION IN CRITICAL CARE
Fluid Responsiveness
Although not the focus of this chapter, inferior vena cava (IVC) measurements and pulse pressure
variation are often used in the critical care setting to determine fluid responsiveness in both spontaneously
breathing and intubated patients. Before interpreting IVC measurements with regard to fluid
responsiveness on bedside examination, clinicians should confirm normal RV function. In the setting of
RV failure, increased pulse pressure variation likely reflects RV systolic dysfunction exacerbated by
positive ventilation, which can be confirmed by assessing the reduced IVC variation.19
Sepsis and Septic Shock Management
Sepsis and septic shock are extremely widespread and old clinical problems, causing hundreds of
thousands of deaths in the United States each year.6 When RV dysfunction is observed in sepsis, it may
herald worse clinical outcomes.19 Sepsis has several effects on the RV and may have a direct circulating
inflammatory effect that induces myocardial and specifically RV depression in about 30% of patients. The
myocardial depression of sepsis is generally reversible within 14 days in patients who survive; however,
nonsurvivors of sepsis are found to have nonreversible RV failure.6 RV depression may progress to RV
failure in this context when airway pressures are increased secondary to positive pressure ventilation.
Furthermore, when associated with acute respiratory distress syndrome (ARDS), sepsis can cause
abnormally high pulmonary vascular resistance and acute RV failure. It has been suggested that
biventricular failure can be treated with inotropic support, and that isolated RV failure may be treated
with norepinephrine to provide increased aortic pressure and, therefore, adequate coronary perfusion
pressure.17 Serial transthoracic echocardiographic examinations may be useful in determining an adequate
response to these treatment modalities.20
Respiratory Illness and RV Function

ARDS can cause acute cor pulmonale in the setting of hypoxia and hypotension. The effects of positive
pressure ventilation on the RV can be monitored using transthoracic echocardiography to guide ventilator
strategy.19 In ARDS, the pulmonary vasculature undergoes pressure changes as a result of hypoxic
pulmonary vasoconstriction. Positive pressure ventilation has variable effects on pulmonary vascular
resistance (PVR). If the lungs are hyperinflated, PVR is increased with the risk of RV failure from acute
cor pulmonale. However, positive end-expiratory pressure can also cause decreased PVR if it reverses
hypoxic vasoconstriction (HPV).21 Furthermore, once patients are recovering from ARDS, RV dysfunction
can limit ventilator weaning because of diminished oxygen delivery capacity.22
Ventilator weaning and ARDS are not the only contexts in which respiratory diseases can have a negative
impact on the RV. Obstructive diseases such as asthma and chronic obstructive pulmonary disease can
also have a negative impact on RV function. In asthma exacerbations, patients can develop hyperinflation
with retained air causing direct compression of the heart, as well as a decrease in venous return, preload,
and stroke volume. During forceful inhalations, large decreases in intrathoracic pressure can variably
increase venous return and cause RV volume overload. In this setting, systemic pressure drops
disproportionately (>10 mm Hg) during inhalation (pulsus paradoxus).23 Patients with obstructive lung
disease can develop auto–positive end-expiratory pressure, which causes elevated PVR and worsens RV
stroke volume because of elevated RV afterload.24 On bedside echocardiography in the acute setting, RV
EF will drop. However, for patients with long-standing lung disease, such as chronic obstructive
pulmonary disease, the findings on bedside echocardiography will more likely be evidence of long-
standing pulmonary hypertension with abnormally elevated RV diameters, elevated RV pressures, and
depressed EF.25
Pulmonary, Fat, and Gas Emboli

In critical care, use of bedside echocardiography to assist with the diagnosis and treatment of acute
pulmonary embolism has been an area of frequent study. Early identification of RV compromise is
essential because of the high mortality rate from acute RV failure.26 Patients with massive pulmonary
embolisms commonly develop acute cor pulmonale.17 Initially, the McConnell sign (severe RV free-wall
hypokinesis with an intact apex) was touted as having a high specificity for pulmonary embolism;
however, more recent studies have shown that the McConnell sign is not unique to pulmonary embolism.27
Use of the RV FAC has been found to be an independent predictor of heart failure and death in patients
with massive pulmonary embolism; therefore, bedside echocardiography can be extremely useful for
prognostication. The TAPSE technique is thought to be less reliable in the setting of acute pulmonary
embolism because of the often regional nature of the RV failure in this setting, in which a regional
functional measure may overestimate RV function.11 Also, in about 15% of massive pulmonary
embolisms, right heart emboli with extension into the RV (usually starting in the right atrium) may be seen
on bedside echocardiography. 28
In the setting of a pulmonary embolism, a downward spiral of events can lead to RV compromise. The
embolism can cause an increase in pulmonary vasculature impedance, which will compromise RV stroke
volume if great enough. Tachycardia can initially serve as a compensatory mechanism. In time, the
mobilized preload reserve will cause an increase in RV pressure in which RV wall stress will increase,
RV oxygen supply will decrease, and possible subsequent RV ischemia follows. Vasoconstrictors may be
helpful in restoring aortic pressure and increase coronary perfusion. Increasing RV preload can cause a
resultant drop in RV function and cardiac output.28
Once a diagnosis of massive pulmonary embolism with cardiogenic shock has been made, thrombolytic
therapy is considered the best treatment. In PE with RV dysfunction but no systemic hypotension, the role
of thrombolytic therapy remains unclear, with a recent meta-analysis suggesting potential mortality
benefit. Serial examinations can help determine if the RV function is worsening over time and may help
guide treatment. If bedside echocardiography shows no evidence of RV dysfunction in the
hemodynamically stable patient, then use of thrombolytic therapy is at the clinician’s discretion, but
generally not recommended.26,29-31
In addition to pulmonary thrombotic emboli, venous gas emboli and fat emboli can also pose significant
challenges to RV integrity. Usually less than 50 mL of gas injected into the systemic venous system can
cause an abrupt increase of PVR with RV EF reduction and potential systemic cardiovascular
collapse.32,33
Postpartum ARDS and cor pulmonale from amniotic fluid “emboli” may also contribute to RV
dysfunction. This entity is most likely a misnomer for what is now thought to be an anaphylactoid or
hypersensitivity reaction to amniotic fluid entering the maternal bloodstream, causing an acute increase in
PVR and respiratory distress in addition to disseminated intravascular coagulation, confusion, and even
seizures. Bedside echocardiography will demonstrate RV volume/pressure overload, but the clinical
constellation should be carefully weighed, because an acute pulmonary embolism in this patient
population remains high in the differential, as does sepsis from chorioamnionitis.34
E X P E RT T I P
Remember to maintain a broad differential diagnosis when bedside clinical exam shows
evidence of RV dysfunction, including both chronic and acute causes.
Myocardial Infarction and Cardiac Arrest

On bedside echography, a myocardial infarction involving RV territory can demonstrate worsening RV
function. An RV infarct will appear different from acute cor pulmonale in that there will likely be regional
(rather than global) wall motion abnormalities, and pulmonary arterial pressure is less likely to be
elevated. A myocardial infarction involving the RV can have a different appearance on bedside
echocardiography depending on the artery involved. If the proximal right coronary artery (proximal to the
marginal branches) is involved, then hypokinesis is present in the lateral and inferior wall. In infarcts of
the posterior descending artery, hypokinesis is seen in the inferior segments. In lesions affecting the left
anterior descending artery, RV anterior wall hypokinesis is most commonly seen. Patients with LV
dysfunction related to myocardial infarction can develop concomitant RV dysfunction. RV dysfunction is
one of the best predictors of outcome for myocardial infarctions regardless of whether the RV dysfunction
resulted from an infarction. As with other clinical scenarios in which regional wall motion abnormalities
are likely to be present, RV FAC is preferred over TAPSE to assess RV function, because TAPSE may
underestimate the degree of RV compromise.11Clinicians also should be mindful that RV function may be
depressed secondary to a localized pericardial effusion, and the usual clinical signs of tamponade, such
as a pulsus paradoxus, will be absent.35
In pulseless electrical activity arrests, bedside echocardiography has also been proposed as a useful tool
to assist in rapid diagnosis. A focused examination can help in the diagnosis of cardiac tamponade and
pulmonary embolism. Notably, 5% of cardiac arrests may be the result of pulmonary emboli and are
commonly associated with significant RV enlargement of more than 25 mm when seen on bedside
transthoracic echocardiography.36
Chronic Pulmonary Hypertension

Chronic pulmonary hypertension is a common problem in patient presentations to critical care units. Using
bedside echocardiography to understand the hemodynamic status of such patients can be extremely helpful
because depression of RV function is a poor prognostic indicator.2,37 Echocardiographic signs of chronic
pulmonary hypertension also include increased RV wall thickness.10 Another sign of primary pulmonary
hypertension is isolated RV pressure overload, indicated by septal flattening throughout the cardiac cycle,
with the exception of LV end-systole in the parasternal short-axis view.11 In the setting of pulmonary
hypertension, FAC or TAPSE is useful to estimate RV function.37 A special consideration in this group of
patients is the increased propensity to develop fluid overload and worsening RV function or failure.
Frequent bedside echocardiographic monitoring of the RV in this setting can be an excellent clinical tool
to guide management.37
C AVE AT
Remember that TAPSE is not a good approximation of RV function in the setting of regional RV
wall motion abnormalities.
In conclusion, this chapter has demonstrated that bedside evaluation of the RV using echocardiography can
be useful in many common clinical scenarios in the care of critically ill patients. RV morphology is unique
and complex, which has historically made understanding its physiologic and pathologic implications
elusive. Using the skills presented in this chapter, clinicians should have an armamentarium of expeditious
bedside evaluation tools to illuminate the differential diagnosis, clues to chronicity, potential treatment
strategies, and insight into patient prognosis.
KEY POINTS
RV morphology can be assessed using multiple methods: RV morphology, wall thickness, and
RV:LV ratio.
RV function can be assessed at the bedside using FAC or TAPSE methodology.
RV pressure and volume overload can be detected in the short-axis view by flattening of the
intraventricular septum.
RV dysfunction can occur acutely or chronically, from multiple pathologies.
REFERENCES
1. Haddad F, Hunt SA, Rosenthal DN, Murphy DJ. Right ventricular function in cardiovascular disease: I, anatomy, physiology, aging, and
functional assessment of the right ventricle. Circulation. 2008;117:1436-1448.
2. Sheehan F, Redington A. The right ventricle: anatomy, physiology and clinical imaging. Heart. 2008;94:1510-1515.
3. Ten Wolde M, Söhne M, Quak E, MacGillavry MR, Buller HR. Prognostic value of echocardiographically assessed right ventricular
dysfunction in patients with pulmonary embolism. Arch Intern Med. 2014;164:1685-1689.
4. Strumpher J, Jacobsohn E. Pulmonary hypertension and right ventricular dysfunction: physiology and perioperative management. J
Cardiothorac Vasc Anesth. 2011;25:687-704.
5. Hoeper M, Granton J. Intensive care unit management of patients with severe pulmonary hypertension and right heart failure. Am J Respir
Crit Care Med. 2011;184:1114-1124.
6. Court O, Kumar A, Parrillo J, Kumar A. Clinical review: myocardial depression in sepsis and septic shock. Crit Care. 2002;6:500-508.
7. Ho SY, Nihoyannopoulos P. Anatomy, echocardiography, and normal right ventricular dimensions. Heart. 2006;92(suppl 1C):i2-i13.
8. Damiano RJ, La Follette P, Cox JL, Lowe JE, Santamore WP. Significant left ventricular contribution to right ventricular systolic function.
Am J Physiol. 1991;261:H1514-H1524.
9. Shaver JA, Nadolny RA, O’Toole JD, et al. Sound pressure correlates of the second heart sound: an intracardiac sound study. Circulation.
1974;49:316-325.
10. Horton KD, Meece RW, Hill JC. Assessment of the right ventricle by echocardiography: a primer for cardiac sonographers. J Am Soc
11. Rudski LG, Lai WW, Afilalo J, et al. Guidelines for the echocardiographic assessment of the right heart in adults: a report from the
American Society of Echocardiography endorsed by the European Association of Echocardiography, a registered branch of the European
Society of Cardiology, and the Canadian Society of Echocardiography. J Am Soc Echocardiogr. 2010;23:685-788.
12. Jurcut R, Giusca S, La Gerche A, Vasile S, Ginghina C, Voigt JU. The echocardiographic assessment of the right ventricle: what to do in
2010? Eur J Echocardiogr. 2010;11:81-96.
13. Anavekar NS, Gerson D, Skali H, Kwong RY, Yucel EK, Solomon SD. Two-dimensional assessment of right ventricular function: an
echocardiographic-MRI correlative study. Echocardiography. 2007;24:452-456.
14. Sade LE, Gülmez O, Ozyer U, Ozgül E, Ağildere M, Müderrisoğlu H. Tissue Doppler study of the right ventricle with a multisegmental
approach: comparison with cardiac magnetic resonance imaging. J Am Soc Echocardiogr. 2009;22:361-368.
15. Louie EK, Rich S, Levitsky S, Brundage BH. Doppler echocardiographic demonstration of the differential effects of right ventricular
pressure and volume overload on left ventricular geometry and filling. J Am Coll Cardiol. 1992;19:84-90.
16. Ryan T, Petrovic O, Dillon JC, Feigenbaum H, Conley MJ, Armstrong WF. An echocardiographic index for separation of right ventricular
volume and pressure overload. J Am Coll Cardiol. 1985;5:918-927.
17. Jardin F, Vieillard-Baron A. Monitoring of right-sided heart function. Curr Opin Crit Care. 2005;11:271-279.
18. Bleeker GB, Steendijk P, Holman ER, et al. Acquired right ventricular dysfunction. Heart. 2006;92(suppl 1):i14-i18.
19. Vignon P. Hemodynamic assessment of critically ill patients using echocardiography Doppler. Curr Opin Crit Care. 2005;11:227-234.
20. Le Tulzo Y, Seguin P, Gacouin A, et al. Effects of epinephrine on right ventricular function in patients with severe septic shock and right
ventricular failure: a preliminary descriptive study. Intensive Care Med. 1997;23:664-670.
21. Pinsky MR. Cardiovascular issues in respiratory care. Chest. 2005;128(5 suppl 2):592S-597S.
22. Teixeira C, da Silva NB, Savi A, et al. Central venous saturation is a predictor of reintubation in difficult-to-wean patients. Crit Care Med.
2010;38:491-496.
23. Mannam P, Siegel MD. Analytic review: management of life-threatening asthma in adults. J Intensive Care Med. 2014;25:3-15.
24. Mughal MM, Culver DA, Minai OA, Arroliga AC. Auto-positive end-expiratory pressure: mechanisms and treatment. Cleve Clin J Med.
2005;72:801-809.
25. Grichnik KP, Hill SE. The perioperative management of patients with severe emphysema. J Cardiothorac Vasc Anesth. 2003;17:364-387.
26. Tapson V. Acute pulmonary embolism. N Engl J Med. 2008;358:1037-1052.
27. Casazza F, Bongarzoni A, Capozi A, et al. Regional right ventricular dysfunction in acute pulmonary embolism and right ventricular
infarction. Eur J Echocardiogr. 2005;6:11-14.
28. Wood KE. Major pulmonary embolism: review of a pathophysiologic approach to the golden hour of hemodynamically significant pulmonary
embolism. Chest. 2002;121:877-905.
29. Kucher N, Boekstegers P, Müller OJ, et al. Randomized, controlled trial of ultrasound-assisted catheter-directed thrombolysis for acute
intermediate-risk pulmonary embolism. Circulation. 2014;129:479-486.
30. Chatterjee S, Chakraborty A, Weinberg I, et al. Thrombolysis for pulmonary embolism and risk of all-cause mortality, major bleeding, and
intracranial hemorrhage: a meta-analysis. JAMA. 2014;311:2414-2421.
31. Meyer G, Vicaut E, Danays T, et al. Fibrinolysis for patients with intermediate-risk pulmonary embolism. N Engl J Med. 2014;370:1402-
1411.
32. Muth C, Shank E. Gas embolism. N Engl J Med. 2000;342:476-482.
33. Akhtar S. Fat embolism. Anesthesiol Clin. 2009;27:533- 550.
34. Neligan PJ, Laff JG. Clinical review: special populations—critical illness and pregnancy. Crit Care. 2011;15:1-10.
35. Spodick DH. Acute cardiac tamponade. N Engl J Med. 2003;349:684-690.
36. Hernandez C, Shuler K, Hannan H, Sonyika C, Likourezos A, Marshall J. C.A.U.S.E.: Cardiac arrest ultra-sound exam—a better
approach to managing patients in primary nonarrhythmogenic cardiac arrest. Resuscitation. 2008;76:198-206.
37. Price LC, Wort SJ, Finney SJ, Marino PS, Brett SJ. Pulmonary vascular and right ventricular dysfunction in adult critical care: current and
emerging options for management—a systematic literature review. Crit Care. 2010;14:R169.
Chapter 6
Volume Expansion and Fluid Responsiveness
Xavier Monnet, MD, PhD; Jean-Louis Teboul, MD,
PhD
OBJECTIVES
Explain the concept of fluid responsiveness and emphasize its importance for clinical practice
Review available echocardiographic methods for detecting fluid responsiveness
Detail the advantages and limitations of echocardiographic evaluation of fluid responsiveness
INTRODUCTION
Predicting whether volume expansion will result in a significant increase in cardiac output is one of the
major practical management issues for patients with acute circulatory failure. Many studies have shown
that only 50% of hemodynamically unstable patients respond to volume expansion,1 and the risks of
excessive fluid administration are clearly established, especially in patients with sepsis and acute
respiratory distress syndrome (ARDS).2
It is now well demonstrated that static measurements (such as central venous pressure) of cardiac preload
do not reliably predict the response of cardiac output to volume expansion. In contrast, fluid
responsiveness can be predicted when dynamic changes in cardiac preload induce significant changes in
cardiac output or surrogates. For this purpose, many functional indices have been developed in recent
years. In this chapter, we summarize echocardiographic indices of fluid responsiveness.
CASE STUDY
Mrs. T. was a 68-year-old woman who was admitted to the ICU with septic shock and community-
acquired pneumonia. Upon admission, she presented with hemodynamic failure (arterial pressure: 80/40
mm Hg, anuria, hyperlactatemia) and respiratory failure (Pao2/Fio2 ratio: 110 mm Hg under Fio2 = 100%
under mechanical ventilation, bilateral infiltrates on chest radiograph). Before admission to the ICU, the
patient had already received 2,000 mL of saline and was receiving norepinephrine (1.2 mg/h). A few
minutes after admission, the dose of norepinephrine was increased to 2 mg/h. This was motivated by the
low diastolic pressure, indicating a strong vasodilation. Her blood pressure increased to 90/50 mm Hg.
Why Was Echocardiography Performed at This Stage?

Echocardiography was performed with 2 goals. The first was to evaluate cardiac function. Even though
the septic origin of shock was clear, it was necessary to evaluate cardiac function. In particular, the
systolic function of the left ventricle could have been altered because of either a previous cardiopathy or
a sepsis-related cardiac dysfunction. The subsequent treatment of the patient would not have been the
same if the contractile function of the left ventricle had been normal or severely depressed.
The second goal was to evaluate fluid responsiveness. In this patient with septic shock, who had already
received a significant amount of fluid, the positive response of cardiac output to fluid administration was
not certain. In addition, the severe impairment of oxygenation because of ARDS indicated that excessive
fluid administration was very risky.
Because no continuous hemodynamic monitoring was in place at this early phase of patient management,
we used echocardiography to assess fluid responsiveness.
How Was Echocardiography Performed? What Did It Show?

We performed transthoracic echocardiography through the apical window. The visual estimation of the
left ventricular ejection fraction was normal. We measured the velocity time-integral (VTI) of the left
ventricular outflow tract (LVOT) before and during a passive leg raising (PLR) test. It increased from 16
to 20 cm, that is, by 25%. This is far above the diagnostic cutoff that must be considered as positive for
the PLR-induced changes in cardiac output (10%). Then, we administered volume expansion. It increased
the LVOT VTI to 21 cm and the arterial pressure to 110/52 mm Hg.
This case illustrates how echocardiography can be used to assess fluid responsiveness before
administering volume expansion in patients in whom fluid overload is deleterious, especially at a phase
of management when continuous monitoring of cardiac output is not already in place.
CONCEPT OF FLUID RESPONSIVENESS

In a patient with acute circulatory failure, volume expansion is administered to increase cardiac output by
increasing cardiac preload. Such a response occurs only when stroke volume is dependent on cardiac
preload. However, preload dependence is not constant: the Frank-Starling relationship between stroke
volume and cardiac preload is not linear (Figure 6-1).
Figure 6-1. Frank-Starling Relationship
Abbreviations: EEO, end-expiratory occlusion test; PLR, passive leg raising.
The slope of the relationship between cardiac preload and stroke volume depends on the ventricular function. Challenging preload and
observing the resulting effects on stroke volume (or surrogates) enables assessment of the degree of fluid responsiveness.
An increase in cardiac preload can result in a significant increase in cardiac output only if the heart is
operating on the initial steep part of the curve. Ventricular function also influences the degree of fluid
responsiveness. Indeed, the Frank-Starling curve has the steepest slope when ventricular function is
preserved (Figure 6-1). The Frank-Starling relationship applies both to the left and right ventricles. Thus,
volume expansion induces a significant increase in stroke volume only if both ventricles are in a preload-
dependent state.
INDICES FOR DETECTING FLUID RESPONSIVENESS

Volume expansion may not lead to a significant increase in cardiac output and may induce deleterious
effects, therefore, it should be performed only when it has a reasonable probability of having the desired
effect.
Context of Occurrence of Circulatory Failure

To predict fluid responsiveness, the first simple criterion to consider is the clinical context of circulatory
failure (Figure 6-2). For example, fluid responsiveness is extremely likely in a patient with unresuscitated
hemorrhagic shock. Similarly, in the initial, unresuscitated phase of septic shock, arterial and venous
vasodilation create a relative hypovolemia that is almost always fluid responsive.
However, when the cause of shock is less clear, and/or after initial resuscitation, cardiac preload
dependence cannot be easily predicted. The decision to perform volume expansion must be based on
hemodynamic criteria that predict its efficacy (Figure 6-2). These criteria are of 2 types: static, based on
a simple measure of cardiac preload, and dynamic, based on observations of the effects of a change in
preload. 1,2 In this chapter, we describe the echocardiographic measures relevant to this question.
Static Ultrasound Indices of Cardiac Preload

It is now clearly demonstrated by a large number of studies and a meta-analysis that no static measure of
cardiac preload reliably predicts the response of stroke volume to volume expansion.2 Echocardiographic
preload indices include the left end-diastolic volume and area, the ratio of peak velocities of E and A
waves of mitral flow, the ratio of the peak velocity of the E wave of mitral flow and the E´ (or Ea) wave
of the mitral annulus on tissue Doppler, and the ratio of the E wave of mitral flow and velocity of left
ventricular filling (Vp). Although these echocardiographic indices correctly estimate left ventricular
preload, they do not identify which patients are preload dependent.
This fact is primarily explained by simple observation of the Frank-Starling relationship (Figure 6-1). A
given level of cardiac preload can be associated with either preload dependence (steep portion of the
Frank-Starling curve) or preload independence (flat portion of the relationship). Therefore, only very low
values of static preload indices (eg, end-diastolic left ventricular area below 5 cm2/m2) reliably predict
the response of cardiac output to volume expansion.
In this respect, ultrasound indices of preload do not differ from other static indicators of cardiac preload,
such as central venous pressure, pulmonary artery occlusion pressure, ventricular ejection time measured
by the esophageal Doppler, or the global end-diastolic volume measured by transpulmonary
thermodilution; none of these static preload indices reliably predict fluid responsiveness.1,2
Figure 6-2. Decisional Algorithm for the Prediction of Fluid Responsiveness
Abbreviations: ARDS, acute respiratory distress syndrome; IVC, inferior vena cava; SVC, superior vena cava.
Respiratory Variability in Stroke Volume

Given the limits of static markers of cardiac preload, other indices have been developed for predicting
volume responsiveness. These indices afford a functional investigation of the Frank-Starling relationship
(Figure 6-2). The first functional indices of preload dependence that were developed are based on the
effects of positive pressure mechanical ventilation on cardiac preload.
Physiologic Principle
Under positive pressure ventilation, each respiratory cycle induces changes in the right atrial pressure,
which is the backward pressure for venous return. The subsequent variation in right atrial pressure results
in more variation of stroke volume if the right ventricle is operating on the rising portion rather than on the
plateau of the Frank-Starling curve.2 The volume of blood ejected by the right ventricle at each systole is
the volume of blood that fills the left ventricle—with a lag phase of 2 to 4 heartbeats because of the
transit through the pulmonary circulation. Then the resulting cyclic variation in left ventricular preload
induces a cyclic variation in left ventricular stroke volume if the left ventricle is preload dependent. Thus,
positive pressure mechanical ventilation should induce large fluctuations in the left ventricular stroke
volume if both ventricles are preload dependent. However, if 1 of the 2 ventricles is not preload
dependent, cyclic variations in stroke volume will have low or zero amplitude.2
Application to Cardiac Ultrasound
Echocardiography estimates the left ventricular stroke volume by analyzing its ejection flow. When the
sampling window of pulsed Doppler is placed in the outflow track of the left ventricle, it measures the
average red blood cell velocity during each systole. The integral of this signal vs. time (VTI) is
proportional to stroke volume (it is the height of a cylinder of blood whose cross-sectional area is that of
the LVOT).
This beat-to-beat measure allows the assessment of the cyclic effects of mechanical ventilation on stroke
volume. Because peak velocity is proportional to the VTI, variability in stroke volume can be assessed
simply by measuring changes in aortic peak velocity (rather than VTI itself) (Figure 6-3). In patients with
acute circulatory failure, it has been shown that when the aortic peak velocity, as measured with
transesophageal echocardiography, was greater than 12%, cardiac output reliably increased after volume
expansion.3
Limitations of Use
The primary limitation to the use of respiratory variation of LVOT velocity is inherent in the ultrasound
technique. In particular, it is sometimes difficult to keep the Doppler sample window in the LVOT during
breathing movements, especially if rapid and large. The risk is of attributing respiratory variations of
LVOT flow to the hemodynamic effects of ventilation when they are simply caused by the motion of the
ultrasound beam away from the blood flow.
Moreover, this method shares the limitations of all indices based on respiratory variation in stroke
volume. It cannot be used in cases of cardiac arrhythmias or spontaneous ventilation (even in patients
receiving mechanical intubation) (Figure 6-2). For this technique to be accurate, patients must be
paralyzed or deeply sedated; such patients are becoming less common in contemporary critical care
environments given a rising focus on early mobility and patient wakefulness. Indeed, in such cases,
changes in stroke volume primarily reflect the irregularities of the cardiac or respiratory cycles rather
than preload dependence. This is true for the variation of the LVOT velocity as well as of any other
surrogate for stroke volume, such as arterial pulse pressure.2,4
Figure 6-3. Doppler Trace of the Left Ventricular Outflow Tract
Typical Doppler trace of the left ventricular outflow tract (LVOT) blood flow in a patient who responds to fluid administration by a significant
increase in cardiac output. The respiratory variation of the LVOT blood velocity (ΔVpeakAo) is decreased by volume expansion.
Moreover, when tidal volume is low5 and/or when respiratory compliance6 is low, as during ARDS,
changes in right ventricular preload induced by mechanical ventilation might be too low to generate
significant variations of stroke volume, even if the patient is preload dependent (Figure 6-2).6
Finally, when the thorax and/or the pericardium are open, respiratory variability indices may not reliably
predict response to volume expansion.2
Respiratory Variability in the Diameter of the Venae Cavae

The use of respiratory variability of the venae cavae to predict fluid responsiveness is based on the
principle that the diameter of the venae cavae depends on the intramural pressure (which itself depends
on the circulating blood volume) and the extramural pressure (intra-abdominal pressure for the inferior
vena cava, intrathoracic pressure for the superior vena cava). Significant respiratory changes in the
diameter of the venae cavae indicate that positive pressure ventilation affects systemic venous return,
suggesting preload dependence.
E X P E RT T I P
When the variation of vena cava diameter is important, simple visual estimation is sufficient
and measurement is not required.
Respiratory Variability of the Inferior Vena Cava

The variations in the diameter of the inferior vena cava are easily measured with transthoracic
echocardiography (Figure 6-4). In the subcostal window, the vessel can be seen on 2-dimensional
ultrasonography within the liver, upstream of its drainage into the right atrium. Motion mode, with the
cursor through the inferior vena cava about 1 to 2 cm upstream of the cavoatrial junction, allows accurate
measurement of the diameter of the inferior vena cava over time, enabling straightforward calculation of
respiratory variability (Figure 6-2).
Two studies have shown that, in patients receiving mechanical ventilation, respiratory variations in the
diameter of the inferior vena cava were higher in responders than in nonresponders to volume
expansion.7,8 The variation can be calculated as ([maximum diameter – minimum diameter] / maximum
diameter) or ([maximum diameter – minimum diameter] / mean of maximum and minimum diameters). If
the diameter of the vein varies significantly with mechanical ventilation, fluid responsiveness is likely.7,8
Early evidence suggests that inferior vena cava collapsibility may be useful in spontaneously breathing
patients, albeit with different thresholds than for patients passively receiving mechanical ventilation.9
Figure 6-4. M-Mode Trace of the Inferior Vena Cava
Typical M-mode trace of the inferior vena cava in a fluid responder. Volume expansion annuls the respiratory variation of the vena cava
diameter.
If the inferior vena cava cannot be seen through the subcostal view, it is possible to find it through the
liver by placing the probe on the right side of the thorax.
Respiratory Collapsibility of the Superior Vena Cava

For the superior vena cava, the diagnostic value of respiratory variability was reported in a study in
patients who have acute circulatory failure and are receiving mechanical ventilation.10 The response to
volume expansion was more likely when the superior vena cava collapsibility index ([maximum diameter
– minimum diameter] / maximum diameter) was greater than 36%.10 Notably, intermediate values of
superior vena cava collapsibility were rarely observed in this study: values clustered at very high or very
low collapsibility.
Limitations of Use
In some critically ill patients with poor subcostal windows (especially from obesity, recent abdominal
surgery, or bowel obstruction), the inferior vena cava may be difficult to image. Superior vena cava
collapsibility can only be measured with transesophageal echocardiography, which requires special
expertise; serial measurements may be difficult to achieve.10
Unlike the respiratory variability of aortic velocity, respiratory variability of diameter of the venae cavae
can be used in patients with cardiac arrhythmias. In contrast, as with the variability of the LVOT velocity,
it is invalid in the case of spontaneous breathing (Figure 6-2). The influence of tidal volume (and lung
compliance) on the diagnostic reliability of venae cavae variability in patients with ARDS has not been
tested but is likely. Finally, experts believe that intra-abdominal hypertension invalidates inferior vena
cava variability measurements, but this has not been formally established.
The Passive Leg Raising Test

In cases in which respiratory variability indices are not valid, the PLR test can be used as an alternative.
The elevation of the lower extremities relative to the horizontal position causes the transfer of a volume
of venous blood into the thorax. This postural maneuver induces a significant increase in right and left
ventricular preload, which can be used to evaluate preload dependence.11 The increase in cardiac preload
induced by PLR does not depend on cardiac rhythm or intrathoracic pressure variations, so PLR is an
alternative to indices based on respiratory variability where they are not valid (Figure 6-2).
Clinical Use
Several studies have demonstrated that a significant increase in stroke volume during PLR predicts fluid
responsiveness with good diagnostic accuracy.11 This is true in patients with cardiac arrhythmias,
spontaneous ventilation, or ARDS.4 A meta-analysis has confirmed the robustness of these findings.12
Multiple studies have measured the effects of the PLR test on LVOT flow assessed with
echocardiography. An increase in the LVOT flow velocity of more than 10% to 15% during PLR predicts
the response to volume expansion with good reliability (Figure 6-5).13-18 The maximal effects of PLR on
cardiac output occur rapidly, within 1 to 2 minutes. After 5 minutes, these effects decrease in some
patients, especially those with severe vasodilation and capillary leak. One study has shown that the
effects of PLR can also be assessed with femoral artery peak velocity, another surrogate of stroke
volume.14 If these results are confirmed by other studies, the femoral artery method would have the
advantage of allowing a simple ultrasound assessment of the PLR test—assessment of LVOT velocity
requires careful attention to probe position and insonation angle.
The specifics of the PLR technique are important to consider. 11 It is better to perform the test starting from
the semirecumbent position (with the trunk inclined at 45°) rather than lying down (with the torso in a
horizontal position) (Figure 6-5). Indeed, in this way, the PLR maneuver allows the mobilization of the
large abdominal venous volume, in addition to the venous blood of the lower limbs. This method
significantly increases the test sensitivity,19 and in our view, is the only one that can ensure that PLR
causes a sufficient increase in cardiac preload to assess preload dependence.
E X P E RT T I P
Performing the PLR test with 2 operators is most convenient. While 1 operator is adjusting the
bed position, the other one carefully keeps the ultrasound beam in the same position in the
LVOT. This allows the operator to be sure that any changes in VTI are related to hemodynamic
changes and not to the change in the angle of insonation.
Figure 6-5. Passive Leg Raising Test
Abbreviation: PLR, passive leg raising; VTI, velocity time integral.
Passive leg raising test assessed on echocardiography. In this fluid responder, the PLR test induces a significant increase in the velocity time
integral of the left ventricular outflow tract blood flow.
E X P E RT T I P
The PLR test must be performed by adjusting the bed position, not by holding and raising the
patient’s heels. Awakening the patient and the pain that it may induce would interfere with the
hemodynamic effects related to changes in cardiac preload.
Limitations of Use
When transthoracic ultrasound is used for PLR, test completion is sometimes hampered by the difficulty in
maintaining the probe stationary relative to the thorax during postural change. Furthermore, it is
reasonable not to use the PLR test in patients with intracranial hypertension. It has been suggested that
intra-abdominal hypertension could create an obstacle to the transfer of blood from the lower limbs
toward the cardiac chambers through the inferior vena cava.20 One study21 suggested that the PLR test was
unreliable in patients with an intra-abdominal pressure higher than 16 mm Hg, but this study did not
measure intra-abdominal pressure during PLR. Thus, this possible limitation of the PLR test needs further
confirmation. Finally, this test often cannot be used during active surgery or unstable pelvic or lower
extremity fractures.
The End-Expiratory Occlusion Test

During mechanical ventilation, inspiration cyclically increases the backward pressure of venous return,
thus reducing the cardiac preload. Stopping mechanical ventilation at end-expiration for a few seconds
interrupts this cyclic reduction: end-expiratory occlusion (EEO) thereby induces a transient increase in
cardiac preload. Observing the resulting effects on stroke volume allows one to assess preload
dependence (Figure 6-2).22 If cardiac output increases by more than 5% during a 15-second EEO, fluid
responsiveness is likely.2 In these studies, the effects of the EEO test were assessed with pulse contour
analysis-derived cardiac output. Whether echocardiography could be used for this purpose, by observing
changes in LVOT blood flow during the EEO test, is likely but remains to be demonstrated. The EEO test
can be used in patients with cardiac arrhythmias and with ARDS, regardless of the level of positive end-
expiratory pressure. It can be used in patients with mild spontaneous breathing activity, provided that the
spontaneous breathing does not interrupt the inspiratory hold.
Fluid Challenge
When no other index is available, it may be best to test fluid responsiveness by administering a small
volume of fluid, observe its effects on cardiac output, and expect that a larger volume expansion will
exert similar effects. This can be performed serially, stopping volume expansion when a small volume
expansion no longer leads to an increase in cardiac output. Importantly, the time for bolus administration
matters—if it is too long, for instance more than 30 minutes, many events could occur during fluid
administration that would make it difficult to attribute the observed hemodynamic changes to the only fluid
challenge. (In general, fluid boluses should be administered within 5-15 minutes.) The question is what
should be considered a “small” volume of fluid.
The disadvantage of usual volume expansion is that it consists of infusing 300 to 1,000 mL of fluid. This
volume is far from negligible. Indeed, performing volume expansion several times a day, as commonly
occurs in early shock, inevitably contributes to fluid overload, which is an independent predictor of
mortality in sepsis23 and ARDS.24
A new method of “mini fluid challenge” has been proposed.25 The effects of 100 mL of colloid on stroke
volume predicted the response of cardiac output to a subsequent 500-mL volume expansion. These
changes in stroke volume were estimated with echocardiography.25 Smaller amounts of fluid have even
been proposed.26,27 Nevertheless, small amounts of fluid can only induce small changes in stroke volume
and cardiac output. Thus, this test requires a precise technique for measuring stroke volume. Whether
echocardiography is precise enough in nonexpert hands is far from certain and, at the very least, requires
further confirmation.
In recent years, several tests have been developed to detect cardiac preload dependence to guide decision
making about volume expansion. These tests enable volume expansion only when it can be reasonably
hoped that it will significantly increase cardiac output. In turn, avoiding unnecessary volume expansion
should decrease harmful volume overload. Many of these tests for preload dependence can be performed
with the help of echocardiography. In particular, ultrasound can be used for assessing respiratory
variation of the velocity of the aortic flow and the diameter of the superior and inferior venae cavae.
Echocardiography can also be used to measure the effects of PLR. Whether EEO and “mini” fluid
challenge are valid and reliable in nonexpert hands is yet to be confirmed. Fluid responsiveness is 1
piece of the puzzle that can be provided by echocardiography during acute circulatory failure.
KEY POINTS
Predicting fluid responsiveness is particularly important in patients with sepsis and ARDS. It
allows clinicians to administer fluid with the certainty that it will induce the expected increase in
cardiac output. It may reduce fluid overload.
Strong evidence demonstrates that static markers of preload do not predict volume responsiveness.
Respiratory variation of the aortic blood flow velocity in passively breathing patients receiving
mechanical ventilation cannot be used in cases of cardiac arrhythmias, spontaneous breathing
activity, and ARDS with low tidal volume and/or low lung compliance.
The respiratory variation of the inferior vena cava and/or the collapsibility of the superior vena
cava indicate fluid responsiveness in patients receiving controlled mechanical ventilation.
Echocardiography can be used to assess the effects of the passive leg raising test. It indicates fluid
responsiveness if the VTI of the aortic blood flow increases by more than 10% to 15%.
REFERENCES
1. Marik PE, Monnet X, Teboul JL. Hemodynamic parameters to guide fluid therapy. Ann Intensive Care. 2011;1:1.
2. Monnet X, Teboul JL. Assessment of volume responsiveness during mechanical ventilation: recent advances. Crit Care. 2013;17:217.
3. Feissel M, Michard F, Mangin I, et al. Respiratory changes in aortic blood velocity as an indicator of fluid responsiveness in ventilated
patients with septic shock. Chest. 2001;119:867-873.
4. Monnet X, Rienzo M, Osman D, et al. Passive leg raising predicts fluid responsiveness in the critically ill. Crit Care Med. 2006;34:1402-
1407.
5. De Backer D, Heenen S, Piagnerelli M, et al. Pulse pressure variations to predict fluid responsiveness: influence of tidal volume. Intensive
Care Med. 2005;31:517-523.
6. Silva S, Jozwiak M, Teboul JL, et al. End-expiratory occlusion test predicts preload responsiveness independently of positive end-expiratory
pressure during acute respiratory distress syndrome. Crit Care Med. 2013;41:1692-1701.
7. Barbier C, Loubieres Y, Schmit C, et al. Respiratory changes in inferior vena cava diameter are helpful in predicting fluid responsiveness in
ventilated septic patients. Intensive Care Med. 2004;30:1740-1746.
8. Feissel M, Michard F, Faller JP, et al. The respiratory variation in inferior vena cava diameter as a guide to fluid therapy. Intensive Care
Med. 2004;30:1834-1837.
9. Lanspa MJ, Grissom CK, Hirshberg EL, et al. Applying dynamic parameters to predict hemodynamic response to volume expansion in
spontaneously breathing patients with septic shock. Shock. 2013;39:155-160.
10. Vieillard-Baron A, Chergui K, Rabiller A, et al. Superior vena caval collapsibility as a gauge of volume status in ventilated septic patients.
Intensive Care Med. 2004;30:1734-1739.
11. Monnet X, Teboul JL. Passive leg raising: five rules, not a drop of fluid! Crit Care. 2015;19:18.
12. Cavallaro F, Sandroni C, Marano C, et al. Diagnostic accuracy of passive leg raising for prediction of fluid responsiveness in adults:
systematic review and meta-analysis of clinical studies. Intensive Care Med. 2010;36:1475-1483.
13. Lamia B, Ochagavia A, Monnet X, et al. Echocardiographic prediction of volume responsiveness in critically ill patients with spontaneously
breathing activity. Intensive Care Med. 2007;33:1125-1132.
14. Preau S, Saulnier F, Dewavrin F, et al. Passive leg raising is predictive of fluid responsiveness in spontaneously breathing patients with
severe sepsis or acute pancreatitis. Crit Care Med. 2010;38:989-990.
15. Maizel J, Airapetian N, Lorne E, et al. Diagnosis of central hypovolemia by using passive leg raising. Intensive Care Med. 2007;33:1133-
1138.
16. Biais M, Vidil L, Sarrabay P, et al. Changes in stroke volume induced by passive leg raising in spontaneously breathing patients: comparison
between echocardiography and Vigileo/FloTrac device. Crit Care. 2009;13:R195.
17. Guinot PG, Zogheib E, Detave M, et al. Passive leg raising can predict fluid responsiveness in patients placed on venovenous
extracorporeal membrane oxygenation. Crit Care. 2011;15:R216.
18. Brun C, Zieleskiewicz L, Textoris J, et al. Prediction of fluid responsiveness in severe preeclamptic patients with oliguria. Intensive Care
Med. 2013;39:593-600.
19. Jabot J, Teboul JL, Richard C, et al. Passive leg raising for predicting fluid responsiveness: importance of the postural change. Intensive
Care Med. 2009;35:85-90.
20. Malbrain ML, Reuter DA. Assessing fluid responsiveness with the passive leg raising maneuver in patients with increased intra-abdominal
pressure: be aware that not all blood returns! Crit Care Med. 2010;38:1912-1915.
21. Mahjoub Y, Touzeau J, Airapetian N, et al. The passive leg-raising maneuver cannot accurately predict fluid responsiveness in patients with
intra-abdominal hypertension. Crit Care Med. 2010;38:1824-1829.
22. Monnet X, Osman D, Ridel C, et al. Predicting volume responsiveness by using the end-expiratory occlusion in mechanically ventilated
intensive care unit patients. Crit Care Med. 2009;37:951-956.
23. Vincent JL, Sakr Y, Sprung CL, et al. Sepsis in European intensive care units: results of the SOAP study. Crit Care Med. 2006;34:344-353.
24. Jozwiak M, Silva S, Persichini R, et al. Extravascular lung water is an independent prognostic factor in patients with acute respiratory
distress syndrome. Crit Care Med. 2013;41:472-480.
25. Muller L, Toumi M, Bousquet PJ, et al. An increase in aortic blood flow after an infusion of 100 ml colloid over 1 minute can predict fluid
responsiveness: the mini-fluid challenge study. Anesthesiology. 2011;115:541-547.
26. Wu Y, Zhou S, Zhou Z, et al. A 10-second fluid challenge guided by transthoracic echocardiography can predict fluid responsiveness. Crit
Care. 2014;18:R108.
27. Guinot PG, Bernard E, Defrancq F, et al. Mini-fluid challenge predicts fluid responsiveness during spontaneous breathing under spinal
anaesthesia: an observational study [published online ahead of print October 14]. Eur J Anaesth. 2015;32:645-649.
Chapter 7
Advanced Cardiac Ultrasound Evaluation
Sasikanth Adigopula, MD; Myriam Amsallem, MD;
Anne-Sophie Beraud, MD
OBJECTIVES
Describe what an advanced cardiology ultrasound can add to a focused examination
Describe the indications for obtaining formal cardiology consultation
Use additional echocardiographic measures to guide treatment in complex patients
Understand the indications of transesophageal echocardiography
Understand the limitations of echocardiographic examinations
INTRODUCTION
The basic echocardiographic techniques for evaluating left ventricular (LV) function were discussed in
Chapter 4. Basic critical care echocardiography focuses on becoming familiar with the standard
quantitative and qualitative assessment of LV size and function and on the echocardiographic principles of
estimating cardiac output (CO). Advanced cardiac ultrasound can enhance the basic evaluation by
identifying pathologic conditions that often require formal cardiology consultation. A more complete
understanding of the application of advanced interpretations and limitations to echocardiography also
maximizes the critical care physician’s communication with the cardiologist. Advanced cardiac
ultrasound principles can therefore serve to reduce the interaction and possible wait time when specialty
consultation is required.
CASE STUDY 1
A 52-year-old man is admitted to the ICU for septic shock, and his blood pressure is 70/30 mm Hg. He is
receiving norepinephrine, and is now started on epinephrine. Despite escalating doses of epinephrine and
norepinephrine, the patient continues to have hypotension. His blood pressure drops further and a quick
bedside cardiac echocardiogram is performed. The parasternal long-axis image is shown in Figure 7-1.
What Is the Most Likely Cause of the Patient’s Worsening Hypotension?

The likely cause of this patient’s hypotension is left ventricular outflow obstructions worsened by
inotropy and chronotropy, as indicated by the thickened intraventricular septum. This patient has
hypertrophic cardiomyopathy with an exceedingly small left ventricle end-diastolic cavity. In addition, the
patient has systolic anterior motion of the mitral leaflet, causing a more severe dynamic left ventricular
outflow tract (LVOT) obstruction. With increasing inotropy, stroke volume (SV) and CO worsen because
of the dynamic obstruction of the LVOT. Switching from epinephrine to phenylephrine decreases the
gradient across the LVOT, increases afterload, and helps SV and CO. This demonstrates in a simple way
how a quick bedside echocardiogram and a higher level of understanding echocardiography can be
diagnostic and guide therapy in the management of complex ICU cases.
CASE STUDY 2
A 53-year-old man was admitted to the critical care unit for routine postoperative care after coronary
artery bypass graft surgery. Twelve hours after surgery, he was found to be hypotensive with his systolic
blood pressure in the 70s. A quick bedside transthoracic echocardiography (TTE) was performed. The
subcostal view is shown in Figure 7-2.
Figure 7-1. Case Study 1 Parasternal Long-axis View

Red arrow indicates a thickened intraventricular septum. Red star shows systolic anterior motion of the mitral leaflet.
Figure 7-2. Case Study 2 Subcostal View
Abbreviations: RA, right artium; LA, left atrium; RV, right ventricle.
Red asterisk indicates thick, heterogenous, echodense blood clot.
What Is the Most Likely Cause of the Patient’s Hypotension?

The subcostal view shows a thick, heterogenous, echodense blood clot compressing the free wall of the
right ventricle (RV) below the liver, explaining the hypotension. This echocardiographic appearance is
different from the common dark, anechoic, homogenous appearance (resembling the echocardiographic
appearance of blood in the cardiac chambers) of pericardial effusion causing tamponade.
Worsening hemodynamics in a patient after cardiac surgery can be indicative of a new potential life-
threatening complication. In this case, the pericardiac hematoma causing tamponade physiology was
quickly noted on the TTE and the patient was taken to the operating room for surgical evacuation.
INDICATIONS FOR FORMAL CARDIAC CONSULTATION

An initial echocardiographic evaluation of a patient can provide useful information for both diagnostic
and therapeutic processes. Although there are numerous situations in which formal cardiac consultation in
echocardiography is helpful, some of the common indications for formal cardiology consultation in the
ICU are listed below.
Acute chest pain syndrome

Discussion of diastology when evaluation is technically difficult
Moderate to severe valvular pathology
History of prosthetic heart valves
History of congenital heart disease
Suspicion of infective endocarditis (IE)
Lack of correlation between echocardiographic findings and clinical presentation
Pregnancy
Acute Chest Pain

Evaluation of a patient with acute chest pain includes the following:
New regional wall motion abnormalities (RWMAs), suggesting acute myocardial infarction
New severe mitral regurgitation, indicating a possible acute large myocardial infarction
Aneurysm of the thoracic aorta, new severe aortic regurgitation, which suggests possible aortic
dissection
Suspicion of Acute Coronary Syndrome

Under most medical ICU scenarios, determining the overall basic function of the LV and RV is sufficient
to help guide management. However, when patients develop chest pain or when troponin levels rise and
acute coronary syndrome is suspected, advanced echocardiographic techniques can be very helpful based
on a careful evaluation for RWMA.1 RWMA occurs within the first 30 minutes of acute coronary
syndrome and has high sensitivity and specificity.2,3 RWMA can also be seen in conditions not related to
coronary artery disease, including the presence of a bundle branch block and dyssynchrony caused by
pacemakers. New RWMA helps the astute clinician to distinguish between the first set of mildly elevated
troponins from a suspected acute coronary syndrome and a troponin leak from increased myocardial
demand.
Figure 7-3. Parasternal Short-axis View of LV in
Patient with Myocardial Infarction
Figure 7-4. Parasternal Long-axis View of LV in

Patient with Aortic Dissection
Figure 7-3, taken in end-systole, shows the thinned and ballooned anteroseptal wall of the LV compared
with the normal lateral and inferior walls. There are a total of 17 LV wall segments including the apical
cap. The different walls and segments of the LV are seen in different views, including the parasternal
long-axis, apical 4-chamber, and apical 2-chamber views. When evaluating for RWMA, remember to
look for both systolic wall motion and endocardial thickening of each segment of the LV wall in the
shortand long-axis views. The wall segments are graded as normal, hypokinetic, akinetic, dyskinetic, or
aneurysmal (Table 7-1).
Table 7-1. Systolic Wall Motion and Endocardial Thickening of LV Wall Segments
Systolic Wall Motion Endocardial Thickening
Normal Normal Normal (>30%)
Hypokinesia Reduced Reduced (<30%)
Akinesia Absent Absent
Dyskinesia Outward Thinning
Aneurysmal Outward Absent and thinning
Suspicion of Aortic Dissection

Aortic dissection is an emergent situation in which each minute to diagnosis and treatment can be very
crucial. Although transesophageal echocardiography (TEE) is highly sensitive and specific (>95%) for a
diagnosis of aortic dissection, a quick TTE can be very helpful too.4 TTE has a specificity of more than
95% and a sensitivity of only about 50% to 60%.5,6 Still, if the TEE setup is in place and ready to go, do
not delay any further by performing a TTE.
When viewing the ascending aorta using TTE, the left parasternal long-axis view is best. When viewing
the aortic arch, it is best to image the suprasternal notch (Figure 7-4). The quick 4-step approach to
identifying aortic dissection using TTE would be to first quickly look at the aortic root, second look at the
aortic valve, and third look for the flap and true and false lumen,7 as follows:
Step 1: Aortic root – The first thing that is usually prominent is a dilated aortic root. It is usually more
than 4.2 cm, while a normal aortic root is 3 to 4 cm.
Step 2: Aortic valve – Look for aortic regurgitation, aortic valve cusp prolapse, midsystolic closure of
the aortic valve, and diastolic fluttering motion of the mitral valve (MV) (secondary to the aortic
regurgitation jet on the MV).
Step 3: Aortic flap – The tear in the aortic intima leads to blood entering the media. This is the false
lumen. The flap appears as a thin mobile, linear structure. The true lumen expands in systole.
Step 4: Look for associated abnormalities including pericardial effusion and possible tamponade, left-
sided pleural effusion, LV RWMA because of extension of the aortic dissection that involves the
coronary arteries, and compression of the left atrium (LA) by the expanding aorta.
Using contrast agents usually enhances visualization of endocardium and helps to better appreciate
segmental wall motion abnormalities.
Advanced Evaluation of Diastolic Function
A detailed description of evaluating LV and RV diastolic function is discussed in Chapter 8. Here we will
focus on technically difficult scenarios and some advanced concepts. At certain times in an ICU, the LV
“squeezing function” seems appropriate but the patient has dyspnea and it is unclear whether the etiology
is primarily a cardiac or pulmonary process. When patients present with multiple complex medical
issues, it may be beneficial for the intensivist to have additional skills in echocardiography to evaluate LV
and RV diastolic function. For the intensivist, diastology represents a noninvasive evaluation of LA
pressure. Fundamentally, diastology measures the pressures between the LV and LA chambers. Recall that
clinical scenarios other than diastolic dysfunction, like mitral stenosis, can affect the measured pressure
gradient between the 2 chambers (Table 7-2).
Table 7-2. Etiologies of Diastolic Dysfunction in an ICU
Systolic dysfunction
Hypertension
Coronary artery disease
Hypertrophic cardiomyopathy
Restrictive cardiomyopathy
Constrictive pericarditis
Valvular disease (mitral regurgitation, tricuspid regurgitation, aortic stenosis)
Tachycardia-induced cardiomyopathy
Septic cardiomyopathy
The severity of diastolic dysfunction is generally graded as follows:
Mild (grade I): Impaired relaxation

Moderate (grade II): Pseudonormalization
Severe (grade III): Restrictive filling pattern
In the ICU setting, the impaired relaxation phase of diastolic dysfunction is not clinically significant
because the LA pressure is grossly normal (Figure 7-5). Hence, in this chapter, we will concentrate on the
moderate and severe diastolic dysfunction – pseudonormal and restrictive filling patterns.
Figure 7-5. Grades of Diastolic Dysfunction
Abbreviation: LAP, left atrial pressure.
3 Steps in Evaluating Diastology

Step 1: Pulsed-Wave Doppler of Mitral Inflow. In the apical 4-chamber view, place the pulsed-wave
Doppler sample volume 1-3 mm between the mitral leaflet tips. Obtain measurements at end expiration
(to reduce variation induced with respirations) and calculate the average of 3 consecutive cardiac cycles.
The peak early filling velocity (E) and late diastolic filling velocity (A) are measured and E/A ratio is
calculated. The E wave reflects the pressure gradient between the LV and LA during early diastole, and
the A wave reflects the pressure gradient between the LV and LA during late diastole.8 In normal diastolic
function, E is greater than A and the ratio is 1 to 1.5. As ventricular compliance starts to decrease, the E
wave gets smaller than the A wave (impaired relaxation phase). As the LA pressure increases with
continued decreased ventricular compliance, the E wave is again bigger than the A wave (pseudonormal
phase). This occurs until the LA pressure steeply increases to the point where the inflow velocity is
characterized by high E wave velocity and small A wave velocity, and the ratio of E to A is more than 2
(restrictive phase) (Figure 7-6).
Figure 7-6. Doppler Mitral Inflow Velocity
Step 2: Tissue Doppler Imaging of Septal and Lateral Mitral Annulus. In the apical 4-chamber view, the
sample volume is placed within 5 mm of both the septal and lateral mitral annulus, and the early diastolic
velocity (E′) and late diastolic velocity (A′) are measured. Normal mitral E′ velocity is more than 10
cm/s, with the lateral E′ velocity slightly higher than the septal E′ velocity. As the LV relaxation is
impaired, the E′ velocity decreases. Septal E′ velocity less than 8 cm/s and lateral E′ velocity less than 10
cm/s indicates an LV impaired relaxation phase. The E/E′ ratio correlates with wedge pressure values and
indicates LA pressure and, therefore, diastolic dysfunction. If E/E′ ratio is less than 8, then the LA
pressure and LV end-diastolic pressure is essentially normal. E/E′ ratios from 8 to 15 indicate moderate
diastolic dysfunction, and E/E′ values more than 15 indicate severe LV diastolic dysfunction with high LA
and LV end-diastolic pressures (Figure 7-7).9
Figure 7-7. Mitral Annular Velocity
Step 3: Pulmonary Vein Inflow Pattern. In the apical 4-chamber view, a sample volume of 2 mm is placed
within the pulmonary veins. Obtain measurements at end expiration and calculate the average of 3
consecutive cardiac cycles. The peak systolic velocity (S) and the peak diastolic velocity (D) are
measured, from which the S/D ratio is derived. Under normal conditions, the S wave is greater than the D
wave or similar in size (often termed “codominant”). The systolic velocity is affected by LA pressure,
preload, and the gradient between the LA and pulmonary vein.10 In the impaired relaxation phase, the S/D
ratio is preserved, but as the diastolic dysfunction gets to moderate and severe, the S wave gets smaller
and the D wave predominates (Figure 7-8).
Figure 7-8. Pulmonary Venous Flow
Other measures, including isovolumic relaxation time, deceleration time, propagation velocity, time
constant of LV isovolumic relaxation, and myocardial performance index, are complex and require
advanced training to be appropriately interpreted and useful in the ICU setting.
KEY POINTS
Heart failure with preserved ejection fraction is a clinical diagnosis. Diastolic dysfunction seen on
echocardiography does not necessarily indicate that the patient has diastolic heart failure.
Atrial size is enlarged in moderate or severe diastolic dysfunction. Changes in diastolic patterns
over time can aid in fluid management of ICU patients.
Mitral inflow velocity is affected by heart rate and preload. In tachycardia, the E and A waves
merge, which can preclude diastolic function evaluation. In atrial fibrillation, the atrial contraction
during the late phase of diastole is not consistent, usually indicating that the A wave is absent.
Mitral annulus velocity is less affected by loading conditions (unlike inflow velocity). However,
segmental wall motion abnormalities can affect the accuracy of annulus velocity measurement and
interpretation. Mitral annulus calcification, mitral stenosis, prosthetic mitral valves, and mitral rings
reduce E′ velocities, whereas severe mitral regurgitation can increase E′ velocity.
Pulmonary vein inflow velocities can be affected by atrial arrhythmias, heart rate, preload, and
mitral regurgitation. In patients younger than 35 years old whose LA pressure and LV end-diastolic
pressure are low, the low pulmonary vascular-LA gradient leads to a low S and a dominant D
velocity. These patients have normal diastolic function. In patients with atrial fibrillation, the S
velocity is usually lower and, hence, the S/D ratio is <1 because of the loss of atrial contraction.
Diastolic function cannot be assessed based on these alone in patients with atrial fibrillation.
DETECTION AND ASSESSMENT OF VALVULAR HEART DISEASE
Detection of gross valvular heart disease (ie, absence vs. suspicion of disease) can easily and reliably be
assessed with limited training during a focused examination. However, precise evaluation of regurgitation
or stenosis, as well as assessment of prosthetic valve function, requires experience and time (Table 7-
3).11-13
Calculating CO
Determining CO in the intensive care setting is usually an important and a very helpful tool. This can be
quickly calculated noninvasively using echocardiography.
We know that CO (cardiac output) = SV (stroke volume) × HR (heart rate). The hydraulic orifice formula
states that the flow across a fixed orifice is equal to the cross-sectional area (CSA) × flow velocity. The
flow velocity, or velocity time integral (VTI), represents a distance. Multiplying an area × distance =
volume. Using this formula, we can calculate the following:
SV = CSA of LVOT × VTI

CSA = πr² (assuming LVOT is circular)
CSA = π (d/2)² = 3.14 (d²/4) = 0.785 × d²
SV = 0.785 x d² × VTI
Flow velocity is variable during ejection in a pulsatile cardiovascular system. Hence, we use VTI. VTI is
the sum of individual pulsed-wave Doppler velocities integrated over time. It is equal to the stroke
distance – the average distance blood travels with each beat of the heart. This is obtained by tracing the
Doppler velocity signal and is the area enclosed by the baseline and Doppler spectrum (Figure 7-9).
Figure 7-9. Pulsed-wave Doppler of LVOT

Table 7-3. Evaluation for Gross Valvular Heart Disease
Basic Evaluation Advanced Examination

MR Color Doppler in parasternal long-axis and Color Doppler in multiple views
apical 4-chamber views: assess for backward
color flow from LV to LA
Timing of regurgitation
Analysis of pulmonary vein flow
Quantitative analysis: PISA
Mechanism of regurgitation11
MS Mitral valve calcifications Mean transvalvular gradient
Restriction of mitral valve opening Functional valve area (PHT)
Acceleration "aliasing” through the valve Valve planimetry
Description of valvular and
subvalvular anatomy
AR Color Doppler in parasternal long-axis and Color Doppler in multiple views
apical 5-chamber views: assess for backward
color flow from aorta to LV
Intensity of Doppler signal
LV diastolic pressure: PHT,
deceleration slope
Quantitative analysis: PISA
Mechanism of regurgitation
Telediastolic velocity in aortic
isthmus
AS Aortic valve calcifications Mean transvalvular gradient
Restriction of aortic valve opening Maximum blood velocity through
the valve
Acceleration “aliasing” through the valve Aortic valve area (continuity
equation)12
Prosthetic aortic or Presence of prosthetic valve Position
mitral valve Mobility
Intra- or perivalvular regurgitation
Transvalvular gradient
Abnormal additional valvular
images13
Abbreviations: AR, aortic regurgitation; AS, aortic stenosis; LA, left atrial; LV, left ventricular; MR, mitral regurgitation; MS, mitral stenosis;
PHT, pressure half time; PISA, proximal isovelocity surface area.
C AVE AT S
The LVOT diameter must be accurately measured because the errors are squared in the formula.
The Doppler beam interrogation angle must be within 20° of the direction of flow because
lower velocities can falsely lower CO.
In atrial arrhythmias, use average VTI over 6 cardiac cycles.
The formula to calculate SV assumes that the LVOT is circular in shape.
TTE has limited sensitivity in detecting vegetations and complications related to IE.
Other structures that can be mistaken for IE include Lambl excrescence in the aortic valve,
valve masses, valve thrombus, prosthetic sutures, and localized valve calcification.
Figure 7-10. Parasternal Long-axis View of LV

Figure 7-11. Measuring LVOT Diameter
Measuring the LVOT diameter accurately is very important. In the parasternal long-axis view, measure
LVOT diameter in midsystole within 1 cm of the ventricular side of the aortic valve (Figures 7-10 and 7-
11).
Calculating Pulmonary Vascular Resistance

Calculating pulmonary vascular resistance (PVR) can be helpful while managing severe heart failure
cases in the ICU. The most accurate way of measuring PVR is by floating a pulmonary artery (PA)
catheter and measuring mean pulmonary artery pressure (mPAP) and pulmonary capillary wedge pressure
(PCWP) and using the following formula:
PVR = (mPAP - PCWP)/CO
However, PVR can be estimated using Doppler echocardiography. Using the principle of pressure =
resistance × flow, we know that resistance = pressure/flow. Therefore, we have this formula:
PVR = PA pressure/PA flow
Substituting PA pressure with tricuspid regurgitation velocity (TRV) and PA flow with right ventricular
outflow tract (RVOT) VTI, we derive the following:
PVR = TRV/RVOT VTI
where TRV is measured in meters per second, and RVOT VTI is in measured in centimeters.
The TR jet velocity is obtained using continuous-wave Doppler to capture the highest velocity in meters
per second in multiple views, with the beam aligned as perpendicular as possible to the TR jet. Agitated
saline can be used to enhance poor Doppler signals. In patients with atrial fibrillation, an average of 5
measurements must be used. The RVOT VTI is obtained similarly to the LVOT VTI described earlier. A
pulsed-wave Doppler is placed in the proximal RVOT just within the pulmonary valve imaged from the
parasternal short-axis view when the pulmonary valve is closed. The commonly used formula in
echocardiography literature is:
PVR = 10 (TRV/RVOT VTI) + 0.16 Wood Units
A TRV/RVOT VTI cutoff value of 0.175 has a sensitivity of 77% and a specificity of 81% to determine
PVR >2 Wood Units (Figure 7-12).14
Figure 7-12. Parasternal Short-axis View of Basal RV
Abbreviations: RVOT, right ventricular outflow tract; PV, pulmonary vein; PA, pulmonary artery.
Congenital Heart Disease: Atrial Septal Defect

The types of atrial septal defect (ASD) include secundum ASD, primum ASD, sinus venosus ASD, and
coronary sinus ASD. ASD accounts for 40% of adults with congenital heart disease.15 It is more common
in women. The interatrial septum is often well visualized in the subcostal view. In patients who are
obese, the apical 4-chamber view is helpful (Figure 7-13).
The shunt is predominantly left to right, but often we find bidirectional shunting as well. A “bubble study”
is performed by injecting saline contrast. In the common type of left-to-right shunt, a negative contrast
effect or washout of bubbles in the RA side of the septum is noted. In the bidirectional shunt, bubbles
enter from the RA to LA within 3 cardiac cycles of their appearance in the RA (Figure 7-14).
Figure 7-14. Apical 4-Chamber View with the “Bubble Study”
E X P E RT T I P S
Clues to the presence of an ASD include:
• Abrupt discontinuity of the septum and slight thickening at its termination.
• Hypermobility of the interatrial septum.
• RA and RV overload displacement of the septum toward the LV.
• Use of peripheral vein injection of agitated saline, which can help identify ASDs.
KEY POINTS
Artifactual echocardiogram dropout of the interatrial septum, caused by the parallel orientation of
the echocardiographic beam to the atrial septum and the thinness of the fossa ovalis, can lead to a
false image of ASD.
Color flow can be used to assess flow across the ASD, but must be interpreted with caution because
slightly off-axis views of an imperfect picture from the LVOT can look similar to a true ASD. Use
the Nyquist limit at 30 to 40 cm/sec for optimal visualization of color flow across the shunt.
TTE can reasonably detect secundum ASDs and primum ASDs. TEE would be helpful to detect
sinus venosus ASDs and coronary sinus ASDs.
The negative contrast that is seen in the common type of left-to-right shunt can sometimes be caused
by inferior vena cava inflow.
The ratio of right heart stroke volume (Qp) to left heart stroke volume (Qs) gives us the flow across
the shunt: Qp = CSA of PA × VTI of PA, Qs = CSA of LVOT × VTI of LVOT.
INFECTIVE ENDOCARDITIS
Infective endocarditis encompasses infection of the endothelial lining of the heart valves, valve annulus,
chordae tendineae (MV, tricuspid valve), or aortic root. IE is usually a clinical diagnosis but
echocardiography can be critical in this setting. Integrating echocardiographic data with clinical data and
microbiology is vital (Table 7-4).
About two-thirds of patients with IE have predisposing heart disease, and about one-third have normal
valves that developed IE. Usually those with left-sided IE have preexisting heart disease and those with
right-sided IE have a predisposition to intravenous drug abuse. Left-sided IE is more common than right-
sided IE (about 65%-70% and 10%, respectively, with the remaining 20%-25% seen in prosthetic
valves).15 The most common valve affected by IE is the aortic valve, followed by the MV. In cases with
right-sided IE, the tricuspid valve is affected in about 80%-85%. In the younger population, the most
common predisposing causes are MV prolapse and intravenous drug abuse. In patients older than 65 years
of age, the most common predisposing causes are pacemakers, defibrillators, prosthetic heart valves,
aortic valve sclerosis or stenosis, and mitral regurgitation.16 Although vegetations can be seen on TTE,
evaluation with TEE, particularly for the MV, is recommended (Figures 7-15 and 7-16).
This chapter’s focus is on echocardiography, therefore the etiology, typical organisms, clinical features,
and laboratory data of IE are not discussed.
Features seen significantly better with TEE include fistula, abscesses, leaflet perforation, aneurysms,
pseudoaneurysms, and infections involving prosthetic valves.17
Figure 7-15. TTE Showing Vegetation Attached to the Aortic Valve

Figure 7-16. TTE Showing Vegetation Attached to the Mitral Valve
Table 7-4. Modified Duke Criteria
Major Criteria Minor Criteria

Positive blood cultures for infective endocarditis Predisposition
Positive echocardiogram for infective endocarditis Fever
New valvular regurgitation Vascular phenomena
Immunologic phenomena
Microbiologic evidence
E X P E RT T I P S
Vegetations are usually seen on the lower pressure side of the valve (ie, atrial side of the MV
and tricuspid valve and ventricular side of the aortic and pulmonary valves).
Inspect each valve in multiple planes with a narrow sector scan.
Vegetations are usually pedunculated or prolapsing. They are echodense and homogenous in appearance.
Chronic vegetations can appear calcified, and in situ abscesses can present as echolucent.
Indications for TEE

In most circumstances, TTE will provide enough information to make a clinical decision in the ICU.
However, there are conditions, such as those included in Table 7-5 and mentioned below, when TEE
provides valuable information and is clearly the superior choice.
Suspected acute aortic pathology (ie, dissection, transsection, intramural hematoma)

Suspected prosthetic valve dysfunction
Suspected complications of endocarditis (eg, fistula, abscess)
Evaluation for left atrial/left atrial appendage thrombus in a patient with atrial fibrillation/atrial flutter
to facilitate clinical decision-making regarding anticoagulation, cardioversion, or ablation
Evaluation for cardiac source of embolus
Unexplained hypotension (sepsis, cardiogenic, mitral regurgitation, tamponade, RV infarct, pulmonary
embolism)
Unexplained hypoxemia
Suspected complications after a myocardial infarction (ie, acute mitral regurgitation, ventricular septal
defect, free wall rupture with cardiac tamponade)
Newer Modalities
Newer modalities such as 3-dimensional (3D) echocardiography, strain, and speckle tracking have
limited roles in the field of echocardiography in the ICU. Data supporting these modalities are sparse and
not supportive for routine use.
Compared with 2D echocardiography, 3D TTE provides accurate estimation of LV volumes and ejection
fraction. 3D TEE also has a crucial role in preoperative assessment of IE, especially in the presence of
prosthetic valves and prosthesis valve dysfunction (such as paraprosthetic regurgitation). It is particularly
useful in the guidance of interventional procedures in structural heart disease.18
Speckle tracking is a semiautomated means of measuring myocardial strain and strain rate in which a
unique acoustic pattern is generated from an ultrasound interrogation of the tissue. This can detect
longitudinal, circumferential, or radial displacement. The advantage of speckle tracking over tissue
Doppler is the lack of dependence on the angle of incident ultrasound beam.19
Strain allows more early detection of systolic dysfunction20 (even when LV ejection fraction appears
within normal ranges), and LV and RV strain alterations have been shown to be linked to a worse
prognosis in several conditions such as amyloidosis and pulmonary hypertension. Strain also allows for
segmental evaluation of the LV myocardial function and more accurate visualization of RWMAs.
Table 7-5. Indications for TEE in Diagnosing IE
Inadequate image quality seen on TTE

Prosthetic heart valves
Absence of vegetations on TTE in a patient with a high pretest likelihood of IE
Severe valve dysfunction
New heart block
Two or more jets of regurgitation from a single valve
Congenital heart disease
Pacemakers and defibrillators
IE with suspected valvular complications
IE going for valve repair or replacement
Abbreviations: IE, infective endocarditis; TEE, transesophageal echocardiography; TTE, transthoracic echocardiography.
REFERENCES
1. Douglas PS, Garcia MJ, Haines DE, et al. ACCF/ASE/AHA/ ASNC/HFSA/HRS/ SCAI/SCCM/SCCT/SCMR 2011 appropriate use
criteria for echocardiography. A report of the American College of Cardiology Foundation Appropriate Use Criteria Task Force, American
Society of Echocardiography, American Heart Association, American Society of Nuclear Cardiology, Heart Failure Society of America,
Heart Rhythm Society, Society for Cardiovascular Angiography and Interventions, Society of Critical Care Medicine, Society of
Cardiovascular Computed Tomography, and Society for Cardiovascular Magnetic Resonance Endorsed by the American College of Chest
Physicians. J Am Coll Cardiol. 2011;57:1126-1166.
2. O’Gara PT, Kushner FG, Ascheim DD, et al. 2013 ACCF/ AHA guideline for the management of ST-elevation myocardial infarction: a
report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation.
2013;127:e362- e425.
3. Amsterdam EA, Wenger NK, Brindis RG, et al. 2014 AHA/ ACC guideline for the management of patients with non– ST-elevation acute
coronary syndromes: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on
Practice Guidelines. Circulation. 2014;130:2354-2394.
4. Evangelista A, Avegliano G, Elorz C, et al. Transesophageal echocardiography in the diagnosis of acute aortic syndrome. J Card Surg.
2002;17:95-106.
5. Willens HJ, Kessler KM. Transesophageal echocardiography in the diagnosis of diseases of the thoracic aorta: part I. Aortic dissection,
aortic intramural hematoma, and penetrating atherosclerotic ulcer of the aorta. Chest. 1999;116:1772-1779.
6. Willens HJ, Kessler KM. Transesophageal echocardiography in the diagnosis of diseases of the thoracic aorta, part II- -atherosclerotic and
traumatic diseases of the aorta. Chest. 2000;117:233-243.
7. Hitatzka LF, Bakris GL, Beckman JA, et al. 2010 ACCF/AHA/ AATS/ACR/ASA/SCA/SCAI/SIR/STS/SVM guidelines for the diagnosis
and management of patients with thoracic aortic disease. A report of the American College of Cardiology Foundation/American Heart
Association Task Force on Practice Guidelines, American Association for Thoracic Surgery, American College of Radiology, American
Stroke Association, Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, Society of
Interventional Radiology, Society of Thoracic Surgeons, and Society for Vascular Medicine. J Am Coll Cardiol. 2010;55:e27-e129.
8. Yamada H, Goh PP, Sun JP, et al. Prevalence of left ventricular diastolic dysfunction by Doppler echocardiography: clinical application of
the Canadian consensus guidelines. J Am Soc Echocardiogr. 2002;15:1238-1244.
9. Nagueh SF, Appleton CP, Gillebert TC, et al. Recommendations for the evaluation of left ventricular diastolic function by echocardiography.
J Am Soc Echocardiogr. 2009;22:107- 133.
10. Jensen JL, Williams FE, Beilby BJ, et al. Feasibility of obtaining pulmonary venous flow velocity in cardiac patients using transthoracic
pulsed wave Doppler technique. J Am Soc Echocardiogr. 1997;10:60-66.
11. Zoghbi WA, Enriquez-Sarano M, Foster E, et al. Recommendations for evaluation of the severity of native valvular regurgitation with two-
dimensional and Doppler echocardiography. J Am Soc Echocardiogr. 2003;16:777-802.
12. Otto CM, Lind BK, Kitzman DW, Gersh BJ, Siscovick DS. Association of aortic valve sclerosis with cardiovascular mortality and
morbidity in the elderly. N Engl J Med. 1999;341:142-147.
13. Nishimura RA, Otto CM, Bonow RO, et al. 2014 AHA/ACC guideline for the management of patients with valvular heart disease: a report
of the American College of Cardiology/ American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2014;63:e57-
e185.
14. Abbas AE, Fortuin D, Schiller NB, et al. A simple method for noninvasive estimation of pulmonary vascular resistance J Am Coll Cardiol.
2003;41:1021-1027.
15. Hoffman JI, Kaplan S. The incidence of congenital heart disease. J Am Coll Cardiol. 2002;39:1890-1900.
16. Haldar SM, O’Gara PT. Infective endocarditis: diagnosis and management. Nat Clin Pract Cardiovasc Med. 2006;3:310-317.
17. Kini V, Logani S, Ky B, et al. Transthoracic and transesophageal echocardiography for the indication of suspected infective endocarditis:
vegetations, blood cultures and imaging. J Am Soc Echocardiogr. 2010;23:396-402.
18. Hung J, Lang R, Flachskampf F, et al. 3D echocardiography: a review of the current status and future directions. J Am Soc Echocardiogr.
2007;20:213-233.
19. Seo Y, Ishizu T, Atsumi A, Kawamura R, Aonuma K. Three-dimensional speckle tracking echocardiography. Circ J. 2014;78:1290-1301.
20. Reant P, Chasseriaud W, Pillois X, et al. Early detection of left ventricular systolic dysfunction using two-dimensional speckle tracking
strain evaluation in healthy subjects after acute alcohol intoxication. Echocardiography. 2012;29:927- 932.
Chapter 8
Assessment and Implications of Diastolic
Dysfunction in Critical Illness
OBJECTIVES
Discuss the physiology of diastolic dysfunction
Discuss the incidence and implications of diastolic dysfunction in critically ill patients
Describe the echocardiographic evaluation of diastolic function
INTRODUCTION
Although the entity of heart failure with preserved ejection fraction (HFPEF), once called “diastolic heart
failure,” has become familiar in general cardiology, the relevance of diastolic dysfunction to the
management of critically ill patients is just beginning to be understood. Diastolic function is increasingly
recognized as an important part of the cardiac evaluation of patients in the ICU, where the attention is less
on a clinical syndrome, heart failure, and more on the heart’s capacity to respond to dynamic physiologic
stress throughout its cycle. Diastole is proving increasingly important to our understanding of the heart’s
response to physiologic perturbations. While the ventricle performs most of the work of cardiac filling in
healthy patients, in pathologic states left atrial hypertension performs more of that work, especially in
early diastole. Because the pulmonary circulation is the venous reservoir from which the left heart fills,
the filling of the left heart has profound implications for pulmonary function and respiratory failure.
Both intrinsic ventricular function and cardiac loading conditions define diastolic function.
Echocardiography provides an ideal, noninvasive method for evaluating most components of diastolic
function. Understanding diastolic function can allow a clinician to understand the mechanism of heart
failure, estimate left ventricular end diastolic pressure noninvasively, evaluate the etiology of pulmonary
edema, and monitor the response to serial volume expansion interventions.
CASE STUDY
E.S. is a 63-year-old morbidly obese woman presenting to the emergency department with perforated
diverticulitis. Her initial transthoracic echocardiogram (TTE) in the emergency department shows mild
left ventricular hypertrophy (LVH), a normal ejection fraction without wall motion abnormalities, an
early-atrial flow velocity (EA) ratio of 0.6, and an E′ velocity of 7 cm/s. She becomes extremely
hypotensive on induction of anesthesia for laparotomy; on intraoperative transesophageal echocardiogram
(TEE), her pulmonary venous inflow (PVI) is systolic dominant, with an EA ratio of 0.7 and an E´
velocity of 6.5 cm/s. She is volume resuscitated with 3 L of crystalloid, and her PVI becomes codominant,
with an EA ratio of 1.2. Her oxygen saturation decreases, requiring an increase in fraction of inspired
oxygen on the ventilator. She remains hypotensive, however, and receives another 2 L of crystalloid. PVI
becomes diastolic dominant, and her EA ratio is 1.8. The surgery is successfully completed and she is
transferred to the ICU with vasopressor therapy. In the ICU, progressive hypoxemia requires an increase
in positive end-expiratory pressure on the ventilator. TTE shows progressive dilation and dysfunction of
the right ventricle with apical sparing. She develops worsening shock, requiring increasing doses of
norepinephrine and resulting in the multiple organ dysfunction syndrome.
What Happened To This Patient?

Some authors suggest that a substantial proportion of apparent acute respiratory distress syndrome is the
result of overly aggressive volume expansion. As I will discuss in this chapter, the initial TTE seen in the
case study showed intrinsic dysfunction of the ventricle during diastole, manifested by slow É velocity, a
low EA ratio, and normal, systolic-dominant PVI. By the middle of surgery, however, she was already
showing signs of left atrial hypertension, with increasing EA ratio and shift in PVI to diastolic dominant.
Although ischemia can cause diastolic dysfunction, normal systolic function and the clinical context argue
against coronary stenosis or obstruction in this case. However, vigilance is always required to avoid
missing such events among critically ill individuals. The acute cor pulmonale is concerning but is most
likely from high mean airway pressures and left atrial hypertension.
By the conclusion of this chapter, the relevant findings on E.S.’s echocardiograms should all be clear.
Diastolic function is often considered an advanced or complex topic, but by starting with basic
physiology and first principles, diastole is reasonably straightforward.
DEFINITION OF DIASTOLE
From the Greek word for “expansion” (once a cosmologic term to describe the expansion of the
universe), diastole by convention refers to the period from the closure of the aortic valve to the closure of
the mitral valve. Consistent with the ventricle-focused framing of cardiac function, diastole is the period
in which the ventricle fills with blood.
Because diastole includes multiple physiologic processes and therapeutic contexts, it provides a window
into heart function that is important for the management of critically ill patients. Because of its complexity,
diastole can initially be difficult to understand, but it is basically the transfer of blood from the atrium to
the ventricle via pressure differences. Throughout, I will emphasize the concept that the atrium and
ventricle contribute to building pressure differences; in health the ventricle predominates, whereas in
illness, left atrial hypertension plays a role, at the cost of venous congestion of the lungs.
I believe that the right ventricle is extremely important and generally underemphasized. In this chapter, I
will describe diastole in terms of the left ventricle, both for ease of exposition and because relatively
little is known about diastole in the right ventricle.
INCIDENCE OF DIASTOLIC DYSFUNCTION

Among community dwellers, symptomatic heart failure is common, especially later in life. In the
cardiology literature, older references to “systolic” or “diastolic” heart failure have been replaced by
heart failure with reduced ejection fraction (HFREF) and HFPEF. The change in nomenclature makes
good sense because measurable diastolic and systolic dysfunction are observed in both HFPEF and
HFREF. Within the terms of this nomenclature, HFPEF is increasingly common, especially among older
individuals.1
Less is known about the incidence of diastolic dysfunction among critically ill patients than in outpatient
populations, in part because the definitions were derived in community-dwelling cohorts. In the acute
setting, loading conditions may change rapidly, and apparent diastolic dysfunction may represent a
preload deficit or hypervolemia rather than a chronic pathologic state. With those caveats, estimates of
incidence of diastolic dysfunction among patients with sepsis ranges from approximately 30% to 60%. An
Israeli study identified diastolic dysfunction in about half of the patients, while our Utah study identified
diastolic dysfunction in about a third of patients, with isolated (ie, in the setting of normal systolic
function) diastolic dysfunction occurring in 23% to 40% of patients newly admitted to the ICU.2,3
PHYSIOLOGY OF DIASTOLE
Diastole represents the conjunction of 2 main inputs: the intrinsic function of the ventricle, and loading
conditions in the atrium and ventricle. While other factors, including age, heart rate, pericardial
constraint, and ventricular interdependence may affect diastology, in barest essentials, the balance
between the intrinsic diastolic function of the ventricle and the loading conditions of the atrium generates
a driving pressure that opens the mitral valve and drives blood flow from the atrium to the ventricle.
C AVE AT
Age-related changes can obscure standard relationships between diastolic parameters and
loading conditions.
As is true throughout the cardiovascular system, pressure gradients generate blood flow during diastole.
In this case, the pressure in the donating chamber, the atrium, minus the pressure in the receiving chamber,
the ventricle, generates the pressure gradient that drives diastolic blood flow. Because the mitral valve
area is large, small pressure gradients can generate substantial flow. The average normal transmitral
gradient is less than 5 mm Hg and commonly in the 2 to 4 mm Hg range. If the atrial pressure is 7 mm Hg
and the ventricular pressure is 4 mm Hg, for example, the pressure gradient is 7 – 4 = 3 mm Hg. The
identical pressure gradient can be generated with a left atrial pressure of 15 mm Hg and a ventricular
pressure of 12 mm Hg, a dramatically different situation in terms of the venous circulation of the lung,
which must empty into the left atrium. In the uncommon case of severe mitral stenosis, the ventricle may
even generate “negative” (less than atmospheric) pressures to facilitate flow across the stenotic valve.
Figure 8-1 displays relevant components of diastole.
Figure 8-1. The Anatomy of Diastole: Pressure Differences Drive Blood Flow
By convention, diastole is divided into 4 phases: isovolumic relaxation, early diastolic filling, diastasis,
and late (atrial) diastolic filling. Diastole ends shortly thereafter, as the ventricle begins to contract at the
beginning of the isovolumic contraction phase of systole. During isovolumic relaxation, the left ventricle
enlarges until the intraventricular pressure first drops below left atrial pressure, at which time the passive
mitral valve opens. The pressures in the left ventricle continue to drop; the balance between the pressure
in the left atrium and the lower pressures in the left ventricle defines the pressure gradient that drives the
flow of blood from the atrium to ventricle.
This early diastolic flow is termed “E,” and the spectral Doppler envelope of that flow is called the “E
wave.” Among healthy individuals, early flow is responsible for 70% to 80% of total diastolic filling. As
blood flows into the ventricle, the lower pressure in that receiving chamber starts to rise slightly, until it
is almost equal to the atrial pressure. The balancing of pressures leads to a temporary pause, called
“diastasis,” in which very little blood flows. Shortly thereafter, atrial contraction transiently increases the
pressure in the atrium, which leads to more flow (in healthy individuals about 20% of total diastolic
blood flow) into the ventricle. This flow during atrial contraction is called “A” for atrial, and the spectral
Doppler envelope is called the “A wave.” In basic clinical practice, we emphasize the early and atrial
phases of diastole, with much less attention paid to isovolumic relaxation and diastasis. Figure 8-2
outlines this process graphically.
Figure 8-2. Schematic of the Phases of Diastole
Abbreviations: LV, left ventricular; LA, left atrial; IVRT, isovolumic relaxation time; DT, deceleration time.
Blood can be induced to flow from the atrium to the ventricle either by increases in the pressure of the
donating chamber, the atrium, or by decreases in the pressure of the receiving chamber, the ventricle. A
healthy ventricle performs most of the work of diastole through brisk, vigorous relaxation, an active
process. For example, during healthy exercise, ventricular relaxation is augmented via a catecholamine-
mediated process, allowing a brisker and earlier generation of lower ventricular pressures. In disease
states, the atrium performs more of the work–by developing left atrial hypertension–of early diastolic
filling, but the atrium is ill-equipped to perform that work because it is intimately connected with the
pulmonary venous circulation, which poorly tolerates increases in venous pressure. In many respects, the
problems of diastolic dysfunction arise because the ventricle fails to do work that is therefore imposed
upon the atrium. The atrium, in turn, passes the hypertension to the pulmonary circulation, resulting in
venous congestion in the lungs. This stage represents the risk associated with volume expansion, which
sometimes improves hypotension at the expense of pulmonary edema.
MECHANISMS OF INTRINSIC VENTRICULAR DIASTOLIC FUNCTION

Systole and diastole are intimately interconnected. Diastole provides the “preload” for the heart, and
without adequate filling, systole will generate a much lower stroke volume than it would with adequate
diastolic filling. Systole therefore depends on diastole for preload. Furthermore, the vigor of systole (ie,
contractility) and the afterload imposed on the ventricle during systole define in part the vigor of early
diastolic relaxation.
Because of the intrinsic stiffness of the myocardium, substantial potential energy is stored at the end of
systole. When active contraction ceases, the heart’s tendency to rebound toward its unstressed state will
create a large increase in volume of the chamber and a concomitant decrease in pressure. This process of
releasing potential energy is commonly called “elastic recoil” and is a major driver of ventricular
diastolic function. This is a key mechanism by which better systole makes for better diastole.
At the end of systole, myosin cross bridges are strongly attached. Those cross bridges can either detach
slowly or quickly, a calcium-dependent process called “lusitropy.” While elastic recoil defines how
much work can be done by the ventricle, lusitropy defines how quickly that work can be performed, like
the speed with which a drag racer releases the brake on her car. Snappy release of the brake is good
lusitropy, and a slow release of the brake represents poor lusitropy. Elastic recoil and lusitropy are the
key determinants of the “snap” of early diastole.
Finally, the stiffness of the ventricle can play an important role in diastole. A pathologically stiff heart is
poorly compliant: a small amount of blood flow into the ventricle rapidly increases the pressure in the
ventricle. The pressure gradient’s driving flow is quickly obliterated in that setting, leading to a short
deceleration time, as discussed below.
Advanced age, diabetes, end-stage renal disease, hypertension, and coronary or valvular heart disease all
commonly cause diastolic dysfunction via a myriad of mechanisms at the macro and micro levels. While
LVH is not synonymous with diastolic dysfunction, thicker hearts are more prone to dysfunction, both at
rest and under stress. On echocardiography, LVH can be a clue to investigate the presence of diastolic
dysfunction.
In the ICU, tachycardia and changes in loading conditions may have substantial effects on diastolic
function. In addition, septic cardiomyopathy is common, contributing to both systolic and diastolic
dysfunction. Interleukin-1b and nitric oxide metabolism are the usual candidates for the “myocardial
depressant factor,” a now obsolete hypothesis that a single chemical was responsible for myocardial
dysfunction during sepsis, whereas now it is appreciated that septic cardiomyopathy represents in many
respects the effects of multiple organ dysfunction syndrome on the heart. Cytotoxic effects,
microcirculatory dysfunction, mitochondrial dysfunction, microthrombi, and other factors combine to
create a myocardium in sepsis that is swollen, stiff, and slow to relax. Stress cardiomyopathy (sometimes
termed “catecholamine cardiomyopathy”; a subset of this phenomenon has been called “Takotsubo
cardiomyopathy”) may also play a role among critically ill patients. This phenomenon is generally
associated with systolic dysfunction, but diastolic dysfunction plays an important role in the syndrome as
well. Although at physiologic levels, such as in exercise, increased catecholamines improve both systolic
and diastolic function, at markedly elevated levels, these hormones can cause substantial cardiac
dysfunction.
ASSESSMENT OF DIASTOLIC FUNCTION

Relevant academic societies have published guidelines for the assessment of diastole.4,5 Although full
evaluation of diastolic function requires cardiac catheterization and advanced imaging modalities,
echocardiography has dramatically improved the noninvasive evaluation of diastole.
In essence, the grading systems in use attempt to describe, in clinically meaningful categories, the
interplay between the atrium and ventricle in effecting the flow of blood across the mitral valve. The
ventricle relaxes more poorly and becomes stiffer, and left atrial hypertension becomes more pronounced,
as the grades increase. Historically and conventionally, diastolic function is divided into grades 0 to 3,
with some authors advocating a distinction between grades 3a (reversible with diuresis or Valsalva
maneuver) and 3b (nonreversible). Grade 0 is normal function (normal ventricle, normal left atrial
pressure), grade 1 is “impaired relaxation” (poor ventricular relaxation, normal left atrial pressure;
ventricle still compliant), grade 2 is “pseudonormal” (poor ventricular relaxation plus left atrial
hypertension; ventricle still compliant), and grade 3 is “restrictive” (all aspects dysfunctional). Grades
are generally assigned on the basis of echocardiographic parameters, with greatest attention paid to the E′
, and the E:E′ and EA ratios, as displayed in Figure 8-3.
C AVE AT
Remember that all assessments of diastolic function must be integrative—discordance of

individual measures is quite common.
Clinicians often want to know the ventricle’s loading conditions, the “cardiac preload.”
Echocardiographic evaluation of the heart allows assessment of the ventricle’s function and the net
resulting flow. Because the ventricular and atrial contribution generate the pressure gradients driving
early diastolic flow, the measurement of the ventricular component and the net flow allow us to infer the
atrial contribution, which is a surrogate for cardiac preload and the risk of pulmonary venous congestion.
Overall blood flow is measured as the E wave peak velocity (recall that E represents early diastolic
flow). Measurements are made from the apical 4 chamber, with a pulse wave gate at the leaflet tips of the
mitral valve, within the left ventricle. Care should be taken not to place the sample volume too apically,
as the velocities will be slower and flow more dispersed. The Doppler angle should be kept below 20
degrees; an average measurement from 3 cardiac cycles is ideal. Figure 8-4 displays appropriate
positioning and the resulting velocity time integral trace.
Figure 8-3. Classification of Diastolic Function

Reproduced with permission Brown SM, Pittman JE, Hirshberg EL, et al. Diastolic dysfunction and mortality in early severe sepsis and septic
shock: a prospective, observational echocardiography study. Crit Ultrasound J. 2012;4:8. Copyright © 2012 Brown et al; licensee Springer.
The ventricular contribution to diastolic filling is measured with the E´ wave peak velocity (explained
below). To appreciate how echocardiography can be used to understand diastolic function requires a
basic understanding of the processing of ultrasound waves by ultrasound machines. Filters are
mathematical techniques to ignore certain kinds of signals on the basis of their characteristics. Most
Doppler echocardiography uses filters tuned to blood flow. Blood flow represents quiet, tiny objects
moving very quickly. These fast red blood cells are the metaphorical equivalent of a hummingbird. For
normal Doppler imaging, filters ignore the loud and slow signals associated with the movement of the
ventricle. The loud, slow-moving cardiac muscle is the metaphorical equivalent of an elephant. Tissue
Doppler imaging (TDI) is just the inversion of the usual filtering strategy: instead of listening to the quiet,
fast signal from red blood cells (the hummingbird), TDI listens to the loud, slow signals from the
ventricle (the elephant). The E wave, measured with typical spectral Doppler, is obtained with normal
filters. It measures early diastolic blood flow. The E´ wave, measured with TDI, is obtained with the
filters inverted. It measures the velocity of the ventricle during early diastole, a reasonable surrogate for
intrinsic ventricular function. The E´ velocity is measured in TDI mode in the A4C, with the pulse wave
gate placed at the septal annulus, ensuring that the Doppler angle is less than 20 degrees. (In research
applications, the average of the septal and lateral annulus measurements is taken; in practice, the lateral
annulus is a little harder to interrogate for novices, so I advocate the septal annulus for basic clinical
applications.6 By convention, manufacturers use blue and red imaging to indicate that TDI is in use.
Figure 8-5 shows a sample evaluation of the medial (or septal) annulus by TDI.
E X P E RT T I P
The septal mitral annulus is often easier to use for measuring E’. Remember that those
velocities run about 2 cm/s slower than the lateral annulus; the cutoff for normal septal annulus
velocity is 8.6 cm/s.
Figure 8-4. Method for Measuring Mitral Inflow

Abbreviation: PW, pulsed-wave Doppler.
Figure 8-5. Method for Measuring Mitral Annulus Velocity

Abbreviations: PW, pulsed-wave Doppler; TDI, tissue Doppler imaging.
Note that the echocardiographic image is measuring the lateral annulus
Imaging of the E and E´ peak velocities generally allows classification of diastolic function. Figure 8-3
displays the characteristic waveforms of each grade of diastolic function.
The ratio of the E velocity (the fastest rate of blood flow during early diastole) to the E´ velocity (speed
at which the ventricle moves in early diastole) is a reasonable surrogate for left atrial pressures, the atrial
component of early diastole. A typical E velocity is about 60 to 90 cm/s, whereas normal E´ is more than
8 cm/s and more commonly around 10 cm/s. In general, an E:E´ ratio less than 8 indicates normal left
atrial pressure, an E:E´ ratio greater than 15 generally indicates elevated left atrial pressure, and ratios in
between are indeterminate. Thus a patient with an E velocity of 110 cm/s and an E´ velocity of 7 cm/s has
an E:E´ ratio of 16, compatible with elevated pressure and either pseudonormal (grade 2) or restrictive
(grade 3) diastolic dysfunction. The ratio of the peak velocities of the early and atrial flow, the “EA
ratio,” is primarily useful to identify impaired relaxation, though it can also help to distinguish
pseudonormal from restrictive. Normally the EA ratio is between 0.8 and 1.5. An EA ratio less than 0.8 is
consistent with impaired relaxation and no other grade. Pseudonormal function is called “pseudo”
precisely because the EA ratio is normal despite the fact that the atrium does the work of the ventricle
during early diastole. In restrictive diastolic dysfunction, left atrial hypertension is even worse and,
importantly, the atrial contraction in late diastole is less able to generate a pressure gradient, so the EA
ratio can become even higher.
The deceleration time of the E wave—the time lapse between peak E velocity and the diastasis, at which
flow velocity is zero—helps to identify a poorly compliant ventricle. A small amount of blood flow and
resulting increase in ventricular volume is associated with a substantial increase in pressure in a poorly
compliant ventricle. This rapid increase in pressure in the receiving chamber causes a drop in the
pressure gradient. As a result of the rapid loss of the pressure gradient, velocities quickly drop too. This
deceleration time is normally longer than 160 msec. Shorter deceleration times suggest a noncompliant
ventricle, which is associated with the restrictive physiology of grade 3 diastolic dysfunction.
E X P E RT T I P
The mitral valve inflows can be obtained even when the 2-dimensional images on A4C are not
clear. When the EA ratio is 0.8, the diagnosis is clear: impaired relaxation.
On TTE, you can use color Doppler to identify the orifice for the PVI and then place the pulse wave
cursor at that inflow.
Other techniques may be relevant to defining diastolic dysfunction. Somewhat more advanced (and
generally seen best on TEE) is the PVI, as mentioned in the case study. Inflow into the left atrium
generally occurs in health during ventricular systole, as the atrium expands by the movement of the base of
the heart. By convention, this is called “systolic dominant” PVI. (Though it is not physiologically
accurate, it may be easiest to remember that normal PVI is systolic dominant because the right ventricle
pushes blood into the left atrium during systole.) As PVI transitions from systolic to codominant or
diastolic dominant, left atrial pressures have risen. Some more cutting edge techniques (eg, speckle-
tracked untwisting, intraventricular pressure gradients) exist for describing diastolic function; I will not
discuss them here. Although left atrial dilation, a marker of chronic left atrial hypertension, figures
prominently in outpatient assessment of diastolic function,5 it is less relevant in the acute setting.2
Several important caveats and disclaimers apply to echocardiographic assessment of diastolic function.
First, mitral stenosis and prosthetic mitral valves (and to a lesser extent, severe mitral annulus
calcification) invalidate mitral inflow measurements, because the assumptions include no obstruction to
flow. Second, patients with tachycardia often demonstrate fusion of the E and A waves, making it difficult
to distinguish them. However, the E:E´ ratio is still generally accurate in that setting if the fused wave is
assumed to be the E wave peak velocity. Third, moderate or severe mitral regurgitation increases
diastolic flows, and data to guide the use of the E:E´ ratio in that setting are fewer. Fourth, in atrial
fibrillation there is no A wave, and the interbeat interval will change dramatically from beat to beat. The
E:E´ ratio is still valid in atrial fibrillation, but measurements should be taken from beats with a similar
preceding interbeat interval to be sure that the E and E´ are comparable. Fifth, in the presence of regional
wall motion abnormalities, E´ will be unreliable. Using mean septal and lateral velocities or
measurements from the normal regions is preferred in that setting. Finally, constrictive pericarditis
increases E´ velocities, thereby invalidating the assumptions associated with the E:E´ ratio.
The most important caveat is the need to interpret data contextually and in an integrated fashion. The
various proposed measures of diastolic function have been derived in community-dwelling patients. Even
in that population, there may be discordance: PVI may not match EA ratios and deceleration times may not
fit perfectly with the E:E´ ratio. To make a final classification will require multiple inputs, interpreted in
clinical context.7 No single measure will definitively assign a grade of diastolic dysfunction at a given
time in a given patient. The parameters used to define diastolic function will be harder to interpret in
older patients, given the changes in cardiac function expected with age.
IMPLICATIONS OF DIASTOLIC DYSFUNCTION

The prognosis of symptomatic HFPEF is approximately as poor as the prognosis of symptomatic HFREF.8
Because most interventional studies of heart failure therapy have focused on HFREF, urgent research is
required among patients with HFPEF. This is true among both community-dwelling individuals and
critically ill patients.
The implications of diastolic dysfunction among critically ill patients are less clear. In a recent Israeli
cohort of 262 patients, worse E´ velocity was clearly associated with higher mortality.3 Another study of
21 patients suggested worse outcomes with worse grades of diastolic dysfunction. 9 Intriguing early
evidence suggests that diastolic dysfunction is closely tied to troponin elevation.10 However, in a cohort
of 78 patients, grade 1 dysfunction was associated with worse survival than higher grades, presumably as
an indication of persistent preload deficit.2 Assessments of diastolic function may improve the
classification of conditions such as pulmonary edema or right-sided heart failure, settings in which left
atrial hypertension is a key diagnostic determinant.
Whether diastolic function has therapeutic implications is an important, parallel consideration. Use of PVI
via TEE is common during surgical anesthesia, and many practitioners feel that the transition from
systolic dominant to codominance or diastolic dominance is associated with higher left atrial pressure
and the need to stop volume expansion. A rising E:E´ ratio during volume expansion likely indicates the
same phenomenon: the development of left atrial hypertension. Titration of volume expansion to such
intermediate outcomes has not been tested in rigorous controlled trials powered to patient-relevant
outcomes, but such techniques are a reasonable candidate for study. Much work remains to be done
generally in terms of establishing the evidence base for critical care echocardiography; diastolic
evaluation is similar to other components.11
KEY POINTS
Ventricular diastolic dysfunction is common and important, both as part of HFPEF and when present
among critically ill patients.
Diastole represents the movement of blood from the donating atrium to the receiving ventricle,
driven by pressure differences between the chambers.
In health, the ventricle does most of the work in diastole through active relaxation. In disease, the
atrium may have to do substantial work during early diastole through left atrial hypertension,
resulting in pulmonary venous congestion.
Echocardiographic evaluation of diastolic function allows the evaluation of ventricular function,
through the E´ velocity, and resulting flow, via the E velocity, thereby allowing a basic estimation of
the degree of left atrial hypertension using the E:E´ ratio.
More research is required to determine the therapeutic implications of diastolic dysfunction among
critically ill patients.
REFERENCES
1. Owan TE, Hodge DO, Herges RM, et al. Trends in prevalence and outcome of heart failure with preserved ejection fraction. N Engl J
Med. 2006;355:251-259.
2. Brown SM, Pittman JE, Hirshberg EL, et al. Diastolic dysfunction and mortality in early severe sepsis and septic shock: a prospective,
observational echocardiography study. Crit Ultrasound J. 2012;4:8.
3. Landesberg G, Gilon D, Meroz Y, et al. Diastolic dysfunction and mortality in severe sepsis and septic shock. Eur Heart J. 2012;33:895-
903.
4. Paulus WJ, Tschope C, Sanderson JE, et al. How to diagnose diastolic heart failure: a consensus statement on the diagnosis of heart failure
with normal left ventricular ejection fraction by the Heart Failure and Echocardiography Associations of the European Society of
Cardiology. Eur Heart J. 2007;28:2539-2550. Sec 2
5. Nagueh SF, Appleton CP, Gillebert TC, et al. Recommendations for the evaluation of left ventricular diastolic function by
echocardiography. J Am Soc Echocardiogr. 2009; 22:107-133.
6. Vargas F, Gruson D, Valentino R, et al. Transesophageal pulsed Doppler echocardiography of pulmonary venous flow to assess left
ventricular filling pressure in ventilated patients with acute respiratory distress syndrome. J Crit Care. 2004;19:187-197.
7. Gutsche AR, Lanspa MJ, Hirshberg EL, et al. Redefining diastolic dysfunction in severe sepsis and septic shock [abstract]. Am J Respir
Crit Care Med. 2014;189:A5493.
8. Kitzman DW, Little WC, Brubaker PH, et al. Pathophysiological characterization of isolated diastolic heart failure in comparison to systolic
heart failure. JAMA. 2002; 288:2144-2150.
9. Sturgess DJ, Marwick TH, Joyce C, et al. Prediction of hospital outcome in septic shock: a prospective comparison of tissue Doppler and
cardiac biomarkers. Crit Care. 2010;14:R44.
10. Landesberg G, Jaffe AS, Gilon D, et al. Troponin elevation in severe sepsis and septic shock: the role of left ventricular diastolic
dysfunction and right ventricular dilatation. Crit Care Med. 2014;42:790-800.
11. Brown SM, Kasal J. Bedside ultrasound in the intensive care unit: where is the evidence? Semin Respir Crit Care Med. 2015;36:6 (in
press).
Chapter 9
Thoracic Ultrasound: Pleural Effusion and Pneumothorax
Chapter 10
Pulmonary Edema and Consolidation
Chapter 9
Thoracic Ultrasound: Pleural Effusion and
Pneumothorax
Mark P. Hamlin, MD, MS; Ryan D. Clouser, DO
OBJECTIVES
Discuss the differences in transmission of ultrasound energy through different tissues as a foundation for
understanding how to distinguish normal from abnormal pleural anatomy
Gain an essential understanding of normal pleural anatomy on ultrasound, including lung sliding, A- and B-line
artifacts, and rib shadows
Show ways to rapidly and accurately rule out pneumothorax or pleural effusion with ultrasound at the bedside
Describe the characteristic findings of pneumothorax on ultrasound, including loss of lung sliding, barcode
(stratosphere) sign, and lung point
Discuss the limitations of thoracic ultrasound in ruling in pneumothorax
Describe characteristics of pleural effusion on ultrasound, including assessment of the size of effusion and selection
of safe location for thoracentesis
Describe how to use real-time ultrasound during thoracentesis; demonstrate positioning options in the critically ill
patient, including the seated, lateral decubitus, and supine positions
INTRODUCTION
The use of ultrasound for diagnosing pleural effusion was described by Joyner and colleagues1 in a
classic JAMA article in 1967. Groups of enthusiasts were publishing articles in the 1990s on the use of
ultrasound in identifying pneumothorax. However, the broad application of ultrasound by nonradiologists
at the bedside has exploded during the last 15 years. Some of the original resistance to using thoracic
ultrasound was based on the belief that the highly reflective aspects of the aerated lung tissue limited its
utility. Although it is true that the drastically different propagation velocities of sound in air (330 m/s) vs.
soft tissue (1,540 m/s) make imaging inflated lungs difficult, ultrasonographers found that they were able
to use the reflective properties of the pleura to demonstrate the absence of fluid or air within the pleural
space. Early lung ultrasound was performed with low-frequency ultrasound probes. Current higher-
frequency probes allow sufficient resolving power to not only visualize motion at the pleura with
respiration, or in response to blood pumping into the pulmonary vasculature, but to actually resolve the
individual layers of the pleura sliding back and forth, and even show irregularities of the pleural surface
of the lung. Bedside ultrasound can rapidly rule out the presence of a pneumothorax or pleural effusion
with nearly 100% negative predictive value, and when present, differentiate pleural effusion from
pneumothorax. Beyond that, the size of an effusion can be evaluated at the bedside, and one can easily
select a safe location to perform thoracentesis without injuring nearby organs or vasculature. The size,
ease of use, and portability of current ultrasound machines brings this technology to the patient’s bedside
in the ICU, operating room, emergency department, or general ward.
PNEUMOTHORAX
Case Study 1
A 31-year-old man presents to the emergency department after a restrained motor vehicle collision. He is
alert, oriented, and complaining of shortness of breath. His chest radiograph does not show pneumothorax
(Figure 9-1). He is taken immediately for a computed tomography (CT) scan to evaluate for other injuries,
and a left-sided pneumothorax is clearly seen (Figure 9-2). A chest tube is placed, and the patient’s
shortness of breath resolves.
How Could the Use of Bedside Ultrasound Have Changed Patient Management?
Ultrasound performance in diagnosis of pneumothorax has been well established. Compared with chest
radiography (CXR), ultrasound is a superior method. One study in supine trauma patients showed that
when compared with chest CT as the gold standard, ultrasound identified 53 of 53 pneumothoraces seen
on CT, whereas CXR identified only 40, missing close to 25%.2
Examination Technique
Anatomic Considerations
When performing thoracic ultrasound to rule out pneumothorax it is essential to remember the anatomy of
the thoracic cage, and not be misled by the patient’s surface anatomy, which can be altered by excessive
muscle development or obesity. The thoracic cage is typically wider transversely than anteroposteriorly.
It becomes progressively narrower as you move superiorly, and the upper ribs have a downsloping
pattern that allows the muscles to push the sternum up and out, increasing the anteroposterior dimension of
the chest, facilitated by the costrochondral cartilaginous attachments anteriorly. Understanding these
anatomic relationships is essential when performing thoracic ultrasound, to know how to orient the probe
perpendicular to the pleura in all areas of the chest.
E X P E RT T I P
Ensure proper orientation of the probe before thoracentesis to minimize injury to adjacent
organs.

Figure 9-1. Supine Chest Radiograph
This image appears to show full lung inflation bilaterally.
Figure 9-2. Left-Sided Pneumothorax
This computed tomography scan through the midthorax shows a left-sided pneumothorax that was missed on chest radiography. This illustrates
the limitations of chest radiography in the diagnosis of pneumothorax in trauma patients.
Probe Orientation
Although different texts may recommend orientation of the probe toward either the patient’s head or feet,
the authors prefer to orient the probe so that when visualizing the patient and the ultrasound screen at the
bedside, the image orientation matches the patient’s orientation. This allows easy identification of the
superior and inferior aspects of the rib, which is essential during thoracentesis to prevent injury to the
neurovascular bundle during needle insertion.
Finding the Ribs and the Pleural Line

Identification of the pleura is facilitated by imaging with the probe perpendicular to the long axis of the
ribs and pointing directly at the pleura. In adults, the pleural line can be found approximately 0.5 cm deep
to the superficial surface of the rib. Ribs are easily identified by their highly reflective (white)
appearance, and the acoustic shadowing below (Figure 9-3).
The exceptions to this shadowing are when the probe is held in the immediate parasternal area over the
costrochondral cartilages, or when visualizing the thorax in young patients whose ribs are not fully
calcified (Figure 9-4)
Being perpendicular to the pleura is essential because the pleura is a specular reflector (mirror-like), and
ultrasound energy that hits this at an angle will not return to the transducer. Figure 9-5 shows images of the
chest taken perpendicular to the pleura, and tilted 30 degrees off perpendicular (Videos 9-1 and 9-2 ).
Figure 9-3. 2D View of Ribs with Acoustic Shadowing

Two-dimensional (2D) view showing typical appearance of ribs with acoustic shadowing on either side with bright visceral/parietal-pleural
interface in between.
Figure 9-4. 2D Thoracic Image of an Infant
In young children, the lack of ossification of the ribs allows transmission of ultrasound energy, similar to costrochondral cartilages in adults. In
this 2-dimensional (2D) view, multiple black spherical objects are ribs, and bright pleura is seen as a continuous wiggling line deep to the ribs.
Note the sharp pleural line in Figure 9-5A, and the diffuse, blurry pleural line in the 30-degree angled
image. After initial identification of the pleura, the sonographer can rotate the probe 90 degrees from this
position into a new position parallel with the long axis of the ribs, to allow imaging of a larger area
between the ribs. This maneuver is particularly useful when evaluating the extent of a pleural effusion or
assessing the extent of airless lung (pneumonia, atelectasis, pulmonary contusion) with a lower-frequency
probe.
Be Systematic
Several recommendations have been published on the best approach to examine the chest with ultrasound,
and the 8-zone approach described here is included in the international evidence-based recommendations
on lung ultrasound published in 2012.3 Comparison of the right and left hemithorax at the same relative
position can be helpful in rapidly identifying pathology, essentially using the patient as his or her own
“control.” In addition, the generalization that “air rises and fluid falls” can be helpful in ruling out an
acute pneumothorax or pleural effusion. It is important to realize that chronic, complex effusions may be
nondependent (Figure 9-6).
The 8-zone lung ultrasound examination extends laterally from the parasternal line to the anterior axillary
line, and then to the posterior axillary line. The chest is further divided into upper and lower lung fields,
as shown in the image. This provides 4 zones in each hemithorax: upper anterior, lower anterior, upper
lateral, and basal lateral. It is important to add text labels to images during acquisition, which can be done
easily with most ultrasound systems, to allow follow-up and to track changes over time.
Thoracic Ultrasound Findings

2-Dimensional (B-Mode)
Lung Sliding. The juxtaposition of the visceral and parietal pleura, and its back-and-forth movement with
respiration, can be visualized with high- and low-frequency probes. This to-and-fro motion has been
termed “lung sliding.”4 Lung sliding rules out the presence of any other substance in the pleural space (air,
liquid, tumor). Normally a small amount of fluid in the pleural space acts as a lubricant, but this is not
typically appreciated as it is evenly distributed around the lung, forming a very thin layer. Lung sliding
can be appreciated only when the patient is breathing either spontaneously or assisted via invasive or
noninvasive mechanical ventilation. Lung sliding can be absent without air or fluid in the pleural space if
the patient is apneic, esophageally intubated, or extremely hyperinflated (severe asthma exacerbation,
positive end-expiratory pressure [PEEP], or auto-PEEP). The presence of some disease states of the lung
or pleura including, but not limited to, pleural adhesions, pneumonia, acute respiratory distress syndrome
(ARDS), or pulmonary fibrosis can also lead to loss of visible lung sliding. In the setting of mainstem
intubation, lung sliding can occur over 1 hemithorax but be absent on the other. In summary, lung sliding is
sensitive for determining the absence of pneumothorax, but the absence of lung sliding can have a broad
differential diagnosis beyond pneumothorax or pleural effusion (Videos 9-3 and 9-4 ).
Figure 9-5. Ultrasound Image of Chest

A) In this image, the probe is held at 90 degrees to the pleura (perpendicular). B) In this instance, the probe is tilted 60 degrees to the pleura.
Diffuse, darker, indistinct visceral/parietal-pleural line is seen if the probe is not held perpendicular to the pleura.
Lung Pulsations. When the heart ejects blood into the pulmonary vasculature, a translational motion of the
lungs is noted along the chest wall. This can be observed as short sliding movements that correspond to
the pulse, but not respiration. These can be observed in apneic patients, indicating that there is direct
contact between the visceral and parietal pleura, thus excluding pneumothorax or pleural effusion (Video
9-5 ).
Figure 9-6. 8 Standard Zones of the Chest
A-Lines. When ultrasound waves strike a strong specular reflector that is perpendicular to the beam, a
large amount of the acoustic energy is reflected back toward the probe. This creates the bright white
interface that allows easy identification of the visceral/parietal-pleural interface. Some of this energy
comes back and is reflected off the skin-probe interface (or connective tissue layers between the probe
and pleura) and travels back down through the tissues to be bounced off the pleura again. This leads to
sound taking a longer time to return to the probe, and is interpreted by the machine as coming from an
acoustic interface further from the probe. The machine plots the bright line, or lines, farther down through
the sector at an equal distance from the primary reflective surface. In lung ultrasound, these reverberation
artifacts are called “A-lines.” This can occur with any strong specular reflector that is perpendicular to
the ultrasound beam, and can lead to a series of repeated lines that appear deep to the pleural line. A-
lines are present in normal lungs as well as pneumothorax, but are typically absent in simple effusions
(Figure 9-7).
Figure 9-7. A-Lines in Patient with Pneumothorax
A) Multiple bright A-lines below the pleura in a patient without pneumothorax. B) Multiple A-lines in a patient with pneumothorax.
B-Lines. B-lines (also called “comet tail artifacts”5) are bright lines that are parallel to the ultrasound
beam being sent out from the probe. Although occasionally seen in the dependent areas in normal lungs,
they are more typically seen in patients with pulmonary edema, fibrosis, or other interstitial or alveolar
lung pathologic processes. The number and spacing of B-lines have been considered useful in assessing
severity of pulmonary edema. Differentiating cardiogenic edema from inflammatory diseases of the lung,
such as ARDS or pneumonia, requires additional characteristics. This will be covered in Chapter 10.
The genesis of B-lines (also known as a “ring down artifact”) is thought to be the ultrasound energy
reflecting off the fluid in the interlobular septa of the lung. Although the exact mechanism is not clear,
bright, laser-like reverberations appear, which extend to the bottom of the screen without fading. B-lines
erase the A-lines they cross. B-lines originate from the visceral pleura and move with it during breathing.
If the B-lines appear to be coming directly from the visceral/parietal-pleural interface, the presence of
pneumothorax or pleural effusion can be ruled out.3 B-line sliding at the level of the visceral/parietal-
pleural interface should be considered equally reassuring as lung sliding in this regard (Figures 9-8 and
9-9, Videos 9-6 and 9-7 ).
Figure 9-8. Three Widely Spaced B-Lines
The middle B-line is clearly erasing A-lines.
Figure 9-9. Closely Spaced B-Lines
Pleura is visible deep to the rib, indicating that the probe is over the costrochondral cartilage.
B-lines can often be appreciated in the posterior portion of the diaphragm during the focused assessment
with sonography in trauma (FAST), or deep to the pericardium during the parasternal long-axis view of
the echocardiographic exam. Like B-lines seen on the chest surface, B-lines seen in these alternative
locations also rule out the presence of fluid or air in the pleural space at that level. In cases of pleural
effusion with associated pulmonary edema, B-lines are often seen emanating from the visceral pleura,
combined with a dark (nonechogenic) space between the parietal pleura and the surface of the lung
(Figure 9-10).
Figure 9-10. B-Lines from Visceral Pleura
This image shows B-lines coming from the visceral pleura with anechoic space between parietal and visceral pleural effusion. B-lines still
originate from the visceral pleural edge even when visceral and parietal pleura are not touching.
Figure 9-11. Seashore Sign

Seashore sign (2-dimensional and M-mode), microcurvilinear probe.
M-Mode (Motion Mode)
The evaluation of the pleural interface with M-mode can be very helpful in differentiating normal from
abnormal. The M-mode cursor is placed between the ribs and then plotted over time. The normal
appearance is a series of white lines of varying brightness between the transducer and the parietal pleura
(easy to identify by comparing the depth from the skin to the pleura on the 2-dimensional [2D] image, then
looking at the same depth on the M-mode). Beyond the parietal-pleural line, the moving aerated lung
creates an appearance similar to grains of sand (if viewed with a high-frequency probe) or small pebbles
(with a lower frequency). This is described as the “seashore sign,” because it looks like a series of
waves coming in and hitting a sandy beach (Figure 9-11).6
M-mode cannot penetrate the ribs in adults. It is critical to line up the M-mode indicator in the interspace,
not over a rib. Allowing the hand holding the transducer to slide on the chest during acquisition can
erroneously lead to the diagnosis of an absent seashore sign in a patient with normal lungs.
In situations in which there is no aerated lung moving under the pleura, the appearance of linear
reverberation artifacts (normally seen superficial to the pleural line) will continue below. Because of its
appearance of white and dark lines of varying thicknesses, this has been described as looking like a
barcode (“barcode sign”) or jet contrails in the sky (“stratosphere sign”). Although this pattern is seen in
pneumothorax, it is not specific for this diagnosis (Figure 9-12).
Pitfalls of M-Mode. The lung must be moving below the probe in order to see the seashore sign. If the
patient is apneic, breath-holding, or mainstem-intubated, no motion of the lung will be seen and, therefore,
no sandy beach-appearing area will be present. Lung pulsations/cardiac oscillations will also cause the
intermittent appearance of sand deep to the pleural line and indicate the lung in apposition with the chest
wall.
E X P E RT T I P
Use of M-mode can add certainty when ruling out pleural pathology in larger patients, when it
can be challenging to see lung sliding or lung pulsations well.
Figure 9-12. Barcode Sign

A) Barcode (stratosphere) sign (2-dimensional and M-mode), linear probe. B) Barcode (stratosphere) sign (2-dimensional and M-mode), low-
frequency phased-array probe.
Figure 9-13. Hand/Probe Motion Creating Artifact That Can Be Mistaken for Lung Point Sign
M-mode showing that a barcode sign can be made to look like a lung point by moving the probe hand. Note the “sandy” appearance superficial
and deep to the pleural line compared with the depth of the pleural line on targeting the 2-dimensional image. Presence on both sides of the
pleura should alert the sonographer to this artifact.
Figure 9-14. Lung Point

Lung point in patient with partial pneumothorax, M-mode.
Wiggling the transducer can create an appearance similar to the sandy beach. This can be differentiated
from a true seashore sign by means of a sandy appearance between the transducer and the pleural line. It
is very important to hold the transducer very steady during M-mode acquisition (Figure 9-13).
C AVE AT
Use anterior chest wall scanning and M-mode to rule out pneumothorax after thoracentesis.
Lung Point. Lung point is a pattern that is 100% specific for pneumothorax.6 Lung point is seen when the
sonographer holds the probe steady at 1 point on the chest and sees a transition from absent lung sliding to
the appearance of lung sliding with inhalation. On some occasions with 2D imaging, the lung can be seen
coming up and touching the parietal pleura. In patients with B-lines, the B-lines can be seen to appear and
disappear as the lung surface makes contact with the chest wall and then drops away.
Lung point is created by the lung increasing in size with inhalation and displacing the air between the lung
and the chest wall. It is not seen in complete pneumothorax because the lung will not inflate enough to
come into contact with the chest wall. When applying M-mode at the same point, it is possible to see the
appearance and disappearance of the sandy (granular) appearance below the pleural line during the
respiratory cycle (Figure 9-14).
E X P E RT T I P
In the lower portion of the thorax, the parietal pleura of the chest comes in contact with the
surface of the parietal pleura on the surface of the diaphragm (anterior and posterior
diaphragmatic reflections, or zone of apposition), and this can be incorrectly interpreted as
absent lung sliding or even the lung point.
A recent study evaluated the value of ultrasound in providing semiquantitative measurement of the size of
pneumothorax.7 The authors of that study evaluated supine patients with ultrasound and CT. Using a 3-
dimensional CT volumetric measurement of pneumothorax volume as the gold standard, they found that
demonstrating a lung point at, or posterior to, the midaxillary line was the point at which the
pneumothorax was identified as being larger than 15% of the volume of the hemithorax (the accepted
threshold of many providers for chest tube drainage); this study showed an 83.3% sensitivity and 82.4%
specificity. The authors of this chapter recommend that lung point only be diagnosed in a patient who
presents with lung sliding in the dependent areas of the chest, without lung sliding in the most
nondependent area, and then shows an area with intermittent lung sliding in between.
When a patient is between breaths (or breath-holding, not ventilated) the normal lung can show a barcode
sign. Demonstration of the seashore sign in a dependent area with breathing indicates that the lung is being
ventilated. It is easy to demonstrate this “fake lung point” by placing the transducer on your own chest,
taking a breath, then holding it while the M-mode is recording. You will see an abrupt termination of the
seashore sign with transition of barcode, similar to a lung point. One clue that this is not a true lung point
is the presence of lung pulsations with a brief sandy beach sign.
In addition, it is important to recognize the appearance of the diaphragmatic reflections that can appear to
be demonstrating lung point as the diaphragm descends during inspiration and the lung moves into that
space (area of apposition) (Video 9-8 ).
Case Study 2
A 45-year-old man undergoing laparoscopic repair of a hiatal hernia in steep reverse Trendelenburg
position develops increased airway pressures intraoperatively. Evaluation indicates an increase in both
peak and plateau pressures of approximately 15 cm of water and a subsequent drop in blood pressure.
There also has been a reduction in the need for volatile anesthetic, and phenylephrine boluses are
required to maintain adequate blood pressure. The surgeon evaluates the abdominal side of the diaphragm
and states that the diaphragm is not bulging, and doubts that the patient has had any passage of carbon
dioxide into the pleural space. Intraoperative ultrasound performed near the apices of the lungs bilaterally
shows asymmetric findings, absent lung sliding, and absent seashore sign on the right only. The patient’s
blood pressure was maintained with phenylephrine, so confirmatory CXR was performed, which showed
a large right pneumothorax. An angiocatheter was placed over the 4th rib anteriorly for decompression of
carbon dioxide. Return of lung sliding was demonstrated over the entire hemithorax after 800 mL of air
was removed, leading to an improvement in the patient’s pressure and an uneventful recovery. Figure 9-15
shows the M-mode appearance of the barcode/stratosphere sign (Figure 9-15A) when there was absent
lung sliding prior to decompression, and the return of the reassuring seashore sign on M-mode after
decompression (Figure 9-15B).
Figure 9-15. Barcode and Seashore Signs

A) Barcode sign in patient with intraoperative pneumothorax. B) Seashore sign seen in same location after the pneumothorax was evacuated
with an angiocatheter.
Evidence for Use of Ultrasound for Pneumothorax

It is easier to rule out pneumothorax than to rule it in. Multiple studies have evaluated the relative
sensitivity and specificity of ultrasound to diagnose pneumothorax. In addition to the trauma series
described,2 which showed that CXR missed 25% of pneumothoraces, a report of 184 patients undergoing
percutaneous needle biopsies of the lung showed ultrasound to be far superior to CXR. After needle
biopsy, all patients underwent evaluation with CT, ultrasound, and CXR.8 In a series of 45
pneumothoraces, CT scan and ultrasound identified 45 and 44 pneumothoraces, respectively; in
comparison, CXR identified only 19 of these 45 pneumothoraces. Recent meta-analyses9,10 showed that
lung ultrasound had superior diagnostic performance compared with CXR in the diagnosis of
pneumothorax. These studies showed that CXR is inferior to ultrasound when used to exclude this life-
threatening condition in critically ill patients. The lack of portability of CT leaves thoracic ultrasound as
the most appropriate diagnostic tool, with very high sensitivity, portability, and immediacy of results.
Figure 9-16 shows an algorithm that can be used when applying lung ultrasound to determine the presence
or absence of pneumothorax.
Figure 9-16. Pneumothorax Algorithm

Information taken from Volpicelli G, Elbarbary M, Blaivas M, et al. International evidence-based recommendations for point-of-care
ultrasound. Intensive Care Med. 2012;38:577-591.
PLEURAL EFFUSION
Critically ill patients develop pleural effusions for a multitude of reasons during their time in the ICU.
Large pleural effusions can compress dependent lung areas and increase atelectasis formation, increase
the work of breathing, increase hypoxemia, cause pleuritic chest pain, and delay the discontinuation of
mechanical ventilation. Pleural effusions can be missed easily with a supine portable CXR. Although CT
scanning is the gold standard for the evaluation of effusion, it is labor intensive, time consuming, and at
times unsafe to transport a critically ill patient for this study. Because of these factors, bedside lung
ultrasound is an indispensable tool to both diagnose and safely treat pleural effusion. It often becomes
necessary to look for effusion to make it easier to discontinue mechanical ventilation, to rule out an
infected effusion (empyema), or to perform an evaluation for hemothorax in a trauma patient. Assessment
of the pleura for the presence or absence of a pleural effusion is simple with the use of ultrasound and is
much more sensitive than CXR. As concerns about exposure to diagnostic radiation increase, lung
ultrasound has this added advantage over the use of CXR and CT scanning. Lichtenstein et al11
prospectively compared the diagnostic accuracy of auscultation, CXR, lung ultrasound, and chest CT in
32 patients with ARDS and 10 healthy volunteers based on the presence of pleural effusion, lung
consolidation, and ARDS (alveolar-interstitial syndrome). The authors found that lung ultrasound had a
diagnostic accuracy of 93% for pleural effusion, 97% for consolidation, and 95% for alveolar-interstitial
syndrome.
The larger the patient, the more important it is for the probe to be perpendicular to the pleura.
Frequently, inexperienced sonographers will be frustrated and unable to acquire diagnostic images
because they are imaging the pleura tangentially, which degrades the image by loss of energy return. This
error additionally increases the depth of travel to and from the pleura, necessitating a lower-frequency
probe, which will give a lower-resolution image.
In contrast, CXR was only 47% accurate for the diagnosis of pleural effusion, 75% for consolidation, and
72% for alveolar-interstitial syndrome. Another prospective study12 compared the performance of lung
ultrasound to detect pleural effusion with that of bedside CXR. This study evaluated 42 patients receiving
mechanical ventilation and found that lung ultrasound had a sensitivity, specificity, and diagnostic
accuracy of 100% for pleural effusion compared with chest CT. CXR performed significantly worse, with
a 65% sensitivity, 81% specificity, and 69% diagnostic accuracy.
Ultrasonographic evaluation of pleural effusion can be performed with high-frequency linear,

microcurvilinear, standard curvilinear, or phased-array probes. Although a high-frequency linear probe
has the best resolution, it is limited by inadequate depth of penetration and acoustic shadowing of the ribs.
The phased-array (cardiac) probe and the microcurvilinear probes have the advantage of a small footprint
with a divergent beam, allowing better determination of the size of an effusion through a single rib
interspace. The large curvilinear probes allow better overall assessment of effusion and surrounding
structures, and can span several interspaces at the same time. Sonographers typically use the large
curvilinear or phased-array probes to assess the size of the effusion and relationship to surrounding
structures. Images can be obtained with the patient in the supine, seated, or lateral decubitus positions.
Scanning around the 4th to 6th intercostal spaces laterally or posteriorly can be performed to quickly
locate a pleural effusion. It is often useful to palpate a rib space and then place the ultrasound probe
between 2 ribs to initiate scanning. We orient the indicator of the ultrasound probe so that the image on the
screen will be in the same orientation as the patient. This can be seen in Figure 9-17, which shows the
head of the patient (in lateral decubitus) to the right, and the machine facing the person performing the
procedure with the right side of the screen corresponding to the patient’s head. To do this, we begin
imaging with a low-frequency probe to give a large field of view, find the diaphragm to determine which
side is cephalad (liver or spleen will be caudad to the diaphragm), and rotate the probe to make the
screen match the patient’s position. Once the diaphragm has been located, we can easily note the presence
of anechoic pleural fluid and the presence or absence of consolidated/atelectatic lung within that space
(Figure 9-18).
As we begin scanning, rib shadows are noted as obvious dark hypoechoic streaking artifact oriented
vertically across ultrasound monitor. While obtaining images, it is useful to first attempt to identify the
structures that are adjacent to the lung and pleura. Pleural effusion will typically be located along the
dome of the diaphragm in the most dependent areas of the patient’s hemithorax. A simple pleural effusion
will display as a homogeneous dark area adjacent to the lung and diaphragm, and often allow
identification of the thoracic spine above the diaphragm (“spine sign”) (Figure 9-19).
Figure 9-17. Right Lateral Decubitus Position for Draining Left-Sided Effusion
Patient with left pleural effusion, in right lateral decubitus position with head to the right. The ultrasound screen is in front, facing the operator,
with the right side of the image corresponding to the cephalad direction of patient.
Figure 9-18. Collapsed/Consolidated Lung Floating in Effusion

It is possible to image through the lung when the lung is not filled with air.
In moderate to large pleural effusions, it is common to visualize atelectatic lung floating in the anechoic
fluid. Atelectatic or consolidated lung can be identified on lung ultrasound because the absence of
aeration allows transmission of the ultrasound energy through the lung, which will often have a similar
ultrasound appearance as that of the liver. Another useful sign is the absence of the mirror image artifact
of the liver that can often be seen in patients without pleural effusion on the thoracic side of the diaphragm
(Figure 9-20). After changing to a high-frequency linear probe, the thickness of the effusion can be
determined with both 2D and M-mode (Figure 9-21).
Ultrasound can also be useful to characterize the quality of pleural fluid. For example, a very dark,
anechoic collection surrounding the lung will most often be consistent with a free-flowing transudative
effusion, whereas a hypoechoic “fuzzy” looking collection could be a more complicated exudative
effusion. It is also often possible to notice septations within pleural effusions on ultrasound, which can
indicate a more complicated collection. This appearance is common in parapneumonic effusions,
empyemas, and subacute hemothoraces that have not been adequately drained. Yang et al13 reported on the
ultrasound appearance of 320 pleural effusions and described the effusions as either anechoic, complex
nonseptated, complex septated, or homogenously echoic. The authors reported that all transudative
effusions had a uniform anechoic appearance. The presence of fibrin stranding, varying degrees of
septations, or diffusely echoic-appearing fluid were all found to be exudative in nature. A similar study
evaluating pleural effusions in febrile medical ICU patients found that all patients with empyema had
ultrasound findings of a complex septated or nonseptated pattern with hyperechoic features or a
homogenously echogenic pattern (Figure 9-22).14
Figure 9-19. Spine Sign

Right thorax/diaphragm/liver showing a spine sign.
Figure 9-20. Normal Appearance of Chest in Absence of Effusion, Mirror Image Artifact of Liver
Liver and diaphragm in a healthy patient, showing the presence of mirror image artifact of liver above the diaphragm. This finding rules out
pneumothorax. This is also a nice example of the inability to visualize the spine above the diaphragm because of aeration of lungs (absence of
the “spine sign”).
Figure 9-21. Appearance of Effusion with High Frequency Linear Probe
Anechoic space between the parietal pleura and visceral pleura (M-mode). The jagged edge occurs because of cardiac oscillations, with larger
waves representing the “sine wave sign.”
Figure 9-22. Complex Pleural Effusion with Septations

Complex pleural effusion showing multiple septations and high-density material against the spine.
Several studies have looked at various methods to quantify the amount of pleural fluid noted during lung
ultrasound. Vignon et al15 performed a prospective study on the ability of ultrasound to detect and assess
the volume of pleural effusion in the ICU. A study group underwent lung ultrasound and had interpleural
distances measured in the supine position at the lung base and the apex. The basal expiratory interpleural
distance greater than 45 mm (right) and 50 mm (left) was correlated with a pleural effusion greater than or
equal to 800 mL, with a sensitivity of 94% and 100%, respectively, and a specificity of 76% and 67%,
respectively. Balik et al16 evaluated 92 pleural effusions with ultrasound and subsequent thoracentesis
and found that pleural effusion volume (expressed in milliliters) could be calculated by multiplying the
maximal distance (in millimeters) between the parietal and visceral pleura at the lung base by 20. The
authors also had a 100% success rate of drainage with ultrasound guidance and zero episodes of bleeding
or pneumothorax.
E X P E RT T I P
Use real-time ultrasound when performing thoracentesis to avoid injury because of the shifting
of fluid over time.
The lateral decubitus position allows for ease of approach to thoracentesis and may minimize the risk of
endotracheal tube and central line displacement.
THORACENTESIS
Thoracentesis can be associated with serious and potentially life-threatening complications, including
hemorrhage and pneumothorax. The early use of ultrasound-guided pleural taps involved a radiologist
coming to the bedside, performing an ultrasound and marking the chest, and then leaving. This was a great
improvement over percussion of the chest, but it still potentially left the patient at risk for injury because
of shifting of fluid over time with changes in patient position. Use of real-time ultrasound has made needle
thoracentesis of pleural effusions a very easy, fast, and safe procedure. In addition to assessing the quality
and quantity of pleural fluid, ultrasound-guided thoracentesis is an indispensable tool for the intensivist.
Real-time ultrasound guidance can also be used to place pigtail drainage catheters with ease and safety. A
prospective study of 605 patients undergoing 941 ultrasound-guided thoracenteses by interventional
radiologists found that the incidence of pneumothorax was less than 3% and bleeding complication rate
was 0.2%. Only 8 of 24 patients with postprocedure pneumothorax required a chest tube.17 A small
prospective study by Lichtenstein et al18 showed that ultrasound-guided thoracentesis could be performed
safely even in mechanically ventilated patients. The group performed 45 procedures in patients with
ultrasound evidence of pleural effusion and obtained fluid in 44 of 45 procedures. The authors reported
rapid access to fluid (<10 seconds) in 40 of 45 cases and were able to drain the effusions in supine
patients in 22 of 45 procedures.
Ultrasound-guided thoracentesis may be easily performed at the patient’s bedside in the ICU with very
simple setup. The patient can be positioned in several ways—seated, supine, or the lateral decubitus
position with the effusion side facing up toward the operator. The lateral decubitus position alleviates
tension on ventilator tubing and may minimize risk of endotracheal tube dislodgement while performing
the procedure. This is the authors’ preferred position.
Setup typically involves placing the ultrasound machine directly across from the operator for ease of
viewing. The patient is then placed in the desired position and the area of the thorax is cleaned thoroughly
with chlorhexidine and allowed to dry to create a sterile field. While the chlorhexidine preparation is
drying, the operator will scrub and don sterile attire. The patient is then covered with sterile towels or a
large fenestrated sterile drape to create a sterile work field. If using ultrasound as a marking tool, it is
best to mark the area immediately before sterilizing the procedure site or alternatively using a disposable
sterile sleeve over the ultrasound probe to locate the largest pocket of effusion for sampling. If a
prolonged period passes between marking a site and performing thoracentesis, the effusion could drain
into a more dependent area, raising the risk of pneumothorax. Once a large pocket of effusion is located,
anesthetize the area with a local anesthetic such as lidocaine (Figure 9-17).
Typically the site with the largest diameter of fluid is the best site to perform thoracentesis. As actively
practicing intensivists, we are performing thoracentesis most commonly for therapeutic indications. The
authors use a minimum size pocket of fluid of 1.5 to 2 cm. Draining smaller effusions is unlikely to
provide a respiratory benefit to the patient, and increases the risk of puncture of the lung or injury to
adjacent structures. If a small effusion sample is needed for diagnostic purposes (culture, laboratory
analysis, flow cytometry) we consult our radiologists to perform the thoracentesis.
When determining the size of an effusion it can be helpful to use M-mode and measure the distance from
the parietal to the visceral pleura. On M-mode, the lung pulsations and respiratory motion give the sandy
beach area a jagged edge and a sine wave-like pattern of movement. The lung itself shows larger
oscillations during breathing – the sinusoid sign. Figure 9-21 shows both the jagged, tooth-like movement
of the pleura from cardiac oscillation and the lower frequency sinusoidal waves of breathing in an M-
mode performed with a high-frequency linear probe.
Before inserting the thoracentesis needle, it is useful to palpate the rib space and ensure easy guidance of
the needle over the top of the rib, to avoid the neurovascular bundle underneath the rib. In thin patients,
we use real-time ultrasound guidance of needle insertion into the pleural space with a linear or
microcurvilinear probe. For larger patients, it is often necessary to use the phased-array or large
curvilinear probe for better penetration. The lower-frequency probes have poor near-field resolution and
can make it hard to visualize the needle (Figure 9-23).
C AVE AT
Avoid thoracentesis on small fluid collections <1.5 cm.
After the effusion has been drained, it is helpful to repeat the ultrasound scan of the pleural space to
evaluate for residual fluid. The anechoic space becomes smaller, thus providing reassurance that the
effusion was completely or almost completely drained. Once the procedure is complete, it is easy to
switch to a high-frequency linear or microcurvilinear probe, place the patient in the supine position, scan
the anterior thorax for the presence of lung sliding, and thus rule out pneumothorax. This quick anterior
chest scan should be repeated if the patient has any change in respiratory status over time because post-
thoracentesis pneumothoraces can develop slowly.
Figure 9-23. Real-Time Needle Guidance with Ultrasound
Real-time ultrasound imaging during thoracentesis, allowing concurrent visualization of effusion and passage of needle, limiting the risk of injury
to the lungs or surrounding organs.
KEY POINTS
Bedside lung ultrasound rapidly and accurately rules out the presence of pneumothorax.
Images may be obtained with linear, phased-array, or curvilinear probes.
Imaging perpendicular to the pleura is essential, and is based on knowledge of anatomy.
Absence of lung sliding or B-lines is abnormal, but the presence of lung point is the only sign that is
specific for pneumothorax.
Bedside lung ultrasound is highly sensitive and specific for the presence of pleural effusion.
Images are best obtained with a curvilinear or phased-array probe.
The patient can be positioned in a supine, seated, or lateral recumbent position.
The volume of effusion can be estimated based on measured distance between visceral and parietal
pleura.
The type of effusion and its complications (empyema, hemothorax, or adhesions) can be judged by
the presence or absence of septation and degree of the echocardiographic signal.
REFERENCES
1. Joyner CR, Herman RJ, Reid JM. Reflected ultrasound in the detection and localization of pleural effusion. JAMA. 1967;200:399-402.
2. Blaivas M. A prospective comparison of supine chest radiography with bedside ultrasound for the diagnosis of traumatic pneumothorax.
Acad Emerg Med. 2005;12: 844-849.
3. Volpicelli G, Elbarbary M, Blaivas M, et al. International evidence-based recommendations for point-of-care lung ultrasound. Intensive
Care Med. 2012;38:577-591.
4. Lichtenstein D, Menu Y. A bedside ultrasound sign ruling out pneumothorax in the critically ill: lung sliding. Chest. 1995;108:1345-1348.
5. Lichtenstein D, Meziere G, Biderman P, et al. The comet-tail artifact: an ultrasound sign of alveolar-interstitial syndrome. Am J Respir Crit
Care Med. 1997;156:1640- 1646.
6. Lichtenstein D, Meziere G, Biderman P, et al. The lung point: an ultrasound sign specific to pneumothorax. Intensive Care Med.
2000;26:1434-1440.
7. Volpicelli G, Boero E, Sverzellati N, et al. Semi-quantification of pneumothorax volume by lung ultrasound. Intensive Care Med.
2014;40:1460-1467.
8. Garofalo G, Busso M, Perotto F, et al. Ultrasound diagnosis of pneumothorax. Radiol Med. 2006;111:516-525.
9. Alrajhi K, Woo MY, Vaillancourt C. Test characteristics of ultrasonography for detection of pneumothorax. Chest. 2012;141:703-708.
10. Alrajab S, Youssef AM, Akkus NI, et al. Pleural ultrasonography versus chest radiography for the diagnosis of pneumothorax: review of
the literature and meta-analysis. Crit Care. 2013;17:R208.
11. Lichtenstein D, Goldstein I, Mourgeon E, et al. Comparative diagnostic performances of auscultation, chest radiography, and lung
ultrasound in acute respiratory distress syndrome. Anesthesiology. 2004;100:9-15.
12. Xirouchaki N, Magkanas E, Vaporidi K, et al. Lung ultrasound in critically ill patients: comparison with bedside chest radiography. Intensive
Care Med. 2011;37:1488- 1493.
13. Yang PC, Luh KT, Chang DB, et al. Value of sonography in determining the nature of pleural effusion: analysis of 320 cases. AJR Am J
Roentgenol. 1992;159:29-33.
14. Tu CY, Hsu WH, Hsia TC, et al. Pleural effusions in febrile medical ICU patients: chest ultrasound study. Chest. 2004;126:1274-1280.
15. Vignon P, Chastagner C, Berkane V, et al. Quantitative assessment of pleural effusion in critically ill patients by means of ultrasonography.
Crit Care Med. 2005;33:1757- 1763.
16. Balik M, Plasil P, Waldauf P, et al. Ultrasound estimation of volume of pleural fluid in mechanically ventilated patients. Intensive Care Med.
2006;32:318-321.
17. Jones PW, Moyers JP, Rogers JT, et al. Ultrasound guided thoracentesis: is it a safer method? Chest. 2003;123:418- 423.
18. Lichtenstein D, Hulot JS, Rabiller A, et al. Feasibility and safety of ultrasound guided thoracentesis in mechanically ventilated patients.
Chapter 10
Pulmonary Edema and Consolidation
OBJECTIVES
Identify interstitial and alveolar-interstitial patterns on ultrasound
Identify atelectasis and consolidation patterns on ultrasound
Utilize differences in the patterns to differentiate among disease processes
INTRODUCTION
The interface between fluid and air creates such high acoustic impedance that it prevents investigation of
what lies beyond the interface. If the lung tissue is visualized, that is pathologic, air is absent. Otherwise,
much is to be learned from an analysis of artifacts, both physiologic and pathologic.1 The character of the
air-fluid interface changes as the amount of fluid increases, and the resulting artifacts can provide useful
information. Ultimately, the power of chest sonography is in the immediate integration of findings with the
clinical assessment at the bedside.
CASE STUDY
A 63-year-old woman with a history of hypertension and depression develops worsening dyspnea and
hypoxia on the first postoperative day after an elective plastic surgery (face lift and abdominoplasty).
Bedside diagnostic sonography is performed at the point of care, and the consulting physician
immediately correlates findings to the clinical course (Figures 10-1 and 10-2). The echocardiogram
discloses normal left and right ventricular function, and the inferior vena cava is collapsible;
measurements indicate normal right atrial pressure.
How Do We Interpret These Findings?

Ultrasound has identified a B-pattern in 5 of 8 hemithorax quadrants. The pleura is irregular with tiny
subpleural hypoechoic abnormalities, and sliding is reduced. The patient has a sonographic alveolar-
interstitial pattern in a diffuse, nonhomogeneous distribution. Focused echocardiogram indicates normal
left ventricular function and no evidence of volume overload or pulmonary hypertension. This is
compatible with noncardiogenic pulmonary edema, or acute respiratory distress syndrome (ARDS). On
computed tomography (CT), one can appreciate the patchy nature of ARDS, and how the sonographic
appearance has a normal pattern in some regions and interstitial-alveolar syndrome in other regions.
A representative CT image of the patient, with the probe position correlating to area 1 on each
hemithorax, is shown in Figure 10-3.
LUNG SONOGRAPHY
The thorax should be scanned in at least 8 regions in a critically ill supine patient (Figure 10-4), including
each hemithorax with a superior and inferior region anteriorly and laterally for a presumed diffuse
process. The thorax should also be scanned posteriorly for suspected regional processes, or when using a
comprehensive grading protocol to assess severity (see Chapter 18).1,2
Figure 10-1. Lung Zones for Insonation

The chest is divided into anterior and lateral parts along anterior and posterior axillary lines, and further into superior and inferior parts along
nipple line. The 8-zone examination is standard. (See also Chapter 18. )
Figure 10-2. Ultrasound Images Depicting Areas Presented in Figure 10-1

A) A phased-array probe was used to obtain the images. Areas 1 and 3 on the right hemithorax and area 2 on the left hemithorax disclose A-
lines, a normal finding. B) A phased-array probe was used to obtain the images. Areas 2 and 4 on the right hemithorax and areas 1, 3, and 4 on
the left hemithorax disclose B-lines, an abnormal finding. C,D) Closer examination of the pleura in the abnormal areas shown in B. A linear
probe was used to obtain these images, which illustrate B-lines and subpleural consolidations.
Figure 10-3. Computed Tomography Image of Patient
In this representative computed tomography image of the patient, the probe position correlates to area 1 on each hemithorax.
Figure 10-4. 8-Zone Lung Ultrasound
Abbreviations: PSL, parasternal line; AAL, anterior axillary line, PAL, posterior axillary line.
The 4 chest areas per side considered for complete 8-zone lung ultrasound examination are shown. These areas are used to evaluate for the
presence of interstitial syndrome. Areas 1 and 2 denote the upper anterior and lower anterior chest areas, respectively. Areas 3 and 4 denote
the upper lateral and basal lateral chest areas, respectively.
Volpicelli G, Elbarbary M, Blaivas M, et al. International evidence-based recommendations for point-of-care-lung ultrasound. Intensive Care
Med. 2012;38:577-59; Figure 2. Copyright © 2012 Springer and ESICM, with kind permission from Springer Science and Business Media.
E X P E RT T I P
Do not neglect the posterior lower lobes because the patient is supine; many pulmonary
abnormalities can manifest first in that location. Localized processes may occur only in a dorsal
area. If the cause of respiratory failure is unknown or is determined not to be a diffuse process,
then add 2 zones of scanning for each posterior hemithorax, for a total of 12 zones rather than 8.
Use the linear or microconvex probe to examine pleura! (Both probes give better resolution at
shallower depths than the phased-array probe. The microconvex probe has a smaller footprint and
wider frequency range.)
Figure 10-5. Normal Lung

A-lines at regular intervals from the pleural line, phased-array probe. Rare B-lines are physiologic, especially in dependent areas.
Both the linear probe and the phased-array probe are used for lung sonography. The linear probe, with its
high resolution and reduced scatter, is ideal for examining the pleura and guiding real-time procedures.
The phased-array probe has much deeper penetration, and is useful for examining the deep margins of
consolidated areas or the depth of effusions, for example. Either probe can identify interstitial edema.1,3
The pleural line is a horizontal hyperechoic line in the intercostal space about 0.5 to 1 cm below the outer
surface of the ribs (Figure 10-5).
Lung sliding is the motion of this line with respiration. When viewed in M-mode, this gives the “seashore
sign.” The lack of motion in the subcutaneous tissues gives a horizontal linear appearance akin to waves
coming toward the beach. The movement detected below the pleural lines appears similar to beach sand
on M-mode (Figure 10-6).
A-lines are horizontal reverberation artifacts of the pleural line. A portion of the returning sound pulse is
reflected back to the tissue by the transducer itself, and a ghost echo of the pleural line appears at
multiples of its actual depth (Figure 10-5).
Avoid advanced ultrasound filters (eg, harmonic imaging).
Figure 10-6. Lung Sliding

M-mode showing the seashore sign, linear probe.
B-lines (also described as “lung comets” or “rockets”) are laser-like vertical reverberation artifacts
generated by the interaction between fluid and air bubbles; the exact mechanism of their production is
unclear. B-lines originate from the pleural line and extend to the end of the screen. They obliterate A-
lines, and move with lung sliding (Figures 10-7 and 10-8; Videos 10-1 – 10-3 ).4
Consolidation and atelectasis appear as a subpleural, echo-poor region of lung. As air is excluded from
the alveoli, the alveoli assume a tissue-like density, resembling liver or spleen. This is sometimes called
“hepatization” (Figures 10-9 and 10-10; Videos 10-4 and 10-5 )
Figure 10-7. B-Lines
A,B) Generation of B-lines of 7-mm and 3-mm spacing, respectively. C-F) B-lines viewed with the phased-array probe, showing the spectrum
from normal to approximately 7-mm (spaced) B-lines, to approximately 3-mm (close) B-lines, to white (confluent) B-lines. This correlates with
worsening lung water, with D roughly representing interstitial edema; E, alveolar edema; and F, severe alveolar edema. G) Examination of B-
lines using the linear probe, again highlighting the spacing of the interstitial pattern at about 7 mm.
INTERSTITIAL AND ALVEOLAR PATTERNS

As lung water increases (during cardiogenic pulmonary edema, for example), the fluid appears first in the
perivascular interstitial space, then progressing to involve interlobular septa and then alveoli. This is a
generalization, and not an exactly linear relationship. The presence of B-lines at about 7 mm of spacing
represents thickening of the interlobular septa, as in early pulmonary edema or fibrosis. This thickening
correlates with Kerley B-lines on chest radiography. Closer B-lines, at about 3 mm of spacing, represent
alveolar filling, which correlates with a ground-glass pattern on radiographs. B-lines can also progress to
confluence, described as “white lung” (Figure 10-7 and Video 10-3 ).4,5
Figure 10-8. Comparing Ultrasound and Computed Tomography Findings
A) Acute pulmonary edema with septal thickening. B) Usual interstitial pneumonitis with septal thickening. C) 7-mm B-lines, linear probe. D)
7-mm B-lines, phased-array probe. E) Acute respiratory distress syndrome with ground glass opacities. F) Acute pulmonary edema with
ground glass opacities. G) 3-mm B-lines, linear probe. H) 3-mm B-lines, phased-array probe.
Figure 10-9. Atelectasis and Effusion

Flattened, atelectatic lower lobe floating in a pleural effusion. The echotexture of the lung is similar to that of the adjacent liver; there is a
punctate air bronchogram.
Although this relationship between ultrasound artifacts and the air/tissue/fluid proportions of the lung has
been observed and correlates well with the lung’s radiographic appearance, the exact mechanism of the
B-line artifact generation is unclear.4 One theory is that sound is reflected from all surfaces of the air
bubble, and when there is a group or layers of bubbles, the ultrasound waves become trapped while
reflecting between them, with some returning to the transducer to create the B-lines. More fluid (lung
water) begets more bubbles, which beget more B-lines.6 B-lines can also be created by collapsing rabbit
lungs ex vivo, suggesting that the geometry of the airspaces contributes to ultrasound interactions.7
A diffuse B-line pattern is present in both cardiogenic and noncardiogenic pulmonary edema (ARDS), as
well as in chronic diffuse parenchymal lung disease (interstitial fibrosis). However, the distribution of the
B-lines and other clues can aid in differentiating between these entities. Acute cardiogenic edema tends to
affect the lung parenchyma in a homogeneous fashion, with the dependent areas more affected. ARDS is
less homogeneous, leaving some areas unaffected. Also, the B-line frequency increases along with the
extravascular lung water in cardiogenic edema, but in ARDS, the alveoli are almost invariably affected
and result in an increased frequency (3-mm spacing or confluent) of B-lines in the involved areas.
Cardiogenic edema does not impair lung sliding, and the pleural line is normal. ARDS causes a
thickened, irregular pleural line, often with small subpleural echo-poor consolidations and impaired
sliding ( Video 10-6 ). Pleural effusions are more common and larger in cardiogenic edema than in
ARDS.8 In patients with diffuse parenchymal lung disease, the interlobular septa are thickened by
collagen and fibrous tissue. In advanced fibrosis with honeycombing evident on CT , the B-lines are
separated at about 7 mm of spacing. Areas of ground-glass opacity give B-lines a spacing of about 3 mm
to confluent.9,10 These findings can be compared in Table 10-1.
Figure 10-10. Static and Dynamic Air Bronchograms

A static air bronchogram would maintain a similar appearance throughout the respiratory cycle, which creates a straight line in M-mode. A)
Atelectasis, phased-array probe. B) Static air bronchogram, M-mode. A dynamic air bronchogram would display changes as the air bubbles
move through the bronchus with respiration, creating a moving line in M-mode. C) Consolidation with shred border, phased-array probe. D)
Dynamic air bronchogram, M-mode.
Table 10-1. Sonographic Differential Diagnosis with Diffuse Findings
Cardiogenic Pulmonary Edema Noncardiogenic Pulmonary Diffuse Parenchymal Lung

Edema Disease
B-line frequency Variable, correlates to Numerous 3 mm, always Variable, more likely 7
severity of lung water alveolar involvement mm in advanced disease
B-line distribution Homogeneous and Nonhomogeneous and Nonhomogeneous,
diffuse diffuse, spared areas commonly basilar
Sliding Present Reduced Present
Pleural line Regular Irregular Irregular, thickened
Effusion Likely Possible Possible
Subpleural consolidation Absent Likely Possible
Echocardiogram LV dysfunction, possible Possible RV dysfunction, RV dysfuction in
RV dysfunction LV normal advanced
disease, LV normal
Abbreviations: LV, left ventricular; RV, right ventricular.
Chest sonography has been shown to be at least as effective as chest radiography, if not more sensitive, to
diagnose acute alveolar-interstitial syndromes.11 When used for evaluation of patients with nontraumatic
dyspnea in the emergency department (ED), ultrasound was effective to rule in and rule out an interstitial
syndrome, yielding high concordance with chest radiography.1,12,13
ATELECTASIS AND CONSOLIDATION

As air is excluded from the lung, the parenchyma appears more tissue-like on ultrasound. When acoustic
impedances of soft tissues and the alveolar content are close to one another, as occurs in the case of fluid-
filled (or air-excluded) alveoli, sound can easily propagate and generate a real image of the lung.
Visualization of lung tissue is always pathologic. This can be caused by various conditions, including
infection, infarction, neoplasm, compressive or obstructive atelectasis, and contusion. To be accessible
with chest sonography, the consolidated area must extend to the visceral pleura, with or without effusion
(Figures 10-9 and 10-10; Video 10-7 ).2 Further analysis of the shape, margin, vascularity, and air
bronchograms often allows differentiation among the causes of consolidation. The lung pulse is a sign of
impaired lung inflation, which by definition occurs with complete atelectasis and may occur in other
settings (ie, breath holding) in which lung sliding—respiratory movement—is absent.14 Air bronchograms
are hyperechoic artifacts visible in consolidated lungs. They appear punctate in cross section, or linear,
possibly branching, in long axis. Air bronchograms can be static, as in trapped air, or dynamic if the air
bubbles move with respiration (Figure 10-10; Videos 10-8 and 10-9 ).15
Atelectatic lung does not move with respiration, but it still moves with pulsation of the heart. Atelectasis
can be considered as compressive or resorptive. Compressive atelectasis is commonly caused by a large
pleural effusion, with the shape of the atelectatic lung sharply demarcated and concave, and the movement
of the lung – along with the pulsations of the heart – creating a “waving” of the lung suspended in the
fluid. M-mode can further delineate this “lung pulse” (Figure 10-11; Video 10-7 ). Dynamic air
bronchograms may be seen, because the airways are still open to the atmosphere, but the atelectatic lung
does not slide with respiration. Resorptive atelectasis is a result of airway obstruction; any associated
effusion will be much smaller, and dynamic air bronchograms will not be present. Consolidated lung, as
with pneumonia, will have air bronchograms present in an irregularly shaped echo-poor area. The deep
border will be delineated by an irregular hyperechoic interface with aerated lung, the so-called “shred”
sign (Figure 10-10B; Videos 10-5 and 10-9 ). This will be present unless the consolidation involves
the entire lobe, which has smooth borders.1,16 Contusion and infarction will have the sonographic findings
of consolidation that are indistinguishable from those associated with pneumonia (as would the
radiographs) and will occur in specific clinical settings.
C AVE AT
Abnormalities must reach the pleura to be visualized with ultrasound.
Figure 10-11. Lung Pulse, M-Mode

Atelectatic lung moves with the pulse rather than with respiration.
Chest sonography has a high accuracy for diagnosis of pneumonia. In a study of patients with suspected
community-acquired pneumonia (CAP) the lung ultrasound detected CAP that was missed on two-plane
chest radiography in 12% of cases. Conversely, radiography detected 7% of cases of CAP that were
missed on lung ultrasound. In these cases, the lesion did not reach the pleura.17 In a meta-analysis
comparing lung ultrasound with CT in adult patients presenting to the ED or ICU, ultrasound had a
sensitivity of 93% and a specificity of 98% for detecting pneumonia.18 The diagnosis of a contusion in a
trauma may be obscured by pneumothorax or subcutaneous emphysema.19 A pulmonary infarction will be
associated with echocardiographic findings of pulmonary embolism.20 Table 10-2 describes the
differences between atelectasis and consolidation.
C AVE AT
Always scan the whole chest systematically according to protocol.
Table 10-2. Sonographic Differential Diagnosis with Focal Findings
Atelectasis Pneumonia Contusion Infarction

Lung pulse Present Absent * *
Dynamic air Absent Present * *
bronchogram
Static air Present, frequent Present, infrequent * *
bronchogram
Irregular (shred) Absent Present, unless Present Small subpleural
border lobar consolidations
especially
posterobasal
Effusion Large if Possible Possible, localized Possible, localized
compressive
Sliding Absent Present or reduced Present Present
* The lung pulse and air bronchogram have not been described in contusion or infarction in particular; however, if the affected area is large
enough, the findings would be expected to be similar to those of pneumonia.
KEY POINTS
A few scattered B-lines can be physiologic, especially in dependent areas of the lung.
B-pattern is present in a region if there are 3 or more B-lines in a rib interspace in a longitudinal
plane.
Alveolar-interstitial syndrome is present if 2 or more regions show a B-pattern.
B-lines can be present focally in an abnormal area; for example, consolidation caused by
pneumonia, contusion, infarction and tumor. The remaining lung is normal.
Differential diagnosis of diffuse B-lines includes:
Cardiogenic pulmonary edema
Noncardiogenic pulmonary edema (eg, ARDS)
Diffuse parenchymal lung disease (eg, interstitial pneumonitis)
Differential diagnosis of focal B-lines includes:
Pneumonia
Atelectasis
Contusion
Infarction
Neoplasia
Consolidation (hepatization) occurs when air is excluded from the alveoli, either because of a
filling or collapsing process; as a result, the lung becomes visible to sonography with a tissue-like
echotexture.
The lung pulse appears as movement of the lung tissue with the cardiac cycle.
Air bronchograms are punctate or linear hyperechoic artifacts within the consolidation. Dynamic
air bronchograms are created when air bubbles move in the bronchi during respirations. The
movement can be appreciated in 2D, and appears as a bright sinusoid line on M-mode. Static air
bronchograms, air trapped in a bronchus but not open to the atmosphere, do not move with
respiration. They appear as a steady line on M-mode.
A shred sign is the appearance of the irregular border between a pleural-based portion of nonaerated
lung and the adjacent aerated portion. This is not present if the consolidation involves the entire
lobe, because the lobar border is smooth.
REFERENCES
1. Volpicelli G, Elbarbary M, Blaivas M, et al. International Liaison Committee on Lung Ultrasound (ILC-LUS) for International Consensus
Conference on Lung Ultrasound (ICC-LUS). International evidence-based recommendations for point-of-care lung ultrasound. Intensive
Care Med. 2012;38:577-591.
2. Lichtenstein DA. Lung ultrasound in the critically ill. Ann Intensive Care. 2014;4:1.
3. Volpicelli G. Lung sonography. J Ultrasound Med. 2013;32:165-171.
4. Lichtenstein D, Mézière G, Biderman P, et al. The comettail artifact: an ultrasound sign of alveolar-interstitial syndrome. Am J Respir Crit
Care Med. 1997;156:1640- 1646.
5. Lichtenstein DA, Mezière GA. Relevance of lung ultrasound in the diagnosis of acute respiratory failure: the BLUE protocol. Chest.
2008;134:117-125.
6. Soldati G, Copetti R, Sher S. Sonographic interstitial syndrome: the sound of lung water. J Ultrasound Med. 2009;28:163-174.
7. Soldati G, Smargiassi A, Inchingolo R, et al. Lung ultrasonography may provide an indirect estimation of lung porosity and airspace
geometry. Respiration. 2014;88:458- 468.
8. Copetti R, Soldati G, Copetti P. Chest sonography: a useful tool to differentiate acute cardiogenic pulmonary edema from acute respiratory
distress syndrome. Cardiovasc Ultrasound. 2008;6:16.
9. Hasan AA, Makhlouf HA. B-lines: transthoracic chest ultrasound signs useful in assessment of interstitial lung diseases. Ann Thorac Med.
2014;9:99-103.
10. Moazedi-Fuerst F, Kielhauser S, Brickmann K, et al. Sonographic assessment of interstitial lung disease in patients with rheumatoid
arthritis, systemic sclerosis and systemic lupus erythematosus. Clin Exp Rheumatol. 2015 Jul-Aug;33 Suppl 91:87-91.
11. Lichtenstein D, Goldstein I, Mourgeon E, et al. Comparative diagnostic performances of auscultation, chest radiography, and lung
ultrasonography in acute respiratory distress syndrome. Anesthesiology. 2004;100:9-15.
12. Kreuter M, Mathis G. Emergency ultrasound of the chest. Respiration. 2014;87:89-97.
13. Zanobetti M, Poggioni C, Pini R. Can chest ultrasonography replace standard chest radiography for evaluation of acute dyspnea in the ED?
Chest. 2011;139:1140-1147.
14. Lichtenstein DA, Lascols N, Prin S, et al. The “lung pulse”: an early ultrasound sign of complete atelectasis. Intensive Care Med.
2003;29:2187-2192.
15. Lichtenstein D, Mezière G, Seitz J. The dynamic air bronchogram: a lung ultrasound sign of alveolar consolidation ruling out atelectasis.
Chest. 2009;135:1421-1425.
16. Reissig A, Copetti R. Lung ultrasound in community acquired pneumonia and in interstitial lung diseases. Respiration. 2014;87:179-189.
17. Reissig A, Copetti R, Mathis G, et al. Lung ultrasound in the diagnosis and follow-up of community-acquired pneumonia: a prospective
multicentre diagnostic accuracy study. Chest. 2012;142:965-972.
18. Chavez MA, Shams N, Ellington LE, et al. Lung ultrasound for the diagnosis of pneumonia in adults: a systematic review and meta-
analysis. Respir Res. 2014;15:50. 19. Soldati G, Testa A, Silva FR, et al. Chest ultra-sonography in lung contusion. Chest. 2006;130:533-
538.
19. Soldati G, Testa A, Silva FR, et al. Chest ultra-sonography in lung contusion. Chest. 2006;130:533-538.
20. Mathis G, Blank W, Reissig A, et al. Thoracic ultrasound for diagnosing pulmonary embolism. Chest. 2005;128:1531- 1538.
Chapter 11
General Diagnostic Abdominal Sonography
Chapter 12
Focused Assessment with Sonography in Trauma (FAST)
Chapter 11
General Diagnostic Abdominal Sonography
Brooke Hensley, MD; Julie St-Cyr Bourque, MD;
Vicki E. Noble, MD
Supplemental images referred to in this chapter may be accessed by visiting www.sccm.me/ultcomp.
OBJECTIVES
Understand the indications, methods, interpretation, and evidence behind various abdominal ultrasound examinations
performed at the bedside for critically ill patients
Discuss the abdominal ultrasound examinations performed in the gallbladder, kidneys, bladder, small bowel, abdominal
aorta, and in pregnancy
INTRODUCTION
Bedside ultrasonography is a powerful tool that can assist clinicians in rapidly identifying or ruling out
intra-abdominal pathology.1 This chapter will serve as a guide for clinicians to answer specific questions
using ultrasound in a clinical context in order to tailor a patient’s care. Specifically, we will focus on
gallbladder, kidneys, bladder, bowel, aorta, and pregnancy ultrasound evaluation.
CASE STUDY
A 38-year-old woman with hypothyroidism, nephrolithiasis, and a previous remote laparoscopic
appendectomy is admitted to the ICU with sepsis of unclear source. The patient reportedly had a normal
abdominal computed tomography (CT) scan 3 days earlier for undifferentiated abdominal pain, nausea,
vomiting, and fevers. She now presents with worsening abdominal pain, decreased urine output, and
intermittent subjective fevers. Her vital signs are as follows: temperature, 101.2°F; blood pressure,
102/78 mm Hg; heart rate, 110 beats/min; respiratory rate, 20 breaths/min; and oxygen saturation, 98% on
room air. On physical examination, the patient is neurologically intact, has dry mucous membranes,
diffuse abdominal tenderness with voluntary guarding without rebound or marked distension, and no skin
changes. Laboratory abnormalities are remarkable, with a white blood cell count of 18,000/µL, normal
liver function tests, acute kidney injury with a creatinine of 4.2 mg/dL (371.3 mmol/L), blood urea
nitrogen 38 mg/ dL (13.6 mmol/L), lactate 3.9 mg/dL (0.43 mmol/L), and a negative finding of beta human
chorionic gonadotropin(β-HCG). Chest radiograph was normal. The patient has not yet provided a urine
sample, but the leading differential diagnosis was reported as urosepsis. Outside hospital records are
pending, including the abdominal/pelvic CT scan that was reported to be unrevealing.
In the ICU, resuscitation with crystalloid and broad-spectrum antibiotics, previously started in the
emergency department, were continued. Bedside abdominal ultrasound was performed by the intensivist
and revealed that the patient was anuric without urinary retention or hydronephrosis and also had a
distended gallbladder with stones, gallbladder wall thickening, and pericholecystic fluid. No sign of
associated bowel dilatation or pneumobilia was present. General surgery was consulted and the patient
improved after appropriate interventions.
PATIENT POSITIONING AND PROBE SELECTION

The abdominal ultrasound examinations detailed in this chapter will be described with the patient in a
supine position. Ultrasound is advantageous over other diagnostic modalities in the critical care setting
because it does not require the patient to be moved either in the bed or outside the unit.2 Aside from the
bowel section, where the linear probe can be of use if the patient’s body habitus permits, all other
examinations described here are performed with either the low-frequency curvilinear or phased-array
cardiac probe. Unless otherwise specified, the probe marker should be oriented to the patient’s right
when in a transverse plane, and to the patient’s head in the sagittal and coronal planes.
GALLBLADDER
Indications
A focused right upper quadrant ultrasound should be considered in patients with undifferentiated right
upper quadrant pain, epigastric/chest pain, nonspecific abdominal discomfort, or sepsis with an unclear
source.3 This section will describe ultrasound findings of cholelithiasis, common bile duct (CBD)
obstruction, and acute cholecystitis.
Image Acquisition
Place the patient in a supine or left lateral decubitus position. The gallbladder may be viewed via any of
the following 3 approaches, in the following order:
Subcostal: Sweep from epigastric region to midclavicular line with the probe marker toward the
patient’s right (Figure 11-1).
Intercostal: Midclavicular line between the lower rib spaces with the probe marker toward the
patient’s head. Rock and fan the probe until the gallbladder is visualized through the intercostal space
(Figure 11-2).
Right midaxillary line: Morison pouch focused assessment with sonography in trauma (FAST) view
with the probe marker toward the patient’s head, then fan anteriorly (Figure 11-3).
Once the gallbladder is visualized, completely fan through it in 2 orthogonal planes: longitudinal (long
axis) and transverse (short axis).
Cholelithiasis
The diagnosis of cholelithiasis is simply made by visualizing stones within the gallbladder. The
gallbladder neck must be fully interrogated, because gallstones in this region are common and easily
missed.4 Cholelithiasis can be identified in the setting of biliary colic or acute biliary disease. However,
cholelithiasis is often asymptomatic and discovered incidentally, so it is important to use ultrasound
findings in clinical context.5 Gallbladder stones can cause shadowing and are hyperechoic, gravity
dependent, and mobile (Figure 11-4). (Keep in mind that one rare exception to gravity-dependent stones
are ones that are ulcerated into the anterior wall.)
E X P E RT T I P
Polyps may mimic stones but do not shadow, are not gravity dependent, and are immobile
(Supplemental Image 11-1 ).
Supplemental Image 11-1. Gallbladder Polyps
A) Longitudinal view. B) Transverse view.
Figure 11-1. Subcostal Approach

Figure 11-2. Intercostal Approach
Figure 11-3. Midaxillary Approach

Figure 11-4. Cholelithiasis
A) Longitudinal view. B) Transverse view.
E X P E RT T I P S
Rotate the probe marker in a more oblique position, as necessary, to obtain an adequate view.
If possible, ask the patient to inspire and hold his/her breath. As the diaphragm descends with
inspiration, the liver moves inferiorly toward the costal margin, subsequently pushing the gallbladder into
view. Placing the patient in a left lateral decubitus position will further improve the image by bringing the
gallbladder closer to the anterior abdominal wall.
Use color Doppler to differentiate the CBD from vascular structures. The CBD does not have detectable
flow.
CBD Obstruction
CBD obstruction may be found in cholecystitis, choledocolithiasis, biliary strictures, pancreatic, or other
malignancies causing mass effect. The diagnosis is made by measuring the CBD.3 A duct greater than 6 to
7 mm may be the only ultrasound abnormality appreciated on examination. The CBD may be found by
following the neck of the gallbladder proximally and identifying it in a longitudinal plane (Figure 11-5),
or finding the “exclamation point” view (Figure 11-6 and Supplemental Image 11-2 ). The CBD is an
anechoic tubular structure with bright echogenic walls. A normal, thin CBD can be difficult to find, but the
easiest way to do so is by first locating the portal vein. The CBD will be located directly anterior to the
portal vein (Figure 11-6), and it should be measured from inner wall to inner wall.
Supplemental Image 11-2. Exclamation Point
Abbreviations: GB, gallbladder; PV, portal vein; CBD, common bile duct.
Figure 11-5. Common Bile Duct, Longitudinal View

Longitudinal view of the common bile duct anterior to the portal vein.
Figure 11-6. Gallbladder Ultrasound with Color Doppler

Abbreviations: GB, gallbladder; CBD, common bile duct; PV, portal vein.
Color Doppler on GB “exclamation point” view to differentiate the CBD and PV. The CBD is the discrete anechoic stripe without color flow,
anterior to the PV.
Figure 11-7. Gallbladder Sludge

Hyperechoic debris within the gallbladder lumen. A) Longitudinal view. B) Transverse view.
Figure 11-8. Gallbladder Wall Thickening
Gallbladder wall thickening (seen here at 0.92 cm) with pericholecystic fluid (*) shown as an anechoic stripe.
Figure 11-9. Distended Gallbladder

Abbreviation: RUQ, right upper quadrant.
Distended gallbladder >10 × 5 cm with sludge and wall thickening.
Figure 11-10. Acute Cholecystitis

Acute cholecystitis demonstrating (A) stones, (B) wall thickening, and (C) pericholecystic fluid.
C AVE AT S
Gallbladder wall thickening may be found secondarily in patients with cirrhosis, ascites, HIV,
congestive heart failure, renal failure, pancreatitis, hepatitis, long-term total parenteral nutrition,
or neoplastic infiltration and can be a nonpathologic finding in these patients.6
Acalculous cholecystitis is a rare disease, but should be considered in toxic-appearing, critically

ill patients with multiple comorbidities and findings of gallbladder wall thickening and
pericholecystic fluid without stones.7
Cholecystitis
Cholecystitis is often a challenging diagnosis that may be easily overlooked. Physical examination
findings or abnormal laboratory values alone have poor sensitivity and specificity. Cholecystitis may not
always be evident on CT, but an early diagnosis may be established with bedside ultrasound.5 Ultrasound
findings suggestive of acute cholecystitis, which should be specifically noted during the examination,
include:
Presence of stones or sludge

Presence of pericholecystic fluid seen as an anechoic stripe
Anterior gallbladder wall thickening beyond 3 to 4 mm. The gallbladder wall should always be
measured anteriorly. An artifact known as “posterior acoustic enhancement” causes the structures
behind a fluid-filled structure to appear brighter. Therefore, the posterior wall through the fluid-filled
gallbladder often causes a falsely thickened appearance.
Positive sonographic Murphy sign, with pain causing cessation of inspiration while applying pressure
only directly over (not around) the gallbladder
CBD dilated more than 6 to 7 mm
Gallbladder distended more than 10 × 5 cm
The presence of stones along with any one of the aforementioned sonographic findings should raise the
suspicion of acute cholecystitis (Figures 11-7 – 11-10; Supplemental Image 11-3 ).6
Supplemental Image 11-3. Anterior Gallbladder Wall Thickness

Anterior gallbladder wall measurement with normal thickness <3 mm.
KIDNEYS
Indications
A bedside renal ultrasound is most useful to evaluate for the presence of hydronephrosis.8
Hydronephrosis may be present in acute conditions such as urinary obstruction from urinary retention,
nephrolithiasis, ureteral stent malfunction, or malignant mass effect. Hydronephrosis can also be seen at
baseline in patients with benign prostatic hypertrophy or pregnancy.
Image Acquisition
Place the probe marker at the right midaxillary line with the probe marker toward the patient’s head
(Figure 11-11).
Slide the probe caudally/cranially and fan anteriorly/posteriorly until the kidney is adequately
visualized in the center of the screen.
Obtain a long-axis view of the kidney and slowly fan through to visualize the renal pelvis, calyces, and
vasculature. Hydronephrosis is seen as anechoic areas in the renal pelvis and is categorized as mild,
moderate, or severe depending on the degree of confluence of the calyces and pyramids (Figure 11-
12).
Mild hydronephrosis: Dilatation of the renal pelvis and calyces, without parenchymal atrophy
Moderate hydronephrosis: Blunting of the fornices, flattening of the papillae, and mild cortical
thinning
Severe hydronephrosis: Gross ballooning of the renal pelvis and calyces with loss of borders, renal
atrophy, and cortical thinning
Figure 11-11. Midaxillary Approach for Renal Ultrasound
E X P E RT T I P S
Always compare the ultrasound findings to those of the contralateral kidney.
Place the color Doppler on the renal structures to help differentiate true hydronephrosis from
renal vasculature. Hydronephrosis will not have any flow within it (Supplemental Image 11-4 ).
Supplemental Image 11-4. Moderate Hydronephrosis with Color Doppler
The renal vasculature is differentiated from true hydronephrosis, highlighted with color flow. Hydronephrosis will not have detectable flow
within it.
Figure 11-12. Hydronephrosis
A) No hydronephrosis. B) Mild hydronephrosis. C) Moderate hydronephrosis. D) Severe hydronephrosis.
BLADDER
Indications
Ultrasound of the bladder is useful to determine a patient’s postvoid residual (PVR) (Figure 11-13) to
assess for urinary retention.8 When a patient is anuric or in renal failure, he or she may have a simple
obstruction requiring a catheter placement. If a patient already has a Foley catheter, an ultrasound
examination is helpful to determine the location of the Foley balloon and whether bladder drainage is
adequate (Figure 11-14).8 Renal stones that have migrated to the bladder, or are more commonly seen at
the ureterovesicular junction (UVJ), may also be visualized.9
Image Acquisition: PVR

Transverse image: Place the probe at the patient’s midline in the suprapubic region, with the probe
marker pointing to the patient’s right.
Completely fan in the caudal and cranial direction, then freeze the screen to record and save the
maximum dimensions of depth and width.
Longitudinal image: Place the probe at the patient’s midline in the suprapubic region, with the probe
marker pointing to the patient’s head.
Completely fan left and right, then freeze the screen to record and save the maximum length dimension.
PVR: Some ultrasound machines have built-in software that needs to be activated to calculate the PVR
based on the 3 dimensions obtained. You may also calculate the estimated PVR by rounding the
measurements to the nearest whole number and using the following equation:
Estimated PVR (mL) = Depth (cm) × Width (cm) × Length (cm) × 0.75
A PVR greater than 250 mL is considered abnormal.
Image Acquisition: UVJ Stone

Transverse image: Place the probe at the patient’s midline in the suprapubic region, with the probe
marker pointing to the patient’s right (same as step 1 for PVR above).
Completely fan in the caudal and coronal directions, and focus on the bilateral UVJs visualized as 2
small, raised regions at the bottom of the screen. A stone may be visualized at the UVJ as a
hyperechoic shadowing structure (Supplemental Image 11-6 ).
To increase the sensitivity of identifying an equivocal or smaller UVJ stone, place color Doppler over
the UVJ. A “twinkling” artifact produced by the stone may be visualized (Supplemental Image 11-7
).10
Supplemental Image 11-6. UVJ Stone

Stone at the right ureterovesicular junction (UVJ) seen as a hyperechoic rounded structure with shadowing.
Supplemental Image 11-7. Left UVJ Stone
A) Without color Doppler. B) With color Doppler, revealing a more apparent “twinkling” left UVJ stone.
E X P E RT T I P
Blood clots within the bladder can be visualized as hyperechoic debris in the lumen
(Supplemental Image 11-5 ).
Supplemental Image 11-5. Obstructed Foley Balloon

Obstructed Foley balloon shown with blood clots (hyperechoic debris) within the bladder. A) Transverse view. B) Longitudinal view.
Figure 11-13. Bladder Ultrasound, Transverse and Longitudinal Views
The postvoid residual (PVR) can be calculated automatically using embedded programming, or it can be estimated with the following formula:
PVR = Depth × Width × Length × 0.75. The estimated PVR in this case is approximately 7 × 5 × 5 × 0.75 = 131.25 mL.
SMALL BOWEL
Indications
Bowel ultrasound is of particular value when a small bowel obstruction (SBO) is suspected. When the
ultrasound beam encounters air, dispersion occurs, making it difficult to identify deeper structures. That is
why ultrasonography of the normal bowel can be quite challenging. When the bowel is filled with solid or
fluid content, it becomes easy to visualize with an ultrasound examination.11 This is why it has been
proven that ultrasound is actually very sensitive and specific to diagnose SBO.12-14 It is a good alternative
to plain radiography because it can be done in the supine position, at the bedside, is repeatable, and is
free of ionizing radiation. Furthermore, it has the ability to help differentiate a mechanical obstruction
from an ileus, a simple from a high-grade bowel obstruction, and will sometimes also diagnose the cause
of the obstruction. One of the key features to look for when imaging the bowel for a suspected obstruction
is the classic back-and-forth movement of its intraluminal content, which will be described in further
detail later in this chapter.
Figure 11-14. Foley Balloon in Bladder

A) Suspended in urine (seen as anechoic fluid) from an obstructed catheter that is incompletely draining. B) With a completely decompressed
bladder that is draining appropriately. A Foley balloon is identified as a well-circumscribed circular structure. If the Foley balloon is clearly seen
in the bladder lumen and surrounded by urine, it is failing to properly drain.
Image Acquisition
To identify dilated loops of bowel, first proceed with a short abdominal screening, which consists of
placing the probe in 4 distinct regions on the abdomen (Figure 11-15):
Epigastric area with the probe in a transverse orientation

Right paracolic gutter with the probe in a longitudinal orientation
Left paracolic gutter with the probe in a longitudinal orientation
Suprapubic area with the probe in a transverse orientation
Figure 11-15. Short Abdominal Screening for Small Bowel Obstruction
Short abdominal screening technique for diagnosis of small bowel obstruction. A) Epigastric area. B) Right paracolic gutter area. C) Left
paracolic gutter area. D) Suprapubic area.
Once dilated loops of bowel are identified, if time permits, perform more detailed sonography of the
abdominal cavity, which can help better differentiate the type of obstruction. This more comprehensive
technique is called the “lawnmower” or “Zamboni” technique15 (Figure 11-16) and consists of the
following steps:
Transverse view: Place the probe in a transverse orientation in the right upper quadrant and proceed
down and up the abdominal wall, applying graded compression every 2 to 3 cm until the probe is in
the left lower quadrant and the whole abdomen has been covered.
Sagittal view: Proceed in the same fashion but with the probe in the sagittal orientation starting in the
left lower quadrant and moving left and right on the abdominal wall until the probe is back in the right
upper quadrant.
Simple SBO vs. Ileus

The ultrasonographic diagnosis of an SBO (Figure 11-17) relies on the identification of bowel loops that
are:
Predominantly fluid filled but can also have echogenic material or “fecalization” of bowel contents in
the lumen
Dilated, with a bowel loop diameter >25 mm (measured from outer wall to outer wall)
Noncompressible
Not edematous, with a bowel wall thickness <3 mm (measured from the outside aspect of the wall to
the inside aspect of the same wall)
In addition to these, identification of 2 other findings will help further define the obstruction as being of
mechanical origin rather than an ileus.16 These are as follows:
Transition point: A transition point will appear as a collapsed empty bowel next to dilated proximal
bowel loops.
Classic “pendulous” or “back-and-forth” movement of the intraluminal bowel content: As peristaltic
activity is present, the bowel content will initially be pushed forward in the lumen but will be seen
coming right back once it has reached the obstruction.
Figure 11-16. “Lawn-Mower” or “Zamboni” Technique for Small Bowel Obstruction

A) Transverse orientation. B) Sagittal orientation.
Figure 11-17. Simple Small Bowel Obstruction Showing Dilated Loops of Bowel
Dilated loops of bowel demonstrating a diameter >25 mm compatible with a diagnosis of small bowel obstruction.
Figure 11-18. High-grade Small Bowel Obstruction with Bowel Wall Edema
Bowel wall edema (>3 mm) suggesting a high-grade small bowel obstruction.
Findings suggestive of an ileus are usually different from those encountered with a mechanical obstruction
and include bowel loops that are:
Predominantly filled with air but can also be fluid filled
Nondilated: Bowel loop diameter smaller than 25 mm
Lacking peristaltic activity
Although lack of peristaltic activity usually orients us to the diagnosis of a paralytic ileus, careful imaging
of multiple loops of bowel is necessary because this can also be seen in other circumstances. One of these
is when a mechanical obstruction is present and part of the dilated bowel is necrotic. In that case the
loops that remain adequately perfused will still exhibit peristaltic activity next to 1 or several aperistaltic
loops. This can also occur with localized ileus where only part of the bowel will not exhibit peristaltic
activity, as is sometimes seen in bowel overlying an inflammatory process such as appendicitis.
High-Grade Obstruction
Strangulated bowel is a time-sensitive diagnosis, therefore identification at the bedside using
ultrasonography is of great value because it can expedite further imaging and time to surgery. These
criteria are as follows17:
Intraperitoneal free fluid: Free fluid identification either in its usual distribution on the FAST
examination (see Chapter 12) or more subtly localized between the loops of bowel as the amount of
free fluid seen in this context is variable (Supplemental Image 11-8 ).
Bowel wall edema: Bowel wall thickness >3 mm (measured from the outside aspect of the wall to the
inside aspect of the same wall) (Figure 11-18).
Lack of peristaltic activity (refer to the previous section for a more detailed explanation).
Pneumatosis of the bowel wall: Pneumatosis will have the same look as the classic “string of pearls”
sign described on plain radiography except that because air is hyperechoic, it will appear as small
white bright beads lining the bowel wall (Figure 11-19).
Supplemental Image 11-8. Intraperitoneal Free Fluid Between Dilated Loops of Bowel
Figure 11-19. Bowel Wall Pneumatosis

Bowel wall pneumatosis exhibiting the classic increased echogenicity of the bowel wall. A) Short-axis view. B) Long-axis view.
Figure 11-20. Abdominal Wall Hernia

Abdominal wall hernia showing interruption in the peritoneal lining with protrusion of bowel content. Red asterisks indicate peritoneal line, and
white arrows show peritoneal lining interruption.
Causative Lesion
At times this more comprehensive abdominal ultrasound will demonstrate the cause of the bowel
obstruction.18 Etiologies such as an abdominal wall hernia, an intussusception, or a gallstone ileus, to
name a few, are readily visible with ultrasound. These will be indicated by the following:
An abdominal wall hernia will be seen as an interruption in the normally continuous peritoneal line
through which bowel loops can protrude and become incarcerated (Figure 11-20).
An intussusception, although much more common in the pediatric population, can sometimes be the
cause of bowel obstruction in adults, particularly when an underlying tumor or Meckel diverticulum is
present. The sonographic appearance of an intussusception is that of a bowel loop within another loop,
giving us the classic “target sign” appearance in the short-axis plane (Supplemental Image 11-9 ).
A gallstone ileus will usually demonstrate a large gallstone in the bowel lumen (please refer to the
gallbladder discussion earlier in this chapter). This will more often be seen at the level of either the
duodenum or the ileocecal valve. If this is suspected, an ultrasound of the gallbladder and liver should
be performed, because features of cholelithiasis or cholecystitis may be present, as well as
pneumobilia secondary to the gallbladder-duodenum fistula created on passage of the gallstone to the
bowel lumen.
Supplemental Image 11-9. Intussusception

A) Classic “target” sign appearance in the transverse view. B) Longitudinal view showing loops of bowel intertwined. Red asterisk indicates
intussusceptum border; blue arrows show intussuscipiens border.
Intraperitoneal Free Air

Finally, ultrasound can demonstrate intraperitoneal free air. This will appear as a reverberation artifact
with an A-line pattern just as one would see in a normal lung examination (see Chapter 10). The
difference is that this reverberation artifact will arise from the peritoneal line (Figure 11-21).
One major pitfall is mistaking normal bowel gas originating from the intestinal lumen with free air
because they both appear similar, especially if the bowel wall touches the peritoneum. It is possible to
distinguish both by placing the patient in the left lateral decubitus position. In that position, because free
air travels to the most superior portion of the abdominal cavity, the reverberation artifact should move
toward the right upper quadrant and can usually then be appreciated between the liver and the diaphragm,
where gas circumscribed in the bowel lumen should not be able to travel. It is also helpful at times to
change to a high-frequency linear probe because a higher resolution can help better differentiate the origin
of these A-lines.
Figure 11-21. Intraperitoneal Free Air
Intraperitoneal free air with its classic A-line pattern. Yellow asterisks indicate free air.
ABDOMINAL AORTA
Indications
Bedside imaging of the abdominal aorta, particularly in a patient exhibiting signs of shock, can be
lifesaving because every minute counts when faced with a ruptured abdominal aortic aneurysm (AAA) or
one on the verge of rupturing. The literature reports that as many as 17% of symptomatic nonfasting
patients who undergo bedside ultrasound for an AAA diagnosis will have an inconclusive study because
of nonvisualization of part of the aorta. This number goes up to 29% when bedside ultrasonography is
used as a screening tool in an asymptomatic high-risk population. Hence, if bedside ultrasonography of
the aorta is inconclusive and AAA is of concern, one should not hesitate to get a CT scan of the abdomen.
Image Acquisition
As with all point-of-care sonography scanning protocols, the abdominal aorta should be imaged in 2
orthogonal planes.
Transverse view: Place the probe in a transverse orientation with the probe marker toward the
patient’s right in the epigastric area at a 90-degree angle to the skin (Figure 11-22). Slowly move the
probe down on the abdomen to image the abdominal aorta from its most proximal portion to the
bifurcation of the iliac arteries. Because we ideally want to start imaging the abdominal aorta at its
most proximal portion, a good trick is to flatten the probe on the abdominal wall until a subxiphoid
view of the heart is seen (see Chapter 3). Once the heart is in view, slowly lift the probe from the
abdominal wall and watch as the most proximal part of the aorta comes into view.
Longitudinal view: From the transverse view of the aorta, turn the probe 90 degrees until it is in a
sagittal orientation with the probe marker oriented toward the patient’s head and the aorta is seen in the
long axis. It is important to see the vessel elongating as the probe is turned to ensure the vessel viewed
in the long axis is the aorta and not the inferior vena cava (IVC), as they course right next to each other
in the abdomen. Although most AAAs will be identified on the transverse sweep, it is always
recommended to proceed with a longitudinal view, because “saccular” or “berry” aneurysms can be
missed on transverse imaging (Figure 11-23). This type of aneurysm represents about 5% of all AAAs
and is more likely to be seen in the setting of trauma, aortic infection, aortic ulcer, or prior aortic
surgery.
Figure 11-22. Scanning Technique for Abdominal Aorta Imaging
Figure 11-23. Longitudinal View of Aorta

A) Normal aorta. B) Saccular or “berry” aneurysm (green asterisks).
When the probe is in the transverse orientation, the first structure to look for, which will serve as our
landmark to find the aorta, is the vertebral body with its shadow. The abdominal aorta lies anterior and
slightly to the left of this vertebra. Both the aorta and IVC will come into view and it is important to be
able to reliably identify the 2, because measuring the wrong vessel could be devastating. The aorta can be
distinguished from the IVC by the following features (Supplemental Image 11-10 ):
Supplemental Image 11-10. Anatomic Positioning of the Aorta

Abbreviation: IVC, inferior vena cava.
Positioning of the aorta and IVC in relation to the vertebral body.
The aorta lies anatomically to the left of the IVC and should thus appear to its right on the screen (when
the probe marker is oriented to the patient’s right). It is important not to solely rely on this criteria
because it is possible to mistakenly orient the probe marker to the patient’s left, which would bring the
aorta to the left of the IVC on the screen.
The aorta will be round, whereas the IVC is often elliptical in shape.
The aortic wall is thick, whereas the IVC has a thin wall.
The aorta will exhibit arterial pulsations. At times these pulsations will be transmitted to the IVC
because of the proximity of these 2 vessels. Pulsed-wave Doppler can be quite helpful in these
circumstances to distinguish between the arterial and venous flow patterns. The aorta will exhibit a
characteristic triphasic arterial pattern with high peak velocities, whereas the IVC will show a more
continuous-wave pattern with respiratory variations and lower peak velocities.
Once the aorta is identified, it is important to image and measure it in 3 different segments:
The proximal aorta branches into 2 major arteries – the celiac trunk and the superior mesenteric artery
(SMA).
The celiac trunk is the first to branch out of the aorta. As it separates into the splenic and main hepatic
arteries, it gives a characteristic appearance called the “seagull sign” (Supplemental Image 11-11
).
Sliding the probe slightly inferiorly on the abdomen will show the SMA. It appears as a small thick-
walled vessel superiorly to the aorta on the screen (Supplemental Image 11-12 ). At times it is
also possible to identify the splenic and left renal vein as they course above and below the SMA,
respectively.
The midaorta will come into view as the probe is slid inferiorly from the level at which the SMA is
identified.
The distal aorta, bifurcating into the iliac arteries, will be the last segment of the aorta seen as the
probe is moved further down on the abdominal wall (Supplemental Image 11-13 ).
Supplemental Image 11-11. Proximal Aorta at the Celiac Trunk

Proximal aorta at the level of the celiac trunk showing the classic “seagull sign.”
Supplemental Image 11-12. Proximal Aorta: SMA
Abbreviations: IVC, inferior vena cava; SMA, superior mesenteric artery.
Supplemental Image 11-13. Distal Aorta Bifurcating into Iliac Arteries

A) Distal aorta. B) Iliac arteries.
When imaging the abdominal aorta is challenging, here are some tips to improve your views:
When bowel gas is the problem, either apply deep constant pressure over the area of interest or slide
the probe slightly to the right or left and angle it toward the aorta. This will often move the bowel gas
out of the way.
When the abdominal wall is muscular or tense, it is often hard to exert the amount of pressure needed
to image the aorta appropriately. In this case, if possible, have the patient bend his/her knees, because
this can make the abdomen softer and thus help with image acquisition.
Figure 11-24. The Importance of Accurate Aortic Measurement
Example of the importance of measuring the aorta from outer wall to outer wall in order not to miss a mural thrombus.
AAA
To avoid missing an AAA, the aortic diameter should be measured at each of the 3 portions that were just
described, as well as at the level of the iliac arteries. The correct measurement includes the walls of the
aorta and iliac arteries (Supplemental Image 11-14 ). This is of the utmost importance because
measuring only the aortic lumen may miss the identification of an aortic aneurysm when a mural thrombus
is present (Figure 11-24).
Supplemental Image 11-14. Aortic Diameter

Correct measurement of the aortic diameter including the aortic walls.
The normal values are as follows:

The aorta can measure up to 3 cm.
Each iliac artery can measure up to 1.5 cm.
The aortic diameter measurement is usually performed in the anteroposterior dimension. For the best
accuracy with this measure, it is important that the ultrasound beam be at a 90-degree angle to the aorta.
Any other angle will falsely increase the diameter because the beam will now be cutting the aorta in an
oblique fashion.19 Although this would increase the sensitivity of the examination, overestimating the
diameter of the aorta can lead to unnecessary additional testing that is not beneficial in the critical care
setting. When the lateral borders of the aorta are well defined on the screen, measuring the right-left
diameter will remove any contribution of the probe angle on this measurement.
Identification of an AAA on abdominal ultrasound should be followed by a FAST examination to look for
intraperitoneal free fluid. However, it is important to remember that about 95% of AAAs will rupture in
the retroperitoneum, which will not indicate a positive result on the FAST examination. Hence, it is
important to remember that a patient experiencing shock with an enlarged aorta on ultrasound may be
exsanguinating from a ruptured AAA even if the FAST examination result is negative.
Other features can help us diagnose a ruptured AAA in the absence of intraperitoneal free fluid. These are
as follows:
Periaortic fluid will appear as an anechoic stripe surrounding the AAA.

Retroperitoneal fluid can be seen as an anechoic fluid collection overlying the vertebral body that
serves as our landmark to identify the aorta. This fluid will follow the vertebral contour, demonstrating
its retroperitoneal location.
Aortic Dissection
When imaging the abdominal aorta, it is also possible to demonstrate a dissection by seeing an intimal
flap inside the aortic lumen. A dissection flap will appear as a hyperechoic line coursing through the
lumen of the vessel and moving with each pulsation (Figure 11-25).
If a flap is seen on the transverse screen of the aorta, it is important once again to confirm it in the
longitudinal plane, because artifact can sometimes produce false images. If an intimal flap is still present,
it can be beneficial to continue the ultrasound examination by imaging the aortic root and the left carotid
artery because the dissection can extend to these vessels.
Parts of the thoracic aorta can be imaged in 2 ways using the cardiac probe:
The parasternal long-axis view of the heart serves as a good window to image the aortic root as well
as 1 slice of the descending thoracic aorta. If the aortic dissection extends from the proximal thoracic
aorta, it is possible to visualize the intimal flap with this view (Supplemental Image 11-15 ).
The suprasternal notch view consists of placing the probe in a transverse plane in the suprasternal
notch and orienting it caudally (Supplemental Image 11-16 ). This will enable imaging of the aortic
arch where a dissection flap can also be demonstrated at times (Supplemental Image 11-17 ).
Supplemental Image 11-15. Aortic Dissection at the Aortic Root
Abbreviations: LV, left ventricle; RV, right ventricle; LA, left atrium; root Ao, aortic root; desc Ao, descending aorta.
Parasternal long-axis view of the heart showing a dissection flap within the aortic root.
Supplemental Image 11-16. Suprasternal Notch View Technique

Probe positioning to obtain a suprasternal notch view.
Supplemental Image 11-17. Suprasternal Notch View
Abbreviation: Ao, aortic.
A) Normal aortic arch. B) Dissection flap through the aortic arch.
Figure 11-25. Aortic Dissection

Aortic dissection diagnosed by seeing a flap within the aortic lumen. A) Transverse view. B) Sagittal view.
Finally, to complete imaging, visualization of the left carotid lumen is of great interest, because an aortic
dissection can extend to this vessel and can help distinguish DeBakey type A from type B dissections.
Placing the probe in the transverse plane on the left side of the neck will show the carotid artery and
should demonstrate an intimal flap if one is present. Repeating the examination in the longitudinal view is
important because a greater portion of the carotid lumen is then imaged, decreasing chances of missing a
flap (Supplemental Image 11-18 ).
Supplemental Image 11-18. Carotid Artery Imaging Demonstrating Intimal Flap

A) Transverse view. B) Longitudinal view.
PREGNANCY
Indications
Every woman of childbearing age presenting with abdominal pain, vaginal bleeding, and/or shock should
be screened for pregnancy. Classically a urine or serum β-HCG level will be measured. In addition,
bedside sonography should be performed, which can be of immediate help in diagnosing an intrauterine
pregnancy (IUP) and thus increase or decrease suspicion of an ectopic pregnancy.
Image Acquisition
To look for pregnancy and pregnancy-related disorders (Figure 11-26), obtain the following images:
Transverse view: Place the probe in the suprapubic region in a transverse orientation and fan the
uterus completely until it disappears both superiorly and inferiorly.
Longitudinal view: Place the probe in the sagittal plane in the suprapubic region and fan the uterus
completely until it disappears both to the right and left.
To ensure timely identification of the uterus and bladder, always start with the probe immediately
proximal to the pubic symphysis and aim caudally. This will ensure imaging of the most inferior part of
the pelvis where the uterus (until the second trimester of pregnancy) and bladder lie. Of note, it is
possible to see the pubic bone with its shadowing on the screen in the longitudinal view.
C AVE AT
Ectopic pregnancies can sometimes progress to an advanced stage in the first trimester before the
pregnant woman has any symptoms. At this stage it is even possible to see an ectopic fetal pole
with a heartbeat. As this obvious pregnancy is displayed on the screen it is possible to mistakenly
interpret it as being within the endometrial lining if a careful assessment of the entire area is not
performed. By always confirming the bladder and uterus juxtaposition first, it becomes evident
when the pregnancy is in an extrauterine location.7
Figure 11-26. Transabdominal Pelvic Ultrasound, Transverse and Longitudinal Views
Scanning technique for pelvic ultrasonography. A) Transverse orientation. B) Longitudinal orientation.
The first landmark to identify is the bladder. This serves 2 purposes:
A full bladder is very helpful because it acts as an acoustic window for the ultrasound beam to
penetrate and reach the organ of interest.
It also serves to confirm the position of the uterus, which is adjacent to the bladder, to avoid
mistakenly diagnosing an ectopic pregnancy as an IUP20 (Figure 11-27).
Another great way to confirm that you are imaging the uterus is to follow it down to the cervix and vaginal
stripe. By doing so, you will make sure the pregnancy is within the uterine cavity and not an ectopic
pregnancy in another anatomic structure.
IUP
To diagnose a definitive IUP, the following structures must be identified:
A gestational sac appears as an anechoic pocket of fluid in the decidual reaction.

A yolk sac looks like a small hyperechoic ring in the gestational sac. A fetal pole appears as an
echogenic oval structure in the gestational sac, and can be seen alongside the yolk sac early in the
pregnancy.
When all structures are present, these will form the classic “double-ring sign” (Figure 11-28). The
absence of any of these structures should raise concern for an abnormal pregnancy like an ectopic
pregnancy.
Figure 11-27. Vesicouterine Juxtaposition
Figure 11-28. “Double-Ring” Sign

Definitive intrauterine pregnancy showing the classic “double-ring” sign: decidual reaction (d), gestational sac (*), yolk sac.
It is important not to confuse the double-ring sign with the “double decidual sign.” The double decidual
sign is sometimes seen in early pregnancy within the decidual reaction. The decidua appears as 2 separate
hyperechoic concentric rings (the decidua parietalis and the decidua capsularis) separated from each
other by a thin anechoic stripe. These are not within the gestational sac but rather surround it and as such
should be distinguished from the double-ring sign. Although the radiology literature uses this sign as a
marker of an early IUP to rule out ectopic pregnancies, we do not recommend point-of-care sonographers
to use this in the same way because this sign is not always present and could lead to erroneous diagnoses.
Rather, we recommend focusing on the presence or absence of a double-ring sign to make conclusions
about the presence or absence of an IUP.
Ectopic Pregnancy
Ectopic pregnancies can have various ultrasound presentations. They can present with:
An empty uterus.
A small, empty intrauterine gestational sac termed the “pseudogestational” sac, which develops
secondary to hormonal stimulation from the ectopic pregnancy. A small gestational sac can also be
seen with a very early pregnancy or a miscarriage, and the decision to obtain an endovaginal or pelvic
ultrasound will depend on the patient’s presentation and β-HCG value.
An IUP that is eccentrically located and not within the endometrial lining. This form of ectopic
pregnancy, which is called “cornual” or “interstitial,” can easily be missed, and as such a high index of
suspicion is required. Diagnosing this type of ectopic pregnancy is possible with bedside sonography
by measuring the myometrial mantle, which is the thinnest portion of the uterine wall surrounding the
pregnancy. Although several measurements have been reported, we recommend using a minimal
thickness of 8 mm as a cutoff. This will be more sensitive in identifying possible cornual ectopic
pregnancies, which can be devastating if left undiagnosed (Supplemental Image 11-19 ).
A normal definitive IUP. This rare form of pregnancy is called a “heterotopic” pregnancy. This is when
2 pregnancies develop, one being a normal, definitive IUP while the other is in an extrauterine
position. These are very difficult to diagnose and require a high level of suspicion based on the β-
HCG value and the patient’s risk factors.
Supplemental Image 11-19. Suspicion of “Cornual” Ectopic Pregnancy

Myometrialmantleis < 8 mm.
E X P E RT T I P S
It is important to measure the “myometrial mantle” and refer for consultative ultrasound any
suspected case of “cornual ectopic pregnancy.” The reason for this is that these abnormal
pregnancies tend to grow until late in the first trimester before rupturing, and when they do
rupture, bleeding is usually significant.
Heterotopic pregnancies are usually rare in the general population. The main risk factors that increase the
chance of having such a pregnancy are chlamydial infection and fertilization treatments such as in vitro
fertilization.
Figure 11-29. Ovarian Mass
Ovarian masses visualized during transabdominal pelvic ultrasound. The uterus outline is shown with an asterisks; the ovarian mass outline with
arrows.
Although the optimal approach to image the adnexa is transvaginally with an endocavitary probe, in the
presence of ovarian pathology, it is possible to visualize the adnexa during a transabdominal pelvic
ultrasound. If an ovarian mass is noticed during a pelvic ultrasound, the diagnosis will depend on the
patient’s β-HCG result as well as the findings on the uterine ultrasound. In a patient with a positive β-
HCG result and an empty uterus with a visible ovarian mass, this should definitely increase your
suspicion of an ectopic pregnancy. In a case in which the patient has a positive β-HCG as well as a
definitive IUP diagnosed on pelvic ultrasound, the possibility of a heterotopic pregnancy will vary greatly
depending on the patient’s risk factors for such a diagnosis. If the patient has a negative β-HCG result,
then several ovarian pathologies are possible, ranging from a simple cyst to a hemorrhagic cyst (Figure
11-29). Simple cysts have smooth walls and an anechoic center, whereas hemorrhagic cysts have smooth
walls with more heterogeneous grey internal echoes. A large heterogenous ovarian mass with an
irregularly appearing wall and heterogeneous grey internal echoes, especially if calcifications are
present, should raise the clinical suspicion for a mass or tumor. Most importantly, if there is any concern
about an ovarian mass found on a transabdominal pelvic ultrasound, a complementary study (either a
transvaginal ultrasound or a consultative radiologic study) should be performed.
Whenever an ectopic pregnancy is suspected, a FAST examination should be performed to detect

intraperitoneal free fluid which, if present, should raise concern for a ruptured ectopic pregnancy, which
is a true emergency.
Viable Pregnancy
When a definitive IUP is diagnosed and a fetal pole with a heartbeat is seen, measuring its frequency can
help determine the viability of the pregnancy. The recommended method to measure the heart rate is via
the M-mode. When the M-mode line is placed on the beating fetal heart, the pulsations will appear as
regularly spaced vertical blurred lines. Measuring the distance between these lines will enable most
ultrasound machines to calculate the heart rate (Supplemental Image 11-20 ). Using Doppler on the
gravid uterus is not recommended because of increased energy output and its unknown effect on
developing tissues. The normal fetal heart rate is 110-160 beats/min, but in the early part of the first
trimester a heart rate around 90 beats/min can be normal. Of note, a heart rate <90 beats/min after 6 to 7
weeks of gestation usually carries a poor prognosis.
Supplemental Image 11-20. M-Mode Technique to Measure Fetal Heart Rate
KEY POINTS
Several abdominal organs can be imaged using bedside ultrasound, including the bowel when it is
obstructed.
Potentially dangerous abdominal pathologies such as choledocholithiasis, abdominal aortic
aneurysm, and ectopic pregnancies can be quickly diagnosed with point-of-care ultrasound.
Diagnosing pathologies quickly and at the bedside can be very advantageous to patients and
physicians by reducing the need for additional imaging and sometimes expediting definitive care.
REFERENCES
1. Bassler D, Snoey ER, Kim J. Goal-directed abdominal ultrasonography: impact on real-time decision making in the emergency department.
J Emerg Med. 2003;24:375-378.
2. Kendall JL, Hoffenberg SR, Smith S. History of emergency and critical care ultrasound: the evolution of a new imaging paradigm. Crit
Care Med. 2007;35:S126-S130.
3. Internal Clinical Guidelines Team (UK). Gallstone Disease: Diagnosis and Management of Cholelithiasis, Cholecystitis and
Choledocholithiasis. London, England: National Institute for Health and Care Excellence (UK); 2014. NICE Clinical Guidelines No. 188.
4. Cooperberg PL, Gibney RG. Imaging of the gallbladder. Radiology. 1987;163;605-613.
5. Kendall JL, Shimp RJ. Performance and interpretation of focused right upper quadrant ultrasound by emergency physicians. J Emerg Med.
2001;21:7-13.
6. Ralls PW, Colletti PM, Lapin SA, et al. Real-time sonography in suspected acute cholecystitis: prospective evaluation of primary and
secondary signs. Radiology. 1985;155:767- 71.
7. Babb RR. Acute acalculous cholecystitis: a review. J Clin Gastroenterol. 1992;15:238-241.
8. American College of Emergency Physicians. Policy Statement on Emergency Ultrasound Guidelines. October 2008. Available at:
http://www.acep.org/workarea/downloadas- set.aspx?id=32878. Accessed May 12, 2015.
9. Eisner BH, Reeses A, Sheth S, et al. Ureteral stone location at emergency room presentation with colic. J Urol. 2009;182:165-168.
10. Fujii Y, Kino M, Kimata T, et al. Significance of twinkling artifact on ultrasound in the diagnosis of cystine urolithiasis. Pediatr Int.
2013;55:e49-e51.
11. Pon MS, Scudamore C, Harrison RC, et al. Ultrasound demonstration of radiographically obscure small bowel obstruction. AJR Am J
Roentgenol. 1979;133:145-146.
12. Jang TB, Schindler D, Kaji AH. Bedside ultrasonography for the detection of small bowel obstruction in the emergency department. Emerg
Med J. 2011;28:676-678.
13. Taylor M, Lalani N. Adult small bowel obstruction. Acad Emerg Med. 2013;20:528-544.
14. Ogata M, Mateer J, Condon R. Prospective evaluation of abdominal sonography for the diagnosis of bowel obstruction. Ann Surg.
1996;223:237-241.
15. Jang T, Deaver M. Small bowel obstruction. In: Mallin M, Dawson M, eds. Introduction to Bedside Ultrasound. Vol 2. Lexington, KY:
Emergency Ultrasound Solutions; 2013:224- 230.
16. Ogata, M. General surgery applications. In: Ma OJ, Mateer JR, Blaivas M, eds. Emergency Ultrasound. New York, NY: McGraw-Hill;
2007:279-340.
17. Hefny AF, Corr P, Abu-Zidan FM. The role of ultrasound in the management of intestinal obstruction. J Emerg Trauma Shock. 2012:5:84-
86.
18. Schmutz GR, Benko A, Fournier L, et al. Small bowel obstruction: role and contribution of sonography. Eur Radiol. 1997;7:1054-1058.
19. Noble V. Abdominal aorta ultrasound. In: Noble V, Nelson B, eds. Manual of Emergency and Critical Care Ultrasound. 2nd ed. Cambridge,
England: Cambridge University Press; 2011:115-131.
20. Wiss R. Obstetrical EDE. In: Socransky S, Wiss R, eds. Point-of-Care Ultrasound for Emergency Physicians, “The EDE Book.” Sudbury,
ON: The EDE 2 Course Inc; 2012:48-70.
Chapter 12
Focused Assessment with Sonography in
Trauma (FAST)
Rachel E. Beard, MD; Stephen R. Odom, MD
OBJECTIVES
Describe the evolution in the diagnostic workup of blunt abdominal trauma
Describe the evidence supporting and opposing the use of FAST
Describe the technique of FAST and E-FAST
Point out the limitations and caveats in the utilization of FAST
INTRODUCTION
Trauma remains a major cause of morbidity, mortality, and years of life lost. It is the sixth leading cause
of death worldwide, and the fifth leading cause of significant disability.1 The worldwide prevalence of
blunt abdominal trauma among all patients admitted with trauma remains unclear, and reports range
anywhere from 6% to 65%.2 Damage to solid abdominal organs affects the liver 36% of the time, the
spleen 32% of the time, and the kidney 24% of the time, and nonoperative management of such injuries is
increasingly successful.1 Blunt trauma often occurs in the setting of high-mechanism injuries and
polytrauma. The management of these cases is extraordinarily complex and physical examination without
the use of imaging such as abdominal ultrasonography has been shown to be inadequate for evaluating
abdominal injuries.3 Missed abdominal injuries and unwarranted suspicion for the diagnosis can both
have severe consequences, necessitating adjuncts to the initial examination and survey to improve
management.
CASE STUDY
A 22-year-old helmeted man was involved in a motorcycle accident at approximately 55 miles per hour.
He was not wearing body armor. He complains of abdominal and left chest pain, with shortness of breath
and difficulty breathing. His blood pressure is 85/40 mm Hg, his heart rate is 90 beats/min, his
respiratory rate is 25 breaths/min, and his oxygen saturation is 88% on a nonrebreather mask at a flow
rate of 15 L/min.
THE EVOLUTION OF FAST

One of the initial tests used to detect abdominal injury in patients with trauma was diagnostic peritoneal
lavage (DPL). It could be used quickly in a trauma setting by making a small incision a few centimeters
inferior to the umbilicus and aspirating peritoneal fluid. Additional sterile fluid could be instilled into the
peritoneum and withdrawn after it was allowed to dwell for a moment. Its diagnostic usefulness was
limited to scenarios in which there was a sizable hemoperitoneum early on. In addition, intermediate tests
were difficult to interpret.4
A number of studies demonstrated the superior sensitivity and specificity of DPL and established criteria
for positivity (Table 12-1). However, it had disadvantages, including a high false-positive rate that led to
nontherapeutic laparotomies. It also failed to evaluate the retroperitoneal space or the diaphragm, and
failed to identify specific organ injury.2,5-7
The foundation for the use of ultrasound in the diagnosis of abdominal diseases was described by Holm
and Mortensen8 in the 1960s. The initial description of ultrasound for use in the trauma setting was
described in the 1980s in a series that described 314 consecutive patients who underwent sonography
after trauma, of whom 71 had positive findings and subsequent laparotomy. Their report of only two false-
positive results endorsed its usefulness.9 Subsequently, the use of what became known as the focused
assessment with sonography in trauma (FAST) protocol became more widespread over the next several
decades, initially in Europe and Asia and then in North America. It is a noninvasive diagnostic modality
and can be rapidly used at the bedside in many different settings by various practitioners. It is also
inexpensive, portable, and avoids computed tomography (CT) with intravenous contrast and ionizing
radiation. These qualities make the use of ultrasound in the trauma setting widely appealing, and it has
increasingly replaced the use of DPL for the detection of free intra-abdominal fluid in the trauma setting.4
FAST, however, is unable to assess hollow viscous injury and is unreliable for evaluating solid
abdominal injuries. Although CT is a useful adjunct, specifically for the assessment of retroperitoneal
structures and gradation of solid organ injury, it cannot be performed in the initial resuscitation, nor
should it be used in the assessment of unstable patients – as can FAST.6
The influential organizations in the field of trauma management, including the American College of
Emergency Physicians (ACEP) and the American College of Surgeons, have endorsed the use of FAST
and constructed guidelines for its use. In 2008, ACEP approved its updated policy statement on
emergency ultrasound guidelines, a revision of its original guidelines published in 2001.10 ACEP
specified 11 core applications for ultrasound in the emergency setting, with trauma being the foremost
(Table 12-2). It also outlined the specific goals of an emergency ultrasound curriculum in the setting of
trauma (Table 12-3). The American College of Surgeons vocalized its support for FAST when it issued
the ninth edition of the Advanced Trauma Life Support guidelines in 2012, which designated DPL as an
optional skill station and mandated the teaching of the new FAST skill station if DPL is not taught, in
order to assess the abdomen as a source of potential blood loss.11
C AVE AT
The FAST examination can miss injuries of the diaphragm, retroperitoneum, intestine, and solid
organ injuries without hemoperitoneum.
Table 12-1. Criteria for Positive Diagnostic Peritoneal Lavage7
Red blood cell count >100,000/mL

White blood cell count >500/mL
Gram stain showing the presence of bacteria
Presence of feces, vegetable fibers, bile, alkaline phosphatase (>6 IU/L) or amylase (>175 IU/L).
Table 12-2. Core Emergency Ultrasound Applications10
Trauma
Intrauterine pregnancy
Abdominal aortic aneurysm
Cardiac
Biliary
Urinary tract
Deep vein thrombosis
Soft tissue/musculoskeletal
Thoracic
Procedural guidance
Table 12-3. Emergency Ultrasound Curriculum: Trauma10
Describe the indications, clinical algorithms, and limitations of bedside ultrasound in blunt and penetrating thoracoabdominal trauma.
Define the relevant local anatomy including the liver, spleen, kidneys, bladder, uterus, pericardium, and lung bases.
Understand the standard ultrasound protocol required when evaluating for hemoperitoneum, hemopericardium, hemothorax, and
pneumothorax.
Recognize the relevant focused findings and pitfalls related to the detection of hemoperitoneum, hemopericardium, and hemothorax.
Describe how volume status can be evaluated and monitored by evaluating left ventricular function and inferior vena cava compliance.
THE EVIDENCE BEHIND FAST

The validity of FAST has been demonstrated in many studies. A randomized study of 262 patients with
suspected torso trauma demonstrated that those treated with ultrasonography as a part of their diagnostic
protocol were transported more quickly to the hospital, discharged more quickly from the hospital,
incurred less hospital cost, underwent fewer CT scans, and had fewer overall complications.12 Multiple
larger studies illustrated a high degree of accuracy with FAST. A study published in 1998 reviewed 1,540
patients who had blunt abdominal or penetrating precordial or transthoracic trauma and indicated an
83.3% sensitivity and 99.7% specificity in patients with blunt abdominal trauma, a 100% specificity and
sensitivity in a subset of those patients who were hypotensive, and 100% sensitivity and 99.3%
specificity in patients with precordial or transthoracic wounds.13 An even larger and more recent study of
4,029 patients with blunt abdominal trauma was published in 2007 and showed an overall sensitivity of
85%, specificity of 96%, and accuracy of 95%. It also validated the use of FAST as a method to triage
patients with hypotension directly to the operating room without CT.14
There is, however, a degree of controversy regarding the application of ultrasound in the field of trauma.
A study in 2003 evaluated 359 hemodynamically stable patients with trauma with suspected blunt
abdominal injury and found that, when using CT scan as a confirmatory test for hemoperitoneum, FAST
had a sensitivity of only 42% and positive predictive value of 67%, though it did demonstrate a
specificity of 98% and negative predictive value of 93%.15 Similar predictive values were also
demonstrated by a much larger study published in 2010, which reviewed 2,105 trauma patients who
underwent the FAST examination and demonstrated an overall sensitivity of 43%, a specificity of 99%, a
positive predictive value of 95%, and a negative predictive value of 94%.16 The authors concluded that
owing to the low sensitivity of negative results without confirmation by CT, the use of FAST should be
reserved for hemodynamically unstable patients.16 Even more expanded concerns were echoed in a large
retrospective chart review published in 2014, which evaluated 1,671 patients with blunt trauma, 146 of
whom had intra-abdominal injuries confirmed on CT or laparotomy.17 A FAST scan demonstrated
sensitivity of only 22% in hemodynamically stable patients and 28% in hemodynamically unstable
patients, and the authors suggested that FAST without CT could miss intra-abdominal injuries, and that in
unstable patients, the decision to proceed to negative laparotomy should not be affected by a negative
FAST result. Lastly, a Cochrane Database meta-analysis published in 2013 reviewed 4 randomized trials
with study populations of patients with blunt trauma who were undergoing diagnostic investigations for
abdominal organ injury.2 The study concluded that though the use of ultrasound-based diagnostic
algorithms reduced the number of CT scans, the meaning of this was unclear and that there is overall
insufficient evidence from randomized controlled trials to justify the endorsement of such algorithms in
the setting of blunt abdominal trauma.
Newer techniques, including contrast-enhanced ultrasound, hold initial promise of reliable gradation of
solid organ injury in blunt trauma. In a recent study of 306 consecutive patients with blunt trauma with
solid organ injury, it was determined that the correlation among CT scan, contrast-enhanced ultrasound,
and clinical outcome prediction was good.18 It is still questionable if this can supplant CT scan in the
evaluation of stable patients with blunt trauma.
THE TECHNIQUE OF FAST

Although its overall usefulness in the trauma setting remains a topic for debate, the method for performing
the FAST examination is well described. A prospective study published in 2013 trained a cross-section
of surgeons and surgical trainees in the sequential 4-view examination ultrasound technique. In 476
patients with trauma, the technique demonstrated a 79% sensitivity and 95.6% specificity for the detection
of injury, and it came to be known as the FAST examination (Table 12-4).4,19 A standard 3.5-MHz convex
probe is typically used (Figure 12-1). A cardiac phased-array transducer may be used if available and is
superior for cardiac imaging. Some clinicians may use high-frequency microconvex probes, especially for
pediatric patients. It is essential to obtain adequate views of the pericardium and the 3 dependent
abdominal regions: Morison pouch, defined as the hepatorenal recess that separates the liver from the
right kidney; the splenorenal recess; and the pelvis. To understand probe placement, it is important to
assess the chest for positioning of the probe. The horizontal xiphisternal line (HXL) is a transverse line
drawn at the level of the xiphisternum and extends around the patient’s anterior chest (Figure 12-2).
Figure 12-1.Ultrasound Probe
A standard 3.5-MHz convex probe used for a Focused Assessment with Sonography in Trauma (FAST).
Table 12-4. Essential Steps in the Performance of FAST4,18
A nasogastric tube is inserted before the examination, if needed, but the urinary catheter is withheld so that the distended bladder
provides an acoustic window for visualization of blood in the pelvis.
Using a 3.5-MHz transducer, the FAST surveys are used for blood in the pericardial sac and the 3 dependent abdominal regions,
including the Morison pouch, splenorenal recess, and pelvis.
Ultrasound transmission gel is applied to the pericardial area, right and left upper quadrants, and pelvis. (The pericardial area is
visualized first, so that blood in the heart can be used as a standard to set the gain appropriately for the detection of hemoperitoneum
and hemopericardium.)
The transducer is oriented for sagittal sections and positioned in the subxiphoid region to identify the heart and to examine for blood in
the pericardial sac.
The transducer is placed in the right midaxillary line between the 11th and 12th ribs to identify the sagittal section of the liver, kidney,
and diaphragm.
With the transducer positioned in the left posterior axillary line between the 9th and 10th ribs, the spleen and kidney are visualized.
The transducer is directed for a transverse section and placed 4 cm superior to the symphysis pubis. It is swept inferiorly to obtain a
coronal view of the full bladder and both sides of the pelvis.
Abbreviation: FAST, focused assessment with sonography in trauma.
The location at which this line intersects the anterior axillary line on the right (Figure 12-3) and the
posterior axillary line on the left (Figure 12-4) will mark the initial probe position for the upper
abdominal scans. The first view obtained should be of the subxiphoid region transversely to assess the
pericardial sac, as well as the diaphragm, to evaluate for fluid or tamponade.
The probe is placed on the HXL near the midline, with the indicator placed to the patient’s right side (note
that the typical abdominal configuration on the ultrasound will require that the indicator be placed to the
patient’s right, whereas some cardiac configurations require placement of the indicator to the patient’s
left) (Figure 12-5).
Both the right and left upper quadrant views can be acquired along the horizontal xiphoid line, a
transverse line across the body at the level of the xiphisternum.
Figure 12-2. Horizontal Xiphisternal Line

The horizontal xiphisternal line is a transverse line drawn at the level of the xiphisternum and extends around the patient’s anterior chest.
E X P E RT T I P
Parasternal long-axis view is a good alternative if the subxiphoid view is not optimal (but a
phased-array probe must be used in this case).
Figure 12-3. Initial Probe Placement for Right-sided Upper Abdominal Scans
Right chest with initial probe placement area marked where horizontal xiphisternal line intersects the anterior axillary line.
Figure 12-4. Initial Probe Placement for Left-sided Upper Abdominal Scans
Abbreviation: LUQ, left upper quadrant.
Left chest with initial probe placement marked at the intersection of the horizontal xiphisternal line and posterior axillary line.
Figure 12-5. Probe Placement for Cardiac View

Note that the indicator is placed to the patient’s right side. In most cardiac settings, this will result in a 180-degree flipped view.
Alternately, a cardiac probe can be used (this will require placing the indicator to the patient’s left side). An overhand grip, as shown, can
facilitate the downward tilting of the probe’s tail to see up into the chest.
Increase depth to image the entire heart when acquiring the subxiphoid view.
Figure 12-6. Normal Cardiac View

Abbreviations: RV, right ventricle; RA, right atrium; LV, left ventricle; LA, left atrium.
Note liver and the potential space of the pericardium.
A normal view will include the right atrium and ventricle in the near field with the liver as the acoustic
window (note that this is rotated 180 degrees from the convention for cardiac scanning) (Figure 12-6).
Fluid in the pericardial space is indicated by an anechoic space in the pericardial sac (Figure 12-7).
Tamponade can be inferred in the correct clinical scenario with scalloping of the right ventricle, right
atrial diastolic and ventricular diastolic collapse, and plethora of the inferior vena cava (see Chapter 16).
Next is a longitudinal examination of the right upper quadrant followed by the left upper quadrant, and
longitudinal and transverse scans of the suprapubic region to visualize both the bladder and the space
anterior to the rectum (the pouch of Douglas between the uterus and rectum in women and the space
between the bladder and rectum in men). The paracolic gutters can also be assessed bilaterally.20
Figure 12-7. Cardiac Tamponade

Abbreviations: RA, right atrium; RV, right ventricle; LA, left atrium; LV, left ventricle.
Note pericardial fluid marked with the arrow.
E X P E RT T I P S
Cardiac tamponade is a clinical diagnosis, suggested by right ventricular collapse and dilated
inferior vena cava.
Do not forget to view the paracolic gutters and the inferior poles of the kidneys in the right and left upper
quadrant views.
The Morison pouch is the most dependent region of the peritoneum in the supine patient and the most
sensitive view to detect free fluid.
Probe position for the right upper quadrant is at the point where the HXL meets the anterior axillary line
on the right (Figure 12-8). The Morison pouch (hepatorenal recess), the most dependent portion of the
peritoneum, can be evaluated from this position (Figure 12-9).
Free fluid is seen as an anechoic space between the liver and kidney (Figure 12-10) or inferior to the
right kidney (Figure 12-11). In some small or localized collections of blood, free fluid may also be seen
between the diaphragm and liver only. The probe is positioned at the intersection of the HXL and the
posterior axillary line on the left to identify the spleen (Figure 12-12).
A normal view will include the spleen and the splenorenal recess (Figure 12-13). This view is more
difficult than the right upper quadrant view and occasionally requires a slightly oblique angulation of the
probe to “peek” through the ribs.
Figure 12-8. Probe Placement for Right Upper Quadrant View and Morison Pouch
Probe placement is at the point where the horizontal xiphisternal line meets the anterior axillary line on the right.
Figure 12-9. Morison Pouch, Normal View
Liver and kidney are labeled. The diaphragm is a strong reflector and appears as a bright line (up arrow). The potential space of the Morison
pouch is marked with a left arrow (this is the deepest part of the peritoneum in the supine patient).
The inferior pole of the left kidney is less likely to have fluid, because the splenocolic ligaments prevent
tracking of fluid in the supine patient in the absence of a large amount of fluid. When present, fluid is often
seen above the spleen in this view (Figure 12-14). The probe is placed 2 cm above the symphysis pubis
in the suprapubic region to evaluate the pelvis, ideally before emptying the bladder. If a catheter is in
place, it should be clamped to allow the bladder to fill partially. The indicator on the probe is placed to
the patient’s right for the transverse view and toward the patient’s head for the longitudinal view (Figures
12-15 and 12-16). A normal evaluation will include the rectouterine pouch (of Douglas) and the
vesicouterine pouch in women, and the rectovesical pouch in men in both planes (Figure 12-17).
Figure 12-10. Free Fluid in Morison Pouch

Free fluid is marked in the Morison pouch with a star. Note the fluid’s position between the liver and kidney.
Figure 12-11. Free Fluid at Inferior Pole of Right Kidney
It is important to scan the lower pole of the right kidney, because fluid can collect here as it flows into the paracolic gutter. Note that there is a
small “stripe” of fluid in the Morison pouch, but as seen in this image, a more impressive collection of fluid appears to be at the inferior pole of
the right kidney (star).
Figure 12-12. Probe Placement for Left Upper Quadrant and Spleen View
Probe placement is at the intersection of the horizontal xiphisternal line and the posterior axillary line on the left.
Figure 12-13. Normal View of Spleen

The spleen and left kidney are labeled. The potential space is marked with a circle. The diaphragm is labeled with a right arrow.
Figure 12-14. Free Fluid Seen Above Spleen
Abbreviation: LUQ, left upper quadrant.
The left arrow marks the fluid seen above the spleen.
I M A G E O P T I M I ZAT I O N T I P S
Occasionally, the probe can be turned obliquely to “peek” through the ribs in the splenic view.
The splenic view is a smaller sonographic window, and is more posterior (posterior axillary line) than
the right upper quadrant view (“put your knuckles on the gurney”).
Figure 12-15. Probe Placement for Suprapubic View, Transverse Position

Placement of the probe on the patient’s right for the transverse view.
Figure 12-16. Probe Placement for Suprapubic View, Longitudinal Position
Placement of the probe toward the patient’s head for the longitudinal view.
Figure 12-17. Normal Suprapubic Views

A) longitudinal view; B) transverse view. The bladder, bladder wall, and abdominal wall musculature are labeled in these figures. Fluid may
collect in the spaces around the bladder, marked by yellow dots.
Free fluid can be seen by fanning the probe and observing anechoic space outside the bladder in the
pouches or between loops of bowel (Figure 12-18).
This technique was later modified by the addition of thoracic views during the initial resuscitation, which
proved useful for the detection of pneumothorax, hemothorax, cardiac injury, and pericardial effusion.
This modified technique was first described in the literature in 2004 and became known as the extended
FAST (E-FAST).21 E-FAST has actually been shown to be more sensitive than chest radiography for the
detection of pneumothoraces and pleural effusions in the trauma setting.21,22 To obtain these views, the
probe is positioned longitudinally on the chest wall and perpendicular to the ribs in the anterior
midclavicular line bilaterally (Figure 12-19). A linear array transducer can be helpful in fitting between
spaces. Below 2 contiguous ribs, the pleural line is identified as a thin hyperechoic line that represents
the interface of the 2 pleural surfaces. In the absence of pneumo- or hemothorax, this line should be seen
to slide back and forth with respiratory movements. A pleural effusion is seen as an anechoic wedge
above the liver that obliterates the pleural line, and with a loss of mirror artifact (Figure 12-20), best seen
in the upper quadrant views and poorly seen in the thoracic views. The ultrasound’s M-mode can be used
for this purpose. The absence of sliding of the pleural line with the visualization of parallel lines above
and below it is referred to as “the stratosphere sign” and is suggestive of pneumothorax (Figure 12-21).20
Hemothorax can also be detected using the M-mode to visualize respiratory variation of an intrapleural
fluid collection, a finding referred to as the “sinusoid sign.”20
Figure 12-18. Free Fluid in Pelvis

A) longitudinal view; B) transverse view. Free fluid is marked in these images with an arrow. Note the sharp borders of the fluid marked by a
Figure 12-19. Probe Placement for E-FAST Views

A) right chest; B) left chest. Probe placement for pleural evaluation in the extended focused assessment with sonography in trauma (E-FAST).
Figure 12-20. Pleural Effusion in Right Hemithorax
The fluid is marked with a star. The diaphragm is marked by a left arrow. Note that the spine shadows continue above the diaphragm when
there is fluid in the chest. This is known as the “spine sign,” and is an indirect finding when fluid or dense consolidation of lung tissue conducts
the sound waves. It will be absent above the diaphragm when there is no fluid in the chest (normal). The liver is labeled.
Figure 12-21. Pneumothorax in M-Mode

In the upper, two-dimensional image, note the location of the pleural line. In the absence of pleural sliding (pneumothorax), the resulting M-
mode image will appear as a barcode sign or “stratosphere” sign. A normal finding in M-mode would appear as a “seashore” sign, with a
transition between the chest wall and sliding pleural.
The learning curve of the FAST examination is a subject of ongoing investigation. One retrospective study
assessed the first 75 examinations conducted by emergency physicians learning the technique, and found
that noninterpretable or misinterpreted images were collected 24% of the time in the first 10
examinations. This number dropped to 3.6% for examinations 41 to 50, and 0% for examinations 70 to 75.
Physicians seemed to learn the skills required to interpret FAST images faster than they acquired the
skills to obtain such images. The splenorenal and subxiphoid views seemed to be the most challenging,
and accounted for 80% of the noninterpretable images.23 Another study indicated that the initial error
rates after recent surgery and of emergency physicians in detecting hemoperitoneum with FAST was 17%,
and that this rate dropped to 5% after the first 10 examinations.24 Multiple models for training courses
have been suggested, and trainees undergoing courses of as short as a 1-day duration have been shown to
perform FAST examinations at accuracy levels comparable to physicians with extensive experience.25 In
their 2008 guidelines, ACEP suggested that at least 25 to 50 documented and reviewed ultrasound cases
be performed during the training period in each of the core applications, including trauma (Table 12-2).10
However, training across specialties and practice settings remains far from standardized, and is an area
for growth and improvement in the future. FAST can be executed properly in less than 5 minutes in the
hands of an appropriately trained operator.20
Other drawbacks and limitations of FAST include the requirement of at least 200 mL of fluid for detection
and up to 400 mL for less experienced operators, limiting its accuracy in early hemoperitoneum.26 The
examination fails to reliably detect retroperitoneal injuries or injuries to the diaphragm. With FAST, it is
also difficult to differentiate the densities and qualities of fluid, and may be difficult to differentiate
ascites, urine, and peritoneal dialysate from blood. It is important to note that fluid in the pouch of
Douglas may be physiologic in a woman of childbearing age. Obese patients are difficult to study from a
technical perspective, as are those with overlying subcutaneous air. Overall, it is important to bear in
mind that the FAST examination has an important but limited role in the diagnosis of abdominal and
thoracic trauma, and should be used only to guide initial management and not for definitive diagnostic
purposes, particularly when nonoperative management is planned.
C AVE AT
Obese patients, patients with overlying subcutaneous air, and patients with intra-abdominal
ascites, peritoneal dialysate, or urine present a technical challenge to the application of FAST.
KEY POINTS
Over the past several decades, FAST has become increasingly widely used in the trauma setting,
and has largely supplanted previously used techniques, including DPL.
The use of FAST has been validated in many studies that demonstrate a high degree of accuracy,
though other studies suggest a much lower degree of sensitivity and question its usefulness.
FAST has an important role in the initial assessment of patients with trauma and can help address
life-threatening problems in the resuscitation phase, as well as assist with decisions regarding
management and further diagnostic testing.
FAST has limitations and should not be used for definitive diagnostic purposes, particularly when
nonoperative management of traumatic injuries is planned.
REFERENCES
1. Soreide K. Epidemiology of major trauma. Br J Surg. 2009;96:697-698.
2. Stengel D, Bauwens K, Rademacher G, et al. Emergency ultrasound-based algorithms for diagnosing blunt abdominal trauma. Cochrane
Database Sys Rev. 2013;7:CD004446.
3. Schurink GW, Bode PJ, van Luijt PA, et al. The value of physical examination in the diagnosis of patients with blunt abdominal trauma: a
retrospective study. Injury. 1997;28:261-265.
4. Rozycki GS, Root HD. The diagnosis of intra-abdominal visceral injury. J Trauma. 2010;68:1019-1023.
5. Engrav LH, Benjamin CI, Strate RG, et al. Diagnostic peritoneal lavage in blunt abdominal trauma. J Trauma. 1975;15:854-859.
6. Griffin XL, Pullinger R. Are diagnostic peritoneal lavage or focused abdominal sonography for trauma safe screening investigations for
hemodynamically stable patients after blunt abdominal trauma? A review of the literature. J Trauma. 2007;62:779-784.
7. Davis JW, Hoyt DB, Mackersie RC, et al. Complications in evaluating abdominal trauma: diagnostic peritoneal lavage versus computerized
axial tomography. J Trauma. 1990;30:1506-1509.
8. Holm HH, Mortensen T. Ultrasonic scanning in diagnosis of abdominal disease. Acta Chir Scand. 1968;134:333- 341.
9. Hoffmann R, Pohlemann T, Wippermann B, et al. [Management of sonography in blunt abdominal trauma]. Der Unfallchirurg.
1989;92:471-476.
10. American College of Emergency Physicians. Emergency ultrasound guidelines. Ann Emerg Med. 2009;53:550-570.
11. ATLS Subcommittee; American College of Surgeons’ Committee on Trauma; International ATLS working group. Advanced trauma life
support (ATLS®): the ninth edition. J Trauma Acute Care Surg. 2013;74:1363-1366.
12. Melniker LA, Leibner E, McKenney MG, et al. Randomized controlled clinical trial of point-of-care, limited ultrasonography for trauma in
the emergency department: the first sonography outcomes assessment program trial. Ann Emerg Med. 2006;48:227-235.
13. Rozycki GS, Ballard RB, Feliciano DV, et al. Surgeon-performed ultrasound for the assessment of truncal injuries: lessons learned from
1540 patients. Ann Surg. 1998;228:557-567.
14. Lee BC, Ormsby EL, McGahan JP, et al. The utility of sonography for the triage of blunt abdominal trauma patients to exploratory
laparotomy. AJR Am J Roentgenol. 2007;188:415- 421.
15. Miller MT, Pasquale MD, Bromberg WJ, et al. Not so FAST. J Trauma. 2003;54:52-59; discussion 9-60.
16. Natarajan B, Gupta PK, Cemaj S, et al. FAST scan: is it worth doing in hemodynamically stable blunt trauma patients? Surgery.
2010;148:695-700; discussion 700-701.
17. Carter JW, Falco MH, Chopko MS, et al. Do we really rely on fast for decision-making in the management of blunt abdominal trauma?
Injury. 2015;46:817-821.
18. Lv F, Ning Y, Zhou X, et al. Effectiveness of contrast-enhanced ultrasound in the classification and emergency management of abdominal
trauma. Eur Radiol. 2014;24:2640-2648.
19. Rozycki GS, Ochsner MG, Jaffin JH, et al. Prospective evaluation of surgeons’ use of ultrasound in the evaluation of trauma patients. J
Trauma. 1993;34:516-526; discussion 26-7.
20. Sofia S. Bedside US imaging in multiple trauma patients: 1, US findings and techniques. J Ultrasound. 2013;16:147- 159.
21. Kirkpatrick AW, Sirois M, Laupland KB, et al. Hand-held thoracic sonography for detecting post-traumatic pneumothoraces: the Extended
Focused Assessment with Sonography for Trauma (EFAST). J Trauma. 2004;57:288- 295.
22. Abdulrahman Y, Musthafa S, Hakim SY, et al. Utility of extended FAST in blunt chest trauma: is it the time to be used in the ATLS
algorithm? World J Surg. 2015;39:172- 178.
23. Jang T, Kryder G, Sineff S, et al. The technical errors of physicians learning to perform focused assessment with sonography in trauma.
Acad Emerg Med. 2012;19:98-101.
24. Shackford SR, Rogers FB, Osler TM, et al. Focused abdominal sonogram for trauma: the learning curve of nonradiologist clinicians in
detecting hemoperitoneum. J Trauma. 1999;46:553-562; discussion 562-564.
25. Walcher F, Kirschning T, Muller MP, et al. Accuracy of prehospital focused abdominal sonography for trauma after a 1-day hands-on
training course. Emerg Med J. 2010;27:345- 349.
26. Branney SW, Wolfe RE, Moore EE, et al. Quantitative sensitivity of ultrasound in detecting free intraperitoneal fluid. J Trauma.
1995;39:375-380.
Chapter 13
Ultrasound-Guided
Vascular Cannulation
Chapter 14
Chest Tubes and Thoracentesis
Chapter 15
Paracentesis and
Abscess Drainage
Chapter 13
Ultrasound-Guided Vascular Cannulation
Arun Nagdev, MD; Justin Bosley, MD; Thomas
Heflin, MD
OBJECTIVES
Use ultrasound to survey regional anatomy, and determine the ideal location for central venous cannulation
Describe ideal patient positioning and transducer orientation during ultrasound guidance for central venous
cannulation
Understand simplified techniques to allow both novice and experienced sonographers to rapidly insert and confirm
central venous cannulation
Use ultrasound visualization to become familiar with the often-varied arterial anatomy
Demonstrate reliable patient positioning and transducer placement to allow for increased first-pass success during
arterial cannulation
Describe a simplified needling technique for the novice and more experienced sonographer to rapidly insert and
confirm arterial cannulation
Discuss the technique of ultrasound-guided paracentesis
INTRODUCTION
Evidence supporting ultrasound guidance for vascular access (specifically central access) is fairly
robust,1-5 and convincing data indicate increased success and a decrease in complication rates when it is
used in critical care and emergency medicine. Both the Agency for Healthcare Research and Quality
(AHRQ) and the National Institute for Health and Care Excellence (NICE) have recommended ultrasound
guidance for central venous access.6 With the availability of point-of-care ultrasound systems in most
emergency departments and ICUs, ultrasound guidance for vascular access is quickly becoming a
requisite skill for all emergency and critical care physicians.
This chapter will discuss the 3 most common sites for obtaining ultrasound-guided central venous access:
the internal jugular vein (IJV), the common femoral vein, and the subclavian vein (SCV). A practical
approach to placing each line will be discussed, as will the rationale for the use of each site and any
associated complications. Later in the chapter, we will also discuss the anatomy, indications, and
technique for the 2 most ubiquitous arterial catheterizations: radial and femoral.
CASE STUDY
An obese 73-year-old woman from an assisted living facility arrives at the emergency department in
extremis. She is altered with signs of a respiratory infection. The patient is febrile (38.7°C) and
hypotensive on initial evaluation, and will need aggressive resuscitation. Because of difficulty in
obtaining adequate peripheral intravenous access and the desire to begin vasopressor therapy, a decision
is made to perform central venous cannulation (CVC). Ultrasound guidance is planned to improve success
and reduce error (eg, carotid artery [CA] puncture, pneumothorax).
CENTRAL VENOUS ACCESS

Obtaining venous access is an essential skill for the emergency and critical care physician. CVC is less
often compulsory, but still remains an indispensable skill in the practice of emergency and critical care
medicine. CVC allows multiple critical actions to be performed ranging from the administration of blood
products and vasoactive medications to transvenous cardiac pacing. CVC may also be the lone option in
cases in which standard peripheral access cannot be obtained.
Even the most experienced provider can have difficulty securing rapid and functional access to the venous
system in specific situations (eg, severe dehydration, cardiac arrest, large body habitus, injection drug
users with sclerosed veins, etc). The classic landmark-based technique has been shown to be less
successful, and has more complications compared with ultrasound guidance. Also, ultrasound
visualization of the vascular anatomy before beginning the procedure allows the specific advantage of
determining the ideal location for skin puncture. Specifically, a thrombosed femoral vein can be identified
at the bedside, allowing the clinician to preemptively choose another site. For a patient receiving
anticoagulation therapy, the visualization of complete overlap of the right internal jugular and CA may
allow the clinician to either choose another access site or ultrasound-guided technique (that is more
advanced) to prevent inadvertent arterial puncture and the resulting sequela. Ultrasound guidance for
central venous access has altered the clinical algorithm of obtaining vascular access, making the
procedure easier for the physician and safer for the patient.
INTERNAL JUGULAR VEIN
Rationale
The IJV is the most commonly accessed central vein, and has relatively few contraindications (eg,
respiratory distress preventing supine patient positioning, cervical spine immobilization, prior vascular
neck surgery compromising arterial or venous flow, etc). It arises from intracranial sinuses and exits the
skull via the jugular foramen, presenting a consistently shallow structure that can be easily accessed in
most patients. Because of the high variation of the IJV with regard to the CA, landmark-based attempts
have been shown to be less successful, while having higher complication rates.7 We recommend a simple
survey scan of both IJVs to determine which vein is easiest to cannulate (largest size, least overlap with
the CA, etc). Using a linear transducer, follow the IJV and CA along the path from the clavicle to the angle
of the mandible to find the ideal location for cannulation.
Anatomy
The IJV should lie lateral to the CA in most patients, though vascular variation is high, and a preemptive
survey scan can aid in determining which side of the neck is ideal for cannulation. This simple
ultrasonographic survey shows the degree of CA and IJV overlap (greater overlap is associated with
higher risk of CA puncture) as well as venous patency and size. Simple adjunctive techniques such as
placing the patient in the Trendelenburg position or asking the patient to perform Valsalva maneuvers can
readily demonstrate venous engorgement and improve success of cannulation.8,9 Also, color Doppler may
be used to distinguish IJV and CA when 2-dimensional (2D)/gray scale imaging cannot readily
differentiate these adjacent vessels. These simple preparatory techniques can reduce error and enhance
first-pass success rates when performing CVC in the IJV.10,11
Complications
The most frequent complications of accessing the IJV include inadvertent CA puncture and iatrogenic
pneumothorax. Ultrasound guidance has been shown to reduce rates of complications compared with
landmark-based techniques for both experienced and novice providers.12,13 Multiple governing bodies
and guidelines recommend ultrasound guidance for IJV cannulation, making this procedure a standard in
most ICUs and EDs.14-16
Patient Positioning
The patient’s bed should be raised to a comfortable height. Rotate the patient’s head away from the site of
the planned CVC to allow for maximal exposure of the submandibular to supraclavicular region.17 The
ultrasound system should be placed in a clear line of site for the operator to improve ergonomics (Figure
13-1A).
E X P E RT T I P
For the novice clinician who is new to ultrasound guidance, we recommend the short-axis
approach, wherein the ultrasound probe and direction of needle advancement are orthogonally
oriented. Even though the needle is not visualized during the entire procedure, we feel that this
technique allows for clear visualization of both the IJV and CA during the procedure. For IJV CVC
placement, the steps are described in this chapter, and the outlined approach is applicable to nearly all
vascular access procedures with closely aligned arterial and venous structures.
Figure 13-1. Ultrasound Positioning for IJV Access

Abbreviations: IJV, internal jugular vein; CA, carotid artery; SCM, sternocleidomastoid muscle.
A) The ultrasound screen is in the clear line of sight of the operator. B) A short-axis (out-of-plane) orientation is used for novice providers.
The directional marker is to the patient’s left (yellow arrow).
Ultrasonographic Evaluation
Ensure that the ultrasound system is clearly visible, so that the operator can visualize the area of skin
puncture and the ultrasound screen without requiring significant neck movement. Once the IJV and CA are
identified and differentiated, the ultrasound probe should be centered over the target IJV. We recommend
that the transducer’s directional indicator is oriented to the provider’s left to synchronize the anatomic
orientation of the patient and the ultrasound screen (Figure 13-1B). Ultrasound localization of the target
vessel allows local anesthesia to be instilled in a targeted region just superior.
Procedure
After aseptic preparation of the site is completed, place sterile gel and a sheath over the transducer. With
the covered linear ultrasound transducer, re-identify the IJV and CA near the skin wheal. Using the
nondominant hand, stabilize the transducer (with minimal pressure) on the patient’s neck or clavicle,
keeping the IJV directly in the center of the ultrasound display. If this orientation is maintained, you can
reasonably use the midline of the transducer as a visual marker, demonstrating the location of the
centered, underlying target vessel. Using the “M-mode” (motion mode) line or a “center line” on the
ultrasound system can aid in confirming the midline position of both the IJV and ultrasound transducer.
When placing the ultrasound transducer over the IJV, we recommend very gentle pressure to prevent
venous compression. This can be accomplished by holding the probe with the tips of the fingers and
resting the medial palmar aspect of the hand on the patient.
With the operator at the head of the bed, insert the needle into the skin at a 45- to 60-degree angle to the
frontal plane (ie, angle between the needle and the skin), maintaining constant negative pressure in the
syringe. The needle should be introduced with a “bevel up” orientation to improve needle tip
visualization and allow guidewire insertion (later step). As a simple rule, measure the depth of the target
vessel and insert the needle through the skin an equal distance back from the probe, creating a 45-degree
angle approach to the target vessel.
Once the needle is inserted into the skin, stabilize the probe and slowly advance the needle toward the
IJV. For the very novice provider, we recommend not moving the ultrasound transducer and advancing the
needle until venous flashback is obtained. A more experienced provider can fan the probe distally (away
from the clavicle and toward the needle) to attempt needle tip visualization during needle advancement.
As the needle is slowly advanced deeper into the neck, the probe is fanned more proximally (toward the
clavicle) to visualize the needle tip as it enters the IJV. The needle tip and needle should produce an
echogenic artifact (ie, hyperechoic or white in appearance) with variable amounts of ring-down
reverberation artifact. Incremental advancement toward the vessel should occur in a methodical manner
with the operator aspirating the syringe and carefully noting flashback.
Pressure from the needle alone may compress the vein entirely in some patients, but once the needle tip
has penetrated the vessel wall, the tenting should resolve and the vessel should appear to reopen. At this
point, the provider should feel an easing of the negative pressure applied on the syringe as a blood flash
enters the needle. When flashback is obtained, the guidewire can be passed through the needle and into the
IJV. A transverse image of the target vein should be obtained proximal to the puncture site while noting the
guidewire location. Dilation should only occur after the operator is confident of lack of arterial
cannulation (Figure 13-2).
Figure 13-2. Accessing the IJV
Abbreviations: IJV, internal jugular vein; CA, carotid artery.
A) Needle puncture is the same distance back as the depth of the IJV at a step angle (45-60 degrees). B) Guidewire confirmation in the IJV
on ultrasound.
In-Plane Approach to IJV

More experienced providers may commonly use the in-plane approach to IJV cannulation. In cases with
significant overlap between the IJV and CA (and when other access points to the central circulation are
not possible), this more advanced technique may be a valuable alternative. The operator must be facile
with visualizing the needle in plane, because minimal medial movement of the needle may allow for
inadvertent CA puncture.
Placing the transducer in a longitudinal plane in the neck with the probe marker facing cephalad will
allow for a clear view of the IJV. Often the vein does not run perfectly straight, and subtle adjustments to
the probe must be made to obtain a clear view of the entire vein.
The needle tip is inserted just cephalad to the probe indicator. The needle should be visible as a bright,
hyperechoic structure advancing toward the vein. This technique requires maintenance of a careful long-
axis image of both the needle and IJV, but it allows clear visualization of the approach and cannulation of
the IJV by the needle tip. After IJV cannulation, the in-plane technique also provides a clear view of the
guidewire as it enters the vein (confirming venous cannulation) (Figure 13-3).
Oblique View
An oblique approach has also been described.18 This view allows for in-plane needle visualization
toward a nearly short-axis view of the IJV and the nearby CA. It affords some benefits of both the short-
axis and long-axis approaches, though not for the novice practitioner, because the spatial relationships
between structures and the needle can be more challenging to interpret initially. This technique begins in
the same manner as the short-axis approach described earlier with the directional marker facing the
patient’s left. Once the vessel is identified, the probe is rotated 45 degrees such that the long axis of the
probe will point toward the patient’s sternal notch. If on the right side of the patient’s neck, this will be a
clockwise rotation; if on the left side of the patient’s neck, it will be a counterclockwise rotation. The
needle is then inserted at the lateral end of the ultrasound probe and advanced under in-plane
visualization of the needle toward the obliquely transected IJV. After the guidewire is passed, the CVC
itself is inserted in the usual Seldinger fashion (Figures 13-4 and 13-5).
Figure 13-3. Long-Axis (In-Plane) Technique

Abbreviation: IJV, internal jugular vein. A) A long-axis (in-plane) approach is used with the ultrasound screen in clear view. B) Guidewire
confirmation is noted in the IJV on ultrasound.
COMMON FEMORAL VEIN
Rationale
The common femoral vein, more commonly referred to as the femoral vein, is a reliably accessible
central vein in patients. During acute medical resuscitation in which either chest compressions or active
airway management may be occurring, cannulation of the femoral vein is often ideal. It is also used in
patients with contraindications for accessing other CVC sites (eg, anticoagulation precluding SCV access
or respiratory distress precluding the supine position needed for internal jugular access). Use of the
femoral site may be contraindicated, however, by intra-abdominal processes (eg, trauma, compartment
syndrome) or complicated by patient habitus (eg, obesity). Its care is also more challenging, and unless
diligently maintained, has been suspected of being more prone to infection. It is also limited in its
usefulness for monitoring central venous pressures.
Figure 13-4. Probe Rotation for Oblique View
With the directional marker (yellow arrow) facing caudad, rotate the probe marker clockwise for the right internal jugular vein.
Anatomy
The common femoral vein forms in the femoral sheath, proximal to the joining of the superficial femoral
vein, deep femoral vein, and the saphenous vein. Anatomic variation also exists in the femoral region,
with venous and arterial structures often overlapping completely.7 A rapid ultrasound evaluation of the
femoral region allows for anatomical mapping as well as ensuring a lack of contraindication to
cannulation (vascular thrombosis, fistula, etc). With these techniques, ultrasound has been shown to
enhance first-pass success rates when accessing the common femoral vein site.19,20
Complications
The most frequent complications of common femoral vein line placement are arterial puncture or
cannulation and intraperitoneal or retroperitoneal hemorrhage. Complications of arterial puncture,
reported to occur in as many as 10% of landmark-based femoral CVC placements, include periarterial
hematoma, arteriovenous fistula formation, pseudoaneurysm formation, thrombosis, limb ischemia, and
hemorrhage.21,22 Previous studies have suggested venous thrombosis rates of 10% to 25%, with an
unknown number resulting in thromboembolism.23,24 Previously, infection was thought to present a greater
risk at this site.25 However, more recent work suggests that infection rates vary minimally by site
placement when performed under ideal sterile conditions.26 Overall, the literature has not conclusively
demonstrated that any CVC site is more problematic than others, and each patient’s unique clinical and
anatomical concerns must be taken into account when deciding which central venous access is ideal.
Figure 13-5. Oblique View
Abbreviations: IJV, internal jugular vein; CA, carotid artery.
After the IJV and CA are noted, an in-plane technique is used to access the central circulation. Blue arrows indicate the needle
Patient Positioning
As with all procedures, optimizing patient and provider positioning is essential for success. The femoral
site, the provider, and ultrasound machine are best positioned ipsilaterally to the site of access. The
patient’s leg may be rotated externally to decrease the overlap between arterial and venous structures, and
the reverse Trendelenberg position may be used to augment vein size in hemodynamically stable
patients.27-29
Once optimally positioned, the linear/high-frequency/high-resolution transducer is used to facilitate and

visualize catheter placement in the femoral vein, most often through the well-known Seldinger technique.
The probe marker (pointing to the patient’s right in Figure 13-6) should align with the ultrasound screen.
The technique for needle insertion and advancement described for IJV CVC placement is analogous at the
femoral vein site. We recommend the short-axis out-of-plane technique for ultrasound-guided femoral
vein cannulation. Again, operators who are facile at in-plane needle visualization may prefer this more
advanced method for accurate venous cannulation (Figure 13-7).
Figure 13-6. Transducer Placement to Locate the Femoral Artery
Abbreviations: FA, femoral artery; FV, femoral vein.
Place the transducer on the inguinal ligament. Ensure that the directional marker is toward the patient’s right.
Figure 13-7. Short-Axis (Out-of-Plane) Technique

Abbreviations: CFV, common femoral vein; FA, femoral artery.
A) A short-axis (out-of-plane) technique is used for the femoral vein cannulation. B) Note the steep needle angle and avoidance of the FA
medially and at the saphenofemoral junction.
SUBCLAVIAN VEIN
Anatomy
The SCV is the third site of CVC access to be discussed. It is reliably present in patients, fed from the
brachial vein, which becomes the axillary vein as it passes the teres major muscle, and courses
inferoposteriorly to the clavicle, becoming the SCV at the lateral border of the first rib. The SCV
continues to the medial border of the anterior scalene muscle, where it combines with the IJV to form the
brachiocephalic vein, also referred to as the “innominate vein,” which then joins its contralateral
counterpart to form the superior vena cava. The landmark-based SCV has long been used for emergency
resuscitation when cervical spine pathology or airway emergencies preclude IJV access, and
intrathoracic or intra-abdominal catastrophes preclude femoral vein access. The most frequent
contraindication is respiratory distress, but anticoagulation presents a larger concern at the SCV site,
because inadvertent arterial puncture cannot be extrinsically compressed. However, as suggested, when
central venous access is truly emergent, the SCV presents one of the most readily accessible sites. As
with the IJV and femoral vein, ultrasound guidance can enhance a landmark-based approach and improve
first-pass success.30,31
Complications
Along with arterial puncture and resultant hemorrhage, pneumothorax is also a well-recognized
complication because of the close proximity of the target vessel to the lung pleura. Ultrasound can be
helpful in identifying the relationship between the arterial and venous structures, and their relationship to
the lung pleura.9 In addition to improving success and reducing complications, ultrasound may also
prompt providers to determine the length of catheter needed to reach the junction of the innominate vein
and the right atrial border for the purpose of measuring the central venous pressure in patients with large
body habitus.
Patient Positioning
Place the patient in a supine position with the arm in the most comfortable position for the procedure.
Arm abduction has been shown to not increase axillary vein size or decrease arteriovenous overlap.32
Using a linear ultrasound transducer, locate the axillary vein by placing the probe (directional marker
cephalad) just below the clavicle at approximately its middle third. This will provide a transverse view
of the axillary vein and artery. Initially, identify both the axillary vasculature and the pleura. As at other
vascular access sites, both manual compression and color flow can be used to differentiate between
venous and arterial structures. Follow the axillary vein laterally on the chest until overlap is minimized
and the pleura is out of view of the probe (or distant from the vasculature). Rotate the probe in a parallel
orientation with respect to the vein (probe marker toward the operator) to obtain a long-axis view of the
vein. Gently fan the probe in a cephalad and caudal direction to clearly differentiate the axillary vein from
the axillary artery. Slight movements of the probe will alter the ultrasound image between the vein and
artery, so we recommend that the operator stabilize the probe by resting his/her distal forearm and wrist
against the anterior chest. Note the depth of the vein to ensure that the needle used in CVC will be able to
puncture the vessel. Sterilization and anesthesia should be done as previously described. We recommend
placing the ultrasound screen on the contralateral side to allow the operator to view the screen while
visualizing the needle.
E X P E RT T I P
Place the needle in-line/in-plane with the ultrasound probe, and puncture at a steep angle (45-
60 degrees) at the proximal (lateral) edge of the probe. Immediately after puncture, adjust the
probe to ensure visualization of the needle tip and the axillary vein.
Procedure
Place the needle in-line/in-plane with the ultrasound probe, and puncture at a steep angle (45-60 degrees)
at the proximal (lateral) edge of the probe. Immediately after puncture, adjust the probe to ensure
visualization of the needle tip and the axillary vein. Advance the needle tip slowly, ensuring that the
needle tip can be visualized throughout the course. Once the needle touches the anterior surface of the
vein, subtle/short motions will be needed to puncture the anterior wall. Slow movement will collapse
both walls and the needle may completely traverse the vein. Aspirating blood and visualizing the
guidewire as it enters the vein can confirm intravascular placement. Differentiation between venous and
arterial cannulation can be difficult in certain states (hypotension, mechanical ventilation, etc), and we
recommend central venous pressure monitoring, if possible (Figure 13-8).
In summary, CVC placement in the SCV is increasingly less common, but remains an essential skill for
critical care providers. Although challenges to access it and complications are well-known, placement
can be optimized using ultrasound for preprocedure planning and intraprocedure guidance.
ARTERIAL CATHETERIZATION
Like central venous catheterization, the use of arterial catheters is nearly universal in critical care
medicine. Continuous access and monitoring of arterial blood confers several advantages. Arterial
catheterization is indicated when the provider must obtain repeated arterial blood gas analysis, such as in
respiratory failure. More commonly, arterial catheterization allows blood pressure and cardiac output to
be directly measured in the critically ill patient, such as during shock or hypertensive emergency.
Figure 13-8. Visualizing the Guidewire

Abbreviation: SCV, subclavian vein.
A) With the directional marker facing cephalad, place the ultrasound transducer in the deltopectoral groove to locate the subclavian/axillary
vein. B) A long-axis (in-plane) approach is used to cannulate the vein. Note the blue arrow indicating the direction of the needle.
Although commonly performed, the act of arterial catheterization in the intensive setting is often difficult.
The insertion, especially in patients with difficult anatomy secondary to obesity or edema, often is
difficult and requires multiple attempts.1 Hypotension, one of the most common indications for arterial
catheterization, can increase the difficulty of the procedure. Repeated attempts often become more
difficult secondary to arterial vasospasm, and complications, including thromboembolism, hematoma,
posterior wall puncture, and infection are not uncommon.1
Traditionally, radial and femoral artery catheters have been inserted using anatomic knowledge and
palpation.3 Numerous studies have shown the benefit of ultrasound guidance over the direct palpation
technique in central venous catheterization5 in terms of both increased success and decreased
complication rates. Logically, the same success of direct visualization with ultrasound-guided
catheterization (with considerable reductions in complications and increased first-attempt success when
compared with traditional landmark techniques) has translated to the use of arterial catheters. The first
prospective, randomized controlled trial of radial artery catheterization showed that ultrasound guidance
for arterial cannulation was successful more frequently and took less time than the palpation method.3
More recently, a meta-analysis of 4 trials demonstrated improved rate of successful first attempt for the
ultrasound-guided group compared with palpation.2 Indeed, as studies continue to mount to show the
increased efficacy of ultrasound guidance,12,13,33 the standard of care is rapidly shifting toward its use.
Case Study 2
A 64-year-old man with a history of congestive heart failure presents to the emergency department with an
altered level of consciousness and shortness of breath. Urine and serologic studies suggest urosepsis and
the patient becomes hemodynamically unstable, requiring intravenous vasopressor therapy. An arterial
catheter is needed to reliably measure blood pressure and obtain frequent blood gas measurements.
Ultrasound guidance is used to improve first-pass success.
RADIAL ARTERIAL CATHETERIZATION
Basic Anatomy
The radial artery is the most common site for arterial catheterization.34 Arising from the bifurcation of the
brachial artery in the cubital fossa, it runs distally as the main artery of the lateral aspect of the forearm
(Figure 13-9). Owing to its superficial course at the volar radial carpal region, it is an ideal arterial
insertion site. The dual arterial supply to the hand by the ulnar artery reduces the risk of distal iatrogenic
occlusions.35 However, a few patients lack this collateral circulation, leading to increased risk of distal
ischemia.36 The Allen test, or modified Allen test, can be performed to demonstrate collateral flow
through the superficial palmar arch. It should be noted that studies have demonstrated variable efficacy of
this procedure;37,38 however, we recommend this conservative approach if time allows. In addition, the
radial artery offers the clinician an unhindered site of operation distal to the patient’s torso, allowing
other invasive procedures to occur simultaneously.
Patient Positioning
Provider and patient positioning is the key to success in any procedure. Abduct the shoulder and supinate
the arm if possible, placing the patient’s arm on a height-adjustable table with a small towel roll for wrist
dorsiflexion. We recommend gently securing the wrist with cloth tape to maintain positioning throughout
the procedure. The provider should position the ultrasound system so that minimal head rotation is needed
to visualize both the screen and the wrist (Figure 13-10).
Figure 13-9. Radial Artery
Place a high-frequency linear transducer (5-10 MHz) with the probe marker to match the position of the
marker on the screen in a transverse plane over the wrist crease (Figure 13-11). For the novice
sonographer, we recommend locating the radius and then noting the pulsatile circular vascular structure.
Gentle compression will allow venous compression and a clear view of the radial artery. Color Doppler
is often not needed, but can be used if there is difficulty locating the radial artery. The depth and gain of
the ultrasound system should be optimized, with approximate depth noted (commonly from the depth
markings on the screen) (Figure 13-11). We recommend placing a small anesthetic skin wheal over the
artery.
Figure 13-10. Positioning to Access the Radial Artery

A) Place a roll under the extended wrist. B) Use a linear (high-frequency) transducer to obtain a transverse view of the radial artery. C)
Position the ultrasound system to allow a clear view of both the needle puncture as well as the ultrasound screen, with minimal head
movement.
Figure 13-11. Radial Artery, Color Doppler

A) Note the distal radius and the radial artery. The depth marker should be optimized. B) Color Doppler can be used when the radial artery is
difficult to locate.
Procedure
We recommend arterial catherization with an integral guidewire kit. The guidewire is inseparable from
the intravascular catheter, and allows the Seldinger technique to be performed once arterial flash is noted.
The integral guidewire approach has been shown to have similar efficacy as the separate guidewire
approach, both of which are superior to the direct puncture approach.39 The integral wire design, or
modified Seldinger technique, is the most ubiquitous in modern ICUs and will be the method discussed
here.
Ultrasound preparation before catheter insertion is key to success. The provider should prepare a linear
probe with a sterile probe cover and place the machine in a position of full visibility (which may be on
the opposite side of the patient). Using a depth of 2 cm, scan the site of palpation in the short axis; a thick-
walled, pulsatile structure should be identified and brought to the center of the screen. Doppler may be
used to confirm flow. Compression of the vessel will be more difficult than vein compression and will
further elucidate arterial pulsatile activity.
To ensure that the center of the probe is over the radial artery, place the M-mode line or “center line”
function of the ultrasound system over the vessel of interest. This confirms that the center of the probe will
be exactly over the radial artery, serving as a simple guide for needle insertion (Figure 13-12).
Figure 13-12. Radial Artery, M-Mode

To center the radial artery on the ultrasound screen, the M-mode line can be used. Needle entry should be in the center of the ultrasound
transducer.
The depth of the vessel should then be measured. We recommend placing a small anesthetic skin wheal at
the same distance as the depth, distal to the ultrasound transducer (1%-2% lidocaine with a small-gauge
needle).
Using the ultrasound in the nondominant hand, place the integral guidewire catheter approximately at the
same distance caudal to the center of ultrasound probe with the dominant hand (eg, if the vessel is 1-cm
deep, the needle should be inserted 1-cm caudal to the ultrasound probe). The goal is to keep the target
radial artery in the center of the ultrasound field. The skin is punctured with the needle “bevel up” (which
increases the echogenicity of the needle) and the needle advanced at a 45- to 60-degree angle toward the
linear probe. With the nondominant hand, fan back toward the needle (while keeping the probe in place)
to find the echogenic ultrasound tip (Figure 13-13). Once the needle is inserted into the skin, tissue motion
as well as resultant ultrasonographic artifacts of the needle can aid needle localization. Using this method,
direct visualization of the needle either “tenting” atop the radial artery or inserting into the lumen of the
radial artery is achieved. The hub of the needle is observed for a flash of bright red blood, signifying
successful arterial puncture. Once the flash is successful, lower the integral wire an approximate angle of
10 to 20 degrees from the skin, and insert the needle 1 to 2 mm further to advance the guidewire into the
lumen of the artery. The catheter is then advanced into the artery over the needle and guidewire. Finally,
the needle-guidewire unit is removed and the arterial tubing is connected. Most arterial line kits have a
mechanism to secure the line, and we recommend not using a simple adhesive dressing because
dislodgement of an arterial line could be problematic.
Figure 13-13. Distance From Skin to Radial Artery

Note the distance from the skin to the radial artery on the ultrasound screen. Enter the skin at the same distance distal to the transducer. The
angle of entry of the needle should be steep.
FEMORAL ARTERIAL CATHETERIZATION

The femoral artery is a less common site than the radial artery for catheterization owing to its position,
perceived invasiveness, and increased rate of infection.40 However, it offers several advantages over
radial artery catheterization. Primarily, the femoral artery is much larger than the radial artery (8.2±0.14
mm vs. 2.3±0.4 mm, respectively).41,42 Other benefits include a decreased risk of thrombosis and
accidental removal.40 In cases of multiple unsuccessful attempts at radial artery catheterization, patients
undergoing active cardiopulmonary resuscitation, or in cases of upper extremity trauma/burns, femoral
artery catheterization may be the ideal option.
Basic Anatomy
Arising from the external iliac artery, the femoral artery descends along the anteromedial part of the thigh
in the femoral triangle as the main arterial supply of the lower limb. The femoral artery is easily
identifiable on ultrasound. In the general approach, the femoral artery is determined by dividing the
distance measured between the anterosuperior iliac spine and the pubic tubercle into thirds; it is then
assumed that the femoral artery lies at the midpoint of the middle third section, lateral to the femoral vein
(Figure 13-14).43 Most texts and classic teaching suggest that the structures of the femoral triangle – the
femoral vein, artery, and nerve – are arranged in order from medial to lateral. However, there are
variations in anatomic positioning and alignment of the femoral vein and femoral artery. A recent study
reviewing computed tomography scans of the pelvis in 100 patients showed that a portion of the femoral
vein and the femoral artery overlap in an anteroposterior plane 65% of the time.7 Given this variation,
ultrasound guidance should be assumed to be the gold standard when performing femoral artery
cannulation.
It is reasonable to assume that the use of anatomic landmarks alone puts the provider in a position of
disadvantage; indeed, ultrasound-guided femoral cannnulation has been shown to be as good as
fluoroscopic guidance.44 With this in mind, the use of ultrasound to not only identify landmarks but also to
guide visualization of cannulation of the femoral artery may aid the provider greatly.
Patient Positioning
As with radial artery catheterization, we recommend using ultrasound guidance in the short-axis plane
approach. Owing to the provider positioning, the right-handed provider has easier access to the right
femoral artery and vice versa. However, the site of insertion should be determined using both the patient’s
clinical scenario and preprocedure ultrasound interrogation of bilateral sites.
Place the probe approximately in the middle of the anterior superior iliac spine and the pubic tubercle, 1
cm inferior and parallel to the inguinal ligament (Figure 13-6). The probe marker should face toward the
patient’s right to correspond with the image on the ultrasound screen. The key structures of the femoral
artery and femoral vein should be located. A general scan of the femoral area should be performed to
assess the access site, especially to identify any possible unexpected anatomy (ie, foreign bodies, fistulas,
etc) that may preclude it from being the ideal site for access. The femoral artery and femoral vein are then
differentiated by femoral vein compressibility, femoral vein enlargement using the Valsalva maneuver or
respiratory variability, and absence of femoral vein pulsatility.
Figure 13-14. Femoral Artery
Procedure
Once the femoral artery and femoral vein structures are identified and differentiated, the transducer
should be centered over the target femoral artery. Using a small-gauge needle, place 3-5 mL of local
anesthetic (1%-2% lidocaine) at the same distance, distal from the probe as the depth of the femoral
artery. After an aseptic preparation of the site, the sterile field should be maintained by placing a sterile
transducer sheath over the transducer and using sterile conduction gel on the sterile skin surface and
between the sheath and transducer. Like radial artery catheterization, the goal of the provider throughout
the procedure is to keep the target femoral artery centered on the ultrasound screen, which translates to
keeping the transducer directly centered over the anatomical location of the target femoral artery. If this
orientation is maintained, the provider can reasonably use the midline of the transducer as a visual
marker, thus demonstrating the location of the centered, underlying target vessel. Thus, when the
transducer is properly centered over the target vessel, it may serve as a guide for accurate needle
presentation to the vessel (Figure 13-15).
With femoral catheterization, the needle is inserted into the skin at a 45- to 60-degree angle to the frontal
plane (ie, angle between the needle and the skin) with the tip pointing cephalad while maintaining
constant backpressure on the syringe. Again, the needle should be introduced with a “bevel up”
orientation to allow the most chance of the echocardiogram reflecting back to the transducer, and thus the
best chance of ultrasound visualization. As discussed before, measure the depth of the target vessel and
introduce your needle the same distance back from the transducer at a 45-degree angle to allow the best
chance of your needle intersecting your scanning plane at the target site identified. Once the needle is
inserted into the skin, tissue motion as well as resultant ultrasonographic artifacts of the needle can aid
needle localization.
Figure 13-15. Ultrasound View of Femoral Artery

A) A clear view of the femoral artery is obtained. B) An ultrasound survey scan reveals that the artery travels toward the umbilicus. The
needle is pointed in the same path as the femoral artery.
E X P E RT T I P
Typically, the needle tip is more echogenic (ie, hyperechoic or white in appearance) with
variable amounts of ring-down reverberation artifact. The needle shaft more often has a ring-
down reverberation artifact.
In our experience, the needle tip is typically more echogenic (ie, hyperechoic or white in appearance)
with variable amounts of ring-down reverberation artifact, with the needle shaft more often having a ring-
down reverberation artifact. Once the needle and needle tip localization are identified, slow advancement
toward the vessel is maintained until the needle impinges on the anterior vessel wall, leading to “tenting”
as the wall is compressed under the needle. Of note, only gentle pressure should be applied with the
probe to avoid occluding the vein, which may hamper continuous visualization. After the vessel is
penetrated, the tenting resolves and a blood flash should be visible in the syringe. If the needle advances
excessively into the anterior wall of the femoral artery, an unintentional double wall puncture (ie, needle
piercing the anterior and posterior walls of the artery) can occur, which should be resolved when
suspected by pulling the needle back slowly while keeping gentle suction on the syringe until blood enters
the syringe.
In the separate guidewire approach, the guidewire should be placed, and the guidewire visualized via
ultrasound to confirm placement of the guidewire in the proper vessel. After ensuring proper placement of
the guidewire in the target femoral artery, the usual Seldinger technique may be used for insertion of the
cannula into the femoral artery.
Ultrasound-guidance for both venous and arterial access has become a mandatory skill for emergency and
critical care physicians. Along with increasing procedural success, ultrasound guidance reduces
inadvertent error. A simplified, yet efficacious method for the novice sonographer will allow for rapid
integration into clinical practice and make ultrasound-guidance a vital aspect of daily clinical care.
KEY POINTS
When performing the classic transverse approach to the IJV, always scan both sides of the neck to
ensure patency and degree of overlap.
Before dilation of the central vessel, use ultrasound to confirm that the guidewire is located in the
venous circulation.
Ultrasound-guided subclavian vein cannulation may be an ideal alternative for the more
experienced sonographer, reducing risk of complications.
Ultrasound-guided radial artery cannulation improves rates of success and decreases complication.
Ultrasonographic femoral arterial cannulation is an often-overlooked option in patients who have
signs of underperfussion or shock, and minimal radial pulses.
REFERENCES
1. Shiloh AL, Savel RH, Paulin LM, Eisen LA. Ultrasound-guided catheterization of the radial artery: a systematic review and meta-analysis
of randomized controlled trials. Chest. 2011;139:524-529.
2. Nicholson T, Ettles D, Robinson G. Managing inadvertent arterial catherization during central venous access procedures. Cardiovasc
Intervent Radiol. 2004;27:21-25.
3. Shiver S, Blaivas M, Lyon M. A prospective comparison of ultrasound-guided and blindly placed radial arterial catheters. Acad Emerg
Med. 2006;13:1275-1279.
4. Williams PL, Warwick R. Gray’s Anatomy. 36th ed. Philadelphia, PA: Saunders; 1980:629-765.
5. Barker WJ. Central venous catheterization: internal jugular approach and alternatives, In: Roberts JR, Hedges JR, eds. Clinical Procedures
in Emergency Medicine. 2nd ed. Philadelphia, PA: Saunders; 1991:340-351.
6. Apfelbaum JL, Hagberg CA, Caplan RA, et al. Practice guidelines for management of the difficult airway: an updated report by the
American Society of Anesthesiologists Task Force on Management of the Difficult Airway. Anesthesiology. 2013;118:251-270.
7. Baum PA, Matsumoto AH, Teitelbaum GP, Zuurbier RA, Barth KH. Anatomic relationship between the common femoral artery and vein:
CT evaluation and clinical significance. Radiology. 1989;173:775-777.
8. Armstrong PJ, Sutherland R, Scott DH. The effect of position and different manoeuvres on internal jugular vein diameter size. Acta
Anaesthesiol Scand. 1994;38:229-231.
9. Lewin MR, Stein J, Wang R, et al. Humming is as effective as Valsalva’s maneuver and Trendelenburg’s position for ultrasonographic
visualization of the jugular venous system and common femoral veins. Ann Emerg Med. 2007; 50:73-77.
10. Leung J, Duffy M, Finckh A. Real-time ultrasonographically-guided internal jugular vein catheterization in the emergency department
increases success rates and reduces complications: a randomized, prospective study. Ann Emerg Med. 2006;48:540-547.
11. Mallory DL, McGee WT, Shawker TH. Ultrasound guidance improves the success rate of internal jugular vein cannulation. A prospective,
randomized trial. Chest. 1990;98:157-160.
12. Latham GJ, Veneracion ML, Joffe DC, et al. High-frequency micro-ultrasound for vascular access in young children—a feasibility study by
the High-frequency Ultrasound in Kids Study (husky) group. Pediatr Anesthesiol. 2013;23:529- 535.
13. Brzezinski M, Luisetti T, London MJ. Radial artery cannulation: a comprehensive review of recent anatomic and physiologic investigations.
Anesth Analg. 2009; 109:1763-1781.
14. National Institute for Health and Care Excellence. Guidance on the use of ultrasound locating devices for placing central venous catheters.
Technology Appraisal Guidance No. 49. Available at: http://www.nice.org.uk/guidance/ta49. September 2002. Accessed August 12, 2015.
15. American Society of Anesthesiologists Task Force on Central Venous Access, Rupp SM, Apfelbaum IL, Blitt C, et al. Practice guidelines
for central venous access: a report by the American Society of Anesthesiologists Task Force on Central Venous Access. Anesthesiology.
2012; 116:539-573.
16. American College of Emergency Physicians. ACEP emergency ultrasound guidelines-2001. Ann Emerg Med. 2001;38:470-481.
17. Lieberman JA, Williams KA, Rosenberg AL. Optimal head rotation for internal jugular vein cannulation when relying on external
landmarks. Anesth Analg. 2004;99:982-988.
18. Phelan M, Hagerty D. The oblique view: an alternative approach for ultrasound-guided central line placement. J Emerg Med. 2009;37:403-
408.
19. Hilty WM, Hudson PA, Levitt MA, Hall JB. Real-time ultrasound-guided femoral vein catheterization during cardiopulmonary resuscitation.
Ann Emerg Med. 1997;29:331-336.
20. Kwon TH, Kim YL, Cho DK. Ultrasound-guided cannulation of the femoral vein for acute haemodialysis access. Nephrol Dial Transplant.
1997;12:1009-1012.
21. Getzen LC, Pollak EW. Short-term femoral vein catheterization: A safe alternative venous access. Am J Surg. 1979;138:875-878.
22. Williams JF, Seneff MG, Friedman BC, et al. Use of femoral venous catheters in critically ill adults: prospective study. Crit Care Med.
1991;19:550-553.
23. Meredith JW, Young JS, O’Neil EA, Snow DC, Hansen KL. Femoral catheters and deep venous thrombosis: a prospective evaluation with
venous duplex sonography. J Trauma. 1993;35:187-191.
24. Joynt GM, Kew J, Gomersall CD, Leung VY, Liu EK. Deep venous thrombosis caused by femoral venous catheters in critically ill adult
patients. Chest. 2000;117:178-183.
25. Lorente L, Henry C, Martín MM, Jiménez A, Mora ML. Central venous catheter-related infection in a prospective and observational study
of 2,595 catheters. Crit Care. 2005;9:R631-R635.
26. Marik PE, Flemmer M, Harrison W. The risk of catheter-related bloodstream infection with femoral venous catheters as compared to
subclavian and internal jugular venous catheters: a systematic review of the literature and meta-analysis. Crit Care Med. 2012;40:2479-
2485.
27. Berk D, Gurkan Y, Kus A, et al. Ultrasound-guided radial arterial cannulation: long axis/inplane versus short axis/out-of-plane approaches?
J Clin Monit Comput. 2013; 27:319-324.
28. Stone MB, Price DD, Anderson BS. Ultrasonographic investigation of the effect of reverse Trendelenburg on the cross-sectional area of
the femoral vein. J Emerg Med. 2006;30:211-213.
29. Werner SL, Jones RA, Emerman CL. Effect of hip abduction and external rotation on femoral vein exposure for possible cannulation. J
Emerg Med. 2008;35:73-75.
30. Yeow KM, Kaufman JA, Rieumont MJ, Geller SC, Waltman AC. Axillary vein puncture over the second rib. AJR Am J Roentgenol.
1998;170:924-926.
31. Lalu MM, Fayad A, Ahmed O, et al. Ultrasound-guided subclavian vein catheterization: a systematic review and meta-analysis. Crit Care
Med. 2015;43:1498-1507.
32. Galloway S, Bodenham A. Ultrasound imaging of the axillary vein: anatomical basis for central venous access. Br J Anaesth. 2003;90:589-
595.
33. Ueda K, Puangsuvan S, Hove MA, Bayman EO. Ultrasound visual image-guided vs Doppler auditory-assisted radial artery cannulation in
infants and small children by nonexpert anaesthesiologists: a randomized prospective study. Br J Anaesth. 2013;110:281-286.
34. Scheer B, Perel A, Pfeiffer UJ. Clinical review: complications and risk factors of peripheral arterial catheters used for haemodynamic
monitoring in anaesthesia and intensive care medicine. Crit Care. 2002;6:198-204.
35. Sandhu NS, Patel B. Use of ultrasonography as a rescue technique for failed radial artery cannulation. J Clin Anesth. 2006;18:138-141.
36. Barbeau G, Arsenault F, Dugas L, Simard S, Larivière MM. Evaluation of the ulnopalmar arterial arches with pulse oximetry and
plethysmography: comparison with the Allen’s test in 1010 patients. Am Heart J. 2004;147:489-493.
37. Kohonen M, Teerenhovi O, Terho T, Laurikka J, Tarkka M. Is the Allen test reliable enough? Eur J Cardiothorac Surg. 2007;32:902-905.
38. Jarvis MA, Jarvis CL, Jones PR, Spyt TJ. Reliability of Allen’s test in selection of patients for radial artery harvest. Ann Thorac Surg.
2000;70:1362-1365.
39. Beards SC, Doedens L, Jackson A, Lipman J. A comparison of arterial lines and insertion techniques in critically ill patients. Anaesthesia.
1994;49:968-973.
40. Lorente L, Brouard MT, Roca I, et al. Lesser incidence of accidental catheter removal with femoral versus radial arterial access. Med
Intensiva. 2013;37:316-319.
41. Crisan S. Ultrasound examination of the femoral and popliteal arteries. Med Ultrason. 2012;14:74-77.
42. Ashraf T, Panhwar Z, Habib S, et al. Size of radial and ulnar artery in local population. J Pak Med Assoc. 2010;60:817- 819.
43. Berk WA, Sutariya B. Vascular access. In: Tintinalli JE, Kelen GD, Stapczynski JS, eds. Emergency Medicine: A Comprehensive Study
Guide. 6th ed. New York, NY: McGraw-Hill; 2004:128-129.
44. Seto AH, Abu-Fadel MS, Sparling JM, et al. Real-time ultrasound guidance facilitates femoral arterial access and reduces vascular
complications: FAUST (Femoral Arterial Access With Ultrasound Trial). JACC Cardiovasc Interv. 2010;3:751-758.
Chapter 14
Chest Tubes and Thoracentesis
Mark Munoz, MD; David Feller-Kopman, MD
OBJECTIVES
Review ultrasound examination of the healthy thorax
Illustrate pathologic findings seen on thoracic ultrasound
Discuss considerations in preparation of thoracic procedures
Describe in a stepwise fashion ultrasound-assisted thoracentesis and tube thoracostomy
INTRODUCTION
As with other body sites, ultrasound guidance for thoracic procedures is associated with a significant
reduction in complications and near-misses, as well as improved procedural success, even in the hands of
expert pulmonologists.1 Thoracic ultrasound is superior to chest radiography for detecting pleural fluid
and pneumothorax. Unlike chest computed tomography scanning, thoracic ultrasound can be performed at
the bedside without the need to transport a critically ill patient. In addition, serial examinations are easily
performed to reevaluate patients with changes in their clinical course. As such, the British Thoracic
Society recommends the routine use of ultrasound to guide thoracentesis and tube thoracostomy.2 The
performance of thoracic ultrasound requires extensive practice to develop competence, and includes an
understanding of ultrasound physics, thoracic anatomy, and both image acquisition and image
interpretation. Guided by these principles, the adept operator must first be capable of performing these
procedures without sonography, and then develop the manual dexterity and psychomotor integration to
perform the skills using ultrasound guidance.
CASE STUDY
A 45-year-old intoxicated man presented to the emergency department for evaluation of sharp, pleuritic
chest pain and severe dyspnea after he sustained several punches to the ribs in a bar fight. On arrival, he
was afebrile, with a heart rate of 110 beats/min, blood pressure of 110/65 mm Hg, tachypnea at 30
breaths/min, and an oxygen saturation of 80% on room air. Examination revealed severe bruises to the left
chest. A chest radiograph showed several rib fractures on that side. Several hours later in the emergency
department, he developed tachycardia and hypoxemia, and underwent endotracheal intubation. As he
remained hypoxemic, a 2-dimensional (2D) ultrasound examination of the left hemithorax was performed,
which revealed a large, hyperechoic effusion with the appearance of fluid more hyperechoic in the
posterior costophrenic space than more superiorly (Figure 14-1). A-lines were visualized anteriorly in
the midclavicular line (Figure 14-2), the lung point was not seen, but the lung pulse was identified (Video
14-1 ).
What Is the Most Likely Diagnosis?

The sonographic features of the pleural fluid are consistent with the “hematocrit sign,” suggesting the
presence of a hemothorax. The presence of A-lines without lung sliding anteriorly suggests the presence
of a pneumothorax, but is not specific for this entity and could also be seen in any clinical situation
limiting lung motion, including right mainstem intubation. The presence of a “lung point,” however, would
confirm the presence of a pneumothorax. The absence of a “lung point” makes the diagnosis of
pneumothorax unlikely, unless the pneumothorax is very large. The “lung pulse” confirms that the lung is
in contact with the parietal pleura, and essentially rules out pneumothorax.
Figure 14-1. Hematocrit Sign

Echogenicity of pleural fluid is greater in dependent regions, suggesting free-flowing but dense layering material (commonly blood).
Figure 14-2. A-Lines

A normal finding, horizontal hyperechoic lines are seen beneath the pleurae (arrows).
After pulling back the endotracheal tube, the patient’s oxygenation significantly improved. A left chest
tube was placed and pleural fluid analysis confirmed hemothorax.
EXAMINATION OF THE HEALTHY THORAX

The initial sonographic evaluation of the patient with thoracic disease should always involve a review of
the patient’s history and physical examination findings as well as all available radiologic imaging.
Thoracic ultrasound requires a systematic approach and typically begins with appropriate positioning of
the patient and orientation of the ultrasound probe.
Orientation of the Ultrasound Probe and Probe Selection

All ultrasound probes have an indicator that corresponds to a marker on the screen. By convention, for
thoracic ultrasound, the indicator on the probe should be pointed cephalad, and the marker on the
ultrasound screen should be in the upper left side (Figure 14-3). With this orientation, the diaphragm
should always be seen on the right side of the screen with the caudal view to the right and the cranial
view to the left of the screen.
It is important to select the right probe for the specific sonographic imaging desired. For pleural imaging,
we recommend a phased-array transducer (typically 5-7.5 MHz) because its footprint can fit easily
between the ribs and offers excellent penetration and adequate resolution. A curvilinear (abdominal)
probe can also be used, but because of its larger footprint, more rib shadows will be visualized. When
looking for a pneumothorax, especially in a thin patient, a higher frequency (10-7.5 MHz) linear array
“vascular” probe offers excellent resolution of the visceral and parietal pleura, but has significantly
reduced penetration compared to phased-array and curvilinear probes.
Positioning and Site Selection

Although thoracentesis and tube thoracostomy can be performed in any position, a skilled approach takes
into account patient factors and clinical situation. Ambulatory patients can be placed in various positions
to facilitate procedures, but critically ill patients with multiple forms of life support (ventilator,
hemodialysis, ventricular assist devices) may not be amenable to repositioning. Because of this
variability, operators must remain facile with procedures in multiple positions. When accessing the
pleural space, one should “go where the fluid (or air) is.”
Erect Position
Classic thoracentesis is performed in the erect position, especially in ambulatory or noncritically ill
inpatients. The patient is asked to sit upright facing away from the operator on the examination table or
bed, which is height adjusted to the comfort of the patient and operator. His or her arms are folded
forward either around a pillow or against a nonmoving table to open the scapulae laterally. Some
deconditioned patients may need stabilization from support staff to maintain this position.
Figure 14-3. Standard Orientation
The green probe marker (cephalad) is located on the upper left. In this view, a large hypoechoic effusion is noted (A). Atelectatic lung is
visible (B). The diaphragm is seen as a hyperechoic arc extending from the upper right of the screen to the middle bottom
Once seated, erect positioning allows for complete examination of the posterior and lateral thorax. The
ultrasound unit should be positioned to allow for simultaneous viewing of the ultrasound screen and the
patient with easy access to controls.
Supine Position
The pleural space in critically ill patients can often be approached in the supine position, as pleural fluid
can often be found laterally and air, anteriorly. Patients lie supine on the bed with their head slightly
elevated and their ipsilateral arm raised over their head or across their chest (again, support staff may be
required to assist the patient in this maneuver to maintain field sterility). With the head semiupright,
pneumothoraces theoretically should rise to the most nondependent portion of the hemithorax while free-
flowing fluid should drift down with gravity.
Lateral and Semidecubitus Positioning

Patients with pleural fluid not well visualized in the supine position may be rolled onto their contralateral
side facing away from the operator to augment visualization of smaller effusions. In this position, free-
flowing fluid accumulates near the spine. This approach makes for a more technically challenging
procedure as intercostal vessels take more tortuous courses within 9 cm of the spinous process.3
C AVE AT
Dynamic respiratory motion should be visible at the diaphragm unless diaphragmatic paralysis or
paresis or contralateral mainstem intubation are present.
A semilateral decubitus position is available for patients whose fluid is still not well visualized by the
aforementioned lateral decubitus maneuver. Raising the head of the bed 30 to 45 degrees and raising the
patient’s arm over the head or across the torso permits access to the midaxillary or posterior axillary line
for fluid sampling. Assistants can ease patient comfort by placing pillows or rolled towels behind the
patient to keep him/her in position.
Identification of Key Anatomic Structures
Diaphragm
One should begin the sonographic examination of the thorax by finding the diaphragm. The lower limit of
the thorax is defined sonographically by the hemidiaphragm and spleen on the left, as well as the
hemidiaphragm and liver on the right. The diaphragm is seen as a hyperechoic arc extending from the
upper right of the screen to the middle bottom of the screen (Figure 14-3). Unless there is diaphragmatic
paralysis/paresis or an inverted diaphragm because of a massive effusion, dynamic respiratory changes in
diaphragm position should be visualized.
Depending on the patient’s position, the amount of pleural fluid, the presence of atelectasis or abdominal
pathology, and degree of respiratory variation, the probe position may change significantly. In the
semirecumbent patient, the diaphragm can commonly be seen up to the fifth and sixth rib space. In the
absence of pleural fluid, delineation of the diaphragm is often based on the limits of the spleen or liver. It
is crucial to examine the entire inferior border of the thorax by moving the probe medially or laterally as
well as superiorly or inferiorly. A key caveat is not to confuse ascites with a pleural effusion.
E X P E RT T I P S
The phased-array transducer (typically 5-7.5 MHz) fits easily between the ribs and offers
excellent penetration and resolution.
Assistants can ease patient comfort by placing pillows or rolled towels behind the patient to keep them in
position.
C AVE AT
Examine the entire inferior border of the thorax. This prevents confusion of ascites with pleural
effusion.
An anechoic space between the parietal and visceral pleura does not guarantee the presence of
pleural fluid.
Chest Wall and Pleurae

Examining the chest wall with the probe in standard orientation (described previously), 3 general layers
can be identified. The most superficial layer, consisting of skin, subcutaneous tissue, and fascia, is seen as
multiple lines of soft tissue echogenicity. Deep into this layer sit the intercostal muscle and ribs, which
are represented by a hypoechoic periosteum with a hypoechoic rib shadow (Video 14-2 ). The third
layer represents the parietal and visceral pleurae, which are seen as 2 hyperechoic lines that can be
difficult to identify in the absence of pleural fluid. In the healthy patient, gliding (or sliding) lung, to-and-
fro movement between the pleural lines with respiration, can be seen overlying the lung tissue (Video 14-
3 ).
Lung Parenchyma
The air-filled nature of lung parenchyma makes it a poor conductor of ultrasound signal, limiting the
evaluation of normal lung tissue. The parenchyma itself is represented by a haze of hyperechoic
reverberation artifacts that intensifies with inspiration. Some of these artifacts are well-described in
disease states as well, including A-lines (horizontal, hyperechoic lines beneath the pleural interface;
Figure 14-1) and B-lines (vertical hyperechoic lines projecting downward from the pleura; Figure 14-4).
B-lines, a form of comet-tail artifact, will erase A-lines and move with respiration, and their presence
rules out a pneumothorax at the point of probe contact.
Heart and Great Vessels

When performing ultrasound imaging for pleural effusion on a patient’s left side, it is good practice to
always identify the heart and pericardium, as well as the descending thoracic aorta before performing any
procedures. These are addressed in a separate chapter.
Figure 14-4. B-Lines

Vertical hyperechoic lines, a form of comet-tail artifact, project downward from pleura to the edge of the screen (arrow). These B-lines with
respirophasic artifacts erase A-lines, move with respiration, and rule out pneumothorax (at the area of probe contact). The finding of 3 or more
B-lines in the same intercostal space (lung rockets) is associated with the alveolar-interstitial syndrome.
EXAMINATION OF THE PATHOLOGIC THORAX

A keen understanding of normal anatomy and facility with the sonographic examination should provide the
operator with enough understanding to plan basic thoracic procedures. However, because these are rarely
done in the healthy individual, familiarity with pathologic findings is also required (Table 14-1).
Pleural Effusions and Thickening

Despite being the target of most ultrasound-guided thoracic procedures, pleural effusions may be difficult
to identify. The volume of effusions must be measured with the probe at a perpendicular angle to the chest
wall to prevent over- or underestimation. As little as 5 to 50 mL of fluid can be seen with ultrasound in
the upright position compared with 200 mL required for visualization on the standard posterior-anterior
chest radiogram.4
E X P E RT T I P
B-lines erase A-lines and move with respiration. Their presence rules out a pneumothorax at the
probe contact.
Several signs may aid differentiation of pleural fluid from lung parenchyma. Foremost, dynamic
respiratory change of shape with visualization of mobile echodensities remains the hallmark sonographic
finding of pleural fluid (Video 14-4 ).5 In addition, effusion color change seen on Doppler imaging (the
so-called “fluid-color” sign) may also suggest pleural effusion.6 Furthermore, pleural thickening may
appear anechoic, hypoechoic, or hyperechoic.7 Thus, an anechoic space between the parietal and visceral
pleura does not guarantee the presence of pleural fluid. It should be noted that hyperechoic fluid
represents exudative effusion, whereas hypoechoic fluid can be either transudates or exudates. The
presence of multiple septae ( Figure 14-5) also has been shown to predict the need for more invasive
pleural drainage (tube thoracostomy or surgery).8 Nodules on the visceral or parietal pleura, pleural
thickening more than 1 cm, and diaphragmatic thickening more than 7 mm suggest the presence of a
malignant pleural effusion ( Figure 14-6).7
Table 14-1. Pertinent Findings on Thoracic Ultrasound Examination
Sign Description Significance
Lung sliding To-and-fro movement between the pleural lines with respiration. Normal finding. When present, rules out pneumothorax with 100%
sensitivity in area of probe contact.
Seashore sign M-mode equivalent of lung sliding, in which horizontal waves ebb and Normal finding, suggestive of lung sliding as described before.
flow with respiration.
Stratosphere sign Straight, barcode-like lines on M-mode (as opposed to the seashore Suggests disruption of lung sliding. Seen in pneumothorax (specificity
sign). 60-99%), and also sometimes in interstitial edema, dense
consolidations, fibrosis, contralateral mainstem intubation.
Lung point sign Point at which lung separates from chest wall. Lung portions in contact 100% specific for pneumothorax.
with the chest wall show lung sliding. Separated portions show no
sliding.
Lung pulse sign Pulsatile motion of the visceral pleura against the parietal pleura. A result of pleural apposition, aids in ruling out pneumothorax, and is
associated with complete atelectasis.
A-lines Horizontal, hyperechoic lines beneath the pleural interface. Anterior A-line predominance suggests wedge pressure <13 mm Hg.
B-lines/lung rockets Vertical, respirophasic, hyperechoic lines projecting downward from ≥3 B-lines in 1 intercostal space (lung rockets) suggest the alveolar-
the pleura, which erase A-lines. interstitial syndrome, associated with interstitial edema or subpleural
septal thickening.
Fluid-color sign Effusion color change seen on Doppler imaging. Suggests pleural effusion rather than lung parenchyma.
Septae Reticular, hyperechoic radiations from pleura to parenchyma. Suggests complex effusion that may require more invasive drainage.
Hematocrit sign Pleural fluid echogenicity appears more hyperechoic in the dependent, Suggests hemothorax.
posterior costophrenic space than superiorly.
Pleural nodules and thickening Hyperechoic, globular structures adherent to prominent, hyperdense Nodules, pleural thickening >1 cm and diaphragmatic thickening >7
pleurae. mm suggest the presence of a malignant pleural effusion.
Dynamic air bronchogram sign Branching, hyperechoic structures with respirophasic movement >1 94% positive predictive value for pneumonia.
mm in M-mode.
Figure 14-5. Loculated Pleural Effusion
Septated loculations (arrow) seen in the costophrenic space. The diaphragm and liver are shown for reference (A). The presence of multiple
septations predicts the need for invasive pleural drainage.
Pneumothorax
Ultrasound is generally thought to be more useful for ruling out pneumothorax than for confirming it. The
presence of sliding lung is the most important finding in this evaluation, which rules out pneumothorax
with a sensitivity of 100% at the point of probe contact (Video 14-3 ).9 It is important to examine
several areas on the anterior and lateral chest in the semiupright patient. The M-mode equivalent of lung
sliding has been termed the “seashore” sign ( Figure 14-7).9 When air interferes with the visceral and
parietal pleural interface, sliding lung cannot be seen and on 2D imaging, the presence of A-lines without
lung sliding should prompt the sonographer to look for a pneumothorax. On M-mode, this has been termed
the “stratosphere” sign ( Figure 14-8). Lack of lung sliding is seen in pneumothorax but also in other
disease processes, including any disease that has caused pleural adhesions, dense lung consolidation, and
contralateral mainstem intubation. Specificity therefore ranges from 60% to 99%, performing better
among less critically ill patients.10 The lung point, however, is 100% specific for pneumothorax. This
refers to the identification of the point where the lung separates from the chest wall ( Figure 14-9 and
Video 14-5 ). Where the lung is in contact with the chest wall, lung sliding will be visualized; where it
separates, sliding will be absent. This can be seen in either 2D or M-mode imaging.11 The sensitivity of
the lung point is inversely proportional to the size of the pneumothorax, with a large pneumothorax having
no area of visceral-parietal contact. When the lung point is not seen, observers should try to identify the
“lung pulse,” seen as pulsatile motion of the visceral pleura against the parietal pleura ( Figure 14-1).
Demonstrating pleural apposition, this sign rules out pneumothorax and is also associated with complete
atelectasis.12
Figure 14-6. Visceral Pleural Enhancement
Pleural thickening (arrow) of more than 1 cm, diaphragmatic thickening of more than 7 mm (A), or nodularity suggests a malignant pleural
effusion (B).
Figure 14-7. Seashore Sign

The M-mode equivalent of lung sliding, respirophasic apposition of the visceral and parietal pleurae, creates a wavy line at the pleural interface
(arrow). This is a normal finding that aides in ruling out pneumothorax at the area of probe contact, which is suggested by the stratosphere sign
(Figure 14-8).
Figure 14-8. Stratosphere Sign
In contrast to the seashore sign (Figure 14-7), the presence of air in the pleural interface disrupts normal respirophasic change seen in M-
mode, resulting in straight horizontal lines (arrow).
Figure 14-9. Lung Point

Defined as the point at which the lung separates from the chest wall, as seen in B-mode (A) and M-mode (B). The portion of the respiratory
phase when this occurs is seen between the 2 arrows. This finding is 100% specific for pneumothorax; however, the sensitivity for
pneumothorax is inversely proportional to the size of the pneumothorax because there will be no area of visceralparietal pleural apposition in a
large pneumothorax.
Alveolar-Interstitial Syndrome
The presence of 3 or more B-lines visible in an intercostal space has been deemed “B+ lines” or “lung
rockets.” This sign is associated with the alveolar-interstitial syndrome, a radiographic finding associated
with interstitial edema or subpleural septal thickening.13 In one study of patients receiving mechanical
ventilation, a predominance of A-lines (as seen in healthy patients) was associated with pulmonary
capillary wedge pressures less than 13 mm Hg, with 97% positive predictive value, whereas anterior B-
line predominance was associated with a wide range of wedge pressures.14
Air Bronchograms and Alveolar Consolidation

Alveolar consolidation with air bronchograms is also sometimes visible sonographically. Consolidated
lung is often described as appearing hyperechoic, similar to liver tissue, with a shredded deep border
(Figure 14-10). Air bronchograms appear as hyperechoic, branching, tubular structures within lung
parenchyma.15
The “dynamic air bronchogram sign” describes respirophasic movement of air bronchogram structures,
seen also in M-mode. In one study, movement more than 1 mm was associated with a 94% positive
predictive value for pneumonia.15 A recent meta-analysis of these signs in the diagnosis of pneumonia
found high pooled sensitivity and specificity, 94% and 96%, respectively.16
E X P E RT T I P
The presence of sliding lung rules out pneumothorax with a sensitivity of 100% at the point of
probe contact.
Figure 14-10. Consolidated Lung

Heterogeneously hyperechoic lung (arrow) is seen underlying a multiechoic parapneumonic effusion. The shredded, deep border of the
consolidations is often seen with hyperechoic, branching air bronchograms.
PROCEDURAL APPROACH TO PLEURAL ACCESS

The safest site and position is one with the largest amount of pleural fluid without high-risk structures in
view such as the heart, lungs, or diaphragm (diaphragmatic excursion can be substantial and should be
observed for several cycles). The distance between the skin and the parietal pleura, as well as the
distance between parietal pleura and lung, should be noted with an image saved on screen.
Once a site is selected, the point of approach should be marked with a blunt instrument or marking pen
that will not wash off during site preparation. After marking the site, repeat ultrasound should be
performed to confirm proper site selection with attention paid to the angle of the ultrasound to the chest
wall, as this should be the path of needle insertion. After preparation with chlorhexidine and draping, the
patient must be assisted in maintaining the same position and must be reexamined with ultrasound if
significant movement occurs.
C AVE AT
Repeat ultrasound should be performed after marking the site to confirm selection, taking into
consideration the angle of the ultrasound to the chest wall.
Partial vs. Real-Time Needle Guidance

Most studies do not use real-time ultrasound guidance to visualize needle insertion; however, pleural
access can also be obtained under real-time ultrasound visualization. Currently there are no data
available to suggest that this technique offers improved safety or efficacy. When performed, real-time
ultrasound guidance uses a technique similar to vascular ultrasound access, where the ultrasound probe
can be used in a short or longitudinal axis. The proposed advantages to the use of real-time ultrasound
guidance for pleural procedures include visualizing the needle entering the target in real time, improving
yield, and potentially avoiding vulnerable structures. The major disadvantages cited include costs
associated with disposable needle guides, hazardous insertion angles related to the awkwardness of
holding both probe and needle, and the absence of data supporting the fact that real-time visualization
improves outcomes. The authors recommend this approach for small effusions or when performing
ultrasound-guided needle biopsies of the chest wall or lung nodules.
THORACENTESIS
The principal forms of thoracentesis are diagnostic and therapeutic, named for their procedural goal.
Although indications for these procedures vary substantially, the approach is nearly identical, and will be
discussed together here. It should be noted that we generally prefer using a standard thoracentesis kit, and
perform therapeutic thoracentesis to minimize subsequent procedures for the patient that may be required
depending on the results of diagnostic thoracentesis.
Preparation
1. Ensure that the patient has no procedural contraindications, including laboratory abnormalities
(international normalized ratio >2.0; activated partial thromboplastin time >2.0; platelets <50×103/μL;
serum creatinine >6 mg/dL), anatomic limitations (pleural fluid depth <1 cm from parietal pleura), or
overlying skin infection.
2. Select an appropriate patient position and measure the projected tract of the needle sonographically,
taking into account the depth to the pleura and the depth of the target effusion.
3. For therapeutic thoracentesis, we recommend using a thoracentesis kit containing the items described in
Table 14-2. Diagnostic thoracentesis can be performed using a small-gauge needle and syringe, with
appropriate sterile technique.
4. Select a site, mark, cleanse, and drape the patient in the usual fashion.
E X P E RT T I P
Use a standard thoracentesis kit and perform a therapeutic tap to minimize subsequent
procedures, maximize symptomatic relief, and aid further diagnostic imaging.
Table 14-2. Generic Thoracentesis Kit Contents
Thoracentesis Tube Thoracostomy
8F polyurethane centesis catheter over 18-gauge (G) 19-cm needle with 3-way 14F polyurethane drainage catheter
stopcock 5-mL Luer-lock syringe
5-mL Luer-lock syringe 10-mL Luer-lock syringe
60-mL Luer-lock syringe 60-mL Luer-lock syringe
22-G 1½-inch needle 22-G 1½-inch needle
25-G 1-inch needle 25-G ⅝-inch needle
No. 11 safety scalpel 19-G 1½-inch introducer needle
Polyurethane suction tubing set No. 11 safety scalpel
1-way aspiration/discharge device Polyurethane suction tubing
Chlorhexidine gluconate applicator Pleural evacuation collection system
Two 5-mL ampules of 1% lidocaine 1-way valve
1-L drainage bag Seldinger guidewire
Sterile drape Guidewire dilator
Gauze pads Chlorhexidine gluconate applicator
Two 5-mL ampules of 1% lidocaine
Sterile drape
Gauze pads
Anesthesia
1. Fill the 5-mL Luer-lock syringe with 1% lidocaine, and using the 25-gauge needle, create a 0.1- to 0.2-
mL wheal of lidocaine subcutaneously, making sure to aspirate before injecting.
2. The needle can then be advanced, aiming for the superior edge of the inferior rib (thereby avoiding the
subcostal neurovascular bundle). The operator should drive the motion with his/her dominant hand,
holding the rear syringe and the nondominant hand braced against the body wall, with the thumb and
index finger stabilizing the needle hub.
3. Advance 1 mm, withdraw to verify the absence of blood return, inject lidocaine, and repeat until
pleural fluid is seen on aspiration. The pleural space can be reached in most patients with a 25-gauge
1-inch needle. Inject additional lidocaine to anesthetize the sensitive parietal pleura. Depending on the
patient’s body habitus, the operator may need to withdraw the short 25-gauge 1-inch needle and
exchange it for the longer 22-gauge 1½-inch needle or even a 20-gauge spinal needle.
Diagnostic Thoracentesis
1. Attach the 60-mL Luer-lock syringe to the 22-gauge 1½-inch needle (longer needles may be required
for obese patients) and advance it with the dominant hand aiming for the inferior rib, as described
before. Aspirate through the needle along the anesthetized tract until pleural fluid is seen.
2. Withdraw 30 to 75 mL of fluid for analysis and withdraw the needle. Alternatively, the same can be
achieved using a centesis catheter as described later in this chapter. Place gauze and a bandage over the
site and send the fluid sample for analysis. Obtain a follow-up chest radiograph or use bedside
ultrasound to evaluate for pneumothorax.
Therapeutic Thoracentesis
1. Using the scalpel, create a 4-mm skin incision parallel to the rib axis (protecting the nearby
neurovascular bundle) at the anesthetized site to allow the catheter to pass through subcutaneous tissue.
2. Attach the 60-mL Luer-lock syringe to the 19-cm centesis catheter, and advance it with the dominant
hand aiming again for the inferior rib, as described before. Aspirate along the anesthetized tract until
pleural fluid is seen, at which point the dominant arm is locked against the operator’s body to stabilize
needle location.
3. Using the nondominant hand, advance the catheter forward while keeping the needle in a fixed location.
Withdraw the needle and attach suction tubing to the catheter hub.
4. Attach the 60-mL syringe to the syringe-pump system and begin aspiration. This system is preferred
over vacuum bottles because of higher rates of pneumothorax and difficulty in measuring pleural
pressure with the vacuum design.17 Most thoracentesis kits contain tubes for pleural fluid analysis,
otherwise sterile specimen cups can be used. It is recommended to send fluid in blood culture bottles
as opposed to plastic tubes for microbiology because this will increase the yield approximately 20%.18
If malignancy is suspected, at least 150 mL should be sent for cytopathology.19
5. When ready to remove the catheter, ask the patient to hum or sigh in a prolonged fashion while
removing the catheter to prevent entrainment of atmospheric air to the pleural space. Once removed,
place gauze and a bandage over the site and send fluids for analysis. Obtain a follow-up chest
radiograph or use bedside ultrasound to evaluate for pneumothorax as described before.
TUBE THORACOSTOMY
The selection of a large bore (36-40F used primarily in trauma) or small bore (8-14F pigtail catheters)
depends on the clinical situation and is beyond the scope of this chapter. Small-bore tubes are currently
recommended in most cases, including empyema,20 therefore this discussion will focus on smaller chest
tubes placed using the modified Seldinger technique.
Preparation and Anesthesia

1. Consider procedural contraindications, including laboratory abnormalities (international normalized
ratio >2.0; activated partial thromboplastin time >2.0; platelets <50×103/μL; serum creatinine >6
mg/dL), anatomic limitations (pleural fluid depth <1 cm from parietal pleura), positive end-expiratory
pressure (which may confer a 7% risk of pneumothorax), or overlying skin infection.
2. Obtain a flexible catheter kit with equipment (Table 14-2).
3. Select an appropriate patient position. Tubes are typically inserted posterolaterally for effusions and
from the fifth to sixth intercostal space in the midaxillary line or the second to third intercostal space in
the midclavicular line for pneumothorax.
4. As described before, measure the projected tract of the needle sonographically, taking into account the
depth to the pleura and the depth of the target effusion.
5. Select a site, mark, cleanse, and drape the patient as described before.
6. Anesthesia technique is performed identically to thoracentesis, as described before.
E X P E RT T I P
Send fluid in blood culture bottles rather than plastic tubes for microbiology because this will
increase the yield ~20%. For suspected malignancy, at least 150 mL should be sent for
cytopathology.
E X P E RT T I P
The obese patient may require the longer 22-gauge 1½-inch needle or even a 20-gauge spinal
needle.
Tube Thoracostomy
1. Create a 4-mm skin incision parallel to the rib axis (protecting the nearby neurovascular bundle) at the
anesthetized site to allow the chest tube to pass through subcutaneous tissue.
2. Attach the introducer needle to the 5-mL syringe and insert it along the anesthetized tract, aiming for the
inferior rib as described before. Aspirate until pleural fluid is seen, at which point the dominant arm is
locked against the operator’s body to stabilize needle location.
3. Detach the syringe and advance the guidewire through the tract. The guidewire should advance easily;
resistance may indicate needle malpositioning, creation of a false subcutaneous tract, or organ injury.
4. Withdraw the needle over the wire. At this point, the wire should move easily, confirming the absence
of kinking.
5. Use the dilator to create a tract along the wire vector, advancing into the pleural space. The operator
should feel the tract give way once this is achieved. It is usually not necessary to insert the dilator to
the hub, but just until it enters the pleural space. Ensure again that the wire moves without resistance
within the dilator.
6. Pass the chest tube and stiffening catheter over the guidewire and advance until the tube enters the
pleural space. The guidewire and stiffening catheter are then held stable as the catheter is advanced
further until all tube fenestrations are inside the pleural space. Once placed, remove the stiffening
catheter and guidewire in one motion, leaving only the tube in place.
7. Suture the chest tube into place.
8. Place a 1-way valve onto the end of the catheter or attach it to the pleural evacuation device at the
desired suction setting. Obtain a follow-up chest radiograph or use bedside ultrasound to evaluate for
pneumothorax, as described before.
C AVE AT
Heavy guidewire resistance may indicate needle malpositioning, creation of a false subcutaneous
tract, or organ injury.
KEY POINTS
Preprocedural or diagnostic examination of the thorax should proceed along the common
landmarks, including diaphragm, chest wall, pleurae, lung parenchyma, and the great vessels.
Pathologic lesions can sometimes appear similar to normal anatomy, as with large heterogeneously
echoic effusions and lung tissue. The novice should become familiar with the different appearances
of normal and pathologic structures.
Certain pathologic findings can be difficult to differentiate as well, including pleural effusions,
pleural base masses, pneumothoraces, pneumonia, and atelectasis.
The preparation for most thoracic procedures is identical, with special considerations made for
position and etiology of the lesion, and clinical circumstance.
REFERENCES
1. Gordon CE, Feller-Kopman D, Balk EM, et al. Pneumothorax following thoracentesis: a systematic review and meta-analysis. Arch Intern
Med. 2010;170:332-339.
2. Havelock T, Teoh R, Laws D, et al. Pleural procedures and thoracic ultrasound: British Thoracic Society Pleural Disease Guideline 2010.
Thorax. 2010;65(suppl 2):ii61-76.
3. Yoneyama H, Arahata M, Temaru R, et al. Evaluation of the risk of intercostal artery laceration during thoracentesis in elderly patients by
using 3D-CT angiography. Intern Med. 2010;49:289-292.
4. Qureshi NR, Gleeson FV. Imaging of pleural disease. Clin Chest Med. 2006;27:193-213.
5. Marks WM, Filly RA, Callen PW. Real-time evaluation of pleural lesions: new observations regarding the probability of obtaining free fluid.
Radiology. 1982;142:163-164.
6. Wu RG, Yuan A, Liaw YS, et al. Image comparison of realtime gray-scale ultrasound and color Doppler ultrasound for use in diagnosis of
minimal pleural effusion. Am J Respir Crit Care Med. 1994;150:510-514.
7. Qureshi NR, Rahman NM, Gleeson FV. Thoracic ultrasound in the diagnosis of malignant pleural effusion. Thorax. 2009;64:139-143.
8. Chen KY, Liaw YS, Wang HC, et al. Sonographic septation: a useful prognostic indicator of acute thoracic empyema. J Ultrasound Med.
2000;19:837-843.
9. Lichtenstein DA, Mezière G, Lascols N, et al. Ultrasound diagnosis of occult pneumothorax. Crit Care Med. 2005;33:1231-1238.
10. Husain LF, Hagopian L, Wayman D, et al. Sonographic diagnosis of pneumothorax. J Emerg Trauma Shock. 2012; 5:76-81.
11. Lichtenstein D, Mezière G, Biderman P, et al. The “lung point”: an ultrasound sign specific to pneumothorax. Intensive Care Med.
2000;26:1434-1440.
12. Lichtenstein DA, Lascols N, Prin S, et al. The “lung pulse”: an early ultrasound sign of complete atelectasis. Intensive Care Med.
2003;29:2187-2192.
13. Lichtenstein D, Meziere G, Biderman P, et al. The comettail artifact: an ultrasound sign of alveolar-interstitial syndrome. Am J Respir Crit
Care Med. 1997;156:1640- 1646.
14. Lichtenstein DA, Mezière GA, Lagoueyte J-F, et al. A-lines and B-lines: lung ultrasound as a bedside tool for predicting pulmonary artery
occlusion pressure in the critically ill. Chest. 2009;136:1014-1020.
15. Lichtenstein D, Mezière G, Seitz J. The dynamic air bronchogram: a lung ultrasound sign of alveolar consolidation ruling out atelectasis.
Chest. 2009;135:1421-1425.
16. Chavez MA, Shams N, Ellington LE, et al. Lung ultrasound for the diagnosis of pneumonia in adults: a systematic review and meta-
analysis. Respir Res. 2014;15:50.
17. Feller-Kopman D, Parker MJ, Schwartzstein RM. Assessment of pleural pressure in the evaluation of pleural effusions. Chest.
2009;135:201-209.
18. Menzies SM, Rahman NM, Wrightson JM, et al. Blood culture bottle culture of pleural fluid in pleural infection. Thorax. 2011;66:658-662.
19. Swiderek J, Morcos S, Donthireddy V, et al. Prospective study to determine the volume of pleural fluid required to diagnose malignancy.
Chest. 2010;137:68-73.
20. Rahman NM, Maskell NA, Davies CWH, et al. The relationship between chest tube size and clinical outcome in pleural infection. Chest.
2010;137:536-543.
Chapter 15
Paracentesis and Abscess Drainage
Lori A. Stolz, MD; Srikar Adhikari, MD, MS
OBJECTIVES
Describe the technique for sonographic evaluation of skin and soft tissue infections
Discuss the sonographic anatomy of skin and soft tissues as well as the pathologic changes that are present in
diagnoses of cellulitis, abscess, and other skin and soft tissue infections
Detail the procedure used for ultrasound-guided needle drainage and ultrasound-assisted incision and drainage of
abscesses
Outline the use of ultrasound for evaluation of ascites
INTRODUCTION
Sepsis demands early source control and appropriate antibiotic treatment. Delays in achieving these goals
increase patient mortality and morbidity. With skin and soft tissue infections and spontaneous bacterial
peritonitis, clinicians may be able to diagnose early and treat a source infection. Using bedside ultrasound
to evaluate these conditions and provide procedural guidance has several advantages. First, evaluating
these conditions at the bedside does not require transfer of a critically ill patient to other areas of the
hospital (such as interventional radiology or the operating room) and, therefore, allows better monitoring
and continued delivery of care. Bedside ultrasound also allows clinicians improved diagnostic accuracy
when evaluating soft tissue skin infections and ascites compared with physical examination alone. In
addition, ultrasound guidance provides greater success and fewer complications than blind, landmark, or
other techniques guided by physical examination.
CASE STUDY
A 45-year-old man with a history of diabetes and intravenous drug use presents to the emergency
department with redness, swelling, and pain in the right gluteal region. He has tachycardia and
hypotension, as well as a large, apparent gluteal cellulitis. After appropriate resuscitation and antibiotics,
he continues to decline clinically. Bedside ultrasound of the gluteal area identified a large soft tissue
abscess (Figure 15-1). Bedside incision and drainage were performed, and the patient’s condition
improved.
ULTRASOUND EVALUATION OF SKIN AND SOFT TISSUE INFECTIONS

With the advent and wide reach of methicillin-resistant Staphylococcus aureus (MRSA), skin and soft
tissue infections are becoming more prevalent and more virulent.1 Though physical examination skills are
often relied upon for the diagnosis, including abscess and cellulitis, these findings are often misleading.2
Failure to properly distinguish these 2 entities or to identify cases in which both are present may lead to
treatment failure, disease progression, and unnecessary attempts at incision and drainage. Ultrasound is
very accurate for the diagnosis of skin and soft tissue infections, with high sensitivity for both abscess and
cellulitis. Computed tomography and magnetic resonance imaging are much less useful modalities in the
critical care unit because of the need to transport patients and maintain care during imaging. With bedside
sonography for soft tissue infections, both accurate diagnosis and minimal interruption in patient care can
be achieved simultaneously.
Figure 15-1. Large Soft Tissue Abscess, Gluteal Region

Complex fluid collection requiring incision and drainage is seen in the gluteal region.
Indications for ultrasound evaluation of skin and soft tissue infections include any of the classic signs:
erythema, swelling, pain, and warmth. Even when physical examination findings are convincing for
abscess or cellulitis, evaluation with ultrasound may be warranted. In a study by Tayal et al,3 patients
with clinical suspicion of soft tissue infections who underwent evaluation with bedside ultrasound had a
change in their management in a majority of cases. In patients with soft tissue infection in which no
drainage was believed to be necessary, the management changed to include drainage in 40% of cases. In
cases in which drainage was believed to be necessary, the management changed to no drainage in 73% of
cases. In addition, ultrasound evaluation of obvious abscesses may reveal unexpected findings, structures,
or another diagnosis.4 There are no firm contraindications for ultrasound examination of a suspected soft
tissue infection, but a probe cover should be used to reduce the risk of transmission of infectious agents.
Figure 15-2. High-Frequency Linear Transducer
High-frequency linear transducer used for imaging superficial structures.
Scanning of an area for abscess, cellulitis, or other soft tissue infection involves systematic evaluation of
the area of concern. Typically, a high-frequency linear transducer is used to optimize the image resolution
in the superficial tissues (Figure 15-2). For larger or deeper areas, a lower-frequency curvilinear probe
can be used as needed for greater imaging depth. Before the evaluation of any potentially infected tissue,
the probe should be covered with a clear, occlusive dressing or a probe cover to protect the patient and to
prevent contamination of the probe. Copious amounts of gel should be used for both patient comfort and to
allow improved image resolution in the tissue closest to the probe surface. Alternatively, a stand-off gel
pad can be used. A water bath can be used to visualize distal extremities such as fingers, toes, hands, and
feet (Figure 15-3). By using a water bath for these small and superficial parts of the body, imaging can be
improved and pain lessened in patients undergoing the procedure.5 The area of concern should be
evaluated in 2 orthogonal planes. The unaffected, contralateral area of the body should also be evaluated
in the same manner for comparison.
Figure 15-3. Water Bath Technique for Scanning Distal Extremities

A) Water bath technique. Hand immersed in water and a high-frequency linear transducer touching the surface of the water.
B) B-mode image showing improved image quality with water bath, eliminating near-field acoustic dead space.
A water bath can be used to visualize distal extremities such as fingers, toes, hands, and feet.
The sonographic appearance of normal superficial soft tissues includes an echogenic line in the near field,
which represents the skin and epidermis, followed by a relatively hypoechoic stripe of subcutaneous fatty
tissue. Connective tissue fibers in this layer may appear more hyperechoic compared with the more
hypoechoic fat lobules between them (Figure 15-4). Deeper structures include brighter hyperechoic
fascial planes and striated hypoechoic muscle. Vessels appear as anechoic circular structures in a
transverse plane and as anechoic stripes in the longitudinal plane. Color or power Doppler will
demonstrate vascular flow, though augmentation (whereby the distal structures are compressed to
visualize) may be necessary to visualize blood flow (Figure 15-5). Tendons have a densely striped
appearance representing the parallel fibers when viewed longitudinally and are more echogenic than most
surrounding structures. In the short axis, tendons tend to be ovoid in shape with a stippled appearance.
Nerves appear similarly in that they are hyperechoic and fibrillar, but they are distinguished by a more
“honeycomb” appearance and are slightly more echogenic in nature (Figure 15-6). When in doubt,
dynamic scanning can be used to visualize sonographic movement of tendons.
Cellulitis has a diverse appearance on sonography. Typical sonographic appearance includes increased
thickness of the subcutaneous tissues and increased echogenicity than the surrounding unaffected tissues
and the contralateral side (Figure 15-7). Fluid tracking in the subcutaneous tissues, known as
“cobblestoning,” may be seen depending on the amount of edema and the composition of fat in the
subcutaneous tissue in that area (Figure 15-8). Color Doppler can be used to evaluate for hyperemia in the
tissues, also confirming cellulitis. However, other conditions that cause edema (congestive heart failure,
renal failure, venous stasis, and angioedema) may mimic cellulitis on sonography. These conditions may
also demonstrate increased tissue thickness and cobblestoning. Findings of hyperemia in the tissues on
color or power Doppler imaging may allow differentiation between these other causes of tissue edema
and an acute inflammatory process, such as infection.
Figure 15-4. Sonographic Appearance of Normal Subcutaneous Tissues

Normal subcutaneous tissues appear with hypoechoic fatty tissue, hyperechoic connective tissue, and striated hypoechoic muscle.
Figure 15-5. Doppler Image Demonstrating Flow Within Vessels
Figure 15-6. Hyperechoic and Fibrillar Nerve

Small hypoechoic areas (nerve fascicles) separated by hyperechoic septae (interfascicular perineurium), giving a “honeycomb-like”
appearance (arrow).
Figure 15-7. Hyperechoic Thickened Tissue with Subcutaneous Edema

Figure 15-8. Cobblestoning Appearance of Cellulitis
Figure 15-9. Abscess Cavity with Mixed Echogenicities

Figure 15-10. Hyperechoic Foreign Body in Abscess
Findings of cutaneous abscess include anechoic or mixed isoechoic collections in soft tissues. There is a
loss of normal subcutaneous tissue structure (Figure 15-9). Compression is a key scanning technique that
should be used on any suspected skin and soft tissue infection. This technique aids in distinguishing tissue
from an isoechoic fluid collection, as the fluid may be seen moving or “swirling.” This use of dynamic
testing distinguishes ultrasound as a preferred imaging modality for the diagnosis of soft tissue infection.
Septations, debris, internal echoes, and any potential foreign bodies should be noted (Figure 15-10).
Depth and size of the abscess cavity should be recorded for procedural planning and the skin can be
marked at the identified ideal location for initial incision. Ultrasound is not capable of distinguishing the
type of fluid in a subcutaneous fluid collection. Hematoma, seroma, and abscess may all have a similar
appearance.
C AVE AT
Ultrasound is not capable of distinguishing the type of fluid in a subcutaneous fluid collection.
Hematoma, seroma, and abscess may all have a similar appearance.
Color or power Doppler imaging should be used on any region that is sonographically identified as an
abscess on B-mode imaging. Aneurysm, pseudoaneurysm, arteriovenous malformation, enlarged or
necrotic lymph nodes, and solid tissue masses may all mimic an abscess clinically and sonographically.
These entities can be distinguished through the use of Doppler imaging. An abscess will show no Doppler
signal in the abscess cavity, though the rim may demonstrate enhancement (Figure 15-11). Vascular
structures, such as aneurysm, pseudoaneurysm, and arteriovenous malformation, will demonstrate obvious
vascular flow within an anechoic cavity (Figure 15-12). Lymph nodes and solid tissue masses may be
mistaken for isoechoic abscess on B-mode imaging. Doppler imaging will demonstrate flow within the
suspected lesion for both of these entities (Figure 15-13). Elastography is emerging as a potential adjunct
to standard ultrasound evaluation of potential abscesses and may be capable of identifying abscess
cavities not otherwise visualized with B-mode imaging.6
Figure 15-11. No Doppler Signal within Abscess Cavity

Enhancement seen along the rim.
Figure 15-12. Doppler Image: Flow Suggestive of Pseudoaneurysm
Figure 15-13. Doppler Image: Lymph Node with Hilar Flow
Color or power Doppler imaging should be used on any region that is sonographically identified as an
abscess on B-mode imaging.
Any cellulitis in a patient with toxicity or sepsis warrants consideration for a possible necrotizing
infection. Though the test characteristics of ultrasound for diagnosing necrotizing skin infections are
inferior to those of computed tomography or magnetic resonance imaging, it is a reasonable test to
perform if the clinical diagnosis is uncertain and the patient cannot otherwise be moved for other imaging
studies. Sharply demarcated hyperechoic areas with dense shadowing represents air within the tissues,
and is an ominous finding suggesting necrotizing soft tissue infection (Figure 15-14). Other findings
include diffusely increased subcutaneous tissue thickness and a layer of fluid along fascial planes
measuring more than 4 mm (Figure 15-15).7
ULTRASOUND-GUIDED ABSCESS DRAINAGE

Ultrasound can aid in incision and drainage of an abscess in several ways. First, it can be used for
preprocedural planning. Surrounding structures such as vasculature, nerves, and tendons can be identified
so that they can be appropriately avoided; and the size, extent, depth, and shape of the abscess can be
identified as well. Real-time ultrasound guidance can be used while performing incision and drainage
(Figure 15-16). Following this procedure, the lesion can then be reevaluated with ultrasound to ensure
that adequate drainage has occurred (Figure 15-17).
Figure 15-14. Necrotizing Soft Tissue Infection
Hyperechoic areas with shadowing represent air within the subcutaneous tissues.
Figure 15-15. Necrotizing Fasciitis

Increased subcutaneous tissue thickness and a layer of fluid along fascial planes measuring more than 4 mm suggests necrotizing fasciitis.
C AVE AT
Air within the abscess cavity may obscure evaluation of the deeper tissues after incision and
drainage.
Needle drainage has much higher immediate and delayed failure rates than traditional incision and
drainage.8 Still, in some situations needle drainage may be preferred because of cosmesis, patient
preference, or abscess size. The use of ultrasound to guide the procedure allows the provider to monitor
success of the procedure. The clinician can recognize the difference between inability to aspirate the
purulent material because of viscosity and failure to reach the purulent material with the needle. Real-
time ultrasound guidance recognizes earlier needle drainage failure and allows for faster definitive
treatment. It also ensures avoidance of surrounding structures and potential damage to them during the
procedure. As the fluid is drained, use of real-time ultrasound guidance allows the remaining pockets to
be redirected as needed.
To use real-time ultrasound guidance for needle aspiration of an abscess, the patient is prepared in the
usual fashion with consent, positioning, cleaning of the area, and draping. The ultrasound probe is
covered with a sterile probe cover. After the pocket of fluid is identified and confirmed, surrounding
structures are noted and a path is chosen that avoids these structures and directly accesses the abscess.
Typically an 18- or higher-gauge needle is used. After infiltration of the anesthetic, the needle is advanced
under real-time ultrasound guidance (Figure 15-18). Use of the long-axis view allows for appropriate
visualization of the needle tip at all times, and has been shown to be preferable for other ultrasound-
guided procedures. If the needle appears to be within the abscess cavity and no purulent material can be
aspirated, small amounts of sterile saline can be injected to attempt to clear the needle. The needle can be
redirected to isolated or undrained pockets.
ULTRASOUND EVALUATION OF THE PATIENT WITH ASCITES

Ascites is a common occurrence in critically ill patients with cirrhosis. Patients admitted to the ICU may
require paracentesis for either diagnostic or therapeutic purposes.
Figure 15-16. Ultrasound-guided Incision and Drainage of Abscess

A) Real-time ultrasound guidance used to make an incision. The tip of the blade (arrow) is seen entering the abscess cavity. B) Hyperechoic
hemostat jaws (arrows) dissecting septations are visible.
Figure 15-17. Cutaneous Abscess Pre- and Post-Drainage
A) Hypoechoic abscess seen before drainage. B) Adequate decompression noted after incision and drainage.
Figure 15-18. Hyperechoic Needle in Long-Axis View in Abscess Cavity
Diagnostic paracentesis is used to either diagnose the underlying cause of ascites or to evaluate for
spontaneous bacterial peritonitis (SBP). It is estimated that 10% to 30% of all hospitalized patients with
ascites have SBP, although this is a difficult clinical diagnosis because many cases are occult or have
minimal signs or symptoms. Studies demonstrate that early diagnosis and treatment of SBP reduces
mortality, but the mortality rate overall remains very high.9 Therapeutic paracentesis is performed in
patients with large-volume ascites who are symptomatic or have respiratory compromise because of the
increased intra-abdominal pressure. This procedure is more effective and safer than diuresis for treatment
of tense ascites. Not only is it safe for critically ill patients, but patients with and without mechanical
ventilation demonstrate improved respiratory function after paracentesis.10
Ultrasound can be used for patients with ascites in several ways. Bedside ultrasound can confirm a small
volume of ascites or if they are obscured by patient habitus on examination. Diagnosis is traditionally
done through physical examination, though the classic signs of shifting dullness and presence of a fluid
wave may be unreliable and is only present with larger volumes of ascites. Ultrasound is very sensitive
for the diagnosis of intra-abdominal fluid and is capable of detecting ascites in very small quantities.11
Ultrasound evaluation should be conducted to confirm the presence of ascites when physical examination
findings are equivocal. This evaluation should be performed with the patient in the supine position, using
a low-frequency curvilinear transducer. With the probe in the right and left lower quadrants – where
paracentesis is typically performed – ascites appear as anechoic areas surrounding the bowel and
mesentery. The bowel appears as a circular structure with a hyperechoic rim representing the serosa and
is tethered by isoechoic mesentery.
The focused assessment with sonography in trauma (FAST) examination offers views that can be used to
reliably confirm a clinical suspicion of ascites when the physical examination is unreliable or very small
amounts of fluid are present. Ascitic fluid will be detected in the same locations that are evaluated on a
FAST examination (right upper quadrant, left upper quadrant, and pelvis). In patients with large-volume
ascites, all of these areas may demonstrate free fluid. Ascites appear as anechoic areas in the splenorenal
space, hepatorenal space, subphrenic space, paracolic gutters, and pelvis (Figure 15-19). Ascitic fluid is
indistinguishable from hemoperitoneum on sonography.
ULTRASOUND-GUIDED PARACENTESIS
Ultrasound can be used for preprocedural planning and for real-time ultrasound guidance of paracentesis.
Ultrasound is well-suited for paracentesis guidance because all of the structures that pose a danger during
the procedure are easily visualized on sonography. Use of ultrasound for paracentesis has been shown to
decrease both bleeding complications and the overall cost of care for patients undergoing in-hospital
paracentesis.12
Indications for diagnostic paracentesis include abdominal pain, fever, leukocytosis, unexplained
encephalopathy, and new-onset ascites. Therapeutic paracentesis is indicated for the treatment of tense
ascites with or without respiratory compromise or lower-extremity edema. The only firm contraindication
is disseminated intravascular coagulation and overlying infection. Other relative contraindications to
blind paracentesis, such as adhesions, pregnancy, bowel obstruction, or distension, are invalid when
ultrasound is used. It is not recommended to avoid paracentesis in the presence of coagulopathy because
no demonstrable correlation exists between coagulopathy and bleeding complications.13,14 Overall,
bleeding complications, though sometimes fatal, are rare and include abdominal wall hematoma,
hemoperiteoneum, and hemorrhage. Other potential complications include infection, secondary SBP, and
persistent leak from the puncture site. These complications are exceedingly rare and paracentesis is
considered to be a very safe procedure.
Figure 15-19. Anechoic Ascitic Fluid

A) Ascitic fluid in the right upper quadrant. B) Ascitic fluid in the left lower quadrant.
E X P E RT T I P
An appropriate pocket of fluid without the presence of nearby bowel, mesentery, or super ficial
vasculature can be identified by first using preprocedural planning.
Preprocedural planning with ultrasound is also advantageous. An appropriate pocket of fluid without the
presence of nearby bowel, mesentery, or superficial vasculature can be identified. Typically, though the
bilateral lower quadrants are chosen as paracentesis sites, the midline is another option. Studies have
shown decreased depth of ascitic fluid and increased thickness of the abdominal wall in the midline.15
For the lower quadrants, the preferred location is an area in the lower abdomen that is generally 5 cm
medial and superior to the anterior superior iliac spine and 2 cm lateral to the lateral rectus muscle
border. With ultrasound, a preferred location can be chosen based on visualized anatomy rather than
landmarks (Figure 15-20).
The abdominal wall should be evaluated for vasculature. Vessels within the abdominal wall, such as the
inferior epigastric artery and the large superficial venous collaterals (common in liver disease), are at
risk for damage during the procedure and can be avoided with thorough sonographic evaluation. Vessels
will appear as small anechoic circular, ovoid, or longitudinal structures (depending on the scanning
plane). Evaluation with color or power Doppler may demonstrate arterial or venous flow, which may be
absent in the case of venous structures (Figure 15-21).
The peritoneal cavity should be evaluated for intraperitoneal structures that should be avoided, such as
organs or the bowel, and an area with adequate clearance and volume can be chosen. The fluid depth
visualized at the site of paracentesis correlates with the amount of fluid that can be drained at a given
location, with a 1-L increase in fluid drained for each 1 cm of depth measured.16 If a minimal amount of
ascites is identified in a lower quadrant, the patient can be repositioned into a left lateral decubitus
position while scanning in the right lower quadrant and vice versa. This repositioning allows the bowel
to rise away from the proposed procedural site.
After an ideal location has been identified and marked, appropriate equipment is gathered and the
patient’s consent obtained. Universal precautions and sterile procedures should be maintained throughout
the procedure. After cleaning the skin with appropriate antiseptic, local anesthetic is injected at the
puncture site. The needle used for the procedure should be adequate to reach the peritoneal cavity, and
this distance can be measured before the procedure. A needle alone can be used for a diagnostic tap and a
catheter-over-needle system is most common for large-volume paracentesis.
Figure 15-20. Pre-Procedural Ultrasound Assessment to Identify Appropriate Site for Needle Insertion
Adequate depth of ascites (anechoic appearance) with hyperechoic loops of the bowel.
Figure 15-21. Pre-Procedural Assessment Using Doppler

Color Doppler showing vessels to avoid while introducing the needle.
E X P E RT T I P
Vessels within the abdominal wall, such as the inferior epigastric artery and the large super
ficial venous collaterals (common in liver disease), are at risk for damage during the procedure
and can be avoided with thorough sonographic evaluation.
As the needle enters the skin, creation of a Z-track in which traction is held against the skin while the
needle is advanced may lessen the incidence of persistent leak through the puncture site. After puncture of
the skin, the needle can be observed advancing through the abdominal wall to the peritoneal cavity using
ultrasound (Figure 15-22). Often the tenting of the peritoneum can be visualized with sonography before
entering the peritoneal cavity. If performing a therapeutic tap, a catheter is typically advanced over the
needle. As fluid is drained, ultrasound can be used to investigate any decrease or cease of flow. The
peritoneum can appear caught against the catheter. This can be remedied by injecting a small amount of
sterile saline through the catheter to dislodge the obstruction, allowing free flow of fluid once more.
Following large-volume paracentesis, albumin is indicated for the prevention of circulatory dysfunction.
Figure 15-22. Real-Time Ultrasound Guidance for Performing Paracentesis

B-mode image showing a hyperechoic needle within the ascitic fluid away from bowel loops.
KEY POINTS
The use of ultrasound aids in the diagnosis of cellulitis and abscess with improved diagnostic
accuracy compared with physical examination alone.
The sonographic appearance of cutaneous abscess includes a cavity within the subcutaneous tissues
that can be anechoic, isoechoic, or hyperechoic, has surrounding hyperemia on Doppler imaging,
and may exhibit swirling of contents with compression.
Ultrasound can be used for preprocedural assessment, for real-time needle guidance, and for
ensuring complete decompression during abscess drainage.
Ultrasound can be used to confirm the diagnosis of ascites and for procedural guidance for
paracentesis.
The use of ultrasound guidance for paracentesis leads to decreased complications.
REFERENCES
1. Prusakowski MK, Kuehl DR. Trends in emergency department management of skin abscesses. Am J Infect Control. 2015;43:336-340.
2. Giovanni JE, Dowd MD, Kennedy C, et al. Interexaminer agreement in physical examination for children with suspected soft tissue
abscesses. Pediatr Emerg Care. 2011;27:475-478.
3. Tayal VS, Hasan N, Norton HJ, et al. The effect of soft-tissue ultrasound on the management of cellulitis in the emergency department.
Acad Emerg Med. 2006;13:384-388.
4. Blaivas M, Adhikari S. Unexpected findings on point-of-care superficial ultrasound imaging before incision and drainage. J Ultrasound
Med. 2011;30:1425-1430.
5. Blaivas M, Lyon M, Brannam L, et al. Water bath evaluation technique for emergency ultrasound of painful superficial structures. Am J
Emerg Med. 2004;22:589-593.
6. Gaspari R, Blehar D, Mendoza M, et al. Use of ultrasound elastography for skin and subcutaneous abscesses. J Ultrasound Med.
2009;28:855-860.
7. Yen ZS, Wang HP, Ma HM, et al. Ultrasonographic screening of clinically-suspected necrotizing fasciitis. Acad Emerg Med. 2002;9:1448-
1451.
8. Gaspari RJ, Resop D, Mendoza M, et al. A randomized controlled trial of incision and drainage versus ultrasonographically guided needle
aspiration for skin abscesses and the effect of methicillin-resistant Staphylococcus aureus. Ann Emerg Med. 2011;57:483-491.e481.
9. Kim JJ, Tsukamoto MM, Mathur AK, et al. Delayed paracentesis is associated with increased in-hospital mortality in patients with
spontaneous bacterial peritonitis. Am J Gastroenterol. 2014;109:1436-1442.
10. Phillip V, Saugel B, Ernesti C, et al. Effects of paracentesis on hemodynamic parameters and respiratory function in critically ill patients.
BMC Gastroenterol. 2014;14:18.
11. Von Kuenssberg Jehle D, Stiller G, Wagner D. Sensitivity in detecting free intraperitoneal fluid with the pelvic views of the FAST exam.
Am J Emerg Med. 2003;21:476-478.
12. Mercaldi CJ, Lanes SF. Ultrasound guidance decreases complications and improves the cost of care among patients undergoing
thoracentesis and paracentesis. Chest. 2013;143:532-538.
13. Lin CH, Shih FY, Ma MH, et al. Should bleeding tendency deter abdominal paracentesis? Dig Liver Dis. 2005;37:946- 951.
14. Patel IJ, Davidson JC, Nikolic B, et al. Consensus guidelines for periprocedural management of coagulation status and hemostasis risk in
percutaneous image-guided interventions. J Vasc Interv Radiol. 2012;23:727-736.
15. Sakai H, Sheer TA, Mendler MH, et al. Choosing the location for non-image guided abdominal paracentesis. Liver Internat. 2005;25:984-
986.
16. Irshad A, Ackerman SJ, Anis M, et al. Can the smallest depth of ascitic fluid on sonograms predict the amount of drainable fluid? J Clin
Ultrasound. 2009;37:440-444.
Chapter 16
Tamponade
Chapter 17
The Use of Ultrasound in the Diagnosis of Shock
Chapter 18
Respiratory Failure
Chapter 19
Thromboembolism
Chapter 20
Cardiac Arrest: Focused Echocardiographic Evaluation in Life Support (FEEL)
Chapter 21
Infection: Septic Shock
Chapter 22
Vascular Injuries
Chapter 16
Tamponade
OBJECTIVES
Understand the anatomy of the pericardium and major causes of pericardial effusion
Understand that pericardial tamponade is a clinical diagnosis and depends on presenting signs and symptoms as
well as echocardiographic findings
Know the key echocardiographic findings of pericardial tamponade:
Right atrial systolic collapse
Right ventricular diastolic collapse
Inferior vena cava plethora
Exaggerated changes in transvalvular Doppler blood flow velocities with respiration
INTRODUCTION
The pericardium surrounds the heart and extends to the proximal great vessels.1 The pericardial space is a
potential space between the visceral pericardium and the parietal pericardium. The visceral pericardium
is contiguous with the epicardium, whereas the parietal pericardium forms a sac around the heart.
Normally the pericardial space contains about 10 to 15 mL of fluid that provides basic lubrication.2
Additional fluid or blood can accumulate in the pericardial space because of infection (viral or
bacterial), malignancy, inflammatory states (collagen vascular disease, uremia, radiation, post–cardiac
surgery, or post–myocardial infarction), aortic dissection, or trauma. Both the rate of pericardial fluid
accumulation and the volume of pericardial fluid determine the physiological consequences of effusion
(Figure 16-1). Pericardial tamponade occurs when the intrapericardial pressure increases and exceeds
intracardiac pressures, which impairs filling of the cardiac chambers, leading to decreased cardiac
output. Increased intrapericardial pressure also leads to a condition called “ventricular interdependence,”
in which the compression of the heart by the pericardial effusion limits filling of the ventricular chambers.
When the right ventricle fills during inspiration, it compresses the left ventricle and limits filling. During
expiration, the left ventricle fills and limits filling of the right ventricle. Echocardiography is an essential
modality for the diagnosis of pericardial tamponade. Ultimately, however, pericardial tamponade is a
clinical diagnosis based on echocardiographic findings, increased pulsus paradoxus, jugular venous
distension, tachycardia, tachypnea, and hypotension. In some cases, tamponade is only diagnosed
definitively after pericardial drainage, when hemodynamic instability resolves.
Figure 16-1.
Graph of intrapericardial pressure vs. volume demonstrating the rapid increase in pressure with rapid accumulation of pericardial fluid vs. the
slower increase in pressure with slow accumulation of pericardial fluid. Pericardial tamponade will occur at lower volumes of pericardial fluid
with rapid accumulation, and at larger volumes of pericardial fluid with slow accumulation.
CASE STUDY
A 30-year-old woman with a history of scleroderma and hypertension was admitted to the ICU with upper
respiratory infection of 4 days’ duration that was complicated by hypotension. Initial echocardiography
showed a left ventricular ejection fraction of 45% and a moderate, circumferential pericardial effusion.
The patient required norepinephrine to maintain an adequate blood pressure. She was spontaneously
breathing on supplemental oxygen, initially by nasal cannula, which was then increased to high-flow face
mask. Despite adequate fluid resuscitation, the patient required a higher dose of norepinephrine to support
her blood pressure. Serial echocardiography showed progressively decreased left ventricular systolic
function, a small right ventricle, right atrial collapse during ventricular systole, greater than 25%
variation of Doppler mitral inflow velocity, and greater than 40% variation in tricuspid inflow velocity.
The patient was taken to the cardiac catheterization laboratory for pericardiocentesis. The troponin had
increased to 4.0 ng/mL. Coronary artery anatomy was normal. Left ventricular ejection fraction was 35%
to 40%. Simultaneous right and left heart catheterization was performed and showed ventricular
interdependence consistent with tamponade physiology (Figure 16-2). Pericardiocentesis with drain
placement was performed and 200 mL of serosanguinous fluid was drained. This resulted in immediate
hemodynamic improvement. The drain was kept in place for 3 days. The patient continued to improve.
After the hypotension resolved, she underwent diuresis for fluid overload. She was discharged from the
hospital 5 days after pericardiocentesis, with a follow-up echocardiogram showing no residual
pericardial effusion and a left ventricular ejection fraction of 60%. The final diagnosis was viral
myocarditis causing cardiomyopathy and pericardial effusion leading to pericardial tamponade.
CARDIAC TAMPONADE PHYSIOLOGY

Cardiac tamponade occurs when fluid or blood in the pericardial space compresses the heart and
compromises cardiac output.3 Intrapericardial pressure exceeds cardiac chamber pressure, resulting in
partial chamber collapse. Cardiac chamber pressures vary through the cardiac cycle, and chamber
collapse occurs during the point in the cardiac cycle when pressure is lowest in the given chamber. Right
atrial chamber collapse occurs first and is a sensitive, but not specific, sign of tamponade because right
atrial collapse may occur with a pericardial effusion in the absence of tamponade.4,5 Late diastolic right
atrial collapse can also occur with hypovolemia.5,6 Right atrial collapse that persists into ventricular
systole and/or lasts for greater than one-third of the cardiac cycle is more specific for cardiac tamponade
(Figure 16-3).4,6,7 Right ventricular early diastolic collapse requires a greater intrapericardial pressure
than right atrial collapse and is less sensitive, but very specific.1,5 About 25% of the time, left atrial late
diastolic collapse also occurs. Left ventricular diastolic collapse only occurs under special conditions
such as localized postsurgical tamponade.6,7 The evolution of cardiac tamponade is a spectrum, and
echocardiographic findings and clinical signs may evolve as tamponade worsens. In fully developed
cardiac tamponade, intrapericardial, right atrial, pulmonary artery diastolic, and pulmonary capillary
wedge pressure are all elevated and equalized.2 This is a very late and entirely specific finding.
To identify onset and duration of right atrial or ventricular collapse relative to the cardiac cycle, it
may be necessary to freeze the 2-dimensional image and scroll through frame by frame to correlate
chamber collapse with the cardiac cycle on the electrocardiogram. M-mode can also be used for this
same purpose.
Figure 16-2.
Abbreviations: LV, left ventricular; RV, right ventricular.
Pressure tracings from right and left heart catheterization of a 30-year-old woman with viral myocarditis and pericardial tamponade requiring
norepinephrine for shock. The patient was spontaneously breathing. Tracings show evidence of ventricular interdependence. RV systolic
pressure is increased during inspiration and decreased during expiration. LV systolic pressure is decreased during inspiration and increased
during expiration. There was evidence of equalization of cardiac pressure with right atrial pressure of 22 mm Hg and pulmonary capillary
occlusion pressure of 21 mm Hg.
The relationship between effusion volume and tamponade depends on how quickly the effusion develops.
Cardiac tamponade may occur acutely because of trauma or postsurgical bleeding. In these cases, blood
fills the pericardial space faster than the pericardium can stretch and accommodate the increased volume.
The pericardial reserve volume is quickly exceeded, resulting in an abrupt increase in pressure in the
pericardial space. When fluid accumulates slowly over time in the pericardial space, the pericardium has
time to stretch and accommodate an increasing volume before intrapericardial pressure exceeds cardiac
chamber pressures (Figure 16-1).6 Uremia, collagen vascular disease, infection, and malignancy are
relatively common causes of slow accumulation of pericardial fluid, where large pericardial effusions
can occur before tamponade occurs.
Figure 16-3.
Abbreviations: RV, right ventricle; LV, left ventricle; LA, left atrium; RA, right atrium.
Pericardial tamponade occurs when intrapericardial pressure increases and compromises systemic venous return to the right atrium. This
occurs when the pericardial pressure increases to greater than the intracardiac chamber pressure, and the myocardial transmural pressure that
is normally positive becomes negative. Chamber collapse occurs first on the right side of the heart where intracardiac chamber pressures are
lowest. A) The RA is the first chamber to collapse during late ventricular diastole and extending into ventricular systole. B) The RV is the next
chamber to collapse during ventricular diastole. The LA and LV are also shown.
This figure was published in Textbook of Clinical Echocardiography, 5th edition, Otto ed. Copyright Elsevier 2013.
Although echocardiography is extremely important for diagnosis, cardiac tamponade remains a clinical
diagnosis that depends on evaluation of symptoms and signs. The patient may complain of dyspnea, chest
tightness, or pleuritic chest pain depending on the cause of the pericardial effusion. Signs may include
elevated jugular venous pressure, tachycardia, tachypnea, and hypotension.3 Patients may be unresponsive
to fluid or vasopressors when in profound shock. Ultimately, cardiac tamponade can cause cardiac arrest,
which generally manifests as pulseless electrical activity. A less common finding is electrical alternans
on the electrocardiogram, attributed to the heart swinging in a large fluid-filled pericardial sac.
E X P E RT T I P
The relationship between effusion volume and tamponade depends on how quickly the effusion
develops. Large effusions that accumulate slowly may not cause tamponade, whereas moderate
effusions that accumulate rapidly are more likely to cause tamponade.
An increased pulsus paradoxus—so called originally because heart tones were audible but the radial
pulse was not palpable after inspiration—is an important clinical sign that results from an exaggerated
inspiratory decrease in systolic blood pressure in spontaneously breathing patients.1,3 Normally during
inspiration the relative negative intrathoracic pressure causes increased filling of the right heart whereas
the left heart has decreased filling because of pooling of blood in the pulmonary veins, leading to a
decreased stroke volume.8 This results in a lower systolic blood pressure during inspiration that is no
more than 10 mm Hg lower than expiratory systolic blood pressure. During pericardial tamponade, there
is an increased respiratory variation in right and left ventricular filling. The increased volume and
pressure in the pericardial space limits filling of the cardiac chambers and results in ventricular
interdependence. During inspiration, there is increased filling of the right heart, with the atrial and
ventricular septum bowing toward the left, which significantly impedes left heart filling and results in a
lower stroke volume and systolic blood pressure. A decreased left ventricular filling pressure during
inspiration also contributes to decreased stroke volume. The left heart is shielded from an inspiratory
decrease in intrathoracic pressure during pericardial tamponade because of increased pressure in the
pericardial space, but the pressure in the pulmonary veins still decreases with inspiration. This results in
a decreased pressure gradient from the pulmonary veins to the left heart during inspiration, but the
pressure gradient is restored during expiration. Left heart stroke volume increases during expiration and
the atrial and ventricular septum bows toward the right, impairing right heart filling.9,10 This exaggerated
ventricular interdependence causes increased fluctuations in systolic blood pressure with respiration,
resulting in a pulsus paradoxus of greater than 10 mm Hg.3
Echocardiography provides another window on the same phenomenon by tracking changes in flow into the
right and left ventricles over the course of the respiratory cycle. This application of Doppler
echocardiography to evaluate respiratory changes in transvalvular blood flow velocity in the right and left
heart is discussed below.
ECHOCARDIOGRAPHIC IDENTIFICATION OF PERICARDIAL EFFUSION

Pericardial effusion is identified on 2-dimensional (2D) echocardiography as an echolucent space
adjacent to the cardiac structures that is usually diffuse and symmetric. Acute hemorrhagic pericardial
effusions may have significant echogenicity resulting from thrombus. Chronic pericardial effusions may
have fibrinous strands within the fluid.2 Pericardial effusions can be observed in the left parasternal,
apical, and subcostal windows (Figures 16-4 - 16-7). The subcostal window is generally most sensitive
for detection of a small effusion. The distance of separation between the heart and parietal pericardium
determines the size of a pericardial effusion. A small pericardial effusion has a width of less than 0.5 cm,
a moderate effusion has a width of 0.5 to 2 cm, and a large effusion has a width of more than 2 cm.
Measurements can be made in whichever window provides the best view of the pericardial effusion.
Figure 16-4.
Abbreviations: PE, pericardial effusion; LV, left ventricle; LA, left atrium; RV, right ventricle; DA, descending thoracic aorta.
Left parasternal window, long-axis view, showing a pericardial effusion surrounding the LV, LA, and RV. The pericardial effusion tracks
between the heart and the descending thoracic aorta. A pleural effusion lies posterior to the heart and the descending thoracic aorta.
Figure 16-5.
Abbreviations: PE, pericardial effusion; LV, left ventricle; LA, left atrium; RV, right ventricle; RA, right atrium.
Apical window, 4-chamber view, showing a large PE surrounding the LV, LA, RV, and RA. A large PE is defined as a separation of more than
2.0 cm between the heart and the parietal pericardium (moderate is 0.5-2.0 cm and small is less than 0.5 cm).
ECHOCARDIOGRAPHIC SIGNS OF PERICARDIAL TAMPONADE
Right Atrial Systolic Collapse

Onset of right atrial collapse in late diastole is a sensitive, but not specific, sign of pericardial
tamponade. Right atrial collapse extending into ventricular systole and lasting more than one-third of the
cardiac cycle is highly specific for pericardial tamponade.7 Right atrial collapse is best viewed from the
subcostal 4-chamber or the apical 4-chamber views. It is essential to have electrocardiographic
monitoring when the 2D echocardiography image is acquired so that the image can be frozen and then
reviewed frame by frame to observe the onset and duration of right atrial collapse through the cardiac
cycle (Figures 16-3 and 16-8). M-mode can also be used to identify and determine the duration of right
atrial collapse during the cardiac cycle.
Figure 16-6.
Abbreviations: LV, left ventricle; RV, right ventricle.
Large pericardial effusion observed in the left parasternal window, short-axis view, at the level of the mid–LV. The RV is also shown.
Figure 16-7.
Abbreviations: PE, pericardial effusion; RV, right ventricle; RA, right atrium; LV, left ventricle.
Subcostal window, 4-chamber view. PE is observed between the RV and the diaphragm. The RA and LV are also shown.
Figure 16-8.
Abbreviations: PE, pericardial effusion; RV, right ventricle; LV, left ventricle; RA, right atrium; LA, left atrium.
RA collapse during ventricular systole (white arrow). Image is of a 74-year-old man with ground level falls and hypotension;
echocardiography- guided PE surrounds the heart: RV, LV, and LA.
Right Ventricular Diastolic Collapse

Because the right ventricular end diastolic pressure is generally a bit higher than right atrial end systolic
pressure, right ventricular diastolic collapse generally occurs later in tamponade than right atrial systolic
collapse. Right ventricular diastolic collapse is less sensitive, but highly specific, for pericardial
tamponade (Figures 16-3 and 16-9).1,5 The subcostal 4-chamber view or left parasternal short axis right
ventricular inflow and outflow views are optimal for observing right ventricular diastolic collapse. When
the timing of right ventricular diastolic collapse relative to the cardiac cycle is not obvious, the images
can be viewed frame by frame, or an M-mode recording can be taken through the right ventricular free
wall. Using M-mode, it can be determined where in the cardiac cycle right ventricular collapse occurs
(Figure 16-10). Pulmonary hypertension and right ventricular hypertrophy can delay right ventricular
collapse until the intrapericardial pressure is very high.1
Plethoric Inferior Vena Cava

A dilated and noncollapsing inferior vena cava in spontaneously breathing patients is a sensitive, but
nonspecific sign of pericardial tamponade that represents elevated right atrial pressure.2 As with the
familiar method for estimating central venous pressure by observing maximal diameter and respiratory
collapse of the interior vena cava,11 in the subcostal window, the diameter of the inferior vena cava is
measured about 1 to 2 cm from the cavoatrial junction. A diameter of the inferior vena cava more than 2.1
cm with respiratory collapse less than 50% is indicative of elevated right atrial pressure (Figure 16-11).
C AVE AT
Pulmonary hypertension and right ventricular hypertrophy can delay right ventricular collapse
until the intrapericardial pressure is very high.
Figure 16-9.
Abbreviations: PE, pericardial effusion; RV, right ventricle; LV, left ventricle; RA, right atrium; LA, left atrium.
Subcostal 4-chamber view of RV collapse during diastole (white arrow). Same case as in Figure 16-8. PE, RA, LA, and LV are shown.
Figure 16-10.
Abbreviations: PE, pericardial effusion; RV, right ventricle; LA, left atrium.
Parasternal window, long-axis view, M-mode cursor through the RV free wall showing late diastolic collapse indicative of tamponade
physiology (white arrow). LA systolic collapse is also shown (red arrow). The PE surrounds the heart.
Reciprocal Respiratory-Related Changes in Doppler Velocity of Tricuspid and Mitral Inflow

Spectral Doppler is used to identify marked respiratory variations in velocity of transvalvular tricuspid
and mitral blood flow during cardiac tamponade that occur because of ventricular interdependence
(Figure 16-12). In spontaneously breathing patients with cardiac tamponade, velocity of blood flow
across the tricuspid valve increases during inspiration and decreases during expiration with more than
40% variation, whereas velocity of blood flow across the mitral valve decreases during inspiration and
increases during expiration with more than 25% variation.2,12 A useful way to remember these thresholds
is to consider that the right heart is more tolerant of changes in flow than the left heart; a 40% change in
flow in the left heart would be associated with advanced shock.
To observe a full respiratory cycle and identify respiratory variation in Doppler inflow velocity, it is
necessary to decrease the sweep speed to 25 mm/s. Ideally, the respirometer function on the ultrasound
machine should be used to identify inspiration and expiration. If a respirometer tracing is not available,
then the peak and trough variation in Doppler inflow velocity is assumed to be because of respiration in a
spontaneously breathing patient.
Figure 16-11.
Abbreviations: IVC, inferior vena cava; RA, right atrium.
IVC plethora. The IVC, liver, hepatic vein, diaphragm, RA, and pericardial effusion are shown. The diameter of the IVC should be measured
about 1 to 2 cm from the junction of the right atrium (blue double arrow). A dilated (more than 2.1 cm) and noncollapsing IVC is consistent
with IVC plethora and pericardial tamponade.
To observe a full respiratory cycle and identify respiratory variation in Doppler inflow velocity, it is
necessary to decrease the sweep speed to 25 mm/s.
Figure 16-12.
A) Pulsed-wave Doppler image of tricuspid inflow velocity variation in pericardial tamponade. In this spontaneously breathing patient, Doppler
velocity is highest during inspiration and lowest during expiration. A variation of more than 40% in tricuspid inflow Doppler velocity is
consistent with pericardial tamponade in a spontaneously breathing patient. B) In the same patient, pulsed-wave Doppler image of mitral inflow
velocity is lowest during inspiration and highest during expiration. A variation of greater than 25% in mitral inflow Doppler velocity is consistent
with pericardial tamponade in a spontaneously breathing patient.
THERAPEUTIC OPTIONS
The definitive treatment of pericardial tamponade is drainage of the pericardial fluid. Optimally, this is
performed by a cardiologist in the catheterization laboratory or by a cardiac surgeon in the operating
room.13,14 In emergent situations, drainage of pericardial fluid may need to be performed at the bedside.
Acute traumatic pericardial tamponade may require emergency thoracotomy. Circulatory arrest resulting
from pericardial tamponade may require emergent percutaneous pericardiocentesis; critical care
physicians should be familiar with this procedure.15 Echocardiographic guidance, most often from the
subcostal window 4-chamber view, provides visualization of the needle entering the pericardial space.2
Relative contraindications to emergency pericardiocentesis include myocardial rupture and aortic
dissection, which require surgical intervention.15 Early consultation by cardiology and/or cardiothoracic
surgery is encouraged if pericardial tamponade is suspected. There may be uncertainty regarding whether
hemodynamic compromise is caused by pericardial tamponade. Improvement in hemodynamics after
drainage of pericardial fluid confirms the diagnosis of tamponade.
Medical management of pericardial tamponade pending definitive drainage of the pericardial effusion
may include volume resuscitation and/or vasopressor support. The best predictor of a response to volume
resuscitation is the presence of hypotension.16 Careful evaluation of volume status is important, because
over-resuscitation in a patient with pericardial tamponade may result in increased intrapericardial
pressure and worsening tamponade.6
C AVE AT
Respiratory variation in tricuspid and mitral Doppler inflow velocity may not be present in
patients with cardiac tamponade who are receiving positive pressure ventilation.
KEY POINTS
Cardiac tamponade is a clinical diagnosis that depends on the evaluation of echocardiographic
findings and clinical signs of increased pulsus paradoxus, elevated jugular venous pressure,
tachycardia, tachypnea, and hypotension.
2D echocardiographic findings in pericardial tamponade include the following:
Right atrial late diastolic collapse continues into ventricular systolic systole. Right atrial
collapse is a sensitive sign, and when the duration of right atrial collapse is more than one-third
of the cardiac cycle, it is a specific sign.
Right ventricular early diastolic collapse is a less sensitive but more specific sign for pericardial
tamponade.
Left atrial collapse is less commonly observed.
Left ventricular diastolic collapse only occurs under special conditions such as localized
postsurgical tamponade.
Doppler echocardiographic findings in pericardial tamponade include the following:
In spontaneously breathing patients with cardiac tamponade, the velocity of blood flow across the
tricuspid valve increases during inspiration and decreases during expiration with more than 40%
variation, whereas velocity of blood flow across the mitral valve decreases during inspiration
and increases during expiration with more than 25% variation.
Limitations of echocardiographic findings in pericardial tamponade include the following:
Right atrial and right ventricular collapse may not occur in the presence of elevated right atrial
and ventricular pressure, such as in pulmonary hypertension.
Respiratory variation in Doppler tricuspid and mitral inflow velocities may not occur during
positive pressure ventilation.
Respiratory variation in Doppler tricuspid and mitral inflow velocities may also be seen in
asthma, chronic obstructive pulmonary disease, pulmonary embolus, right ventricular infarction,
and hypovolemia.
REFERENCES
1. Wann S, Passen E. Echocardiography in pericardial disease. J Am Soc Echocardiogr. 2008;21:7-13.
2. Otto CM. Pericardial disease. In: Textbook of Clinical Echocardiography. 5th ed. Philadelphia, PA: Elsevier, Saunders; 2013:254-270.
3. Roy CL, Minor MA, Brookhart MA, et al. Does this patient with a pericardial effusion have cardiac tamponade? JAMA. 2007;297:1810-
1818.
4. Argulian E, Messerli F. Misconceptions and facts about pericardial effusion and tamponade. Am J Med. 2013; 126:858-861.
5. Merce J, Sagrista-Sauleda J, Permanyer-Miralda G, et al. Correlation between clinical and Doppler echocardiographic findings in patients
with moderate and large pericardial effusion: implications for the diagnosis of cardiac tamponade. Am Heart J. 1999;138(4 Pt 1):759-764.
6. Spodick DH. Acute cardiac tamponade. N Engl J Med. 2003;349:684-690.
7. Gillam LD, Guyer DE, Gibson TC, et al. Hydrodynamic compression of the right atrium: a new echocardiographic sign of cardiac
tamponade. Circulation. 1983;68:294-301.
8. Picard MH, Sanfilippo AJ, Newell JB, et al. Quantitative relation between increased intrapericardial pressure and Doppler flow velocities
during experimental cardiac tamponade. J Am Coll Cardiol. 1991;18:234-242.
9. Sharp JT, Bunnell IL, Holland JF, et al. Hemodynamics during induced cardiac tamponade in man. Am J Med. 1960;29: 640-646.
10. Oh JK, Seward JB, Tajik AJ. Pericardial diseases. In: The Echo Manual. Philadelphia, PA: Lippincott Williams & Wilkins; 2006:289-309.
2015;28:1-39.
12. Leeman DE, Levine MJ, Come PC. Doppler echocardiography in cardiac tamponade: exaggerated respiratory variation in transvalvular
blood flow velocity integrals. J Am Coll Cardiol. 1988;11:572-578.
13. Imazio M, Adler Y. Management of pericardial effusion. Eur Heart J. 2013;34:1186-1197.
14. Sagrista-Sauleda J, Merce AS, Soler-Soler J. Diagnosis and management of pericardial effusion. World J Cardiol. 2011;3:135-143.
15. Fitch MT, Nicks BA, Pariyadath M, et al. Videos in clinical medicine: emergency pericardiocentesis. N Engl J Med. 2012;366:e17.
16. Sagrista-Sauleda J, Angel J, Sambola A, et al. Hemodynamic effects of volume expansion in patients with cardiac tamponade. Circulation.
2008;117:1545-1549.
Chapter 17
The Use of Ultrasound in the Diagnosis of
Shock
Cameron Bass, MD; Habib Srour, MD; Alfredo E.
Urdaneta, MD; R. Eliot Fagley, MD
OBJECTIVES
Review the basic ultrasound examination for shock states, including abdominal, pleural, vascular, and cardiac
imaging
Illustrate pathologic findings seen in shock states
Discuss the use of serial ultrasound examinations in shock states
INTRODUCTION
The use of ultrasound in emergency departments and critical care units around the world is
revolutionizing the diagnosis, treatment, and monitoring of patients in shock states. Several goal-directed
ultrasonographic examinations have been described, including the focused assessment with sonography in
trauma (FAST) and focused assessment of transthoracic echocardiography (FATE), among others.1,2 The
benefit to the critically ill patient is in the immediacy and repeatability of these examinations. In the hands
of the intensivist, these features of ultrasonography make it an exceptional tool in caring for the critically
ill.
Many life-threatening diagnoses such as cardiac tamponade, acute right heart failure, catastrophic valve
failure, and aortic dissection may require urgent intervention, and are amenable to ultrasound imaging.
Differentiating among hypoperfusion states can be challenging, and it often requires a sophisticated
integration of history, clinical presentation, physical examination, laboratory work, and imaging that can
be time-consuming when time is of the essence. Further delineation of the source of shock is not only
important to the determination of the course and type of treatment, it may provide earlier operative
intervention, drainage, or removal of the offending agent. Use of ultrasound in shock requires integration
of information from history, physical examination, laboratory findings, and imaging, with information from
serial examinations of multiple ultrasound applications, including cardiac, abdominal, thoracic, and
vascular imaging.3
The goal of ultrasonography in shock is to answer the following questions:
Is there a life-threatening cause for the shock state?

Is the patient euvolemic, hypovolemic, or volume-overloaded?
Is the heart function normal, depressed, or hyperdynamic?
Is there major cardiac valvular pathology?
CASE STUDY
A 22-year-old woman presents to the emergency department for evaluation after a high-speed car crash in
which she was the driver. She complains of chest pain, dyspnea, and feelings of abdominal fullness and
distension. She is afebrile, her heart rate is 115 beats/min, blood pressure 90/40 mm Hg, respiratory rate
28 breaths/min, and her oxygen saturation on room air is 96%. She has bruising and tenderness to
palpation over her anterior chest wall. A chest radiograph shows several rib fractures and a widened
mediastinum.
What Is the Next Best Step?

This patient has a mechanism of injury and physical examination findings that are a concern for traumatic
cardiac or vascular injury, particularly cardiac contusion, aortic injury, intercostal arterial injury,
abdominal vascular injury, hepatic injury, or splenic injury. FAST has been shown to be sensitive and
specific for the identification of aortic dissection, pericardial effusion, pleural effusion, and
hemoperitoneum (see Chapter 12). The patient is in shock, and there is no mention of focal neurologic
injury, so magnetic resonance imaging would not be appropriate at this time. Exploratory laparoscopy
may be appropriate if the findings on FAST support operative intervention, but diagnostic laparoscopy
has been largely replaced by FAST. Although it is possible that the patient has cardiac tamponade,
transesophageal echocardiography (TEE) is inappropriate for evaluation of her abdominal signs,
symptoms, and examination findings.
COMMON CAUSES OF SHOCK AND ASSOCIATED ULTRASOUND FINDINGS
Hypovolemic Shock
Determining volume status in a patient with shock is key to the resuscitation and management in cases of
hemodynamic compromise. Both the initiation of vasoactive agents to raise the blood pressure and
excessive volume administration are associated with poor outcome. Central venous pressure (CVP) is
traditionally taught to be an indicator of right atrial pressure, which is thought to reflect preload and fluid
responsiveness; however, 2 meta-analyses have clearly demonstrated that CVP is a poor surrogate for
volume status.4,5 The pulmonary capillary wedge pressure has also been used to determine volume status
and guide fluid resuscitation; however, the use of pulmonary artery catheters has waned over the past
decade. Other modalities have been examined to determine volume status and fluid responsiveness, but
one of the least invasive and quickest methods is bedside ultrasonography of the inferior vena cava (IVC)
with measurement of its size and variation with respirations. The technique for bedside ultrasonography
of the IVC and the differences in ultrasound findings for a spontaneously breathing, nonmechanically
ventilated patient and a mechanically ventilated patient are discussed in this chapter. An additional
practical way to assess for fluid responsiveness is by evaluating the variation in the left ventricular
outflow tract (LVOT) velocity time integral (VTI) and stroke volume with respirations.6
E X P E RT T I P
One of the quickest and least invasive methods of determining volume status and
responsiveness is bedside ultrasonography of the IVC, measuring both its size and variation
with respirations.
IVC Variability
Measurement. The IVC is measured with the patient in the supine position and with a curvilinear or
phased-array ultrasound probe placed in a long-axis subxiphoid view. In this view, the IVC should be
visualized entering the right atrium (RA) (Figure 17-1). At a point that is 1 to 2 cm caudal to this junction,
the diameter of the IVC during the respiratory cycle can be measured using M-mode.
Figure 17-1. Measurement of IVC Diameter

Abbreviations: RA, right atrium; IVC, inferior vena cava; IVC dia, inferior vena cava diameter.
The diameter of the IVC is measured 1 to 2 cm from the cavoatrial junction. IVC diameter and respiratory variation are indicative of the
likelihood of volume responsiveness. Respiratory variation of more than 50% predicts a high likelihood of volume responsiveness.
Spontaneously Breathing Nonintubated Patient. Spontaneously breathing nonintubated patients breathe via
negative pressure ventilation. As the diaphragm contracts, the ribs expand out. This creates a negative
pressure in the thoracic cavity and pleural space that leads to inflation of the lungs. This negative thoracic
pressure is also transmitted to the intrathoracic vessels. Because the IVC is a thin-walled, compliant
vessel, the negative pressure in the thoracic cavity leads to blood in the intra-abdominal IVC being drawn
into the intrathoracic IVC and delivered to the RA. Thus, the IVC partially collapses during inspiration.
The degree of respiratory variation of the IVC during a respiratory cycle provides insight into volume
status and the likelihood of response to a fluid challenge. A respiratory variation of the IVC diameter of
more than 40% correlates with a CVP of less than 8 mm Hg, with 91% sensitivity and 94% specificity,
and is predictive of responsiveness to a fluid challenge with 70% sensitivity and 80% specificity.7
Mechanically Ventilated Patient. In the mechanically ventilated patient, breathing occurs via positive
pressure ventilation. The mechanical ventilator delivers a volume of gas that inflates the lungs and
expands the thoracic cavity. This delivery of gas creates positive intrathoracic pressure that is transmitted
to the intrathoracic vessels. As previously mentioned, the IVC is very compliant and thus blood in the
intrathoracic component of the IVC is pushed toward the intra-abdominal component of the IVC, leading
to distention of the IVC. The respiratory variability in the distention of the IVC has been demonstrated to
predict volume responsiveness, with variation between 12% and 18% predicting a positive response to a
fluid challenge, with a specificity of 90% and sensitivity of 90%.5 Studies that correlate IVC diameter
with fluid responsiveness have used a variety of mechanical ventilator settings. Tidal volumes, peak
inspiratory pressures, plateau pressures, and positive end-expiratory pressure have been inconsistent, as
one may expect given the heterogeneity of the critically ill population.
LVOT VTI. Another use of bedside ultrasound to determine fluid responsiveness is to determine the
degree of respiratory variation of the LVOT VTI. As previously mentioned, during a positive pressure
ventilation breath, blood is pushed out of the intrathoracic IVC and into the intra-abdominal IVC, leading
to decreased RA filling. This leads to decreased right ventricular stroke volume, which in turn leads to
decreased left ventricular stroke volume. LVOT VTI, also known as “stroke distance,” is the area under
the velocity curve through a valve or conduit over time. It can be conceptualized as the distance a single
red blood cell would travel in 1 heartbeat. The VTI, or stroke distance, can be multiplied by the area of
the conduit to determine stroke volume. Presuming the LVOT area does not change significantly throughout
the respiratory cycle, changes in the LVOT VTI will reflect stroke volume variation and will be directly
related to changes in left ventricle (LV) filling conditions.
Using a transthoracic echocardiographic (TTE) apical 5-chamber view or a TEE deep transgastric view,
a pulsedwave or continuous-wave Doppler cursor is positioned through the LVOT (Figure 17-2). The
LVOT VTI variation is calculated using VTImax – VTImin/[(VTImax + VTImin)/2] × 100 (Figure 17-3).
Patient selection for the LVOT VTI technique does carry limitations. Thus far it has only been validated in
the determination of the likelihood of a positive response to a fluid challenge in patients receiving
mechanical ventilation with at least 8 mL/kg in normal sinus rhythm and with normal intra-abdominal
pressure.7
Figure 17-2. Measurement of Blood Flow Velocity Through LVOT with Spectral Doppler
Abbreviations: LV, left ventricle; LVOT, left ventricular outflow tract; RV, right ventricle; Ao, aorta; LA, left atrium.
Continuous- or pulsed-wave Doppler allows sampling of the velocity of blood flow across the valves and major vessels. The dotted line in the
figure demonstrates the appropriate alignment of a spectral Doppler beam to sample the velocity of blood flow through the LVOT (the pulsed-
wave gate is placed within the LVOT). Variation of more than 12% in the velocity time integral of blood flow through the LVOT has been
correlated with volume responsiveness.
Figure 17-3. Respiratory Variation of Peak Velocity in the LVOT
Abbreviations: LVOT, left ventricular outflow tract; VTI, velocity time integral.
The figure demonstrates variability in the peak of the VTI curve using pulsed-wave Doppler. The full curve can be traced to calculate the
VTI.
Stroke Volume. The degree of variation of the left ventricular stroke volume has been demonstrated to
predict a positive response to a fluid challenge with a change greater than 12%, having 100% sensitivity
and 89% specificity. The calculation of stroke volume and cardiac output requires 2 different
echocardiographic windows. The diameter (DLVOT) of the LVOT is measured on the ventricular side of
the aortic valve, in a parasternal long-axis view. In midsystole, the cross-sectional area of the LVOT
(ALVOT) can be estimated using the formula for the area of a circle: ALVOT = π × (DLVOT / 2).2 To
estimate stroke volume, pulsed-wave Doppler LVOT VTI is measured from an apical 5-chamber view in
TTE or deep transgastric view in TEE. The SV (stroke volume) and CO (cardiac output) calculations are
as follows: SV = ALVOT × LVOT VTI; then CO = SV × HR.7
Causes of Hypovolemic Shock: Hemorrhage and Trauma

Hemoperitoneum. FAST was developed as a rapid, noninvasive, repeatable examination that can identify
hemoperitoneum. In a meta-analysis of penetrating abdominal trauma, FAST had a specificity higher than
94% but a sensitivity ranging widely from 28% to 100%. When used with hemodynamically unstable
patients with blunt abdominal trauma, FAST had a specificity higher than 95% and a sensitivity of 75%
for detecting hemoperitoneum. In hemodynamically stable patients with blunt abdominal trauma, FAST
had a similar specificity of 99%, but a much lower sensitivity of 41% for hemoperitoneum.1,7,8
FAST looks at 4 different anatomic locations: pelvic, hepatorenal recess, perisplenic space, and
subxiphoid (Figure 17-4).2 The right upper quadrant coronal and sagittal images provide a window into
the hepatorenal recess. The hepatorenal recess is the most dependent portion of the upper abdominal
cavity in the supine patient, and free intraperitoneal fluid around the liver or in the hepatorenal space
(Morison pouch) may be well-visualized here. A probe is placed in the right midaxillary line around the
11th to 12th intercostal rib. Free intraperitoneal fluid will be seen in the Morison pouch or along the tip of
the liver.2
The left upper quadrant sagittal section, or perisplenic region, looks for free intraperitoneal fluid around
the spleen, between the spleen and diaphragm, or between the spleen and left kidney. The probe is placed
in the left midaxillary line around the 11th to 12th intercostal rib.2
The pelvic location is the most dependent portion of the peritoneal space, and the focus of this view is to
look for free intraperitoneal fluid around the bladder. The probe is placed in the midline just cephalad to
the pubic symphysis. In men, free intraperitoneal fluid will be found along the posterior bladder wall,
whereas in women free fluid is most likely to be found in the pouch of Douglas (the space between the
uterus and bladder).2
Using the curvilinear probe in the subxiphoid position begins the transition to more extensive monitoring
with cardiac ultrasound and is particularly useful in ruling out cardiac tamponade. Free fluid will appear
as a hypoechoic black stripe between the pericardium and the atrial or ventricular wall. This sonographic
window is discussed in further detail in the TTE section of this chapter.2
Hemothorax. Assessment for the presence of hemothorax is easily performed with ultrasound. A chest
radiograph can identify as little as 200 mL of intrathoracic fluid, but ultrasound is able to identify as little
as 20 mL of intrathoracic fluid. From the traditional FAST views, the presence of intrathoracic fluid can
be rapidly identified. From either the hepatorenal or perisplenic views, the ultrasound probe is brought
cephalad and the diaphragm identified, whereby free intrathoracic fluid will be identified superior to the
diaphragm.
Figure 17-4. Schematic Anatomy of FAST.

Abbreviations: FAST, focused assessment with sonography in trauma; L, liver; K, kidney; RUQ, right upper quadrant; LUQ, left upper
quadrant; GB, gall bladder; IVC, inferior vena cava; D, duodenum; B, bladder; S, spleen; LAX, long axis; SAX, short axis; UT, uterus.
Reproduced with permission from Fagley RE, Haney MF, Beraud A-S, et al. Critical care basic ultrasound learning goals for American
anesthesiology critical care trainees: recommendations from an expert group. Anesth Analg. 2015;120:1041-1053.
Cardiogenic Shock
Bedside echocardiography may guide diagnostic and resuscitative efforts in shock. Although performing
and interpreting a complete echocardiographic examination requires extensive training, intensivists can
correctly identify normal and abnormal LV function with a high degree of certainty after relatively little
formal training. Information obtained from an intensivist’s echocardiogram changes management in up to
half of cases. This may include guiding fluid administration, use of vasoactive medications, and treatment
limitations. Protocol-driven focused echocardiographic examination, particularly TTE examination, can
improve patient care. This is especially true in the setting of cardiac tamponade, cardiac arrest, global
cardiac systolic dysfunction, and ventricular enlargement. Concurrent hemodynamic data analysis may
corroborate diagnoses of myocardial ischemia, cardiac tamponade, isolated RV dysfunction, pulmonary
hypertension, septic shock, or hypovolemia.9
Focused TTE examination is not meant to replace a comprehensive TTE study. Rather, focused TTE
allows quick serial assessments of hemodynamically unstable patients and their responses to
resuscitation. When transthoracic imaging is not adequate, TEE may provide better images. In the acute
setting, TEE is needed for adequate image acquisition only infrequently. When presented with uncertain
TTE and TEE findings, it is advisable to consult with an expert echocardiographer.2
LV and RV Systolic Function

In the assessment of systolic LV function, subjective estimation of LV contractility using TTE is as
accurate and reproducible as calculated measures of ejection fraction. Hypovolemic shock is associated
with decreased end-diastolic and end-systolic ventricular volumes, and when severe, LV cavity
obliteration. In distributive shock states, such as septic shock, impaired contractility can be observed with
or without LV dilatation. In cardiogenic shock, LV hypocontractility and dilatation are often present.
Regional Wall Motion Abnormalities

A more advanced technique for evaluating the patient in shock is to look for regional wall motion
abnormalities on bedside echocardiogram. A complete diagnostic evaluation for myocardial ischemia is
time consuming, and can be difficult owing to body habitus, positioning, dressing locations, or anatomic
variation in some patients. In emergency situations, however, an examination limited to a midpapillary
level short-axis view can identify myocardial regions supplied by each of the major coronary arteries and
may facilitate intervention. With this technique, the examiner is looking for both motion and thickening of
the myocardial wall. The normal myocardium increases in thickness and moves toward the center of
ventricular cavity during systole. Heavily damaged heart muscle can become akinetic or even move
paradoxically (“dyskinesis”). Although many conditions can cause decreased function, careful
observation can differentiate whether the impairment is global or regional. If the regional pattern
corresponds to the area supplied by a single coronary artery, then suspicion for acute coronary syndrome
should be high (Figure 17-5).
Figure 17-5. Coronary Artery Territorial Distribution

Abbreviations: LAD, left anterior descending coronary artery; RCA, right coronary artery.
The LAD, circumflex, and RCA supply specific and predictable areas of the heart. The LAD supplies a significant portion of the anterior and
septal myocardium. The circumflex supplies the anterolateral and inferolateral myocardium, and the RCA supplies the inferior and inferoseptal
myocardium. In periods of myocardial ischemia, various degrees of dysfunction can be appreciated in these regions.
To identify areas of myocardial injury, the practicing intensivist should understand the structured
evaluation and nomenclature of regional wall motion abnormalities (Figure 17-6). The system
recommended by the American Heart Association is the 17-region model, which includes 6 basal
segments assessed on the ventricular side of the mitral valve, 6 midventricular segments assessed at the
midpoint of the papillary muscles, 4 apical segments assessed between the papillary muscles and the
apex, and the apical cap (Figure 17-6). The scoring system awards values of 1 to 5 for each segment
evaluated: 1 is normal (>30% thickening), 2 is mildly hypokinetic (10% - 30% thickening), 3 is severely
hypokinetic (<10% thickening), 4 is akinetic (no appreciable thickening), and 5 is dyskinetic (paradoxical
motion during systole). The walls are named according to their anatomic position, and comprise the basal
and midpapillary anteroseptal, anterior, anterolateral, inferolateral, inferior, and inferoseptal walls. The
apical LV has anterior, lateral, inferior, and septal segments.10
Figure 17-6. Nomenclature for the 17-Segment Model for Regional Wall Motion
Abbreviations: A, anterior; AS, anteroseptal; IS, inferoseptal; I, inferior; IL, inferolateral; AL, anterolateral; S, septal; L, lateral.
The standard nomenclature for the various myocardial segments reflects the coronary arterial supply to the region. A, AS, and AL segments
are supplied by the left anterior descending coronary artery. AL, IL, and I segments are supplied by the circumflex artery. I and IS segments
are supplied by the right coronary artery. The apex receives blood supply from all 3 coronary arteries. The basal segments are those closest to
the mitral valve. The midcavity segments are on the same plane as the papillary muscles. The apical segments are closest to the apical cap of
the left ventricle, where it joins the right ventricle.
Regional wall motion can be evaluated from any view of the heart, but the parasternal views and apical
views offer a more clear delineation of regional blood supply. Acquiring a short-axis view of the heart is
described elsewhere in this chapter, but in this case the focus is shifted specifically to the ventricle of
concern, usually the LV. Figure 17-5 demonstrates the way in which typical blood supply to the LV is
divided. Because the LV contracts and thickens concentrically, it is usually easy to see if 1 region is not
functioning as well as the others. To evaluate the entire ventricle, however, one has to fan from the base to
apex.10 It is important to be mindful of how the other views of the heart intersect the coronary distribution
already described. By rotating the probe 90 degrees and acquiring a long-axis view, it becomes easier to
see inferolateral dysfunction in comparison to apical dysfunction, as might be present in a distal left
anterior descending coronary artery lesion. Acquiring an apical 4-chamber view is an alternative for
doing the same evaluation and often provides a clear view of the apex.
LV Diastolic Function
Assessment of LV diastolic function in the hemodynamically unstable patient can be estimated by
comparing the early diastolic maximal transmitral flow velocity (E) with the early diastolic tissue
velocity of the mitral valve annulus (e′). In an apical 4-chamber or midesophageal 4-chamber TEE view,
pulsed-wave Doppler may be used to measure the transmitral flow velocity, and tissue Doppler may be
used to measure the velocity of the mitral annulus. The e′ velocity is relatively independent of loading
conditions. An e′ velocity less than 8.6 cm/s is indicative of impaired ventricular relaxation, and the
velocity decreases with worsening diastolic dysfunction. The E/e′ ratio can be used to identify patients
with high filling pressures, because E/e′ ratios greater than 7 correlate well with a pulmonary capillary
wedge pressure greater than 13 mm Hg. Very high E/e′ ratios may be indicative of diastolic heart failure,
which could lead to cardiogenic shock.2
RV Function
RV function and RV pressures can also be qualitatively and quantitatively assessed using TTE. The
distance that the base of the anterior leaflet of the tricuspid valve travels throughout the cardiac cycle,
also called the “tricuspid annular planar systolic excursion distance,” provides a reliable estimate of RV
systolic function. The position of the base of the anterior tricuspid valve leaflet is marked at end-systole
and at end-diastole. The distance between the 2 points is measured. A tricuspid valve excursion distance
less than 16 mm indicates severe RV impairment. RV dilatation is defined as a diastolic area greater than
two-thirds the diastolic area of the LV (Figure 17-7), or greater than 42 mm in absolute basal diameter in
4-chamber views.11 Flattening or D-shaping of the interventricular septum, and akinesia of the mid–free
wall of the RV in combination with a normally functioning RV apex (McConnell sign) can also indicate
acute RV dysfunction caused by volume and/or pressure overload and may be present in acute right heart
syndromes, including pulmonary embolism.12,13
E X P E RT T I P
Bedside echocardiography and evaluation for regional wall motion abnormalities is a more
advanced technique. A complete diagnostic evaluation for myocardial ischemia is time
consuming and can be difficult owing to body habitus, positioning, dressing locations, or
anatomic variation in some patients. In emergency situations, an examination limited to a midpapillary
level short-axis view can identify myocardial regions supplied by each of the major coronary arteries and
may facilitate intervention.
Figure 17-7. RV Volume and Pressure Overload
With increases in RV afterload, the ventricle compensates by improving performance, as described by the Starling curve. However, with very
large or acute changes, the RV is unable to compensate. The resulting increase in pressure dilates the RV and pushes the interventricular
septum toward the LV cavity, resulting in a “D-shape.”
Pulmonary Arterial Systolic Pressure

Calculation of pulmonary artery systolic pressures may help confirm a diagnosis of RV failure, especially
when acute left heart failure or pulmonary embolism are suspected. The estimation of pulmonary artery
systolic pressures should be performed routinely in cases of tricuspid valvular regurgitation. Color
Doppler echocardiography is used to identify any tricuspid regurgitation. The tricuspid regurgitation jet
maximum velocity (Vmax) is recorded using continuous-wave Doppler. The pressure gradient (ΔP)
between the RA and the RV in systole is calculated using the modified, simplified Bernoulli equation: ΔP
= 4 × Vmax 2. ΔP is then added to the estimated right atrial mean pressure or CVP reading to estimate the
RV systolic pressure. In the absence of pulmonic valve pathology and/or severe tricuspid regurgitation,
this approach provides a good estimation of systolic pulmonary artery pressure.2,13
Figure 17-8. Aortic Stenosis

Abbreviations: RV, right ventricle; Ao, aorta; LV, left ventricle; AV, aortic valve; LA, left atrium; MV, mitral valve; AS, aortic stenosis.
As the leaflets and annulus of the aortic valve calcify or are otherwise limited in their opening, the velocity of blood flow increases. This
increase in velocity is reflected in an increase in flow acceleration as the blood approaches the stenotic choke point, and an increase in velocity
and appearance of turbulence as the blood exits the stenotic choke point.
Assessment of Severe Valvular Dysfunction

The level of detail in the assessment of valvular dysfunction should be determined by echocardiographic
operator experience and clinical context. Severe mitral or aortic stenosis, and severe acute mitral or
aortic regurgitation may all cause acute hemodynamic decompensation in the critically ill patient. Severe
valvular lesions can be identified by an intensivist.3 Common chronic valvular lesions may complicate
the course of the critically ill patient. TTE assessment of the aortic valve is accomplished using the
parasternal long-axis, parasternal short-axis, apical 5- and 3-chamber, and in some cases subxiphoid
aortic valve short-axis windows. When necessary, the TEE examination involves the midesophageal
aortic valve short-axis, midesophageal aortic valve long-axis, and deep transgastric views. TTE mitral
valve assessment is performed via the parasternal long-axis, parasternal short-axis (basal view), apical
4-chamber, and apical 2-chamber views. TEE interrogation of the mitral valve involves the 4-chamber,
commissural, 2-chamber, and aortic valve long-axis of the midesophageal views, and the transgastric
short-axis (basal) view.2
Aortic Stenosis. Aortic stenosis is detected in long- and short-axis views by identifying calcified left,
right, and/or noncoronary leaflets and restricted leaflet motion. Color flow Doppler will reveal turbulent
flow from the aortic valve into the proximal ascending aorta (Figure 17-8). Continuous-wave Doppler
velocity measurements, taken in the apical 5-chamber view by TTE or the deep transgastric view by TEE,
are necessary to confirm the diagnosis (Figure 17-9). Severe aortic stenosis is defined as peak aortic
velocities greater than 4 m/s, or a ratio of aortic valve-to-LVOT velocities greater than 4:1. In patients
with low cardiac output states, however, measured velocity across the aortic valve may underrepresent
the severity of aortic stenosis because of reduced aortic outflow.14
Figure 17-9. Continuous-Wave Doppler Tracing in Aortic Stenosis

The velocity of blood flow through a stenosed aortic valve (AV) increases significantly. The high-velocity wave, around 4 m/s, is the velocity
through the AV. Velocity through the left ventricular outflow tract (LVOT) is measured with pulsed-wave Doppler in the LVOT. An
AV/LVOT velocity ratio higher than 4:1 indicates severe aortic stenosis.
Figure 17-10. 2D Anatomy and Color Flow Doppler in Aortic Insufficiency
Abbreviations: 2D, 2-dimensional; AI, aortic insufficiency; RV, right ventricle; Ao, aorta; AV, aortic valve; LV, left ventricle; MV, mitral valve;
LA, left atrium.
In AI, a diastolic backflow of blood occurs from the ascending aorta back into the LV via the incompetent AV. Often the pathology is not
evident with 2D transthoracic echocardiography alone, but becomes more obvious with the use of color flow Doppler. Color flow is evident
across the AV in diastole, which begins with the T-wave of the electrocardiogram.
Aortic Insufficiency. Aortic insufficiency can be diagnosed using color flow Doppler (Figure 17-10) and
confirmed using continuous-wave Doppler (Figure 17-11). Moderate to severe aortic insufficiency can be
characterized by a vena contracta diameter greater than two-thirds of the LVOT diameter and
holodiastolic flow reversal in the aortic arch.15
Figure 17-11. Continuous-Wave Doppler in Aortic Insufficiency

Abbreviations: LVOT, left ventricular outflow tract; AV, aortic valve.
When aligned along the axis of the LVOT, the AV, and the ascending aorta, the velocity of blood flow through the incompetent portion of the
AV can be evaluated. The steeper the slope of the aortic insufficiency jet from its highest point in mechanical diastole (just after the T-wave on
the electrocardiogram) to its lowest point in mechanical diastole (just after the S-wave on the electrocardiogram), the more severe the aortic
insufficiency.
Mitral Stenosis. Mitral stenosis may be suspected by calcification or thickening of the mitral valve
leaflets that restrict mitral leaflet excursion (Figure 17-12). The severity of mitral stenosis can be
quantified using continuous-wave Doppler to determine the transmitral velocity and measuring the area
under the VTI curve to determine the mean pressure gradient. A mean transmitral diastolic gradient
greater than 10 mm Hg is indicative of severe mitral stenosis.
Figure 17-12. Color Flow Doppler in Mitral Stenosis

Abbreviations: MV, mitral valve; LV, left ventricle; RV, right ventricle; RA, right atrium; LA, left atrium.
In severe mitral stenosis, color flow Doppler reveals flow acceleration in the diastolic phase of the cardiac cycle as blood in the LA converges
toward the stenotic MV. The larger the area of flow acceleration, the more severe the patient’s stenotic lesion.
Figure 17-13. Mitral Regurgitation

Abbreviations: LV, left ventricle; MV, mitral valve; RV, right ventricle; RA, right atrium; AV, aortic valve; LA, left atrium; Ao, aorta; MR, mitral
regurgitation.
In severe MR, flow acceleration is found on the LV side of the MV throughout systole. In addition, turbulence on the LA side of the MV is
evident. The MR jet may be central, anteriorly directed in cases of anterior leaflet prolapse or posterior leaflet restriction, or posteriorly
directed in cases of posterior leaflet prolapse or anterior leaflet restriction.
Mitral Regurgitation. Mitral regurgitation or insufficiency is assessed by evaluating anterior and posterior
leaflet coaptation and by using color flow Doppler to determine the size, shape, and directionality of the
regurgitant jet (Figure 17-13). It is important to keep in mind that the severity of mitral regurgitation is
affected by LV afterload, which can vary depending on positive pressure mechanical ventilation, positive
or negative inotropic support, vasopressors, or vasodilators. Cardiogenic shock resulting from severe
acute mitral regurgitation is usually caused by papillary muscle rupture, trauma, or endocarditis. Color
flow Doppler is a simple means to visualize systolic regurgitation into the left atrium. Complicated mitral
valve lesions should prompt consultation with a subspecialist echocardiographer.16
Tricuspid Regurgitation. Severe tricuspid regurgitation is an unusual cause of cardiogenic shock. It should
be suspected in scenarios in which systemic perfusion is poor but there are signs of venous hypertension
(eg, hepatic congestion, peripheral edema, and jugular venous distension). Tricuspid regurgitation can be
qualitatively described as severe when the regurgitant jet occupies more than two-thirds the area of the
RA (Figure 17-14).16
Echocardiographic Evaluation During Cardiopulmonary Arrest

During cardiac arrest and in the periarrest period, echocardiography can rapidly provide a large quantity
of critical information that is easier to interpret and more reliable than indirect measures. Examples
include direct visualization of pericardial fluid as a sign of tamponade, and the combination of acute right
ventricular dilatation and the McConnell sign for pulmonary embolism. In both scenarios, TTE may more
rapidly facilitate therapeutic decision making.
The first step in echocardiographic evaluation during cardiac arrest is to compare the rhythm seen on the
electrocardiogram to the ventricular contraction pattern visualized, and the presence or absence of a
palpable pulse: asystole vs. pulseless electrical activity vs. pseudo–pulseless electrical activity
(ventricular electrical and mechanical activity which generates no pulse). The next step is to assess for
the cause of arrest, paying particular attention to evidence of conditions such as cardiac tamponade,
pulmonary embolism, pneumothorax, or aortic dissection. Upon return of spontaneous circulation, a more
complete examination can further explore potential causes of ongoing shock or arrest. Valvular
abnormalities causing arrest would likely be catastrophically severe (see the “Assessment of Severe
Valvular Dysfunction” section, discussed earlier). Acute mitral regurgitation from a papillary muscle
rupture or acute mitral regurgitation and aortic regurgitation from endocarditis could result in profound
shock or cardiac arrest. Severe aortic and mitral stenosis may be rare causes of primary arrest, but they
may prolong arrest or shock states that occur for nonvalvular reasons. After the return of spontaneous
circulation, the ascending and descending aorta should be examined again with TTE or TEE for aortic
dissection. LV and RV dysfunction after return to spontaneous circulation may represent the primary
inciting event or postarrest or posthypoxic myocardial stunning. Echocardiographic findings suggestive of
acute pulmonary embolism as a cause of circulatory collapse include acute RV dysfunction (TTE and
TEE) and clot in the main and right pulmonary artery (TEE).17,18
Figure 17-14. 2D Anatomy and Color Flow Doppler Findings in Tricuspid Regurgitation
Abbreviations: 2D, 2-dimensional; LV, left ventricle; RV, right ventricle; TV, tricuspid valve; LA, left atrium; RA, right atrium; TR, tricuspid
regurgitation.
In severe TR, color flow Doppler reveals flow acceleration in systole as blood converges toward the regurgitant TV. Turbulence is also noted
in the RA.
Hypertrophic obstructive cardiomyopathy and systolic anterior motion of the mitral valve are uncommon
but potentially treatable causes of circulatory collapse. Aortic outflow obstruction or turbulent
subvalvular flow can be generated in patients with small hypertrophic LV who are hypovolemic and/or
tachycardic, and may be assessed by a high continuous-wave Doppler gradient in the LVOT. These high
systolic flow velocities can lead to motion of the anterior mitral leaflet into the aortic outflow tract
(systolic anterior motion), resulting in subaortic obstruction and severe mitral regurgitation. With
correction of hypovolemia, discontinuation of inotropic agents, and increased afterload, this dynamic and
functional systolic outflow obstruction decreases, and can be observed using continuous-wave Doppler in
long-axis views through the LVOT.2
One of the limitations of ultrasound assessment during cardiac arrest is the challenge of imaging the heart
and lungs during chest compressions. Neither TTE nor TEE should interfere with ongoing advanced
cardiovascular life support. However, the use of TEE allows fewer and shorter interruptions in
cardiopulmonary resuscitation and should probably be the primary echocardiographic choice when
equipment is available and a secure airway is otherwise indicated. Echocardiographic evaluation of
circulatory arrest is appropriate as a diagnostic adjunct when treating any patient who has
cardiopulmonary arrest.2
C AVE AT
One of the limitations of ultrasound assessment during cardiac arrest is the challenge of imaging
the heart and lungs during chest compressions. Neither TTE nor TEE should interfere with
ongoing advanced cardiovascular life support.
Cardiac Function in Septic Shock

Myocardial depression with sepsis peaks within the first few days and resolves in survivors by 7 to 10
days. Unlike classic cardiogenic shock, it is associated with low or normal filling pressures. Septic
cardiomyopathy occurs in the majority of patients with septic shock during the first 3 days, with most
cases occurring in the first 48 hours. Often, sepsis-induced decreases in afterload can mask myocardial
dysfunction until administration of vasoconstrictive agents “exposes” a poorly contracting ventricle.
Serial assessments of myocardial function are necessary because myocardial dysfunction can change
rapidly in the early phases of septic shock. The relationship between ventricular function during sepsis
(hyperkinetic or hypokinetic) and survival is not yet clear. Because the ventricular dysfunction of sepsis
affects both left and right ventricles, changes in chamber volumes and pressures should be closely
monitored when trying to establish optimal preload.19
Obstructive Shock
Ultrasound examination for obstructive shock focuses on the specific diagnoses being considered.
Primarily, this involves a search for tension pneumothorax, tamponade, and pulmonary embolism.
Pneumothorax
Bedside ultrasound for pneumothorax is well studied and has been shown to be more sensitive and
specific than supine chest radiography in the trauma population, using chest computed tomography as the
gold standard. The initial examination is based on the presence or absence of lung sliding. This test for
lung sliding and lung point may be performed with any ultrasound probe, but we find that the linear high-
frequency probe is the optimal choice. Lung sliding is an artifact created by normal interface between the
parietal and visceral lung pleura, which disappears when air disrupts that interface. It has high sensitivity,
but low specificity for pneumothorax, because several other conditions, including pleurodesis, acute
respiratory distress syndrome, scarring, and other inflammatory pleuritides can interfere with lung sliding.
In M-mode, normal lung sliding will create a “seashore” image, whereas the absence will create a
“stratosphere” or “bar code” sign. Another sign of importance in the diagnosis of pneumothorax is the
“lung point,” which is defined as a single segment of pleura which changes between the “sliding” and
“nonsliding” appearance with respiration. Although lacking sensitivity, it is considered highly specific for
pneumothorax.20
E X P E RT T I P
To identify a pneumothorax using the lung point sign, the probe is advanced inferiorly space by
space until lung sliding has reappeared.
The image is acquired by applying the probe to the intercostal space with the indicator dot oriented
cranially, creating an image with 2 ribs and the lung space between them. The next step is visualizing the
bright parietal pleural line and the sliding visceral pleura just below. If pneumothorax is indeed present, it
is generally found in the superior portion of the thorax. To identify the lung point sign, the probe is
advanced inferiorly space by space until lung sliding has reappeared.
Pulmonary Embolism and Deep Venous Thrombosis

The ultrasound examination for pulmonary embolism is a topic of debate. The main areas of interest are
the heart and the deep veins. The main finding of increased RV/LV end-diastolic area ratio is more
accurately a sign of RV volume or pressure overload, and so is present in multiple pathological
conditions other than pulmonary embolism. As a result, it is not sufficiently specific to be pathognomonic.
Potentially, serial cardiac examinations showing a sudden change in RV/LV ratio would be of great
interest, but has not yet been demonstrated in a clinical trial.
Ultrasound assessment of the deep veins for thrombosis, however, is a well-established modality. The
highest performance is achieved using a “duplex” modality combining B-mode and Doppler imaging. At
the bedside, however, several studies have demonstrated the usefulness of a compression-only ultrasound
at a limited number of points for the detection of deep vein thrombosis, with exceptional test performance.
Several emergency medicine studies found excellent performance with a 2-point examination involving
only the femoral and popliteal veins, but studies in ICU patients have shown limited sensitivity with 2-
rather than at least 3-point compression examinations.21
The compression examination is performed by locating the femoral vein in cross-section in the inguinal
fossa, and applying pressure until the femoral artery has started to deform. If the vein has completely
collapsed then the study result is negative. Otherwise it is considered a positive finding, even if
echogenic material is not directly visualized in the lumen. This compression is repeated at the branch
point of the deep and superficial femoral veins, and then again at the popliteal fossa (Figure 17-15).
Drawing conclusions from this study can be challenging in the critically ill patient, because historically
20% to 40% of patients with pulmonary embolism do not have deep vein thrombosis at the time of
diagnosis of pulmonary embolism. Similarly, many patients with deep vein thrombosis do not have
pulmonary embolism. Still, in the absence of other explanations for hypotension, it does provide a
justification for therapy or further imaging.
Figure 17-15. Abnormal Femoral Arterial and Venous Ultrasound

When pulmonary embolism is suspected as a cause for obstructive shock with right ventricular failure, examination for deep venous thrombosis
is warranted. The probe is placed caudally to the inguinal ligament, in the inguinal fossa, and the FA and FV are visualized in cross-section.
Pressure adequate to compress the FA is placed using the ultrasound probe, and the FV is examined for compression. If the FV is not
compressible, then thrombus should be suspected.
Figure 17-16. 2D Echocardiogram of Pericardial Effusion Via Subxiphoid Sonographic Window

Abbreviations: 2D, two-dimensional; RV, right ventricle; RA, right atrium; LV, left ventricle; Ao, aorta.
In the presence of pericardial effusion, a large echolucent area separates the heart from the pericardial sac. If the effusion is large enough, it
can obstruct venous inflow by causing dynamic RA and RV compression.
Cardiac Tamponade
Pericardial fluid is quickly and easily visible on ultrasound from several different cardiac windows
(Figure 17-16) using either TTE or TEE. Emergency physicians were able to demonstrate pericardial
effusion with a sensitivity of 96% and specificity of 98% in emergency department patients at risk for
effusion.22 Techniques for acquiring the standard point-of-care views of the heart were described
previously, and all are useful for evaluating a pericardial effusion. Defining an effusion as indicative of
tamponade, however, is more complex. Several findings such as RA collapse, which occurs at a lower
pressure than RV collapse, suggest elevated pressures in the pericardial effusion, but the sensitivity and
specificity of these findings vary widely from study to study. As such, only the absence of a pericardial
effusion can truly rule out cardiac tamponade as a cause of shock.23
IVC imaging has been described previously, and the list of potential causes for an incompressible IVC
includes obstructive shock states, RV failure, LV failure, atrial septal defect, partial anomalous pulmonary
venous return, and tricuspid regurgitation. Technical imaging of the IVC is as described before, and IVC
distention has been described as the most sensitive (97%) albeit least specific (40%) echocardiographic
sign of cardiac tamponade, because any cause of right heart volume overload is a potential confounder. 24
Distributive Shock
Sepsis
As the most common form of shock, septic shock is discussed independently in Chapter 21. Given a
history and presentation compatible with infection and systemic inflammatory response syndrome, certain
findings are typical of septic shock on ultrasound. As stated before, cardiac and vascular examinations
give indications of absolute or relative hypovolemia with collapsible IVC and effacement of the left
ventricular cavity during systole. This is also supportive, though not diagnostic, of the decreased afterload
typical of distributive and vasodilatory shock.19 Pleural ultrasound examination can support volume status
findings with the presence or absence of B-lines. However, these findings may vary in the setting of
sepsis-related cardiomyopathy, where wall motion will be decreased and noncardiogenic pulmonary
edema can lead to a preponderance of B-lines.
Specific to sepsis, ultrasound can assist in diagnosis and source control. Examination of the abdomen for
cholecystitis, ascites, pyelonephritis, or abscess is possible, as is pleural examination for empyema and
pneumonia. Serial ultrasound examination can guide fluid, vasopressor, and inotrope management.25
Neurogenic Shock
The shock resulting from central nervous system injury has a broad range of hemodynamic implications.
Conventional wisdom points to presenting signs of bradycardia, hypotension, and hypothermia. In the
setting of spinal canal hemorrhage, trauma, or epidural abscess, these derangements are possible in
varying degrees, typically related to the level of the injury. In the case of trauma, there typically is a
coexisting hemorrhagic component to the shock. A primary differentiator is the presence of stereotypical
neurologic deficits.
Cardiac ultrasonography generally reveals sinus bradycardia with signs of decreased afterload and
effacement of the LV cavity in systole. Bradycardia is relative and is more pronounced with involvement
of the cardiac accelerator fibers high in the thoracic spinal cord. The LV appears hyperdynamic with
generally preserved diastolic function. These findings are typical for the acute phase of neurogenic shock.
Ultrasound is also useful in serial examinations with the addition of phenylephrine to determine if the
shock is purely distributive or if there is also a cardiogenic component. This is particularly important
because of the frequent need for vasopressor support to improve spinal cord perfusion pressure in the
interest of minimizing neurologic damage.26
E X P E RT T I P
Not all dilated IVCs are created equal. The differential diagnosis for an incompressible IVC
includes obstructive shock states, RV failure, LV failure, atrial septal defect, partial anomalous
pulmonary venous return, and tricuspid regurgitation in addition to volume overload.
KEY POINTS
Ultrasound is becoming increasingly important in the differential diagnosis of shock. The modality
allows for rapid diagnosis of life-threatening causes of shock.
Shock may be classified as hypovolemic, cardiogenic, obstructive, or distributive.
Serial monitoring of ultrasound examinations allows physicians to tailor therapy to a patient’s
needs on a moment-to-moment time scale.
IVC examination and cardiac examination are more reliable and useful measures of intravascular
volume status than many invasive tools.
Causes of cardiogenic shock may be myocardial, valvular, or obstructive in nature. Rapid
assessment of global ventricular function, regional wall motion, valvular structure and function, and
pulmonary artery systolic pressure help narrow the differential diagnosis in cardiogenic shock.
Obstructive shock can be caused by tension pneumothorax or hemothorax, deep venous thrombosis
with pulmonary embolism, or cardiac tamponade, all of which are diagnoses amenable to
identification by ultrasound.
Hallmarks of distributive shock include low systemic vascular resistance and complete LV cavity
effacement in systole. Examples of distributive shock include sepsis and neurogenic shock.
REFERENCES
1. Hsu JM, Joseph AP, Tarlinton LJ, et al. The accuracy of focused assessment with sonography in trauma (FAST) in blunt trauma patients:
experience of an Australian major trauma service. Injury. 2007;38:71-75.
2. Fagley RE, Haney MF, Beraud A-S, et al. Critical care basic ultrasound learning goals for American anesthesiology critical care trainees:
recommendations from an expert group. Anesth Analg. 2015;120:1041-1053.
3. Mayo P. Training in critical care echocardiography. Ann Intensive Care. 2011;1:36.
4. Marik PE, Cavallazzi R. Does the central venous pressure predict fluid responsiveness? An updated meta-analysis and a plea for some
common sense. Crit Care Med. 2013;41:1774-1781.
5. Marik PE, Monnet X, Teboul J-L. Hemodynamic parameters to guide fluid therapy. Ann Intensive Care. 2011;1:1-9.
6. Feissel M, Michard F, Mangin I, et al. Respiratory changes in aortic blood velocity as an indicator of fluid responsiveness in ventilated
7. Muller L, Bobbia X, Toumi M, et al; the AzuRea group. Respiratory variations of inferior vena cava diameter to predict fluid
responsiveness in spontaneously breathing patients with acute circulatory failure: need for a cautious use. Crit Care. 2012;16:R188.
8. Becker A, Lin G, McKenney MG, Marttos A, Schulman CI. Is the FAST exam reliable in severely injured patients? Injury. 2010;41:479-
483.
9. Jensen MB, Sloth E, Larsen KM, et al. Transthoracic echocardiography for cardiopulmonary monitoring in intensive care. Eur J
Anaesthesiol. 2004;21:700-707.
10. Cerquiera MD, Weissman NJ, Dilsizian V, et al. Standardized myocardial segmentation and nomenclature for tomographic imaging of the
heart. Circulation. 2002;105:539-542.
11. Ghio S, Recusani F, Klersy C, et al. Prognostic usefulness of the tricuspid annular plane systolic excursion in patients with congestive heart
failure secondary to idiopathic or ischemic dilated cardiomyopathy. Am J Cardiol. 2000;85:837- 842.
12. Lau G, Ther G, Swanvelder J. McConnell’s sign in acute pulmonary embolism. Anesth Analg. 2013;116:982-985.
13. Mansencal N, Joseph T, Vieillard-Baron A, et al. Comparison of different echocardiographic indexes secondary to right ventricular
obstruction in acute pulmonary embolism. Am J Cardiol. 2003;92:116-119.
14. Baumgartner H, Hung J, Bermejo J, et al. Echocardiographic assessment of valve stenosis: EAE/ASE recommendations for clinical
practice. Eur J Echocardiogr. 2009;10:1-25.
15. 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). Eur J Echocardiogr. 2010;11:223-244.
16. Lancellotti P, Moura L, Pierard LA, et al; European Association of Echocardiography. European Association of Echocardiography
recommendations for the assessment of valvular regurgitation. Part 2: mitral and tricuspid regurgitation (native valve disease). Eur J
17. Labovitz AJ, Noble VE, Bierig M, et al. Focused cardiac ultrasound in the emergent setting: A consensus statement of the American
Society of Echocardiography and American College of Emergency Physicians. J Am Soc Echocardiogr. 2010;23:1225-1230.
18. van der Wouw PA, Koster RW, Delemarre BJ, et al. Diagnostic accuracy of transesophageal echocardiography during cardiopulmonary
resuscitation. J Am Coll Cardiol. 1997;30:780-783.
19. Griffee MJ, Merkel MJ, Wei KS. The role of echocardiography in hemodynamic assessment of septic shock. Crit Care Clin. 2010;26:365-
382.
20. Ding W, Shen Y, Yang J, et al. Diagnosis of pneumothorax by radiography and ultrasonography: a meta-analysis. Chest. 2011;140:859-866.
21. Kory PD, Pellecchia CM, Shiloh AL, et al. Accuracy of ultrasonography performed by critical care physicians for the diagnosis of DVT.
Chest. 2011;139:538-542.
22. Mandavia DP, Hoffner RJ, Mahaney K, et al. Bedside echocardiography by emergency physicians. Ann Emerg Med. 2001;38:377-382.
23. Imazio M, Adler Y. Management of pericardial effusion. Eur Heart J. 2013;34:1186-1197.
24. Himelman RB, Kircher B, Rockey DC, et al. Inferior vena cava plethora with blunted respiratory response: a sensitive echocardiographic
sign of cardiac tamponade. J Am Coll Cardiol. 1988;12:1470-1477.
25. Lichtenstein DA, Meziere GA. Relevance of lung ultrasound in the diagnosis of acute respiratory failure: the BLUE protocol. Chest.
2008;134:117-125.
26. Summers RL, Baker SD, Sterling SA, et al. Characterization of the spectrum of hemodynamic profiles in trauma patients with acute
neurogenic shock. J Crit Care. 2013;28:531-e1.
Chapter 18
Respiratory Failure
Jan Kasal, MD; Chakradhar Venkata, MD
OBJECTIVES
Review the lung ultrasound scanning protocol and basic patterns
Outline the role of lung ultrasound and echocardiography in a protocol for patients with respiratory failure
Review the use of lung ultrasound and echocardiography in mechanically ventilated patients, including
assessment of lung recruitment, liberation from mechanical ventilation, evaluation of the diaphragm, and
detection of acute cor pulmonale complicating acute respiratory distress syndrome
INTRODUCTION
Clinical studies have established the role of lung ultrasound (LUS) for multiple pathological conditions,
such as cardiogenic pulmonary edema, acute respiratory distress syndrome (ARDS), pneumonia, pleural
effusion, and atelectasis. In this chapter, we will review the current understanding of LUS alone and in
conjunction with echocardiography as a diagnostic mode in patients with undifferentiated acute
respiratory failure. LUS can be used to monitor for increased extravascular lung water. In addition to
diagnosing pulmonary edema, it may also guide volume expansion (or the initiation of diuresis). In
patients undergoing mechanical ventilation, LUS can be used to evaluate lung recruitment, manage
difficult-to-wean patients, predict successful extubation, evaluate diaphragm function, and assess the
effect of increased airway pressures on right heart function. Although many recent clinical studies of LUS
have been undertaken, studies of its impact on patient outcomes are still needed. As with any monitoring
device, LUS will only be successful if it is paired with treatment that improves outcomes.
CASE STUDY
A 43-year-old woman with no significant medical history is admitted with respiratory distress. She had a
recent febrile illness and diarrhea. Oxygenation was stabilized initially with a fraction of inspired oxygen
of 0.5. A central line was placed in the right internal jugular vein, but she is now deteriorating. A LUS
obtained on arrival in the ICU shows bilateral confluent anterior B-lines with sliding and posterior
consolidations. The diagnosis of pneumonia with ARDS is made; pneumothorax is ruled out.
The patient continues to deteriorate and is intubated. A repeat chest radiograph reveals diffuse infiltrates.
Positive end-expiratory pressure (PEEP) is initially set at 8 cm H2O but fails to improve her oxygenation,
despite a fraction of inspired oxygen of 1.0. LUS continues to demonstrate bilateral anterior B-lines while
lateral consolidations are unchanged. PEEP is increased stepwise to 18 cm H2O. At this level of PEEP,
B-lines are replaced by A-lines in anterior lung zones. Her arterial blood pressure decreases.
Echocardiography shows normal ejection fraction (EF) and a moderately dilated right ventricle with
septal dyskinesia. Crystalloids and norepinephrine are administered. Further attempts to recruit the lungs
are stopped. The patient continues to receive lung protective ventilation and is placed in a prone position;
the PEEP level is reduced.
Her clinical course is protracted. Results of a workup are positive for Legionella pneumophila. The
patient eventually improves sufficiently to consider pressure support trials, which are started on day 12.
However, she repeatedly fails spontaneous breathing trials, and lung infiltrates are somewhat more
prominent, diffusely. Repeat echocardiography shows an EF of 45%; Doppler data estimate E/e′ (early
diastolic transmitral E to tissue Doppler e′) of 18. Diuresis is intensified. Infiltrates improve but rapid
shallow breathing continues during spontaneous breathing trials. She has diffuse weakness on
examination. Minimal diaphragmatic excursions are seen on ultrasound. Tracheostomy is performed 2
weeks after presentation. Following a prolonged stay in a long-term acute care hospital, the patient
eventually recovers to functional independence.
How Was LUS Useful in This Case?

LUS proved useful for the management of this critically ill woman experiencing respiratory failure. The
intensivist made an initial diagnosis of pneumonia with ARDS while ruling out iatrogenic pneumothorax,
all before performing chest radiography. Subsequently, the intensivist used LUS to help guide PEEP
titration and, when the patient became hypotensive, to diagnose ACP. Later, LUS was important for
evaluating weaning-induced pulmonary edema and assessing diaphragmatic weakness. This case
illustrates a common use of LUS in respiratory failure.
SCANNING PROTOCOL AND BASIC FINDINGS

LUS is conventionally performed in 8 anterior-lateral areas,1 using the anterior and posterior axillary line
as landmarks, further divided into superior and inferior regions. The examination can be extended more
dorsally to visualize possible consolidations or pleural effusions (Figure 18-1). Thus, 12 zones are
sometimes used (eg, in calculation of the re-aeration score).2 The choice of probe depends on the target
and depth of scanning, equipment availability, and patient body habitus. High-frequency linear probes
have high resolution but low penetration, and so are useful for pleural examination and in patients with
thin chest walls. Phased-array probes have lower resolution but deeper penetration and are useful for
examination for consolidation and, in obese patients, pleural effusion. Where available, a microconvex
probe has a narrower footprint and wider frequency range, useful for both superficial and deep disease
processes. During lung scanning, fundamental frequency imaging is preferred; harmonic imaging may need
to be turned off, because it is the default setting in most machines. LUS relies both on direct imaging of
lung tissue (if the lung is consolidated and conducts ultrasound waves well) or, indirectly, on
interpretation of various artifacts (if the lung is aerated).
Figure 18-1. Lung Zones
A) 4-zone examination. B) 8-zone examination is standard. C) 12-zone examination is particularly useful when evaluating for posterior
consolidations and pleural effusions.
Normal Finding
A normally aerated lung does not transmit ultrasound waves. A-lines are caused by reverberation artifact
originating at the pleural line, and are seen horizontally spaced from the pleura in regular intervals. Lung
sliding, or movement of parietal against visceral pleura, is seen on 2-dimensional (2D) mode and on M-
mode (the “seashore sign”).
Pneumothorax
Lung sliding rules out pneumothorax at the examination site. Absent lung sliding can be seen on 2D; M-
mode shows the stratosphere (or “barcode”) sign. Absent sliding is not specific for pneumothorax.
Pleural adhesions, right mainstem intubation, atelectasis, high-frequency oscillatory ventilation, apnea,
and esophageal ventilation all have absent sliding. In ARDS, lung excursion may be subtle. Lung point
sign convincingly rules in pneumothorax.
Pleural Effusion
Pleural effusion is seen as anechoic space, though effusions with exudate (eg, empyema) or blood may be
echogenic.
Consolidation
Consolidation produces a loss of lung aeration. Therefore, consolidated lung tissue conducts ultrasound
waves and subsequently becomes visible, with a tissue-like appearance. Air bronchograms may be seen
within the consolidation, appearing as hyperechoic punctate images. Movement of gas within the
hyperechoic punctate images, the dynamic air bronchogram,3 helps to differentiate resorptive atelectasis
from the consolidation seen in pneumonia. Consolidation may form at any place and is often located at the
so-called posterolateral alveolar or pleural syndrome (PLAPS) point, at the posterior axillary line above
the diaphragm. Specific diseases causing consolidation include atelectasis, contusion, and pneumonia.
Pulmonary embolism (subpleural infarcts) and cancer can form a similar pattern.
B-Lines
Increased extravascular lung water extending to the periphery of the lung will produce B-lines. These are
artifacts thought to arise from the ultrasound beam reverberating from edematous interlobular septa and
alveoli.4 B-lines originate from the pleural surface, move during respiration, extend to the bottom of the
screen without fading, and erase A-lines. If the B-lines are diffuse (several positive regions on both sides
of the diaphragm), cardiogenic or noncardiogenic pulmonary edema should be considered, and much less
commonly, interstitial pneumonias. In moderate edema, well-separated B-lines are seen; in severe edema,
they are coalescent B-lines. If the B-lines are focal, pneumonia is more likely. (For more detailed pattern
descriptions, refer to Chapter 10.)
DIAGNOSTIC PROTOCOLS IN RESPIRATORY FAILURE

A patient experiencing respiratory distress is in a medical emergency demanding rapid and accurate
diagnosis. The differential diagnosis can be narrowed by following a standardized LUS protocol. LUS in
patients with respiratory failure can be classified further using protocols for undifferentiated respiratory
failure and for heart failure. We will review the rationale and method for each, followed by evidence
supporting its use.
Undifferentiated Respiratory Failure: BLUE Protocol

The bedside lung ultrasound in emergency (BLUE) protocol was retrospectively applied to causes of
dyspnea in 301 patients with respiratory failure.5 Specific ultrasound profiles were considered diagnostic
of pulmonary edema, chronic obstructive pulmonary disease (COPD)/asthma, pulmonary embolism,
pneumothorax, and pneumonia.
Method
The chest should be scanned bilaterally, in specific BLUE “points” (Figure 18-2), 3 on each side of chest.
Both of the examiner’s hands are placed next to each other on the chest, with the fingertips pointing
toward the sternum, and the upper hand touching the clavicle. The upper point is in the middle of the
upper hand. The lower point is in the middle of the lower palm. The PLAPS point is at the intersection of
a horizontal line at the level of the lower BLUE point and a vertical line at the posterior axillary line. A
specific clinical diagnosis is then assigned based on an LUS profile (Figure 18-3).
Figure 18-2. Bedside Lung Ultrasound in Emergency (BLUE) Points

Figure 18-3. Bedside Lung Ultrasound in Emergency (BLUE) Profiles
Abbreviations: COPD, chronic obstructive pulmonary disease; ARDS, acute respiratory distress syndrome; DVT, deep vein thrombosis;
PLAPS, posterolateral alveolar or pleural syndrome.
A-lines, B-lines, and consolidations are assessed at specific BLUE points. Sliding helps to differentiate between A and A′ profiles, B and B′
profiles. Lung point and examination for DVT further assist in establishing the diagnosis
The assignments of BLUE profiles and clinical diagnoses are as follows:
Pulmonary edema: B profile (anterior predominant bilateral B-lines with sliding)

COPD/asthma: Normal A profile (anterior predominant bilateral A-lines, with sliding)
Pulmonary embolism: A profile with deep vein thrombosis (DVT)
Pneumothorax: A′ profile (anterior bilateral A-lines, absent sliding), with lung point
Pneumonia (if any of these 4 profiles is present): B′ profile (bilateral B-lines with absent sliding), A/B
profile (predominant B-lines on 1 side, A-lines on other side of chest), C profile (anterior
consolidation), and PLAPS
As the initial major step, the sonographer should evaluate for lung sliding. A patient with bilateral A-lines
(A profile) without consolidation would most likely have COPD/asthma. However, occasionally a
pneumothorax or pulmonary embolism could be missed. Therefore, when encountering an A profile in a
patient with dyspnea, the sonographer should always carefully evaluate for the absence of lung
sliding/presence of lung point to exclude pneumothorax. This pattern of bilateral A-lines without lung
sliding is the A′ profile. In a patient with the A profile, deep veins are scanned for DVT to assess the
probability of pulmonary embolism. As the second major step, the sonographer determines whether B-
lines are present (in practice, sliding will be evaluated simultaneously while examining for either B- or
A-lines). If B-lines are present, it is important to know whether these are distributed unilaterally or
bilaterally (ie, on either or both sides of the chest). The patient in the case study had bilateral B-lines (B
profile) with lung sliding, indicating pulmonary edema/ARDS. On the other hand, a patient with unilateral
B-lines (A/B profile) would be diagnosed with pneumonia. Even without the presence of B-lines (A
profile), the patient still could have pneumonia if there are consolidations anteriorly (C profile) or at the
PLAPS point.
This profile approach does not take into account several other pathologies such as interstitial lung
diseases. In addition, diseases may overlap (eg, pneumonia can coexist with ARDS) and may thus be
difficult to differentiate.
Evidence
Several LUS protocols for evaluating patients with respiratory failure have been published.5-7 These
studies suggested that the results of LUS are accurate and, in some cases, led to reclassifying the clinical
diagnosis. However, no studies directly evaluated the impact of LUS on patient outcomes.
In the retrospective analysis, the BLUE ultrasound diagnosis was accurate in 90.5% of patients. The B
profile was 97% sensitive and 95% specific for pulmonary edema. The A profile without DVT was 89%
sensitive and 97% specific for asthma/COPD. The A profile with DVT was 81% sensitive and 99%
specific for pulmonary embolism. The A′ profile was 88% sensitive and 100% specific for
pneumothorax. The B′ profile, A/B profile, C profile, and PLAPS were overall 94% specific and 89%
sensitive for pneumonia if any of the 4 profiles were present; the individual sensitivities were much
lower. However, the diagnostic standard was based on a chart review using unspecified “standardized
methods” interstitial lung diseases and similar conditions were excluded.
Subsequent studies using BLUE demonstrated acceptable accuracy albeit lower than in the original report.
In a prospective study of 78 ICU patients, LUS combined with echocardiography yielded 83% diagnostic
accuracy compared with the clinical diagnosis.8 Another study prospectively evaluated the clinical
impact of LUS on decision making in 189 patients undergoing mechanical ventilation9 and showed a
change in management in 47% of cases. Another study also found lower accuracy (cardiogenic edema,
65%; pneumonia, 66%; pulmonary embolism, 38%; pneumothorax, 58%), although adding
echocardiography increased the diagnostic accuracy.10
Combined Echocardiography and LUS in Respiratory Failure

Diffuse B-lines may be seen in cardiogenic pulmonary edema, but also in ARDS and less common
conditions such as interstitial pneumonia. Echocardiography can further differentiate among these
conditions.
Method
One possible approach to respiratory failure uses both LUS and echocardiography. Patients may be
evaluated initially according to concepts introduced in the BLUE protocol. When diffuse B-lines are
found (such as in the patient in our case study), echocardiography and additional LUS may further
differentiate cardiogenic pulmonary edema from ARDS and other causes of diffuse interstitial syndrome
(Figure 18-4). For example, a patient with left ventricular (LV) systolic or diastolic dysfunction or
plethoric inferior vena cava would be more likely to have cardiogenic pulmonary edema.
Echocardiography not only establishes the presence of cardiogenic pulmonary edema, but it also can
clarify the mechanism of cardiac dysfunction (eg, systolic, diastolic, or valvular dysfunction). On the
other hand, in the patient with normal echocardio-graphic findings, the diagnosis of ARDS is more likely,
especially if LUS shows an irregular pleural surface, spared areas, or subpleural consolidations. (A
detailed description of echocardiographic techniques for evaluating systolic and diastolic function and
LUS techniques for ARDS can be found in Chapter 8 and Chapter 10.) Evidence of the impact of such an
approach on patient-centered outcomes is limited, nuances in approaches may vary, and more information
will likely be forthcoming in the future.
Figure 18-4. Combining Lung Ultrasound and Echocardiography in Respiratory Failure

Abbreviations: LV, left ventricle; IVC, inferior vena cava; ARDS, acute respiratory distress syndrome.
If diffuse B-lines are found on lung ultrasound, echocardiography and detailed lung ultrasound can help to differentiate cardiogenic pulmonary
edema from ARDS. LV systolic and diastolic function may be evaluated with a visual estimation of the ejection fraction, and diastolic function
with mitral E, A velocity, and e′ velocity.
E X P E RT T I P
Consider integrating more advanced echocardiographic techniques (estimation of left atrial
pressure) and LUS techniques (ARDS vs. cardiogenic pulmonary edema differentiation) when
applicable.
Evidence
Most evidence for LUS protocols in patients with dyspnea with diffuse B-lines comes from studies in
acute decompensated heart failure (ADHF). These protocols use echocardiography in addition to LUS
and are designed to specifically diagnose cardiogenic pulmonary edema. LUS protocols showed
reasonable sensitivity and specificity for ADHF and can be integrated with echocardiography. The
Emergency Thoracic Ultrasound In The Differentiation Of The Etiology Of Shortness Of Breath
(ETUDES) study prospectively used a combination of ultrasound and natriuretic peptide (N-terminal of
the prohormone brain natriuretic peptide) to diagnose congestive heart failure.11 Anderson et al12 found
that incorporating more modalities (LUS, inferior vena cava, and cardiac examination for EF) in the
ADHF diagnosis yielded better specificity (100% vs. 75%), but lower sensitivity (36% vs. 70%) than
LUS alone. The lung and cardiac ultrasound (LuCUS) study13 assessed the combined role of LUS and
cardiac ultrasound in ADHF and its impact on management. LUS had 83% accuracy (better than clinical
gestalt) and changed management in 47% of patients. In the Italian Society of Emergency Medicine
(SIMEU) study14 of 1,005 patients, LUS had better accuracy (sensitivity, 97%; specificity, 97%) than the
clinical workup, chest radiography, or natriuretic peptide concentrations. LUS reclassified the disease in
19%.
ESTIMATION OF EXTRAVASCULAR LUNG WATER
LUS Evaluation of Lung Congestion

Volume expansion is a basic therapy used in critically ill patients. Although often necessary, fluid
administration may result in pulmonary edema. Prior methods for assessing cardiac preload (eg, via
catheters with pressure transducers) are invasive, and their usefulness has not been well demonstrated
after decades. Bedside evaluation, chest radiography, and oxygenation data are used in practice but
sometimes cannot be completely relied upon, even in expert hands. B-lines, the LUS surrogate for
pulmonary edema, can predict extravascular lung water (EVLW) and pulmonary artery occlusion pressure
(PAOP). PAOP reflects hemodynamic, or intravascular, congestion (pressure inside pulmonary
vasculature), whereas EVLW reflects pulmonary congestion directly. EVLW greater than 10 mL/kg has
been established as the threshold for acute lung injury in literature. Knowledge of EVLW may be
important in the management of patients experiencing respiratory failure.
Method
The 8 anterolateral areas are used. Multiple B-lines (at least 3) in a single longitudinal scan, on at least 2
areas per side, represent diffuse interstitial syndrome, or B pattern (seen in cardiogenic pulmonary
edema, ARDS, fibrosis, or interstitial pneumonia). Multiple B-lines limited to fewer than 2 areas per side
are considered focal interstitial syndrome (seen in pneumonia, infarction, contusion) and are of the A
pattern rather than B pattern. Interpretation is as follows: (1) A pattern vs. B pattern is sensitive and
specific for discriminating “dry” vs. “wet” lung (EVLW threshold, 10 mL/kg); (2) B pattern is sensitive
and specific for elevated PAOP if combined with low EF; (3) the ability of B-lines to accurately track the
change of EVLW over time is uncertain.
Evidence
B-lines have been used to differentiate elevated from normal PAOP in ICU patients,15 but several later
studies demonstrated that this correlation does not always hold.16,17 Patients with normal PAOP may
develop B-lines in high altitude pulmonary edema, capillary leak seen in ARDS, or interstitial lung
disease. On the other hand, EVLW correlates well with B-lines. Thus, the main use of LUS is to estimate
lung congestion directly, irrespective of PAOP.
In a multicenter study of 73 critically ill patients (the most common diagnosis being septic shock [n = 19],
followed by cardiogenic pulmonary edema, respiratory failure secondary to COPD, pneumonia, and liver
transplantation) who were monitored by pulse contour cardiac output or pulmonary artery catheter,17 only
1 of 17 patients with an A pattern had increased EVLW. The presence of an A pattern (the absence of B-
lines) had 90.9% specificity (confidence interval [CI] = 78.7%-99.2%) and 94.4% positive predictive
value (CI = 78.7%-99.2%) to detect EVLW less than 10 mL/kg. The ability of LUS to discriminate
elevated PAOP was not as good, but improved when B-lines were combined with impaired LV function
on echocardiography. In 26 critically ill patients with ARDS, B-lines correlated with EVLW.18 The LUS
had a sensitivity of 82% and specificity of 77% to detect EVLW greater than 10 mL/kg. Concordance
between change of EVLW and B-lines was poor (74%), suggesting that invasive monitors would be
necessary to accurately track change of EVLW – contrary to earlier data in patients receiving dialysis.19
C AVE AT
Bilateral B-lines are not specific for cardiogenic pulmonary edema, because these are also
present in ARDS, interstitial lung disease, and pneumonia. In such cases, echocardiography may
help to differentiate cardiogenic pulmonary edema.
Figure 18-5. Fluid Administration Limited by Lung Ultrasonography (FALLS) Protocol

Defining Fluid Tolerance: The FALLS Protocol
Evidence links fluid excess with poor outcomes in critically ill patients.20 During fluid resuscitation,
preload responsiveness diminishes while the risk of pulmonary edema increases. The fluid administration
limited by lung ultrasonography (FALLS) protocol combines echocardiography (to clarify the etiology of
shock) with LUS (to stop fluid resuscitation when pulmonary edema develops).6
Method
After first ruling out cardiogenic or obstructive shock using echocardiography in a patient with acute
circulatory failure, the appearance of B-lines after fluid resuscitation, without hemodynamic
improvement, excludes hypovolemic shock and defines fluid tolerance. A patient whose hypotension
improves with IV fluids but who does not develop B-lines likely was hypovolemic. If B-lines develop,
the patient likely had distributive shock. Importantly, the early diagnosis of pulmonary edema could
theoretically provide a safety margin to stop fluid resuscitation in time and limit hypoxemia related to
excessive fluid administration (Figure 18-5).
C AVE AT
Patients with distributive shock from any cause may develop B-lines early, while still requiring
fluid resuscitation.
Evidence
FALLS is an intriguing concept that has not yet been rigorously tested. Patients with capillary leak may
already have interstitial syndrome, yet significant preload deficit could result in suboptimal fluid
resuscitation in some patients with ARDS who could still benefit from intravenous fluids. Ultrasound-
guided fluid resuscitation following the concept of fluid tolerance must be studied before this approach is
widely adopted.
LUNG RECRUITMENT
In patients with ARDS, PEEP keeps lung regions open that would otherwise collapse. Recruitability may
be predicted to some extent by a ratio of arterial partial oxygen pressure to the fraction of inspired oxygen
of less than 150 and a decrease in dead space with concomitant increase in lung compliance when
applying increased PEEP. In patients with minimal recruitable lung, application of higher PEEP is of little
benefit and may even be harmful. Lung recruitment has been traditionally evaluated by computed
tomography or static pressure-volume curves, which are generally impractical. Alternatively, lung
recruitability may be evaluated with LUS.
Method
Lung recruitment in patients with ARDS results in improved lung aeration. A-lines, then B-lines, and then
consolidation are seen as lung aeration decreases. Four distinct ultrasound patterns can be detected to
assess the degree of aeration.2 These patterns are: (1) A-lines (normal aeration), (2) multiple, well-
separated B-lines (moderate loss of aeration) resulting from interstitial syndrome, (3) coalescent B-lines
(more severe loss of aeration) resulting from the filling of alveoli by pulmonary edema or pneumonia, and
(4) frank consolidation (severe loss of aeration) (Figure 18-6).
Figure 18-6. Aeration Patterns.
A) A-lines (normal aeration). B) Multiple separated B-lines (moderate loss of aeration; interstitial filling). C) Coalescent B-lines (more severe
loss of aeration; alveolar filling). D) Frank consolidation (severe loss of aeration).
Bouhemad B, Mongodi S, Via G, Rouquette I. Ultrasound for “lung monitoring” of ventilated patients. Anesthesiology. 2015;122:437-447.
Copyright © 2015 American Society of Anesthesiologists and Lippincott Williams & Wilkins, Inc.
Using these patterns, two distinct scores can be calculated: the lung aeration and lung re-aeration scores
(Tables 18-1 and 18-2). The aeration score reflects global aeration, a static measure; an increase in the
score indicates decreased aeration. The lung re-aeration score measures dynamic changes in each region
of interest during a recruitment maneuver (eg, a PEEP trial), so a score is obtained before and after the
PEEP change for each region. An increased re-aeration score indicates increased aeration, suggesting that
recruitment has been successful.
Patients with ARDS have heterogeneous distribution of aeration loss within the lungs, and this
heterogeneity may be evaluated with ultrasound. A normal pattern may be seen in anterior and lateral
regions, whereas B-lines and consolidations may be seen in lateral and posterior regions. In patients with
homogeneous distribution (a minority of patients), B-lines and/or consolidations may be seen diffusely.
With increased PEEP, patterns change.
LUS is a clinically useful method for titrating recruitment, preventing lung de-recruitment, or evaluating
PEEP nonresponders. A practical approach to lung recruitment follows these steps21 (Figure 18-7):
On a low level of PEEP, examine 4 anterior regions to evaluate the extent of loss of aeration.
If A-lines are seen (suggesting only focal loss of aeration), the risk of overdistension exists; use lower
levels of PEEP if desired (eg, ≤10 cm H2O).
If diffuse B-lines are seen (suggesting diffuse loss of aeration), use higher level of PEEP if desired (eg,
12-16 cm H2O).
At each level, the clinical response is evaluated by the disappearance of B-lines.
Other parameters (eg, airway pressures, hemodynamics) should be closely monitored as well.
E X P E RT T I P
When evaluating lung recruitment, keep in mind that anterior zones are generally more
recruitable than posterior; diffuse B-lines are generally more recruitable than dense
consolidations.
Table 18-1. Lung Aeration Score

Pattern Points
Normal (N) 0
Well-separated B-lines (B2) 1
Coalescent B-lines (B1) 2
Consolidation (C) 3
Total Score 0-36
Perform a 12-zone lung examination, and score each zone. The sum of all scores is the total aeration score. An increased score indicates
decreased aeration.
Table 18-2. Lung Re-aeration Score

Pattern Change
(PEEP 0 → 15 cm H2 O) Points
C → B1 1
B1 → B2
B2 → N
C → B2 3
B1 → N
C → N 5
Abbreviations: PEEP, positive end-expiratory pressure; C, consolidation; B1, coalescent B-lines; B2, well-separated B-lines; N, normal.
Perform a 12-zone lung examination. After evaluating the pattern before and after an increase in PEEP, the change in each zone is scored.
The sum of all scores is the total re-aeration score. The higher the total score, the larger the increase in aeration. A score ≥8 correlates with
PEEP-induced lung recruitment >600 mL.
Figure 18-7. Titration of PEEP Using LUS

Abbreviations: PEEP, positive end-expiratory pressure; LUS, lung ultrasound.
C AVE AT
Because LUS cannot capture hyperinflation, it cannot be used as the sole method of selecting
PEEP.
Evidence
Early studies used transesophageal echocardiography to evaluate ultrasound densities (consolidations) in
ARDS; the results showed the change in densities with change in PEEP,22 change over time, and change as
a response to prone positioning. The LUS re-aeration score tightly correlated with recruitment as
assessed by pressure volume curves.2 Correlation was more accurate with a greater degree of recruitment
(score ≥8 was associated with lung recruitment >600 mL; a score ≥4 with lung recruitment of 75-450 mL)
and in diffuse rather than focal loss of aeration. Anterior B-lines and lateral consolidations are generally
more recruitable than posterior consolidations.2
LUS IN LIBERATION FROM MECHANICAL VENTILATION

Patients with respiratory failure are typically evaluated for liberation from mechanical ventilation using
standard criteria, such as the rapid shallow breathing index (RSBI), but performance of RSBI is limited.
For instance, it may be difficult to predict who will not be successfully extubated after a successful
spontaneous breathing trial (SBT). Some patients may develop pulmonary edema after extubation, and
others may have unrecognized diaphragm weakness. LUS alone or in combination with echocardiography
can yield important information relevant to liberation from mechanical ventilation.
Method
In difficult-to-wean patients, LUS may identify pulmonary congestion, pleural effusion, atelectasis, and
diaphragm weakness. Patients who have SBT-induced left atrial hypertension may be identified with
echocardiography. For this technique, transmitral diastolic flow is used to obtain early (E) and atrial (A)
diastolic velocity. Tissue Doppler imaging is used to obtain early mitral annulus velocity (e′). The E/e′
ratio is one of the best noninvasive estimates of left atrial pressure.
To estimate left atrial pressure, apical 4-chamber views are obtained. The mitral valve inflow E and A
velocities are measured using pulsed-wave Doppler. Mitral annulus e′ velocities are measured using
tissue Doppler, and the E/e′ ratio is calculated.
To assess risks for extubation failure using combined LUS and echocardiography (Figure 18-8), the
following steps can be used before and during SBT.
1. Perform baseline echocardiography to evaluate for:

Ventricular size and function
Left atrial size (sign of chronically elevated left atrial pressure)
Valvular function
Filling pressures
2. Consider whether any abnormal findings at baseline could be contributing to the failure to wean (see
Chapter 8).
3. Perform baseline LUS to evaluate for:
Presence or absence of EVLW (diffuse B-lines)
Consolidations
Atelectasis
Diaphragm excursion (refer to relevant sections)
4. Consider whether any abnormal finding could be contributing to the failure to wean.
5. Perform dynamic transthoracic echocardiography and LUS to exclude:
Development of EVLW (appearance of diffuse B-lines)
Increase in left atrial pressure (increase of E/e′) induced by the SBT
Evidence
Predicting Postextubation Distress: LUS Approach. It is sometimes difficult to predict which patients will
develop postextubation distress after passing an SBT. Those who developed respiratory distress within
48 hours after extubation had significantly worse lung aeration before and by the end of SBT, though they
had an adequate RSBI. End-SBT LUS scores greater than 17 were highly specific for predicting
postextubation distress, whereas LUS scores of 12 or lower were highly sensitive for excluding
postextubation distress.23
Weaning Failure: Echocardiography Approach. The following may occur during liberation from
mechanical ventilation: increased LV preload, increased LV afterload, and decreased LV compliance.
Patients with left heart disease have an associated increase in left atrial pressures and pulmonary edema
complicating weaning.24 Specifically, the combination of E/A ratio greater than 0.95 and E/e′ ratio greater
than 8.5 (lateral e′ velocity) accurately predicted SBT-induced PAOP elevation greater than 18 mm Hg.25
Patients with weaning-induced PAOP elevation failed an SBT more often that those without PAOP
elevation (100% vs. 64%). The study was conducted in a selected patient population (2 prior
unsuccessful attempts to wean, thus the high failure rates) and required echocardiographic skills, but
offered a useful, noninvasive alternative to a pulmonary artery catheter.
Figure 18-8. LUS and Echocardiography in Liberation from Mechanical Ventilation
Abbreviations: LUS, lung ultrasound; 2D, 2-dimensional; TDI, tissue Doppler imaging; PW, pulsed wave.
Weaning Failure: Combined Echocardiography and LUS Approach. Despite limited evidence,26 the
combination of echocardiography (to estimate LV filling pressure) and LUS (to evaluate for the
development of extravascular lung water and to exclude other issues, such as atelectasis, pleural effusion,
and diaphragmatic paralysis) may offer additional advantages over physical examination and RSBI in the
evaluation of difficult-to-wean patients.
DIAPHRAGMATIC ULTRASOUND
Patients with diaphragmatic paralysis or weakness, or who are asynchronous with mechanical ventilation,
may be difficult to identify. Ultrasound evaluation is a fast and accurate method of assessing the
diaphragm and excluding diaphragmatic dysfunction at the bedside in critically ill patients.
Method
Ultrasound evaluation of the diaphragm is performed using a phased-array probe. The probe is placed in
the anterior axillary line below the costal margin and directed cephalad, medially and dorsally, with the
directional marker pointing cephalad (Figure 18-9). The ultrasound beam reaches the posterior third of
the corresponding hemidiaphragm in a perpendicular direction. The liver is used as the acoustic window
on the right and spleen on the left side. A normal diaphragm is seen as a bright, echogenic line on 2D
imaging. It moves caudally during inspiration, that is, toward the probe, which is upward on the
ultrasound image. During expiration, the diaphragm moves away from the probe. After optimizing the
probe position, M-mode is used to measure the direction of the diaphragmatic motion and magnitude of
excursion. Normal movement is recorded as an upward tracing on M-mode. Amplitude of excursion is
measured on the vertical axis of the tracing from baseline to the point of maximum height during
inspiration. To improve the accuracy of measurement, the probe should be kept as perpendicular as
possible to the diaphragmatic excursion line.
Figure 18-9. Diaphragmatic Ultrasound

A) Diaphragmatic excursions during a spontaneous breathing trial in a 44-year-old woman with acute respiratory distress syndrome and critical
illness polyneuropathy, on ventilator day 39. B) Reducing pressure support from 24 cm to 5 cm correlates with a reduction of diaphragmatic
excursion but remains within normal range (≥10 mm). C) Diaphragmatic thickening in the same patient. Maximum thickness is seen in end
inspiration. Measurements are taken in the zone of apposition in the anterior axillary line using a linear probe, ideally 10 MHz. The diaphragm
thickens during spontaneous breathing. D) The position of the probe for measurement of diaphragmatic excursion. A 3.5 MHz phased-array
probe is placed in the midclavicular or anterior axillary line below the costal margin and directed upward, medially and dorsally with the
directional marker pointing cephalad. The ultrasound beam should reach the posterior hemidiaphragm in perpendicular fashion.
Diaphragm thickness is measured with a high-frequency linear array probe (≥10 MHz) in the zone of
apposition of the diaphragm to the rib cage, the area of the chest wall where the abdominal contents reach
the lower rib cage. The probe is positioned in the midaxillary line between the 8th and 10th intercostal
spaces. The diaphragm is visualized as a nonechogenic central layer bordered by 2 echogenic layers—the
peritoneum and the diaphragmatic pleura (Figure 18-9).
Diaphragmatic excursion is greater in men than in women, and greater on the left than the right. In healthy
volunteers, the lower limit of normal diaphragmatic excursion during quiet breathing, voluntary sniffing,
and deep breathing is 0.9 cm, 1.6 cm, and 3.7 cm for women; and 1 cm, 1.8 cm, and 4.7 cm for men,
respectively.27 Diaphragm thickness varies widely in normal individuals, ranging between 1.8 and 3 mm
at functional residual capacity.
Evidence
Diaphragmatic Paralysis. A paralyzed hemidiaphragm will demonstrate no caudal movement with
inspiration and may have paradoxical (downward) movement on M-mode. In patients with diaphragmatic
weakness, excursion may be reduced. Repeated examinations over a period can provide information
about the recovery of diaphragm function.28
E X P E RT T I P
Evaluation of the true degree of diaphragmatic weakness by measuring lung excursion in
mechanically ventilated patients requires that ventilator support be decreased to a minimum
level. Evaluation of diaphragmatic thickness is possible with the high-frequency probe.
C AVE AT
During ultrasound of the diaphragm, the field of view is often small and frequently obscured by
lung movements or bowel gas. In patients with dyspnea, increased respiratory effort can result in
greater chest wall movement and cause lungs and ribs to obscure the images.
Diaphragm thickness can also be used as a surrogate marker of diaphragmatic weakness or paralysis. A
value of less than 2 mm was reported to be associated with diaphragmatic paralysis.29 However, the
thickness may be normal in acute diaphragmatic paralysis (atrophy has not yet set in—false-negative
result) and low in small individuals (false-positive result).
Weaning from Mechanical Ventilation/Prediction of Successful Extubation. Mechanical ventilation

induces diaphragmatic muscle atrophy,30 hence assessment of diaphragmatic dysfunction in ventilated
patients has been of significant research interest. In 88 mechanically ventilated patients undergoing SBT,
diaphragmatic dysfunction (<10 mm upward vertical excursion or the presence of negative deflection in
M-mode) was associated with a longer weaning time, longer total ventilation time, and higher weaning
failure rate.31
In another study of 55 mechanically ventilated patients undergoing SBT, the liver and spleen
displacements in a craniocaudal direction during respirations were measured. Using a cutoff value of 1.1
cm predicted successful extubation with sensitivity and specificity of 84.4% and 82.6%, respectively,
which was better than traditional weaning parameters.32 Changes in diaphragmatic thickening can also be
used to predict successful extubation. In 63 patients undergoing a weaning trial, a change in diaphragmatic
thickness between end-expiration and end-inspiration (Δtdi%) of 30% or more predicted extubation
success with a sensitivity, specificity, and positive predictive value of 88%, 71%, and 91%,
respectively.33 The aforementioned studies suggest that assessment of diaphragmatic function is a more
sensitive and specific parameter than volume-associated weaning parameters (eg, spontaneous tidal
volume, RSBI) in predicting extubation failure. Patients who maintain adequate tidal volumes by
recruiting accessory respiratory muscles during the breathing trial but who have poor diaphragmatic
excursion are more likely to fail than patients with adequate tidal volumes and good diaphragm
movement.
Assessment of Patient-Ventilator Interactions. In patients receiving assisted mechanical ventilation (eg,

pressure support ventilation), M-mode diaphragm ultrasound provides information about patient-
ventilator synchrony. A dissociation between the diaphragmatic contractions and the triggering and
cycling of the ventilator is seen with ventilator dyssynchrony. This information could be used to adjust the
ventilator settings to optimize the patient-ventilator interaction.
Postoperative Period. Diaphragm ultrasound has been used to assess postoperative pulmonary and
diaphragmatic dysfunction in patients undergoing upper abdominal and cardiac surgical procedures. A
maximal diaphragmatic excursion of less than 25 mm on either side during maximal inspiratory effort was
associated with severe diaphragmatic dysfunction in patients who required prolonged mechanical
ventilator support after cardiac surgery.34 In another study of 35 patients who underwent liver lobectomy,
the amplitude of diaphragmatic excursion measured during deep breathing predicted changes in the vital
capacity measured with spirometry.35
ECHOCARDIOGRAPHY IN ARDS
Acute cor pulmonale (ACP) is a problem often encountered in mechanically ventilated patients with
ARDS. Knowledge of echocardiographic findings is essential for making the diagnosis. ACP is caused by
sudden increase in right ventricular (RV) afterload. Several factors lead to ACP in ARDS, including
distal obstruction of pulmonary vasculature and excessive alveolar stretch from mechanical ventilation.
Alveolar stretch is related to tidal volume or air trapping. Echocardiography is more useful than a
pulmonary artery catheter for evaluating the severity of ACP, including the ability to directly evaluate RV
function. When RV afterload is high, RV contraction is prolonged, so the ventricle continues to push after
LV systole has ended. RV pressure briefly may exceed LV pressure, resulting in leftward displacement of
the interventricular septum, commonly termed interventricular septal dyskinesia. In pressure-overloaded
states, the RV dilates. The heart is enclosed in pericardium with no free space for ventricular dilation, so
RV dilation can occur only at the expense of the left ventricle, which becomes restricted
(echocardiographic pattern of RV dilation, measured semiquantitatively using the ratio of the RV and LV
end-diastolic areas).36
Method
RV Systolic Overload. Interventricular septal dyskinesia first occurs at the end of systole and onset of
diastole (Figure 18-10 and Video 18-1 ). If the RV filling pressure continues to be higher than the LV
pressure, interventricular septal displacement persists through diastole. The sudden return of the septum
toward the RV is produced only when LV pressure exceeds RV pressure at onset of systole/end diastole.
This paradoxical motion of the interventricular septum can be detected from the parasternal short- or
long-axis view using 2D imaging. M-mode of the septum provides an accurate analysis.
RV Diastolic Overload. To quantify RV dilatation, the apical 4-chamber view is used to determine the
ratio of RV and LV end-diastolic areas. The normal RV/LV end-diastolic area ratio is less than 0.6;
moderate dilatation, 0.6 to 0.9; and severe dilatation, 1 or more (Figure 18-11). Using Doppler
examination of tricuspid regurgitation, pulmonary artery systolic pressure can be calculated, but this may
be of limited value because the pressure also depends on RV performance, which can be abnormal
(Figure 18-12).
As RV pressure overload persists, significant changes occur in the configuration of the RV. In the long-axis
view, the RV becomes more rounded and loses its triangular configuration. In the short-axis view, it loses
its crescentic shape and becomes oval because of septal flattening (Figure 18-13). Pulsed-wave Doppler
in the pulmonary artery may show increased and premature peak velocity, with midsystolic velocity
reduction.
Figure 18-10. Septal Dyskinesia

Patient with severe acute respiratory distress syndrome who is receiving positive end-expiratory pressure of 15 cm H2O. The image was
obtained in M-mode from the parasternal long axis. During the onset of left ventricular (LV) diastole, the prolonged right ventricular (RV)
systole causes a shift of the septum into the LV (yellow arrow), which has already entered diastole (black arrow). The septum returns toward
the RV only when LV pressure exceeds RV pressure during the onset of LV systole. This pattern of septal dyskinesia is consistent with RV
systolic overload.
Image courtesy of Xavier Monnet, MD.
Figure 18-11. RV Dilation in Acute Respiratory Distress Syndrome
Apical 4-chamber view. The RV end-diastolic area is greater than the LV end-diastolic area, consistent with severe RV dilation.
Chronic Versus Acute RV Overload. To differentiate acute from chronic RV pressure overload, the RV
free wall can be examined for hypertrophy (Figure 18-14). Subcostal or medially angulated parasternal
long-axis views are used. Normal RV free wall thickness is less than 5 mm. In chronic pulmonary
hypertension, hypertrophy is seen (usually >9 mm at the end diastole). The RV thickness may increase
relatively quickly over time with ongoing RV load. Literature describes an increase in RV diastolic
thickness (6 mm) after 48 hours of mechanical ventilation. Beside chronic pulmonary hypertension, right
ventricular hypertrophy is seen also in infiltrative and hypertrophic cardiomyopathies.
E X P E RT T I P
Consider using the parasternal short-axis view, M-mode, or 2D clip running in slow motion to
appreciate interventricular septum dyskinesia.
Figure 18-12. Estimation of Pulmonary Artery Systemic Pressure in ARDS with Poor RV Function
Estimated pulmonary artery systemic pressure is only 45 mm Hg (likely because of poor right ventricle performance) despite severe dilation of
the right ventricle and septal dyskinesia.
Figure 18-13. Loss of Normal Configuration of RV in ARDS

Parasternal short-axis view of patient in Figure 18-12. During RV pressure overload, the RV becomes oval because of septal flattening
(arrow).
Figure 18-14. RV Hypertrophy in ARDS
Abbreviation: RV, right ventricle.
A 44-year-old woman has severe acute respiratory distress syndrome secondary to pneumonia. She is on day 35 of mechanical ventilation.
Free RV wall thickness (arrow) measured in the subcostal view is 0.77 cm (normal <0.5 cm). She does not have a history of pulmonary
hypertension.
C AVE AT
In mechanically ventilated patients, transthoracic views are often limited. Transesophageal

echocardiography will give better information. LV dilation makes the RV/LV end-diastolic area
ratio unreliable. Bundle branch block may mimic septal paradoxical motion. In RV infarction, the
RV dilation is present, but unlike in ACP, there is frequently LV posterior or inferior free wall
motion abnormality and PA pressures may not be elevated.
Evidence
Echocardiography was instrumental in defining the role of ACP in ARDS. The description of ACP is
based on the RV/LV area ratio.37 In the era of lung-protective ventilation, the incidence of ACP based on
echocardiography in ARDS is 14% to 25%,38,39 increasing with the severity of ARDS.40 If lung stretch
cannot be limited by adjusting ventilator settings, prone positioning can further reduce the incidence of
ACP.41 In larger cohorts, ACP is independently associated with mortality.40 High plateau pressure (>26
cm) appeared particularly harmful in the presence of ACP.40 Even with low tidal volume and plateau
pressure limitation, increasing PEEP increases RV afterload and RV diastolic area, and decreases the
cardiac index.38 It appears logical to titrate ventilator settings (tidal volume, respiratory rate, PEEP) and
fluid therapy to minimize ACP, but this approach has yet to be tested in trials. The use of
echocardiography to guide ventilator settings in ARDS may be warranted in the future.
E X P E RT T I P
Reasonable methods to avoid ACP in ARDS include keeping plateau pressure <27 cm H2O,
limiting tidal volumes, and avoiding hypercarbia. This recommendation is based on limited
evidence.
KEY POINTS
LUS is useful for rapid and accurate evaluation of patients with dyspnea of unknown etiology, but
its impact on patient outcomes warrants further studies.
The degree of lung congestion can be directly evaluated with LUS. The presence of A-lines
(absence of B pattern) makes increased extravascular lung water unlikely.
Lung recruitment can be evaluated with LUS and it can help with titration of PEEP in hypoxemic
patients.
Difficult-to-wean patients can be evaluated for the development of weaning-induced cardiogenic
pulmonary edema, pleural effusions, atelectasis, and diaphragmatic weakness using
echocardiography and LUS.
Diaphragmatic ultrasound is useful to evaluate for diaphragmatic paralysis and patient-ventilator
synchrony.
In patients with ARDS receiving higher PEEP, consider the possibility of ACP. Ventilator settings
can be adjusted in an attempt to reduce or resolve ACP.
REFERENCES
1. Volpicelli G, Elbarbary M, Blaivas M, et al. International evidence-based recommendations for point-of-care lung ultrasound. Intensive
Care Med. 2012;38:577-591.
2. Bouhemad B, Brisson H, Le-Guen M, et al. Bedside ultrasound assessment of positive end-expiratory pressure-induced lung recruitment.
Am J Respir Crit Care Med. 2011;183:341-347.
3. Lichtenstein D, Meziere G, Seitz J. The dynamic air bronchogram: a lung ultrasound sign of alveolar consolidation ruling out atelectasis.
Chest. 2009;135:1421-1425.
4. Lichtenstein D, Meziere G, Biderman P, Gepner A, Barre O. The comet-tail artifact: an ultrasound sign of alveolar-interstitial syndrome.
Am J Respir Crit Care Med. 1997;156:1640-1646.
5. Lichtenstein DA, Meziere GA. Relevance of lung ultrasound in the diagnosis of acute respiratory failure: the BLUE protocol. Chest.
2008;134:117-125.
6. Lichtenstein D. Fluid administration limited by lung sonography: the place of lung ultrasound in assessment of acute circulatory failure (the
FALLS-protocol). Expert Rev Respir Med. 2012;6:155-162.
7. Volpicelli G, Lamorte A, Tullio M, et al. Point-of-care multiorgan ultrasonography for the evaluation of undifferentiated hypotension in the
emergency department. Intensive Care Med. 2013;39:1290-1298.
8. Silva S, Biendel C, Ruiz J, et al. Usefulness of cardiothoracic chest ultrasound in the management of acute respiratory failure in critical
care practice. Chest. 2013;144:859-865.
9. Xirouchaki N, Kondili E, Prinianakis G, Malliotakis P, Georgopoulos D. Impact of lung ultrasound on clinical decision making in critically ill
patients. Intensive Care Med. 2014;40:57-65.
10. Bataille B, Riu B, Ferre F, et al. Integrated use of bedside lung ultrasound and echocardiography in acute respiratory failure: a prospective
observational study in ICU. Chest. 2014;146:1586-1593.
11. Liteplo AS, Marill KA, Villen T, et al. Emergency thoracic ultrasound in the differentiation of the etiology of shortness of breath
(ETUDES): sonographic B-lines and N-terminal pro-brain-type natriuretic peptide in diagnosing congestive heart failure. Acad Emerg Med.
2009;16:201- 210.
12. Anderson KL, Jenq KY, Fields JM, Panebianco ML, Dean AJ. Diagnosing heart failure among acutely dyspneic patients with cardiac,
inferior vena cava, and lung ultrasonography. Am J Emerg Med. 2013;31:1208-1214.
13. Russell FM, Ehrman RR, Cosby K, et al. Diagnosing acute heart failure in patients with undifferentiated dyspnea: a lung and cardiac
ultrasound (LuCUS) protocol. Acad Emerg Med. 2015;22:182-191.
14. Pivetta E, Goffi A, Lupia E, et al. Lung ultrasound-implemented diagnosis of acute decompensated heart failure in the emergency
department: a SIMEU multicenter study. Chest. 2015;148:202-210.
15. Lichtenstein DA, Meziere GA, Lagoueyte JF, Biderman P, Goldstein I, Gepner A. A-lines and B-lines: lung ultrasound as a bedside tool for
predicting pulmonary artery occlusion pressure in the critically ill. Chest. 2009;136:1014-1020.
16. Fagenholz PJ, Gutman JA, Murray AF, Noble VE, Thomas SH, Harris NS. Chest ultrasonography for the diagnosis and monitoring of high-
altitude pulmonary edema. Chest. 2007;131:1013-1018.
17. Volpicelli G, Skurzak S, Boero E, et al. Lung ultrasound predicts well extravascular lung water but is of limited usefulness in the prediction
of wedge pressure. Anesthesiology. 2014;121:320-327.
18. Bataille B, Rao G, Cocquet P, et al. Accuracy of ultrasound B-lines score and E/Ea ratio to estimate extravascular lung water and its
variations in patients with acute respiratory distress syndrome. J Clin Monitor Comput. 2015;29:169- 176.
19. Noble VE, Murray AF, Capp R, Silvia-Reardon MH, Steele DJ, Liteplo A. Ultrasound assessment for extravascular lung water in patients
undergoing hemodialysis: time course for resolution. Chest. 2009;135:1433-1439.
20. Boyd JH, Forbes J, Nakada TA, Walley KR, Russell JA. Fluid resuscitation in septic shock: a positive fluid balance and elevated central
venous pressure are associated with increased mortality. Crit Care Med. 2011;39:259-265.
21. Bouhemad B, Mongodi S, Via G, Rouquette I. Ultrasound for “lung monitoring“ of ventilated patients. Anesthesiology. 2015;122:437-447.
22. Tsubo T, Sakai I, Suzuki A, Okawa H, Ishihara H, Matsuki A. Density detection in dependent left lung region using transesophageal
echocardiography. Anesthesiology. 2001;94:793-798.
23. Soummer A, Perbet S, Brisson H, et al. Ultrasound assessment of lung aeration loss during a successful weaning trial predicts
postextubation distress. Crit Care Med. 2012;40:2064-2072.
24. Teboul JL, Monnet X, Richard C. Weaning failure of cardiac origin: recent advances. Crit Care. 2010;14:211.
25. Lamia B, Maizel J, Ochagavia A, et al. Echocardiographic diagnosis of pulmonary artery occlusion pressure elevation during weaning from
mechanical ventilation. Crit Care Med. 2009;37:1696-1701.
26. Mongodi S, Via G, Bouhemad B, Storti E, Mojoli F, Braschi A. Usefulness of combined bedside lung ultrasound and echocardiography to
assess weaning failure from mechanical ventilation: a suggestive case. Crit Care Med. 2013;41:e182-e185.
27. Boussuges A, Gole Y, Blanc P. Diaphragmatic motion studied by M-mode ultrasonography: methods, reproducibility, and normal values.
Chest. 2009;135:391-400.
28. Matamis D, Soilemezi E, Tsagourias M, et al. Sonographic evaluation of the diaphragm in critically ill patients: technique and clinical
applications. Intensive Care Med. 2013;39:801-810.
29. Gottesman E, McCool FD. Ultrasound evaluation of the paralyzed diaphragm. Am J Respir Crit Care Med. 1997;155:1570-1574.
30. Grosu HB, Lee YI, Lee J, Eden E, Elkermann M, Rose KM. Diaphragm muscle thinning in patients who are mechanically ventilated.
Chest. 2012;142:1455-1460.
31. Kim WY, Suh HJ, Hong SB, Koh Y, Lim CM. Diaphragm dysfunction assessed by ultrasonography: influence on weaning from mechanical
ventilation. Crit Care Med. 2011;39:2627-2630.
32. Jiang JR, Tsai TH, Jerng JS, Yu CJ, Wu HD, Yang PC. Ultrasonographic evaluation of liver/spleen movements and extubation outcome.
Chest. 2004;126:179-185.
33. DiNino E, Gartman EJ, Sethi JM, McCool FD. Diaphragm ultrasound as a predictor of successful extubation from mechanical ventilation.
Thorax. 2014;69:423-427.
34. Lerolle N, Guerot E, Dimassi S, et al. Ultrasonographic diagnostic criterion for severe diaphragmatic dysfunction after cardiac surgery.
Chest. 2009;135:401-407.
35. Kim SH, Na S, Choi JS, Na SH, Shin S, Koh SO. An evaluation of diaphragmatic movement by M-mode sonography as a predictor of
pulmonary dysfunction after upper abdominal surgery. Anesth Analg. 2010;110:1349-1354.
36. Vieillard-Baron A, Prin S, Chergui K, Dubourg O, Jardin F. Echo-Doppler demonstration of acute cor pulmonale at the bedside in the
medical intensive care unit. Am J Respir Crit Care Med. 2002;166:1310-1319.
37. Jardin F, Dubourg O, Bourdarias JP. Echocardiographic pattern of acute cor pulmonale. Chest. 1997;111:209-217.
38. Fougeres E, Teboul JL, Richard C, Osman D, Chemia D, Monnet X. Hemodynamic impact of a positive end-expiratory pressure setting in
acute respiratory distress syndrome: importance of the volume status. Crit Care Med. 2010;38:802-807.
39. Vieillard-Baron A, Schmitt JM, Augarde R, et al. Acute cor pulmonale in acute respiratory distress syndrome submitted to protective
ventilation: incidence, clinical implications, and prognosis. Crit Care Med. 2001;29:1551-1555.
40. Jardin F, Vieillard-Baron A. Is there a safe plateau pressure in ARDS? The right heart only knows. Intensive Care Med. 2007;33:444-447.
41. Vieillard-Baron A, Charron C, Caille V, Belliard G, Page B, Jardin F. Prone positioning unloads the right ventricle in severe ARDS. Chest.
2007;132:1440-1446.
Chapter 19
Thromboembolism
John Hardin, MD; Beatrice Hoffmann, MD, PhD
OBJECTIVES
Discuss the basics of vascular ultrasound and identify the distinction between arteries and veins
Review the epidemiology of deep vein thrombosis
Describe the imaging technique for upper and lower extremity venous systems in the evaluation of deep vein
thrombosis
Discuss elements of imaging in the cardiac apical 4-chamber, cardiac parasternal short-axis, and inferior vena
cava views that assist in the evaluation of clinically significant acute pulmonary embolism
INTRODUCTION
An important goal of point-of-care (POC) ultrasonography in the acute setting is to appropriately evaluate
a patient for deep venous thrombosis (DVT). DVTs have a risk of fragmenting or propagating to become
pulmonary emboli (PE), and carry a significant mortality rate in the acute care setting. Ultrasound in the
acute care setting becomes important in the early detection and treatment of DVT to prevent PE as well as
post-thrombotic syndrome in the postacute setting.
Fortunately, the skills necessary to perform an appropriate extremity ultrasound examination can be
performed with focused training and with an accuracy similar to that of comprehensive vascular
ultrasound.1 DVT ultrasound training is included as an emergency ultrasound indication taught to
emergency medicine postgraduate trainees as well as part of training curricula offered by critical care
societies, emphasizing the importance of POC ultrasound in the diagnosis of peripheral DVT.
Furthermore, with preexisting tools (such as cardiac, lung, and inferior vena cava [IVC] views), POC
ultrasound can be used to evaluate a patient with suspected PE, which may ultimately assist in expedited
diagnosis and treatment.
CASE STUDY
A 52-year-old man with unknown medical history presents after a witnessed collapse. Cardiopulmonary
resuscitation is initiated, and return of spontaneous circulation is achieved in less than 10 minutes. On
arrival at the emergency department, the first echocardiography image shows a dilated right ventricle
(RV) with impaired contractility and apical sparing (Figures 19-1 and 19-2). Although the patient
undergoes successful intubation and ventilation, he remains hypotensive. An electrocardiogram does not
show any changes consistent with ischemia. Further ultrasound imaging reveals a flattened septum in
systole consistent with pressure overload, and a plethoric IVC (Figure 19-3). Two-point compression
ultrasound reveals DVT in the common femoral vein (Figure 19-4). Thrombolytic therapy is initiated and
the patient’s blood pressure improves over the next several hours.
Figure 19-1. Parasternal Long- and Short-Axis Echocardiogram Views in Pulmonary Embolism
A) Massive pulmonary embolism with acute RV dilation and McConnell sign on clip. B) D-shaped LV in short-axis view. White areas indicate
septum; yellow areas, RV; and blue areas, LV.
Figure 19-2. Severe Acute Presentation of Chronic Pulmonary Hypertension

Abbreviations: RV, right ventricle; LV, left ventricle; RA, right atrium.
A) Short-axis view. B) Apical 4-chamber view. C) Parasternal long-axis view. D) Color flow showing severe tricuspid regurgitation, and right
atrial and ventricular septal bowing.
Figure 19-3. Plethoric Inferior Vena Cava, Longitudinal View
Figure 19-4. Common Femoral Vein with Clot

Abbreviations: CFV, common femoral vein; GSV, greater saphenous vein; A, femoral artery branches.
CFV with clot reaching into the GSV.
C AVE AT
Power Doppler sonography is a technique that displays the strength of the Doppler signal in color
rather than speed or direction of signal.
Which Ultrasound Findings in the Case Support the Decision to Initiate Thrombolytic Therapy?
The only ultrasound finding diagnostic of an acute PE is the direct visualization of a clot in transit in the
IVC, RV, or pulmonary artery. The presence of right ventricular dysfunction and dilation on POC
ultrasound could indicate an acute or chronic process like pulmonary hypertension in this patient with an
unknown medical history. Therefore the decision to initiate thrombolytic therapy relies on increasing the
pretest probability of acute PE. The confirmation of DVT on POC ultrasound in this patient increased the
pretest probability that the likely cause of his persistent shock was acute PE and that he would likely
benefit from thrombolysis.
PERIPHERAL DVT
Epidemiology
Classically, the decision to perform an ultrasound to evaluate for peripheral DVT is symptom based. A
patient in the emergency department setting typically presents with edema, pain, and redness of an
affected extremity. Scanning of unaffected extremities is not recommended because although specificity
can be maintained, sensitivity can drop to less than 50%, making it an exceedingly poor screening test.2
Therefore, in the acute setting, DVT scans are typically recommended only if performed on a symptomatic
extremity. However, evidence suggests that contralateral DVTs can be found in up to 34% of the DVT
presentations, particularly in patients with cancer.3 In the ICU, the absolute prevalence of DVT is
unknown, but some reports have found an incidence as high as 60% in patients with trauma and an
incidence between 9% and 21% even in patients receiving appropriate chemoprophylaxis.4-6 DVTs in the
ICU are often clinically silent. Simply being in the ICU raises the pretest probability of DVT and,
therefore, the sensitivity of POC ultrasound for DVT.5
In addition to PE, which is the most feared complication of DVT, post-thrombotic syndrome
(characterized by evidence of venous insufficiency after DVT) can occur in up to 20% to 50% of patients
after a proximal (popliteal and above) thrombus, with the risk increasing the more proximal the extent of
the clot.7
Lower extremity DVT represents approximately 90% of peripheral DVT and, if untreated, has up to a
50% rate of progression to PE.8 Upper extremity DVT represents approximately 2% to 5% of DVT cases
and has a rate of progression to PE of approximately 37%. With appropriate treatment, the risk of lower
extremity DVT progression approaches 0%, but data suggest that even with 3 months of treatment, there is
little change in the progression rate of upper extremity DVT to PE.9
Vascular Ultrasound Basics

The ultrasound techniques used for identifying DVT are similar to general vascular ultrasound techniques.
Distinguishing between an artery and a vein is essential. As such, the ultrasound probe choice and the
ultrasound modalities used are designed to help the clinician identify a vein that appears abnormal. The
linear or vascular probe is the probe of choice, but in cases with greater imaging depths than usual (eg, in
a morbidly obese patient), the curvilinear probe can be used.
Veins are thin-walled structures, typically more oval in shape, and are always located next to a
corresponding circular, thicker-walled artery. Color Doppler can help distinguish between arterial
pulsations and more continuous flow of veins. The venous system is a low-pressure system with large
capacitance that can easily accommodate changes in pressure and flow. Venous flow is continuous, with a
triphasic waveform that can be easily distinguished from the pulsatile nature of an artery with the pulsed-
wave Doppler. During inspiration, negative intrathoracic pressure draws blood from the periphery into
the central circulation. Therefore, respiratory variation of venous flow can also be seen in central veins
with pulsed-wave Doppler. Once the vein is appropriately identified, compression of the vein, color
filling of the entire vessel, augmentation of flow, and respiratory variation can all be used to determine if
DVT is present.
Transducer Type
Linear (preferred)
Curvilinear (for the difficult or obese patient)
Ultrasound Methods
Two-dimensional B-mode (compression ultrasound)
Color Doppler (augmentation, direct visualization, vessel identification)
Pulsed-wave Doppler (augmentation, vessel identification)
E X P E RT T I P S
Use color Doppler to distinguish arterial pulsations from venous flow.
During real-time color Doppler imaging , recall that red and blue do not correspond to artery
and vein. They represent flow toward and away from the transducer, respectively.
Use time-gain compensation to improve imaging at the level of the vein and to reduce posterior acoustic
enhancement.
Power Doppler sonography is a technique that displays the strength of the Doppler signal in color rather
than speed or direction of the signal.
Power Doppler is more sensitive for low flow than its color Doppler counterpart.
General Scanning Technique

Scanning of vessels in extremities follows the same general principles. Two-point compression
ultrasound, as its name implies, involves scanning in the femoral triangle and the popliteal fossa.
Scanning should always include confirmation that the structure identified is continuous by scanning both
cephalad and caudally from the point of initial skin contact. Once you are confident you have identified a
vein and can see the artery next to it, scan proximally to distally—if there is a proximal thrombus, you
have diagnosed DVT.
Techniques to Confirm DVT

The most important ultrasound technique is compression, because this is both necessary and sufficient to
make the diagnosis of and to exclude DVT (Figure 19-5). The desired vein is always located in the
transverse plane (short axis). If compression is performed in the long-axis view, the vein may translate in
and out of the image plane, yielding a false-negative result. Progressive compression is performed until
either (1) complete approximation of the anterior and posterior walls of the vein is achieved or (2)
deformity or significant compression of the corresponding artery occurs without obliteration of the vein
lumen. If the vein is normal, the opposing walls have to touch, and as in the first case, this is a negative
compressive study. In the latter example, the study is positive, indicating that the thrombus within the
lumen is preventing approximation of the vessel walls.
In addition to compression, pulsed-wave, color, and power Doppler imaging can all be used to aid in
vessel identification, whereas color and power Doppler can allow for direct visualization of filling
defects in areas where a thrombus is suspected (Figure 19-6).
Augmentation of flow can also be used to aid in confirming DVT, but cannot be used as a sole indicator
for the presence or exclusion of a thrombus. Augmentation of flow is performed by having the Doppler
gate over the vein and performing a maneuver to increase flow through the vein. In the lower extremity,
the patient can dorsiflex his or her ankle or the ultrasonographer can gently squeeze the ipsilateral calf
while imaging the popliteal or femoral areas. Augmentation in the central veins of the upper extremity is
more challenging, but the patient can make a fist to augment flow of the axillary or basilic veins. In either
case, a normal study will show an increased velocity of blood flow through the vessel (Figure 19-7). An
abnormal study will reveal a blunted effect or no change at all if there is obstruction to the flow of the
vein.
Figure 19-5. Compression Ultrasound of the Upper Thigh

Abbreviations: A, artery; V, vein.
Example of normal compression of arteries and veins in the upper thigh. Black arrows indicate compressed veins.
Figure 19-6. Upper Extremity Color Doppler of the Axillary Vein
Abbreviation: V, vein.
Example of color Doppler (red and blue) used for identifying smaller arteries and veins with blood flow (white arrows) and an axillary vein
with thrombus showing no flow.
Figure 19-7. Normal Augmentation of Venous Blood Flow over the Femoral Vein
Lower Extremity DVT

The lower extremity has a reliable deep network of vessels, but with some anatomic duplication in 30%
to 50% of patients in the femoral and popliteal systems.10 Most studies were based on a limited 2-region
compression evaluation of the symptomatic extremity. Clots will extend into either the deep femoral or
popliteal regions, and will often originate in popliteal fossa. Therefore, complete imaging of the leg,
including the calf vessels, adds little other than time to the examination.11,12 In addition, emergency
department and ICU physicians favorably performed twopoint compression ultrasound to detect DVT
when compared to vascular ultrasound performed by ultrasound technicians and interpreted by
radiologists.8,13
Scanning of the Lower Extremity

The examination should start with the probe positioned at the level of the inguinal ligament. At this
location, the operator should be able to see the common femoral vein either next to the common femoral
artery or next to the already bifurcated artery (the common femoral artery usually bifurcates immediately
cranial to the corresponding vein). The greater saphenous vein usually inserts medially at this point, and
is easily visualized with sonography. Clinicians should be sure to visualize the saphenous vein and
compress it at the point of confluence. Compression and apposition of the venous vessel walls exclude
DVT at this level. The scan should continue to the level of bifurcation into the superficial and deep
femoral vein, and then approximately 10-12 cm distally toward the adductor canal at the level of the
distal femur, with serial compression being performed every 1-2 cm. Representative images only need to
be obtained at 1 or 2 of these areas (Figures 19-4 and 19-8–19-12).
C AVE AT S
The superficial femoral vein is part of the deep venous system.
Always visualize the saphenous vein and the popliteal trifurcation.
Clots in the superficial system can propagate easily into the deep venous system.
Figure 19-8. Normal Compression Ultrasound of the Proximal Thigh

Abbreviations: CFV, common femoral vein; GSV, greater saphenous vein; A, artery.
Normal CFV and GSV without compression (A) and with B) compression. Blue areas indicate veins. Red areas indicate bifurcated common
femoral artery (femoral and profunda femoris).
Figure 19-9. Normal Midfemoral Vein with and without Compression
Blue areas indicate veins, and red areas indicate arteries.
The examiner should then position the patient in either prone or lateral decubitus position to evaluate the
popliteal fossa. The popliteal vein is located superficial to the popliteal artery in this evaluation (Figure
19-9). Compression excludes DVT. This scan should be performed from the cranial aspect of the
popliteal fossa and continue down 4-6 cm below the popliteal fossa, to include the merging of the anterior
and posterior tibial veins with the peroneal vein. These tributaries do not necessarily need to be imaged
in a bedside scan.
Upper Extremity DVT

As with the lower extremity, the venous system has superficial and deep components. Given the frequency
of peripheral venous cannulation, the superficial system is a frequent site for thrombus and
thrombophlebitis. Upper extremity DVT is diagnosed in roughly 19% of hospitalized adult patients.14
Although lower extremity DVTs are thought to have a higher rate of embolization, one study noted that
almost 10% of upper extremity DVTs result in PE.15 More recently, Lamontagne et al16 noted that upper
extremity DVT occurred in 2.2% of medical and surgical patients. Although the presence of upper
extremity DVT was associated with a significant increased risk of PE, the presence of PE did not
translate into an increased risk of death.16
Figure 19-10. Midfemoral Compressive Ultrasound with Clot
A) Midfemoral vein with clot and no flow using color Doppler. B) Same image without color flow and obvious clot in vein.
Figure 19-11. Popliteal Compression Ultrasound without Clot

Abbreviations: V, vein; A, artery.
Normal popliteal vein without compression (A) and with compression (B), and complete opposition of anterior and posterior vessel walls
(arrow) next to the popliteal artery.
Figure 19-12. Popliteal Compression Ultrasound with Clot
Popliteal vein without compression (A) and with gentle compression and clot (B).
Specific Indications for Scanning

Indications for scanning include unilateral arm pain; swelling; redness, especially in the setting of a recent
central venous line in the internal jugular or subclavian veins;recent placement of a port; peripherally
inserted central catheter; or dialysis line placement. Peripherally inserted central catheter lines are
associated with a higher risk for thromboembolism than central venous catheters.17 Patients with
malignancy are particularly susceptible to upper extremity thrombus.9
Scanning of the Upper Extremity

The scanning of the upper extremity should start with the internal jugular vein, which is easily
compressible along its course to the supraclavicular notch, where it is joined by the subclavian vein to
form the brachiocephalic vein. These views are identical to those used in placing an ultrasound-guided
internal jugular central venous catheter. Caution should be used while compressing the internal jugular
vein because its close proximity to the carotid body at the carotid artery bifurcation could potentially
cause a vagal episode. Similar to the lower extremity examination, studies show a high sensitivity and
specificity of sonographic detection of clots with vein compression, 78% to 100% and 82% to 100%,
respectively.18
C AVE AT S
Remember to identify duplication of the venous system.

Use color or power Doppler on noncompressible vessels.
The scan should continue laterally in the supraclavicular position to evaluate the subclavian vein, because
this is noncompressible. Detection of a thrombus will be based on direct visualization, preferably
combined with color, power, or pulsed-wave Doppler (if available). Toward the midclavicle, the
ultrasonographer should move to an infraclavicular approach with the probe to continue imaging the
subclavian vein in the same manner. The vein is then followed into the axilla, where it becomes the
axillary vein after crossing the first rib and then down the arm where it becomes the brachial vein to the
antecubital fossa. As previously indicated, compression should take place at every 1-2 cm during the
course of the examination (Figures 19-13 and 19-14).
The large superficial veins—the basilic on the medial aspect and the cephalic on the lateral aspect—
should also be imaged and compressed along their course if possible, because proximally both of these
veins merge with the axillary vein and can contain DVTs (Figure 19-6).
Figure 19-13. Internal Jugular Vein Compression Ultrasound with Clot

Abbreviations: IJV, internal jugular vein; V, collateral vein; A, carotid artery.
Internal jugular vein and dilated collateral vein, both with clot and noncompressibility on ultrasound.
Treatment of DVT
In negative studies and where follow-up may be difficult, D-dimer can be used to further exclude DVT.
However, if the D-dimer test is positive and the ultrasound study is negative, then ultrasound should be
repeated in 1 week.19
Debate about the treatment of acute DVT is still ongoing. Generally, patients can be treated on an
outpatient basis, unless there is concern about follow-up or other significant comorbidities that require
inpatient admission.
Superficial thrombophlebitis should be treated with nonsteroidal anti-inflammatory drugs and heat.
Anticoagulation is not indicated.
Parenteral Anticoagulation
This treatment can be given with low-molecular-weight heparin (1.5 mg/kg daily preferred over 1 mg/kg
twice daily), fundaparinux, or unfractionated heparin with concurrent administration of a vitamin K
antagonist (VKA). The recommended starting dose of warfarin is 5-10 mg/day with concomitant
parenteral therapy for at least 5 days, and when the therapeutic international normalized ratio has been
achieved for at least 2 consecutive measurements, 24 hours apart.20
Enteral Anticoagulation
Although not endorsed by the American College of Chest Physicians, there is good evidence to suggest
that oral rivaroxaban can be used for initial treatment of acute DVT, at a dosing regimen of 15 mg twice a
day for 3 weeks, then 20 mg daily, without the need for checking the international normalized ratio, though
there is some difficulty in patients with renal insufficiency.21
Figure 19-14. Axillary Vein with Clot Adjacent to Color-filled Axillary Artery
Abbreviation: V, vein.
PE
PE remains the most feared and harmful sequelae of DVT. With an incidence of roughly 7 cases of PE per
100,000 population,22 the mortality can range from 8% in hemodynamically stable patients to 65% in
those requiring cardiopulmonary resuscitation.23 Survivors may have lifelong morbidity in the form of
debilitating pulmonary hypertension. In addition, treatment may require lifelong anticoagulation, resulting
in subsequent hemorrhagic complications.
Workup of PE remains complicated, with scoring systems, such as the modified Wells criteria24 and the
pulmonary embolism rule-out criteria,25 using risk profiles and D-dimer testing to reduce the need for
imaging with ionizing radiation.
Computed tomography (CT) pulmonary angiography remains the current gold standard diagnostic method
used for PE. However, ultrasound is an incredibly useful adjunct in patients who are too critically ill or
unstable to travel to the radiology suite for definitive imaging or in cases in which CT angiography could
be contraindicated, such as pregnancy or a history of life-threatening intravenous contrast allergy.
The primary purpose of the ultrasound examination in this regard is to either identify a clot in the right
heart system and/or signs of RV strain and obstruction in the setting of the correct clinical presentation.
Transducer Type and Optimal Views

Phased-array (cardiac) transducer: apical 4-chamber and parasternal short-axis views
Curvilinear transducer: IVC (if a phased-array probe cannot be used)
General Scanning Technique

The apical 4-chamber, parasternal short-axis, subcostal 4-chamber, and IVC views can all provide
ultrasonographic clues to the possible presence of PE. In each view, the clinician is looking for evidence
of RV strain and obstructive pathology. The apical 4-chamber view is the only view that allows a direct
comparison between the right and left ventricular chamber sizes and is the view in which the McConnell
sign can be identified (Figure 19-1).26 A parasternal short-axis view also allows for the comparison of
ventricular function, and can demonstrate flattening or bowing of the left ventricular septum toward the
left ventricle. This is commonly referred to as a “D-shaped left ventricle.” Flattening of the septum during
diastole is indicative of RV volume overload, and flattening during systole is indicative of increased RV
pressure (Figure 19-1). Because PE is an obstructive process, the subcostal IVC can reveal a large,
plethoric IVC without respiratory variation in size as a result of the significantly increased right-sided
filling pressures. If a completely collapsible IVC is present, alternative sources should be sought for the
patient’s condition.
Echocardiography for Diagnosis of PE

In an apical 4-chamber view of the heart, an RV-LV end-diastolic dimension ratio greater than 0.7 is
associated with a sensitivity of 66% and a specificity of 77% for PE. However, current guidelines suggest
an RV-LV ratio greater than 0.9:1 to define RV strain (Figure 19-2). This view also provides the rare
ability to see a clot in transit between the right atrium and the RV. The McConnell sign (isolated retained
apical kinesis in the setting of a dilated [and akinetic] RV) is frequently reported as the most specific
echocardiographic finding for PE (96%); however, it has exceedingly poor sensitivity (16%).27 To be
clinically useful, pretest probability, clinical context, and the prevalence of PE in the patient population
being scanned needs to be considered before the presence or absence of a McConnell sign can be
accurately interpreted as suggestive of PE. Except in the case of direct visualization of a clot in transit,
echocardiography is not diagnostic of PE. In the right clinical circumstances, the presence of RV strain on
echocardiography in combination with identification of DVT on two-point compression ultrasound in a
clinically unstable patient can be suggestive enough to rationalize immediate treatment for PE.
E X P E RT T I P S
Visualize the entire apex on the apical 4-chamber view.
Failure to visualize the entire apex can lead to inaccurate comparison.
E X P E RT T I P S
A clot in transit is the only definitive echocardiographic diagnosis of PE.
Explore other causes of RV strain or enlargement, such as chronic obstructive pulmonary

disease and pulmonary hypertension.
Continue the scan to include the IVC (PE is an obstructive process).
Treatment of PE
The treatment of PE is complicated and there is some debate remaining on definitive treatment, but it
generally falls under the categories of (1) anticoagulation, (2) thrombolysis, or (3) embolectomy.
Treatment will generally be based on the clinical picture. Minimally symptomatic patients without any
evidence of RV dysfunction or myocardial necrosis (as defined later in this section) can be treated with
anticoagulation alone. Current recommendations suggest subcutaneous low-molecular-weight heparin or
fondaparinux plus a VKA over intravenous unfractionated heparin plus a VKA, but the overall initial
treatment is the same as for DVT—parenteral anticoagulation plus an oral VKA.20
Current research suggests that in a select group of patients, oral anticoagulation with rivaroxaban can be
used to treat acute PE;22 however, this is not currently supported by published guidelines. Treatment of
more severe PE is more complicated and relies on various definitions of severity, which tend to be in
flux.
The American Heart Association (AHA) defines submassive PE as “acute PE without systemic
hypotension (systolic blood pressure >90 mm Hg) but with either RV dysfunction or myocardial
necrosis.” The presence of RV abnormality on ultrasound may therefore be used for risk stratification of
patients with PE. Based on ultrasound, RV dysfunction is further defined as RV dilation (apical 4-chamber
RV diameter divided by LV diameter >0.9) or RV systolic dysfunction on echocardiography or RV dilation
(again, apical 4-chamber RV diameter divided by LV diameter>0.9) on CT.28 However, adjuvant
laboratory testing (troponin, B-type natriuretic peptide, and electrocardiography) should all be used in
making this diagnosis.
In contrast, massive PE is similarly defined by the AHA as “acute PE with sustained hypotension
(systolic blood pressure 90 mm Hg for at least 15 minutes or requiring inotropic support, not due to a
cause other than PE, such as arrhythmia, hypovolemia, sepsis, or left ventricular dysfunction),
pulselessness, or persistent profound bradycardia (heart rate <40 beats/min with signs or symptoms of
shock).”20
Although current AHA guidelines still use the terms “submassive” and “massive” to describe PE, those
denotations have recently fallen out of favor because the clot burden does not correlate well with clinical
acuity or prognostication. Clot burden does, however, lead to an increased incidence of right heart
dilation.29 These definitions have more recently been replaced with “low risk” and “high risk” by the
European Society of Cardiology (ESC). The ESC defines “high risk” as suspected acute PE with shock or
hypotension, and “low risk” as suspected acute PE without shock or hypotension. In these ESC guidelines,
further explanation of shock or hypotension is given as “systolic blood pressure <90 mm Hg or a systolic
pressure drop ≥40 mm Hg for >15 minutes if not caused by new-onset arrhythmia, hypovolemia, or
sepsis.” This dichotomy is based on 30-day mortality figures.30
The peripheral venous system should be distended in order to evaluate the veins – ensure that the
extremities are dependent (reverse Trendelenberg), with arms hanging down in order to provide better
venous distension.
The legs may hang over the side of the bed to improve visualization of the lower extremity venous system.
Generally the more distal the vein, the more easily it is compressed. If you cannot visualize and expect the
vein, reduce the amount of pressure on the probe.
In a massive PE with hypotension, refractory shock, peri-arrest, or arrest, the treatment should generally
lean toward thrombolysis, either systemic or catheter-directed, in centers with this capability. Emergent
mechanical embolectomy can also be considered. Current dosing recommendations for treatment of a
massive or submassive PE (with impending respiratory or circulatory compromise) is 100 mg of
alteplase over 2 hours if there are no contraindications to thrombolysis.
Alternatively, in a cardiac arrest likely caused by PE, there is no definitive recommendation, but studies
suggest a bolus dose of 50-100 mg with or without an intravenous infusion.31 It should be noted that there
is no role for thrombolysis in undifferentiated cardiac arrest.
KEY POINTS
Bedside vascular ultrasound can be quickly performed to evaluate a patient for lower or upper
extremity DVT.
DVTs are associated with increased risk of mortality and significant morbidity.
With the exception of clot in transit, echocardiography is not diagnostic for PE.
In the correct clinical circumstance, the presence of RV strain on bedside echocardiography can
assist in risk stratification of patients with suspected PE.
REFERENCES
1. Burnside PR, Brown MD, Kline JA. Systematic review of emergency physician-performed ultrasonography for lower-extremity deep vein
thrombosis [review]. Acad Emerg Med. 2008;15:493-498.
2. Lensing AW, Doris CI, Mcgrath FP, et al. A comparison of
compression ultrasound with color Doppler ultrasound for the diagnosis of symptomless postoperative deep vein thrombosis. Arch Intern
Med. 1997;157:765-768.
3. Pennell RC, Mantese VA, Westfall SG. Duplex scan for deep vein thrombosis--defining who needs an examination of the contralateral
asymptomatic leg. J Vasc Surg. 2008;48:413-416.
4. Burns GA, Cohn SM, Frumento RJ, et al. Prospective ultrasound evaluation of venous thrombosis in high-risk trauma patients. J Trauma.
1993;35:405-408.
5. Marik PE, Andrews L, Maini B. The incidence of deep venous thrombosis in ICU patients. Chest. 1997;111:661-664.
6. Cook D, Crowther M, Meade M, et al. Deep venous thrombosis in medical-surgical critically ill patients: prevalence, incidence, and risk
factors. Crit Care Med. 2005;33:1565- 1571.
7. Galanaud JP, Kahn SR. Postthrombotic syndrome: a 2014 update. Curr Opin Cardiol. 2014;29:514-519.
8. Kearon C. Natural history of venous thromboembolism. Circulation. 2003;107(suppl 1):I22-30.
9. Prandoni P, Polistena P, Bernardi E, et al. Upper-extremity deep vein thrombosis: risk factors, diagnosis, and complications. Arch Intern
Med. 1997;157:57-62.
10. Pozniak MA, Allan PL. Clinical Doppler Ultrasound. New York, NY: Churchill Livingstone; 2013.
11. Poppiti R, Papanicolaou G, Perese S, et al. Limited B-mode venous imaging versus complete color-flow duplex venous scanning for
detection of proximal deep venous thrombosis. J Vasc Surg. 1995;22:553-557.
12. Crisp JG, Lovato LM, Jang TB. Compression ultrasonography of the lower extremity with portable vascular ultrasonography can
accurately detect deep venous thrombosis in the emergency department. Ann Emerg Med. 2010;56:601-610.
13. Kory PD, Pellecchia CM, Shiloh AL, et al. Accuracy of ultrasonography performed by critical care physicians for the diagnosis of DVT.
Chest. 2011;139:538-542.
14. Mustafa S, Stein PD, Patel KC, et al. Upper extremity deep venous thrombosis. Chest. 2003;123:1953-1936.
15. Becker DM, Philbrick JT, Walker FB. Axillary and subclavian venous thrombosis: prognosis and treatment. Arch Intern Med.
1991;151:1934-1943.
16. Lamontagne F, Mcintyre L, Dodek P, et al. Nonleg venous thrombosis in critically ill adults: a nested prospective cohort study. JAMA Intern
Med. 2014;174:689-696.
17. Chopra V, Anand S, Hickner A, et al. Risk of venous thromboembolism associated with peripherally inserted central catheters: a systematic
review and meta-analysis. Lancet. 2013;382:311-325.
18. Sajid MS, Ahmed N, Desai M, et al. Upper limb deep vein thrombosis: a literature review to streamline the protocol for management. Acta
Haematol. 2007;118:10-18.
19. Kraaijenhagen RA, Piovella F, Bernardi E, et al. Simplification of the diagnostic management of suspected deep vein thrombosis. Arch
Intern Med. 2002;162:907-911.
20. Kearon C, Akl EA, Comerota AJ, et al. Antithrombotic therapy for VTE disease: antithrombotic Therapy and Prevention of Thrombosis,
9th ed—American College of Chest Physicians Evidence-Based Clinical Practice Guidelines. Chest. 2012;141(suppl):e419S-e494S.
21. Bauersachs R, Berkowitz SD, Brenner B, et al. Oral rivaroxaban for symptomatic venous thromboembolism. N Engl J Med.
2010;363:2499-2510.
22. Büller HR, Prins MH, Lensin AW, et al. Oral rivaroxaban for the treatment of symptomatic pulmonary embolism. N Engl J Med.
2012;366:1287-1297.
23. Kasper W, Konstantinides S, Geibel A, et al. Management strategies and determinants of outcome in acute major pulmonary embolism:
results of a multicenter registry. J Am Coll Cardiol. 1997;30:1165-1171.
24. Wolf SJ, Mccubbin TR, Feldhaus KM, et al. Prospective validation of Wells Criteria in the evaluation of patients with suspected pulmonary
embolism. Ann Emerg Med. 2004;44:503-510.
25. Kline JA, Courtney DM, Kabrhel C, et al. Prospective multicenter evaluation of the pulmonary embolism rule-out criteria. J Thromb
Haemost. 2008;6:772-780.
26. Mcconnell MV, Solomon SD, Rayan ME, et al. Regional right ventricular dysfunction detected by echocardiography in acute pulmonary
embolism. Am J Cardiol. 1996;78:469- 473.
27. Lodato JA, Ward RP, Lang RM. Echocardiographic predictors of pulmonary embolism in patients referred for helical CT.
Echocardiography. 2008;25:584-590.
28. Jaff MR, Mcmurtry MS, Archer SL, et al. Management of massive and submassive pulmonary embolism, iliofemoral deep vein thrombosis,
and chronic thromboembolic pulmonary hypertension: a scientific statement from the American Heart Association. Circulation.
2011;123:1788- 1830.
29. Furlan A, Aghayev A, Chang CC, et al. Short-term mortality in acute pulmonary embolism: clot burden and signs of right heart dysfunction
at CT pulmonary angiography. Radiology. 2012;265:283-293.
30. Konstantinides SV, Torbicki A, Agnelli G, et al. 2014 ESC Guidelines on the diagnosis and management of acute pulmonary emobolism. Eur
Heart J. 2014;35:3033-3080.
31. Hayes B. What’s the code dose of tPA? Academic Life in Emergency Medicine website. Available at: http://www. aliem.com/whats-the-
code-dose-of-tpa/. March 14, 2013. Accessed April 13, 2015.
Chapter 20
Cardiac Arrest: Focused Echocardiographic
Evaluation in Life Support (FEEL)
James Fair, MD; Michael Mallin, MD
OBJECTIVES
Describe the practical use of echocardiography in cardiac arrest
Explain the challenges of true and pseudo-pulseless electrical activity
Describe the use of ultrasound in the management of reversible causes of cardiac arrest:
Hypovolemia
Tamponade and pericardiocentesis
Tension pneumothorax
Right heart failure, including pulmonary embolism
Left heart failure, including myocardial infarction
Describe the use of transesophageal echocardiography in cardiac arrest
INTRODUCTION
The use of ultrasound in cardiac arrest presents many challenges, given the time constraints and imaging
difficulties posed by performing high-quality cardiopulmonary resuscitation (CPR). Importance must be
placed on high-quality chest compressions and minimizing interruptions during closed cardiac
compressions. Despite the challenges posed by this environment, ultrasound can be an extremely useful
diagnostic tool in identifying cardiac function during arrest, identifying reversible causes of cardiac
arrest, and guiding the treatment of those reversible conditions. This chapter will focus on the practical
application of ultrasound in the patient experiencing cardiac arrest.
CASE STUDY
A 35-year-old male truck driver with a history of hypertension is brought to the emergency department by
his wife for chest pain and shortness of breath that began about an hour before arrival. The initial systolic
blood pressure is 55 mm Hg, and the patient loses consciousness shortly after being placed in a room. His
pulses are not palpable and closed cardiac compressions are started after he is transferred to the gurney.
The patient quickly regains consciousness, complaining of chest pain as IV access is obtained, an oxygen
face mask is placed, and pulse oximetry and telemetry are started. Initial vital signs are a blood pressure
of 72/35 mm Hg, heart rate of 110 beats/min, oxygen saturation of 85%, respiratory rate of 32
breaths/min, and temperature of 37.2°C. Electrocardiography is called for but the patient loses
consciousness and becomes pulseless again before arrival of the electrocardiography machine.
The patient is given CPR according to American Heart Association guidelines, and the initial rhythm
shows pulseless electrical activity (PEA). The patient undergoes mechanical intubation. While
compressions are under way, an apical 4-chamber echocardiographic view is obtained, and during the
next pulse check it shows a dilated, poorly functioning right ventricle (RV) and an underfilled left
ventricle (LV) (Figure 20-1). Tissue plasminogen activator, 50 mg, is ordered and given 8 minutes into the
echocardiographic code, with a second dose of tissue plasminogen activator given 15 minutes into
echocardiography. Return of spontaneous circulation is achieved after 23 minutes of CPR, with a blood
pressure of 80/60 mm Hg. An epinephrine drip is started and the patient is taken to the interventional
radiology suite for emergent thrombectomy. In the interventional radiology suite, a complete right main
pulmonary artery occlusion is found and the thrombus is removed, with blood pressure rebounding to
124/72 mm Hg on admission to the ICU. After a prolonged 60-day hospital stay because of complications
of RV failure, the patient leaves the hospital completely neurologically intact.
Figure 20-1. Dilated RV in Patient with Pulmonary Embolism

Abbreviations: RV, right ventricle; LV, left ventricle; RA, right atrium; LA, left atrium.
Reproduced with permission Breitkreutz R, Walcher F, Seeger FH. Focused echocardiographic evaluation in resuscitation management:
concept of an advanced life support-conformed algorithm. Crit Care Med. 2007;35:S150-S161. Copyright © 2007 Society of Critical Care
Medicine and Lippincott Williams & Wilkins.
Cardiac arrest treatment follows a protocolized approach based on the importance of high-quality CPR
and early defibrillation of shockable rhythms with minimal interruptions to chest compressions.1 At the
same time, focused echocardiography has been shown to be tremendously useful in cardiac arrest, both
diagnostically and prognostically.2 To incorporate focused echocardiography into the management of
cardiac arrest, a protocolized approach is recommended, which requires focused training effort.3 Both
transthoracic echocardiography (TTE) and transesophageal echocardiography (TEE) can be used. TEE
has been suggested to be better suited for use in cardiac arrest because it does not interfere with chest
compressions, offers better image quality, and acquires images instantly during a pulse check, thus
minimizing interruption of chest compressions.4 However, because TEE is not widely available in most
ICUs and emergency departments, this chapter will focus mainly on the use of TTE.
PRACTICAL APPLICATION
When using TTE during CPR, the preferred views to obtain are the parasternal long-axis and short-axis,
the apical 4-chamber, or the subcostal long-axis views. Apical and subcostal views allow evaluation of
both the right and left heart and can sometimes be obtained during chest compressions. The parasternal
window is challenging because it cannot be obtained until the CPR provider removes his or her hands,
and is unobtainable with mechanical CPR devices. If the parasternal window is used, the
ultrasonographer must apply gel before attempting visualization, and should be prepared to remove the gel
before restarting compressions. This process will limit the time available for scanning during a 10-
second pulse check.
Regardless of the view obtained, it is imperative to not delay the resumption of chest compressions,
because pulse checks should last no longer than 10 seconds. It is advisable that the ultrasonographer or
code team leader count down aloud from 10 during pulse checks to ensure no delay occurs.3 Windows are
sometimes obtainable during compressions, therefore the probe should be placed before the pulse check
so image acquisition is immediate. Images should be saved to the ultrasound machine so that the images
can be analyzed after the pulse check once compressions have resumed, avoiding any delay of
compressions (Table 20-1).
PEA vs. PSEUDO-PEA

Current recommendations classify cardiac arrest into shockable and nonshockable rhythms, with
ventricular tachycardia and ventricular fibrillation representing the shockable rhythms and PEA and
asystole representing the nonshockable rhythms. This classification system relies on 2 criteria: rhythm
analysis and palpation of a pulse. Pulse checks have been shown to be inaccurate, with first responders
only correctly identifying the presence of a carotid pulse in 55% of cases with no time constraints, and
only 15% of cases when limited to the 10 seconds allowed during pulse checks.5 Echocardiography
provides an obvious remedy to these problematic inaccuracies by differentiating organized cardiac
activity capable of perfusing the body underneath the observed rhythm or frank cardiac standstill. PEA has
traditionally been thought to be synonymous with electromechanical dissociation, meaning there is
organized electrical activity without organized contractility (Video 20-1 ). Ultrasound, as well as data-
utilizing invasive arterial blood pressure measurements, has found that in many cases there is often
perfusion despite the lack of a palpable pulse. The term “pseudo-PEA” has thus been coined to describe
the situation when cardiac function is seen on ultrasound or arterial line waveform without a palpable
pulse2,6 (Video 20-2 ). It is also possible for the monitor to falsely show asystole when either
organized contractility or a shockable rhythm is present (Video 20-3 ).
E X P E RT T I P
To minimize interrupting chest compressions, acquire apical 4-chamber or subcostal views
during chest compressions, allowing instant image acquisition during the pulse check. If the
parasternal view is the only adequate window, then have the gel preloaded on the phased-array
probe before the pulse checks and a towel in the other hand ready to wipe the excess gel off the chest
before resuming compressions. Save image clips during pulse checks and evaluate them during
compressions to avoid delaying compressions.
Table 20-1. FEER Protocol*
Phase Step With Command, Element
High-quality CPR, 1. Perform immediate and accurate BLS and ACLS according to AHA/ERC/ILCOR guidelines, with at least 5 cycles of chest compression/ventilation
preparation, team 2. Tell the CPR team: “ I am preparing an echocardiogram”
information 3. Prepare portable ultrasound (let prepare) and test it
4. Accommodate situation (eg, best position of patient and doctor, removal of clothes), be ready to start
Execution, obtaining 5. Tell CPR team to count down 10 secs and undertake a pulse check simultaneously
the echocardiogram 6. Command: “ Interrupt at the end of this cycle for echocardiography”
7. Put the probe gently onto the patient’s subxiphoid region during chest compressions
8. Perform a subcostal (long axis) echocardiogram as quickly as possible. If you cannot identify the heart after 3 secs, stop the interruption and repeat
again 5 cycles later and/or with the parasternal approach
Resuming CPR 9. Command after 9 secs at the latest: “ Continue CPR” and control it
Interpretation and 10. Communicate (after continuation of chest compressions only) the finding to the CPR team (eg, wall motion, heart squeezing, cardiac standstill
consequences [massive], pericardial effusion, no conclusive finding, suspected pulmonary artery embolism, hypovolemia) and explain consequences and follow-up
procedure
Abbreviations: FEER, focused echocardiographic evaluation in resuscitation; CPR, cardiopulmonary resuscitation; BLS, Basic Life Support;
ACLS, Advanced Cardiac Life Support; AHA, American Heart Association; ERC, European Resuscitation Council; ILCOR, International
Liaison Committee on Resuscitation.
*A practical approach is depicted. Because CPR interruption is limited to a maximum of 10 secs within advanced life support, it is necessary
to give clear commands. Note that the echocardiogram is undertaken after clear preparation only in step 8.
Reproduced with permission Breitkreutz R, Walcher F, Seeger FH. Focused echocardiographic evaluation in resuscitation management:
concept of an advanced life support-conformed algorithm. Crit Care Med. 2007;35:S150-S161. Copyright © 2007 Society of Critical Care
Medicine and Lippincott Williams & Wilkins.
To date there is one sizeable study implementing a TTE protocol into CPR that involved 230 patients, of
which 204 underwent the focused echocardiographic evaluation in life support (FEEL). The study found
that the use of ultrasound in cardiac arrest is both feasible as well as beneficial. The FEEL protocol was
studied in a prehospital environment and performed by emergency physicians who underwent a standard
training program, and found that 96% of the images were of diagnostic quality and the use of ultrasound
changed management in 78% of cases. This study supports the inaccuracies of the current classification of
patients as having asystole or PEA, based on rhythm analysis and pulse checks, finding that 58% of
patients initially classified as having PEA and 35% of patients with asystole actually had organized
cardiac activity.2 This is helpful prognostic information, as organized cardiac activity confers a much
better prognosis than true PEA or asystole.7 Patients found to have true PEA, identified by electrical
activity on the monitor with cardiac standstill on echocardiogram, have a very poor prognosis – with
virtually none of them surviving to hospital discharge.8 The FEEL trial also showed that in the peri-arrest
patient, the FEEL protocol helped identify reversible causes of cardiac arrest such as pulmonary
embolism (PE), cardiac tamponade, and hypovolemia.2 Although one would think an earlier diagnosis of
reversible causes would lead to improved survivability, this question has not yet been studied in any large
clinical trials.
C AVE AT
Although cardiac standstill is predictive of poor outcome, this is only true in patients with out-of-
hospital arrest and emergency department ultrasound. Presumably, these patients have had
prolonged downtimes. Data are limited on cardiac standstill visualized in patients having an in-
hospital cardiac arrest.
IDENTIFYING REVERSIBLE CAUSES

A distinct advantage of cardiac ultrasound during arrest care is the ability to identify reversible causes of
arrest that allow for diagnoses not otherwise easily identified. These diagnoses made by cardiac
ultrasound during arrest may lead to therapeutic maneuvers that can be potentially lifesaving. Potential
diagnoses recognizable on cardiac ultrasound include pericardial tamponade, acute myocardial infarction
(MI), PE, hypovolemia, and, potentially, tension pneumothorax.
Cardiac Tamponade
Cardiac tamponade caused by pericardial effusion is a reversible cause of cardiac arrest in which
ultrasound is essential for both the diagnosis and treatment. The development of tamponade physiology
does not depend on the size of fluid accumulation but rather on the speed at which the fluid accumulates,
with fluid collections as small as 50 to 100 mL causing tamponade in some cases. A pericardial effusion
is seen on ultrasound as an anechoic region that surrounds the heart circumferentially and can be
visualized from the parasternal, apical, and subcostal views (Figure 20-2). The parasternal long-axis
view can be useful to differentiate a pericardial effusion from a pleural effusion by identifying the fluid as
tracking either anterior (pericardial) or posterior (pleural) to the descending thoracic aorta. A common
false-positive finding that is mistaken for pericardial effusion is the presence of an anterior fat pad. This
can be differentiated from a pericardial effusion because the fat pad is more echogenic than an effusion
and is limited to the anterior portion of the heart, so it will not wrap circumferentially around the
posterior aspect of the heart. Identifying a possible effusion in multiple views is recommended to avoid
false positives.9
A pericardial effusion of course does not always cause tamponade, and care should be taken to ensure that
tamponade physiology is present before performing an invasive procedure such as pericardiocentesis. In
an arrest situation, there is no time to perform complicated echocardiographic evaluation of tamponade
physiology. In this particular setting, a pericardial effusion causing tamponade should demonstrate
significant RV collapse, resulting in an underfilled LV. Without these findings, the pericardial effusion is
unlikely to be the cause of arrest.
Figure 20-2. Subcostal M-Mode View of Pericardial Effusion with RV Collapse During Diastole
Abbreviation: RV, right ventricular.
A pericardial effusion causes tamponade if the pressure in the pericardium from the effusion rises
sufficiently to overcome the right atrial (RA) pressure and thus the ability of the heart to fill. This
pressure will first cause noticeable changes in chambers of the heart with the lowest pressure. The RA
collapses during systole, and suggests tamponade if it collapses for longer than one-third the duration of
the cardiac cycle. Collapse of the RV during diastole suggests tamponade physiology with greater
specificity but less sensitivity than RA collapse. M-mode obtained through the RV and LV from either the
parasternal or subcostal views can be helpful in clarifying the timing of RV collapse as occurs during
systole or diastole (Figure 20-2). Pericardial tamponade typically causes respiratory variation of inflow
velocities because of ventricular interdependence. This occurs because the space within the pericardium
is limited during tamponade, thus the filling of 1 ventricle impairs filling of the other. This phenomenon
can be observed by placing pulsed-wave Doppler at the tip of the mitral valve (MV) leaflets or tricuspid
valve (TV) leaflets and observing the degree of variation of filling with respiration (Figures 20-3 and 20-
4). During spontaneous ventilation, the RV will fill more with inspiration because of the effects of
negative intrathoracic pressure, causing a higher velocity during inspiration through the TV and a lower
velocity through the MV. The LV will fill more during expiration, causing a higher velocity through the
MV and a lower velocity through the TV. Velocity variations of more than 25% through the MV and more
than 40% through the TV are highly suggestive of tamponade.10
Figure 20-3. Pulsed-Wave Doppler Image, RV Inflow

Marked respiratory variation of right ventricle inflow can be seen in the presence of pericardial effusion, suggesting tamponade in a
Figure 20-4. Pulsed-Wave Doppler Image, LV Inflow
Marked respiratory variation of left ventricle inflow can be seen in the presence of pericardial effusion, suggesting tamponade in a
When performing pericardiocentesis, ultrasound guidance is recommended to decrease complication

rates. A parasternal, apical, or subxiphoid approach is possible, and ultrasound allows identification of
the largest fluid collection as well as avoidance of lung or liver tissue. Once the safest location for
pericardiocentesis is chosen, the needle should be advanced with continuous aspiration under ultrasound
guidance so that the physician is always aware of the location of the needle tip. Gentle fanning back and
forth of the ultrasound beam will help to keep track of the true needle tip. Once the needle is visualized
within the pericardial space, infusing agitated saline may be useful to ensure the correct location, and a
catheter can then be advanced into the pericardial space for further drainage of fluid.11
When using the subcostal window, make small adjustments by fanning back and forth and rotating to
make all 4 heart chambers appear as large as possible. This will give a more accurate representation
of the actual size ratio of the RV to the LV. If the coronary sinus is visualized, the plane is too far inferior.
If the aortic valve is visible, the plane is too far anterior.
Myocardial Infarction
Another reversible cause of cardiac arrest is MI, but this can be difficult to diagnose with
echocardiography given its various possible presentations, depending on the distribution of the infarct. In
a patient presenting with cardiac arrest caused by MI and who has organized cardiac contractility, severe
LV systolic dysfunction with an ejection fraction less than 30% will be the most likely finding on
echocardiography. This can be observed by poor motion of the endocardial walls, a lack of thickening of
the myocardium during systole, and poor MV opening during diastole. LV systolic function can be
evaluated by noncardiologists such as emergency physicians with good correlation with cardiologists.12
Regional wall motion abnormalities (WMA) may be present at the same time. If an MI is related to a
single vessel coronary artery occlusion, then a regional WMA will likely be present. Generally speaking,
anterior, septal, and apical WMAs suggest occlusion of the left anterior descending artery, lateral WMAs
correspond to left circumflex occlusions, and inferior WMAs correspond to right coronary artery
occlusions. However, significant variability exists in coronary artery distribution, and patients may have
preexisting abnormalities related to prior infarcts. Any patient suffering a cardiac arrest without a
sufficient alternative explanation should be considered for emergency catheterization or thrombolysis for
suspected MI.
PE
Massive PE is the cause of a significant number of cardiac arrests. It causes circulatory collapse with the
presence of an abrupt and dramatic increase in resistance in the pulmonary arteries, thus creating pressure
overload of the RV. When PE is the cause of cardiac arrest, the ultrasonographer should expect the right
heart to be dilated and poorly functioning, while the LV will typically be underfilled and hyperkinetic.
Once the patient enters cardiac arrest, the LV may also be hypokinetic because of ischemia, thus
complicating the situation. The RV dilation and hypokinesis should persist, however.
Several echocardiographic tools exist to assess for RV pressure overload. In the setting of massive PE,
the RV size will be dilated, and an RV-LV diastolic ratio greater than 1 indicates increased RV dysfunction
(Figure 20-1). Increased pressure in the RV will also cause flattening of the septum, giving a D-shaped
appearance to the LV if viewed from the parasternal short axis (Figure 20-5). Elevated right-sided
pressures will also cause the inferior vena cava (IVC) to appear dilated with a diameter greater than 2.1
cm, and less than 50% collapsibility with respiration.13 Tricuspid annular plane systolic excursion is
simply the measurement of the distance the tricuspid lateral annulus moves back and forth with each
cardiac cycle. In the case of severely increased RV pressure, the annulus fails to move much because of
the increased pressure the RV faces. Tricuspid annular plane systolic excursion can be measured from the
apical 4-chamber view by placing M-mode with the spike through the tricuspid lateral annulus and
measuring the distance the annulus travels with each beat, with a value lower than 1.7 cm being
abnormal13 (Figure 20-6). Although uncommon, a clot in transit may be visualized within the RA, RV, or
IVC, thus making the diagnosis obvious (Video 20-4 ).
Hypovolemia
Hypovolemia is a common cause of cardiac arrest, with PEA being the most likely initial rhythm. The
easiest way to evaluate the possibility of hypovolemia is to perform ultrasound of the IVC looking for size
and collapsibility. Although there is a body of literature on using IVC ultrasound to predict fluid
responsiveness, hypovolemia causing cardiac arrest will not require subtle measurements and will be
clearly small in a spontaneously breathing patient, with a diameter usually of less than 1 cm, and
collapsible by more than 50%. If the IVC is measured, it should be measured about 1 cm proximal to the
middle hepatic vein, and M-mode can be used to better visualize the degree of collapsibility with
respiration (Figure 20-7). The IVC in this case may be difficult to locate given the fact that it could be
completely collapsed. Other signs of hypovolemia include a small, hyperdynamic, and underfilled RV and
LV with cavity obliteration during systole.14
Figure 20-5. D-Shaped LV Caused by Flattened Septum
This occurs because of elevated right-sided pressures in a patient with pulmonary embolism.
Figure 20-6. Tricuspid Annular Plane Systolic Excursion

In this example, reduced tricuspid annular plane systolic excursion (TAPSE) occurs because of acute pulmonary embolism.
Tension Pneumothorax
Another potential cause of obstructive shock-related cardiac arrest is tension pneumothorax. Ultrasound
has been shown to be superior to supine chest radiography for the identification of pneumothorax, and in
the case of cardiac arrest, a computed tomography scan is not an option.15 In a normal lung, sliding with
each respiration will be observed at the pleural line, which confirms the absence of pneumothorax in that
location. However, in the case of cardiac arrest the patient will not have spontaneous respirations, hence
lung sliding will be absent. Lung sliding should be observed if the patient is given a breath with an
adequate tidal volume, and this can be performed during a pulse check. However, as with
echocardiography in cardiac arrest, care must be taken to ensure ultrasound evaluation is not prolonging
pulse checks to any more than 10 seconds. The presence of B-lines excludes the presence of
pneumothorax in that location. Although a thorough examination of several lung fields is necessary to
exclude a small pneumothorax, a hemodynamically significant pneumothorax capable of causing cardiac
arrest can be excluded with the presence of lung sliding in a single region of that lung ( Video 20-5 ).
The absence of lung sliding with ultrasound has been shown to be an excellent tool for the diagnosis of
pneumothorax in other clinical scenarios. However, this has not yet been studied in the cardiac arrest
population, and there is no current evidence that this method is superior to a physical examination.2
Figure 20-7. Inferior Vena Cava, M-Mode Image

Complete collapse with inspiration is demonstrated in a spontaneously breathing patient.
TEE USE IN CARDIAC ARREST

In multiple case series, TEE has been shown to reliably provide the diagnosis of cardiac arrest and to
guide appropriate interventions, such as fluid resuscitation, pulmonary embolectomy, or
pericardiocentesis.16-18 As mentioned previously, TEE is ideally suited for use in cardiac arrest given its
superior image quality and lack of interference with chest compressions. When using TEE during CPR,
the midesophageal 4-chamber view provides the best single view to evaluate cardiac activity during
pulse checks (Figure 20-8 and Video 20-6 ). This view is also the easiest to obtain, with the TEE
probe simply advanced at 0 degrees on the multiplane until the left atrium comes into view. From there,
slight retroflexion might be required, along with centering the image with rotation; once the view is
acquired, the probe can be left in place throughout the resuscitation. Just as in TTE, images should be
saved during pulse checks and interpreted after compressions have resumed, avoiding any delays in chest
compressions. The same concepts seen in TTE for identifying reversible causes of arrest apply to TEE,
with some minor variations. Regarding evaluation for right heart failure suggestive of PE, the
midesophageal 4-chamber view will provide evaluation of RV size and function, but flattening of the
septum is better evaluated from the transgastric short-axis view. Evaluation of hypovolemia can be made
more easily from the bicaval view with collapsibility of the superior vena cava of 36% or more,
indicating fluid responsiveness in patients receiving mechanical ventilation19 or by assessing LV end-
diastolic area in the transgastric short-axis view.20 However, this technique has only been studied in
patients with sepsis19 or those undergoing cardiac surgery, and is not necessarily applicable to the patient
in cardiac arrest or peri-arrest.
Figure 20-8. Transesophageal Echocardiography, Midesophageal 4-Chamber View

Abbreviations: LA, left atrium; RA, right atrium; RV, right ventricle; LV, left ventricle.
KEY POINTS
Echocardiographic evaluation of the heart during arrest is feasible during pulse checks, but should
not prolong pulse checks and should not last longer than 10 seconds.
Echocardiography can be useful as an adjunct to the pulse check to help differentiate true-PEA from
pseudo-PEA.
Echocardiography is useful for assessing the reversible causes of cardiac arrest, changing
management in most cases.
Hypovolemic shock as a cause of cardiac arrest is suggested by a small, collapsible IVC and a
hyperdynamic, underfilled LV.
Cardiac tamponade is suggested by the presence of a pericardial effusion along with a distended
noncollapsing IVC.
Tension pneumothorax as a cause for cardiac arrest is suggested by the absence of lung sliding
unilaterally.
Right heart failure as caused by pulmonary embolism is likely the cause of cardiac arrest when a
dilated RV is observed with an RV-LV diastolic area ratio >1.
Left heart failure, as is seen after MI or in end-stage systolic heart failure, is likely the cause of
cardiac arrest in the case of a severely decreased ejection fraction.
REFERENCES
1. Neumar RW, Otto CW, Link MS, et al. Part 8: Adult Advanced Cardiovascular Life Support: 2010 American Heart Association Guidelines
for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2010; 122:S729-S767.
2. Breitkreutz R, Price S, Steiger HV. Focused echocardiographic evaluation in life support and peri-resuscitation of emergency patients: a
prospective trial. Resuscitation. 2010;81:1527-1533.
3. Breitkreutz R, Walcher F, Seeger FH. Focused echocardiographic evaluation in resuscitation management: concept of an advanced life
support-conformed algorithm. Crit Care Med. 2007;35(5 suppl):S150-S161.
4. Blaivas M. Update on point of care ultrasound in the care of the critically ill patient. World J Crit Care Med. 2012;1:102- 105.
5. Eberle B, Dick WF, Schneider T, et al. Checking the carotid pulse check: diagnostic accuracy of first responders in patients with and
without a pulse. Resuscitation. 1996; 33:107-116.
6. Paradis NA, Martin GB, Goetting MG. Aortic pressure during human cardiac arrest. Identification of pseudo-electromechanical
dissociation. Chest. 1992;101:213-218.
7. Salen P, Melniker L, Chooljian C. Does the presence or absence of sonographically identified cardiac activity predict resuscitation
outcomes of cardiac arrest patients? Am J Emerg Med. 2005;23:459-462.
8. Blyth L, Atkinson P, Gabb K. Bedside focus echocardiography as a predictor of survival in cardiac arrest patients: a systematic review.
Acad Emerg Med. 2012;19:1119-1126.
9. Otto CM. Textbook of Clinical Echocardiography. 5th ed. Philadelphia, PA: Saunders; 2013:255-262.
10. Klein A, Abbara S, Agler D. American Society of Echocardiography clinical recommendations for multimodality cardiovascular imaging of
patients with pericardial disease. J Am Soc Echocardiogr. 2013;26:965-1012.
11. Silvestry FE, Kerber RE, Brook MM. Echocardiography-guided interventions. J Am Soc Echocardiogr. 2009; 22:213-231.
12. Randazzo MR, Snoey ER, Levitt MA. Accuracy of emergency physician assessment of left ventricular ejection fraction and central
venous pressure using echocardiography. Acad Emerg Med. 2003;10:973-977.
13. Lang RM, Badano LP, Mor-Avi V. Recommendations for cardiac chamber quantification by echocardiography in adults: an update from
the American Society of Echocardiography and the European Association of Cardiovascular Imaging. J Am Soc Echocardiogr. 2015;28:1-
39.
14. Leung JM, Levine EH. Left ventricular end-systolic cavity obliteration as an estimate of intraoperative hypovolemia. Anesthesiology.
1994;81:1102-1109.
15. Blaivas M, Lyon M, Duggal S. A prospective comparison of supine chest radiography and bedside ultrasound for the diagnosis of traumatic
pneumothorax. Acad Emerg Med. 2005;12:844-849.16.
16. Memtsoudis SG, Rosenberger P, Loffler M. The usefulness of transesophageal echocardiography during intraoperative cardiac arrest in
noncardiac surgery. Anesth Analg. 2006;102:1653-1657.
17. Van der Wouw PA, Koster RW, Delemarre BJ. Diagnostic accuracy of transesophageal echocardiography during cardiopulmonary
resuscitation. J Am Coll Cardiol. 1997; 30:780-783.
18. Lin T, Chen Y, Lu C. Use of transoesophageal echocardiography during cardiac arrest in patients undergoing elective non-cardiac surgery.
Br J Anaesth. 2006;96:167-170.
19. Vieillard-Baron A, Chergui K, Rabiller A. Superior vena caval collapsibility as a gauge of volume status in ventilated septic patients.
20. Cheung AT, Savino JS, Weiss SJ. Echocardiographic and hemodynamic indexes of left ventricular preload in patients with normal and
abnormal ventricular function. Anesthesiology. 1994;81:376-387.
Chapter 21
Infection: Septic Shock
Patrick Bender, MD; Robert Hieronimus, MD
Videos referred to in this chapter may be accessed by visiting www.sccm.me/ultcomp
OBJECTIVES
Review the pathophysiology of sepsis and the systemic manifestations of septic shock and severe sepsis
Present a case of sepsis-induced myocardial dysfunction; review the natural history and some of the
echocardiographic findings
Review the echocardiographic assessment of preload and volume status in patients with sepsis
Discuss left and right ventricular dysfunction in sepsis
Discuss the use of echocardiography in guiding hemodynamic management of patients with sepsis
Outline one possible algorithm for guiding sepsis therapy with echocardiography
INTRODUCTION
Sepsis is a maladaptive response to infection that can be refractory to resuscitation (septic shock) and
progress to organ dysfunction (severe sepsis). Septic shock is characterized by systemic vasodilation,
endothelial dysfunction, tissue hypoperfusion, and acidemia. Organ system dysfunction can involve either
a single system in isolation or multiple organ systems together. The heart, lung, kidney, and liver are
commonly involved. Hemodynamic instability in sepsis has been evaluated with a number of direct and
indirect invasive measures including central venous pressure, pulmonary artery occlusion pressure
(PAOP), cardiac output/index, systemic vascular resistance, pulse-pressure variation, and mixed venous
oxygen saturations. Practice patterns over time have seen a movement away from the use of invasive
monitors toward less invasive modalities.
Focused bedside transthoracic echocardiography (TTE) is one such modality that allows the clinician to
gain a wealth of information about the effective circulating volume, systemic vascular resistance, and
cardiac performance in a noninvasive manner. Serial examination may allow a provider to tailor therapy
as hemodynamics change throughout the course of this complex illness, and potentially identify the
etiology of the instability.
The goal of this chapter is to outline the echocardiographic findings that may be present in sepsis and
discuss the ways these findings may help guide management decisions for patients with sepsis. A brief
review of sepsis-induced myocardial dysfunction (SIMD) is provided. Concluding remarks will include a
management algorithm for patients with septic shock that uses the possible findings discussed in this
chapter.
CASE STUDY
DA is a 61-year-old man who was an avid small game hunter and enjoys excursions with his two pet
beagles. His medical history includes a motor vehicle collision in which he sustained a splenic laceration
requiring a splenectomy. Two days before presentation, he was bitten by one of his dogs. He subsequently
presented to our institution with fever, chills, nausea, and weakness. Blood cultures taken at the time of
admission eventually returned positive for Capnocytophagia canimorsis, a gram-negative, rod-shaped
bacterium that is commensal flora in canines.
How Might Echocardiography Be Used to Monitor This Patient?

Broad-spectrum antibiotics, fluid resuscitation, and vasopressors were implemented early in his
admission. Despite treatment, the patient progressed to severe sepsis with associated cardiac, renal, and
hepatic complications. An electrocardiogram showed diffuse nonspecific ST and T wave changes.
Troponin was measured and found to be elevated. He developed acute kidney injury and liver
insufficiency in conjunction with his cardiac abnormalities. TTE revealed a left ventricular ejection
fraction of 30% to 35% with global hypokinesis. After 2 days of intensive management and inotropic
support, the patient stabilized. His organ dysfunction improved and he eventually underwent extubation.
At his follow-up visit roughly 20 days later, the patient demonstrated full recovery of left ventricular
function. Video 21-1 shows the patient’s echocardiography study in the parasternal longaxis and apical
4-chamber views at the time of hospitalization and at his follow-up visit.
SEPSIS-INDUCED MYOCARDIAL DYSFUNCTION

SIMD is a reversible depression of cardiac function that may be seen in patients with sepsis who may not
have coexisting baseline cardiac disease. The precise incidence of SIMD is difficult to say with certainty,
but may be present in up to 40% of patients with septic shock.1 Myocardial depression can be
univentricular, biventricular, or regional. It is typically evident by days 2 to 3 of hospitalization for
sepsis, and resolves with treatment usually around days 10 to 14. Patients with myocardial dysfunction
and sepsis may also exhibit troponin elevation, but typically do not demonstrate myocardial cell death or
reductions in coronary blood flow. It is thought that the leakage of troponin could be secondary to a loss
of myocardial cell membrane integrity or potential microvascular thrombosis, but this remains somewhat
unclear.2
Table 21-1. Assessment of Septic Shock with Echocardiography
Left ventricular function Afterload or SVR (deductive reasoning)
Right ventricular function Preload or volume status
Cardiac output
Diastolic function
Abbreviation: SVR, systemic vascular resistance.
Although the exact pathophysiologic mechanism has been illusive, many cellular abnormalities have been
implicated in SIMD. In vitro and in vivo studies support the role of cytokine mediators of inflammation,
such as tumor necrosis factor alpha and interleukin-1, as mediators in the early phase.3 However, the
cytokine levels quickly decline and do not account for the prolonged suppression of cardiac function.
Molecular signaling within cardiac myocytes is altered in sepsis. The beta-adrenergic pathway,
especially the response to agonism, appears to be reduced in sepsis, and may contribute to the myocardial
dysfunction. Calcium homeostasis has also been identified as contributory; currents and release of
calcium from the sarcoplasmic reticulum, along with the response of the contractile elements, appear to
be reduced in patients with sepsis.1
ECHOCARDIOGRAPHIC ASSESSMENT OF THE PATIENT WITH SEPSIS

Sepsis can influence all of the physiologic factors involved in hemodynamic homeostasis, including
preload, afterload, and myocardial contractility. It is valuable to have a tool at the bedside that can
identify the cause of hemodynamic instability and help target therapy appropriately. Table 21-1 outlines
the measurements that can be assessed using TTE in patients with sepsis.
Assessment of Preload and Fluid Responsiveness

Sepsis is associated with systemic arterial and venous dilation in conjunction with increased endothelial
permeability and extravasation of plasma volume into the extracellular space. This constellation of
changes can lead to the profound hypovolemia and hypotension seen in septic shock. One cornerstone of
therapy that has been shown to reduce mortality in sepsis is early aggressive repletion of volume when
needed.4 Although aggressive volume repletion is appropriate for most patients with sepsis, the use of
echocardiography can help differentiate between patients who would benefit from fluid therapy and those
who would not.
Vena Cava Collapsibility

The inferior vena cava (IVC) carries most of the venous return from the periphery to the right atrium. The
caliber of the IVC changes in response to various factors, including intra-abdominal pressure, right atrial
pressure, and blood volume. The course of the cava through the abdomen is relatively straight, making it
an easily identifiable structure on ultrasound. Mechanical ventilation induces pressure changes in the
thorax and subsequently transmits them to the IVC. During inspiration with positive pressure ventilation,
pressure changes lead to decreased entry of blood from the IVC into the right atrium, thus changing the
volume of blood within the IVC. During exhalation, the intrathoracic pressure decreases and venous
return to the heart is increased accordingly.
Cyclic changes in intrathoracic pressure have a different impact on the caliber of the IVC depending on
the relative volume status of the patient. In the patient who has been adequately resuscitated, the
capacitance of the venous system will have been nearly exhausted. Thus, the pressure changes induced
during positive pressure ventilation have minimal effect on the diameter of the vein walls. This is because
much of the capacitance reserve has been exhausted, and the system is operating in a different portion of
the venous compliance curve.
Contrarily, a patient with hypovolemia will have a great deal of compliance reserve in the venous system.
Thus, cyclic changes in intrathoracic pressure during respiration will induce a greater change in the
appearance of the IVC on ultrasound. When the IVC collapses during positive pressure exhalation or is
distended during inspiration, it can be indicative of systemic hypovolemia and predictive of fluid
responsiveness. Video 21-2 shows dynamic IVC variability during the respiratory cycle. This is an
example of a patient that would likely respond to fluid therapy
Evidence. Feissel et al5 studied IVC diameter changes in patients with septic shock who were receiving
mechanical ventilation. Measurements of the IVC were taken using the M-mode, and cardiac output was
calculated both before and after volume challenge. The change in IVC was calculated as the maximum
diameter minus the minimum diameter normalized by the mean of the two values. The authors found that
fluid challenge in patients with large respiratory variation in IVC diameter throughout the respiratory
cycle induced correspondingly large increases in cardiac output. In this study, the threshold value for
differentiating responders from nonresponders was 12% (positive pressure ventilation, 93%; negative
pressure ventilation, 92%). Similar findings were also confirmed by another group led by Barbier et al6
during the same period, and was published in the same journal issue.
Method. To assess the IVC, the probe should be placed on the abdominal wall in a longitudinal subcostal
view, with the indicator in the cephalad position. The probe can be tilted to the right of the midline, and
the IVC should appear. It is important to distinguish the IVC from the aorta during this period. Once an
adequate image with the IVC in long axis is obtained, M-mode should be activated. The M-mode line
should be positioned perpendicular to the IVC within a few centimeters of the right atrium. Care should
be taken to not include the hepatic vein in the path of the M-mode line. M-mode will give a repetitive
measurement of a single line through the IVC throughout the respiratory cycle. The sweep of the machine
should be changed to a slow speed in order to include the changes in the diameter of the IVC over as
many respiratory cycles as possible. A pressure waveform from the ventilator can be synchronized with
the ultrasound machine, if available, and may help correlate airway pressure changes with changes in the
IVC diameter (Figure 21-1). Maximum and minimum IVC diameters should be measured and IVC
collapsibility then calculated using the equation in Table 21-2. A large change in the IVC indicates that a
patient is likely to be volume responsive.
Figure 21-1. Subcostal Long-Axis View of IVC Entering the Right Atrium
The M-mode cursor was placed within 2 cm of the confluence of the inferior vena cava (IVC) and right atrium. Respiratory variability of the
IVC is demonstrated in this figure, and the dimensions are measured with calipers. The white arrowhead represents the exhalation phase of
positive pressure ventilation and the yellow arrowhead represents the inspiratory phase.
Variation in Aortic Velocity, Stroke Volume, and Cardiac Output

The loading conditions of the right and left ventricles are interdependent. Changes in the right ventricular
preload and ejection are translated into changes in left ventricular preload and ejection once blood
transits through the pulmonary circulation to the left side of the heart. Accordingly, the stroke volume of
the left ventricle and the velocity at which it is ejected through the aortic valve will change. This
phenomenon has been well studied and is the basis for pulse-pressure variation on arterial waveform
analysis in patients receiving mechanical ventilation.
Evidence. Slama et al7 reported animal data on aortic velocity time integral variation as a marker of
volume responsiveness. They demonstrated progressive variation in the aortic velocity time integral and
Vmax using TTE with the progressive incremental removal of increasing fractions of blood from intubated
rabbits. Feissel and colleagues8 studied this subject and hypothesized that respiratory variation in aortic
peak velocity would predict changes in stroke volume after fluid challenge in patients with septic shock.
Using transesophageal echocardiography, aortic velocity was measured using pulsed-wave Doppler
ultrasound. A change in aortic peak velocity of 12% or more during the respiratory cycle predicted a
positive response to fluid challenge (positive pressure ventilation, 91%) (Table 21-2).
Table 21-2. Dynamic Predictors of Fluid Responsiveness
Index Equation % Change Indicative of Volume Responsiveness Reference
∆IVC diameter Dmax insp - Dmin exp 12%

x 100 Feissel et al5
Dmean
∆IVC diameter Dmax insp - Dmin exp 18%
x 100 Barbier et al6
Dmin exp
Aortic ∆Vpeak Vpeak max - Vpeak min ≥12%

x 100 Feissel et al8
Vpeak min
Passive leg raising ∆ Stroke volume 10%-12.5% Préau et al10

Lamia et al11
Maizel et al12
Method. In order to measure the velocity of blood ejected through the aortic valve, an apical 5-chamber
view should be obtained. Upon visualization of the left ventricular outflow tract and the aortic valve,
pulsed-wave Doppler should be directed through the aortic valve. The Doppler signal should be as close
to parallel to the direction of aortic ejection as possible to reduce measurement error. Acquire the
velocity over several respiratory cycles. Again, using slow sweep speed to include several respiratory
cycles is helpful (Table 21-2). Compare the Vpeakmin and the Vpeakmax to calculate the change in Vpeak.
Figure 21-2. Apical 5-Chamber Aortic Velocity

Aortic velocity variation can be measured in the left ventricular outflow tract from an apical 5-chamber view. This figure shows the velocity
variation over multiple respiratory cycles.
Passive Leg-Raising Test

Volume assessment with the aforementioned techniques is not accurate in a large percentage of critically
ill patients who do not receive passive ventilation. As mechanical ventilation technology has become
more advanced, fewer patients are truly dependent on full passive mechanical ventilation. In order to
predict fluid responsiveness in these patients with spontaneous respiratory activity (assisted or
unassisted) or cardiac arrhythmias, the passive leg-raising maneuver can be used.
E X P E RT T I P
It is important to wait for 1-2 minutes between the passive leg raising maneuver and obtaining
the second measurement of stroke volume or cardiac output. This allows time for full
equilibration of the autotransfusion.
An initial intervention in response to hypotension is to position patients in the Trendelenburg position.

This is thought to take advantage of gravitational forces that can augment venous return from the periphery
toward the central circulation. Passive leg raising has been demonstrated with radio-labeled red cells to
mobilize blood to the central circulation.9 This can be thought of as a temporary autotransfusion. Because
the volume of blood mobilized from the lower extremities represents an increase in preload to the heart, it
is thought to predict the response to a fluid bolus.
Evidence. Préau et al10 measured the change in stroke volume, pulse pressure, and femoral artery velocity
in response to passive leg raising in patients with severe sepsis. They found that a change in stroke
volume of 10% or more after passive leg raising was predictive of fluid responsiveness. Lamia et al11
studied passive leg raising in critically ill patients who received mechanical ventilation but demonstrated
spontaneous breathing activity. An increase in stroke volume greater than 12.5% after passive leg raising
predicted a positive response to volume expansion with 500 mL of saline. Interestingly, the static
predictors of left ventricular filling, including left ventricular end diastolic area and E/e', were not
predictive of response to volume challenge. In another study of patients who were being ventilated
spontaneously, Maizel et al12 used TTE to measure stroke volume and cardiac output after passive leg
raising to predict response to volume resuscitation. An increase of more than 12% in either stroke volume
or cardiac output was predictive of volume responsiveness.
Method. The full description of how to measure stroke volume and cardiac output can be found in other
chapters of this text. Initially, the stroke volume and cardiac output must be measured with the patient in
the semirecumbent position, with the head of the bed at a 45° angle. Then passive leg raising is initiated
by lowering the head and torso to a flat position and raising the legs to a 45° angle. It is important to wait
1 to 2 minutes between measurements to allow for the full effect of the autotransfusion. Stroke volume and
cardiac output is then measured a second time and compared to the initial measurement. If the stroke
volume and cardiac output has increased by 10% to 12.5% or more, then the patient is likely to respond to
a fluid challenge. Figure 21-3 depicts the proper technique for conducting a passive leg-raising maneuver.
Figure 21-3. Passive Leg Raising

This is a schematic figure for the technique of passive leg raising.
LIMITATIONS OF ECHOCARDIOGRAPHY IN THE ASSESSMENT OF VOLUME STATUS
Several assumptions are made in inferring the relationship between dynamic parameters in the circulatory
system throughout the respiratory cycle and the ventricular dependence on preload. These assumptions
include mechanical ventilation without spontaneous effort or dyssynchrony, regular cardiac rhythm, and
the absence of elevated intra-abdominal pressure. In addition, ventricular diastolic dysfunction,
pulmonary hypertension, and right ventricular failure can confound the cardiopulmonary interactions used
to assess volume status.
Examination of respirophasic variations in IVC diameter or aortic blood velocity assumes that the
pressure conditions in the thorax and heart rate are uniform. When patients have spontaneous respiratory
activity on mechanical ventilation or dyssynchrony with the ventilator, the pressure conditions within the
thorax are not uniform. In this setting, little information can be inferred from the subsequent changes in
IVC diameter and its relationship to ventricular preload dependence.
Tidal volume size should also be regarded. The aforementioned literature generally studied patients who
were receiving tidal volumes of 8 to 10 mL/kg predicted body weight. With the expanding use of lower
tidal volumes in patients at risk for acute lung injury, including those with sepsis, caution must be taken
when interpreting these respirophasic changes. Lower tidal volumes will have less impact on
respirophasic variation. Briefly changing to tidal volumes of 8 to 10 mL/kg predicted body weight for
evaluation of fluid responsiveness seems a safe and reasonable approach.
In examining aortic blood flow velocities it is assumed that the heart rhythm is regular and that each
cardiac cycle is uniform. The presence of atrial fibrillation or other irregular heart rhythms alters the
examiner’s ability to infer a relation between aortic velocity variation during the respiratory cycle and
ventricular preload dependence. Atrial fibrillation should have less impact on IVC variability. When
calculating cardiac output for patients with atrial fibrillation, it is recommended to use the average of
several stroke volumes.
ASSESSMENT OF VENTRICULAR PERFORMANCE

Septic shock is typically classified as a low-resistance, high-output type of shock. When systemic
vascular resistance and volume status are restored, however, cardiac dysfunction can be revealed. SIMD
can manifest as univentricular or global dysfunction, and may affect systolic function, diastolic function,
or both. Low output and reduced contractility of the left ventricle can be seen commonly. It was initially
believed that a dilation of the ventricles occurred as a compensatory response to maintain cardiac output
in sepsis as an adaptation for preload. These findings were reported in one study, but they were not
verified in subsequent publications and will not be considered further in this text.3
Left Ventricular Systolic Function

Left ventricular dysfunction can contribute significantly to the hemodynamic instability of sepsis.
Manifestations can include regional wall motion abnormalities or global hypokinesis. Care must be taken
to differentiate a coexisting myocardial dysfunction from a new finding that is associated with sepsis.
Evidence. Vieillard-Baron and colleagues13 demonstrated that replacement of vascular tone with
norepinephrine was successful in increasing left ventricular afterload, but frequently unmasked left
ventricular systolic function. In contrast to cardiogenic shock, SIMD is usually not associated with
elevated filling pressures. Depression of the left ventricle is usually defined by an ejection fraction of
40% to 45% or less.13
Method. Initial inspection of the ventricles from a 4-chamber subcostal or apical view provides the
examiner a qualitative sense of wall motion and regional abnormalities. In experienced hands, the
qualitative estimation of ejection fraction is as good as the quantitative estimation.
A 4-chamber view of the heart can be obtained by placing the probe in the apical or subcostal position. It
is relatively easy to gain an impression of global atrial and ventricular shape, size, and motion from these
views. Alternatively, a parasternal short-axis view of the ventricles can be obtained at the midpapillary
level to appreciate the quality of circumferential motion of the ventricles.
The quantitative evaluation of the ventricles begins in the parasternal long-axis view. From this view, the
fractional shortening of the ventricular cavity can be measured by M-mode through the left ventricular
cavity during end-systole and end-diastole. Fractional area change can be performed using planimetry to
measure the left ventricular area at the end of diastole and comparing to the area at end-systole. Fractional
area change and fractional shortening are quickly and easily performed. Screen shots of normal and
abnormal fractional shortening are provided in Figures 21-4 and 21-5, respectively.
Another model that relies on geometric assumptions is the Simpson method of disks. This method assumes
that the left ventricle can be equated to a stack of disks oriented from the apex to the base of the heart on
top of one another, and calculates the sum of their volume. In order to obtain the most precise estimate of
ejection fraction and stroke volume, the dimensions of the left ventricle should be measured from the
apical 4-chamber view and 2-chamber view. During systole and diastole, the cavity area can be measured
using preloaded software. 3D echocardiography is another viable technique for chamber quantification.
However, it is generally time consuming relative to the other methods described. Ultimately, the
qualitative assessment of function by an experienced echocardiographer is probably adequate, and may
even be preferred for speedy assessment at the bedside.
Figure 21-4. Normal Fractional Shortening, Parasternal Long-Axis View

Fractional shortening in a normal subject from the parasternal long-axis view. This image is intended to illustrate the recommended view.
Figure 21-5. Abnormal Fractional Shortening, Subcostal Short-Axis View

Abnormal fractional shortening is demonstrated in the patient from our case presentation. The fractional shortening was measured from a
subcostal short-axis view of the left ventricle on hospital day 2. This image maintains the American Society of Echocardiography–
recommended plane through the right ventricular cavity and interventricular septum. The intracavitary diameter is easily appreciated through
this view.
Diastolic Dysfunction in Sepsis

It is clear that the presence of diastolic dysfunction has adverse consequences. Diastolic dysfunction in
sepsis may have important ramifications in the volume resuscitation of these patients. However, the
precise importance of diastolic dysfunction in patients with sepsis is unknown. The few studies that have
examined diastolic function in sepsis have yielded conflicting results regarding its presence and impact
on patient outcome.
Evidence. The most current study of the topic comes from Brown et al,15 who prospectively evaluated the
level of diastolic function in ICU patients with severe sepsis or septic shock. They hypothesized that left
ventricular diastolic dysfunction would correlate with higher 28-day mortality and took measurements in
the first 6 hours of hospitalization, 18 to 32 hours after admission, and 24 hours after vasopressor therapy
was discontinued. Interestingly, lower grades of diastolic dysfunction were associated with worse
outcomes. A subgroup of patients found to have grade I diastolic dysfunction – defined as an E/A ratio
less than 0.8 and an eʹ value less than 8 cm/sec – early in the course of sepsis seemed to have higher
mortality, which was not consistent with the study hypothesis. Upon further analysis, they also found that
while central venous pressure was elevated and diastolic dysfunction was of a lower grade, this group
incidentally received less volume expansion before admission to the ICU. This may be an area for
improvement in the care of this subgroup.
Method. The role and significance of diastolic dysfunction in septic shock remain unclear. Measurements
and interpretation of diastology can be time consuming and are not currently imperative in the
echocardiographically directed management of patients with sepsis. For further information on the theory
and technique of diastolic function assessment, refer to other chapters of this text.
Right Ventricular Function
Although left ventricular dysfunction is common in SIMD, dysfunction can also be present in the right
ventricle. Pulmonary vascular resistance may be elevated in sepsis, and can lead to acute right ventricular
failure. The right ventricle is not adapted or designed to deal with dramatic changes in afterload and does
not accommodate changes in these variables.
The motion of the interventricular septum during systole and diastole can provide vital information
regarding the right ventricular preload and afterload. Under normal conditions, the septum provides a
buttress for the low-pressure right ventricle to contract against and eject blood. It typically maintains a
rounded appearance and is convex toward the right side such that the left ventricle looks like the center of
a doughnut. When the conditions in the right ventricle change because of either volume or pressure
overload, the motion and appearance of the septum can also change. When volume overload is present,
middiastolic bowing of the interventricular septum toward the left ventricle can be seen, whereas
midsystolic bowing of the septum is more indicative of elevated afterload. Bowing of the septum causes
the left ventricle to take a classic D-shaped appearance in contrast to its normally circular geometry
(Figure 21-6).
Figure 21-6. Qualitative Assessment of Right Ventricular Function

Qualitative assessment of right ventricular function by inspecting the interventricular septal motion throughout the cardiac cycle. Notice how
either pressure or volume stress on the right heart will bow the septum toward the left ventricle. This makes the left ventricle take on a D
shape.
Acute right ventricular failure in the setting of sepsis portends a grim prognosis and is usually associated
with acute respiratory distress syndrome. Right ventricular function is difficult to measure using
mathematical assumptions because of its irregular geometric shape.
Evidence. Tricuspid annular plane systolic excursion (TAPSE) has been studied as a marker of right
ventricular systolic function in the longitudinal direction.16 M-mode and pulsed-wave Doppler were used
to measure the displacement of the right ventricular base during systole and diastole. The largest
amplitude wave toward the probe represents TAPSE and is called the “D wave.” The systolic excursion
of the tricuspid valve can be measured using the peak velocity of the D wave via pulsed-wave Doppler,
or measurement of TAPSE via M-mode measurements (Figure 21-7). The Ueti et al16 study found that
peak velocity of the D wave and TAPSE correlated strongly with radionuclide measurement of right
ventricular function. Assessing for right ventricular dilation in the apical, subcostal, and parasternal
views can also be effective for the assessment of right ventricular dysfunction. The incidence of right
ventricular dilation in sepsis with this method has been reported as anywhere from 11% to 32%.13,17
Figure 21-7. TAPSE in Apical 4-Chamber View

Tricuspid annular plane systolic excursion (TAPSE) demonstrated with an apical 4-chamber view. Notice the cursor lined up at the meeting
point of the tricuspid valve and the free wall of the ventricle. This echocardiographic image retains scale markings, and it is evident that the
movement of the tricuspid annular plane is within the normal value of >16 mm.
Method. The evaluation of the right ventricle and assessment of dysfunction is mostly qualitative and can
be challenging secondary to poor imaging planes and suboptimal definition of this complex structure. With
some effort, the appearance of the right ventricle can usually be appreciated from the apical view. A
qualitative assessment of ventricular dimensions and geometry can be made. The parasternal short-axis
view of the heart provides visualization of the left ventricle, right ventricle, and interventricular septum.
Motion of the interventricular septum throughout the cardiac cycle, along with right ventricular size, can
be appreciated from this view.
Quantitative measurement of right ventricular function can be carried out using TAPSE. In order to do this,
a 4-chamber view is obtained from the apical position. The M-mode cursor should be activated and the
cursor placed at the junction of the tricuspid valve annulus and the free wall of the right ventricle. TAPSE
in this view is defined as the distance of excursion of the right ventricular base from diastole to systole.
The normal value for TAPSE is more than 16 mm, and values less than 16 mm are indicative of poor right
ventricular function.18 This technique is the most attainable, reliable, and rapidly interpretable marker of
right ventricular function to use at the bedside. The American Society of Echocardiography also
recommends tissue Doppler study of the tricuspid valve annulus to obtain a systolic excursion velocity, or
RVS′. This measurement can be performed in the same apical 4-chamber view by pointing the Doppler
cursor to the tricuspid annulus or the middle of the right ventricular free wall. Values for Sʹ less than 10
cm/ sec indicate right ventricular dysfunction.
REDUCED SYSTEMIC VASCULAR RESISTANCE

Vasodilation and low systemic vascular resistance are commonplace in sepsis. There are no good
echocardiographic measurements that definitively assess the state of systemic vascular resistance. The
status of systemic vascular resistance is therefore deduced by the process of eliminating other potential
etiologies that can be assessed with echocardiography. If preload, cardiac output, and cardiac function
appear to be within normal ranges, it can be deductively reasoned that the systemic vascular resistance
may be altered. Echocardiographic findings should be combined with a focused physical examination
with special attention to findings such as bounding pulse pressure and warm vasodilated extremities to
complete the picture.
ECHOCARDIOGRAPHICALLY DIRECTED TREATMENT OF SEPTIC SHOCK

It is well understood that early antibiotics and aggressive hemodynamic control help to improve the
outcomes of patients with sepsis.4 These early interventions are a part of the Surviving Sepsis Campaign
protocol and have become usual care. While such protocols have helped to incorporate critical
interventions initially, it has been difficult to demonstrate a clear difference in outcomes between the
protocol-based approach and usual care. In fact, there have been multiple prospective, randomized
clinical trials (ProCESS, ARISE, and ProMISe trials) that have not shown a clear difference between
these two strategies.19-21 The main outcomes investigated by these studies include mortality, organ
failures, duration of organ support, and length of ICU and hospital stay.
Goal-Directed Fluid Therapy with Echocardiography

Investigation of dynamic predictors, on the other hand, has shown promise in directing therapeutic
management decisions. One meta-analysis conducted by Benes et al22 found that goal-directed fluid
therapy using dynamic predictors (stroke volume variation or pulse-pressure variation) of fluid
responsiveness reduced postsurgical morbidity and ICU length of stay, related to reductions in infectious,
cardiovascular, and abdominal complications. Although this is not the same as using echocardiography to
guide therapy, it takes advantage of similar dynamic indices and is certainly a prelude to the use of
echocardiographic decision-making in patients with sepsis.
We have reviewed the assessment of the physiologic components of blood pressure and how each factor
may be altered in sepsis. Both cardiac output and ventricular contractile performance can be assessed
with TTE. The intravascular fluid status can be determined with the use of IVC diameter changes during
the respiratory cycle. The state of resistance within the vascular system can be deduced from the
condition of the other factors. For example if the cardiac output, contractility, and preload are all
relatively normal in a hypotensive patient with septic shock, the system vascular resistance must altered.
Evidence. Kanji and colleagues23 studied 220 critically ill patients with undifferentiated sepsis in an ICU.
Limited echocardiography was used as an intervention to guide therapy in 110 of these patients. The
authors hypothesized that the use of limited echocardiographic guidance for fluid therapy and inotropes in
patients with sepsis would improve survival at 28 days relative to conventional management. Survival
analysis revealed a significant difference in mortality at 28 days between the 2 groups. In addition, a
statistically significant reduction in risk of acute kidney injury was seen in the group managed with
limited echocardiography. The use of limited echocardiography was found to be associated with a
reduction in fluid administration and increased use of inotropic support for left ventricular hypokinesis.
This was a small study and was not prospectively randomized, but certainly provides some hope of a
future for echocardiographically based goal-directed therapy in sepsis.
C AVE AT
Remember to consider the clinical context and to think about possible coexisting cardiac disease
in approaching and interpreting echocardiographic images.
Figure 21-8. Echocardiographically Guided Hemodynamic Assessment

Abbreviations: BP, blood pressure; CO, cardiac output; SVR, systemic vascular resistance; SV, stroke volume; HR, heart rate; IVC, inferior
vena cava; LV, left ventricle; RV, right ventricle; FS, fractional shortening; FAC, fractional area change; TAPSE, tricuspid annular plane
systolic excursion.
Suggested approach to the echocardiographically guided management of hemodynamically unstable patients with sepsis.
1. We recommend beginning with an assessment of the patient’s volume status. This is because of the frequency of relative hypovolemia and
the relative speed with which the operator can obtain these measurements.
2. Subsequently, we recommend a rapid qualitative assessment of ventricular function.
3. Measurement of stroke volume and cardiac output help to determine the type of shock present (hyperdynamic or hypodynamic).
4. If the cardiac output is normal or high, the patient is likely in a hyperdynamic state with a low systemic vascular resistance. In this scenario,
the addition of vasopressors is an appropriate next intervention.
5. The adequacy of tissue perfusion should be assessed using goals that are defined by the intensivists.
6. If the goals as defined by the intensivists are not met, the echocardiography study should be repeated. It should also be repeated as needed
to determine the adequacy of response to interventions.
Method. Via et al24 proposed a treatment algorithm in a recent review that incorporated relevant
echocardiographic findings from patients with septic shock. This algorithm deconstructed hemodynamic
instability into its components and ruled each one either in or out in a stepwise fashion. We have taken a
similar approach to the problem in our deconstruction of hemodynamic instability and management in
patients with sepsis. Figure 21-8 outlines one approach to echocardiographically guide management of
patients with sepsis.
To be clear, there is no current definitive evidence from prospective randomized clinical trials to support
the hypothesis that echocardiographically guided therapy leads to improved outcomes in patients with
sepsis. However, we believe that echocardiography may offer a more elegant, individualized, and
effective approach to management of sepsis with the tools that we have outlined in this chapter.
Focused TTE is a useful noninvasive tool and demonstrates a great deal of potential for improving the
care of critically ill patients with sepsis. Useful information about the patient’s intravascular volume
status and fluid responsiveness, ventricular systolic function, ventricular diastolic function, and vascular
resistance can be gained. Interpretation of echocardiographic findings in the clinical context can be
completed in minutes and translated into rational treatment decisions. It remains unclear whether the
guidance of hemodynamic therapy with echocardiography leads to improvement in outcomes, but
preliminary data suggest that it may. Focused echocardiography will likely continue to be an indispensible
tool for the clinician caring for critically ill patients with sepsis.
KEY POINTS
Echocardiography is a validated tool to distinguish fluid responsiveness in patients with sepsis.
Ventricular dysfunction including SIMD is easily identifiable with echocardiography and is
frequently an indication for inotropic support.
Diastolic dysfunction is commonly diagnosed with echocardiography in sepsis. The clinical
implication of this finding is currently unclear.
An echocardiographically guided management algorithm allows for individualized and targeted
therapy of hemodynamic instability in sepsis, with an, as of yet, unclear impact on outcomes.
REFERENCES
1. Romero-Bermejo F, Ruiz-Bailen M, Gil-Cebrian J, et al. Sepsis-induced cardiomyopathy. Curr Cardiol Rev. 2011;7:163-183.
2. Maeder M, Fehr T, Rickli H, et al. Sepsis-associated myocardial dysfunction: diagnostic and prognostic impact of cardiac troponins and
natriuretic peptides. Chest. 2006;129:1349-1366.
3. Parrillo J. Pathogenic mechanism of septic shock. N Engl J Med. 1993;328:1471-1477.
4. Dellinger RP, Levy MM, Rhodes A, et al. Surviving sepsis campaign: international guidelines for management of severe sepsis and septic
shock. Crit Care Med. 2013;41:580- 637.
5. Feissel M, Michard F, Faller JP, et al. The respiratory variation in inferior vena cava diameter as a guide to fluid therapy. Intensive Care
Med. 2004;30:1834-1837.
6. Barbier C, Loubieres Y, Schmit C, et al. Respiratory changes in inferior vena cava diameter are helpful in predicting fluid responsiveness in
ventilated septic patients. Intensive Care Med. 2004;30:1740-1746.
7. Slama M, Masson H, Teboul JL, et al. Respiratory variations of aortic VTI: a new index of hypovolemia and fluid responsiveness. Am J
Physiol Heart Circ Physiol. 2002;283:H1729-H1733.
8. Feissel M, Michard F, Mangin, I, et al. Respiratory changes in aortic blood velocity as an indicator of fluid responsiveness in ventilated
9. Rutlen DL, Wackers FJ, Zaret BL. Radionuclide assessment of peripheral intravascular capacity: a technique to measure intravascular
volume changes in the capacitance circulation in man. Circulation. 1981;64:146-152.
10. Préau S, Saulnier F, Dewavrin F, et al. Passive leg raising is predictive of fluid responsiveness in spontaneously breathing patients with
severe sepsis or acute pancreatitis. Crit Care Med. 2010;38:819-825.
11. Lamia B, Ochagavia A, Monnet X, et al. Echocardiographic prediction of volume responsiveness in critically ill patients with spontaneous
breathing activity. Intensive Care Med. 2007;33:1125-1132.
12. Maizel J, Airapetian N, Lorne E, et al. Diagnosis of central hypovolemia by using passive leg raising. Intensive Care Med. 2007;33:1133-
1138.
13. Vieillard-Baron A, Caille V, Charron C, et al. Actual incidence of global left ventricular hypokinesia in adult septic shock. Crit Care Med.
2008;36:1701-1706.
14. Parker M, Shelhamer J, Bacharach S, et al. Profound but reversible myocardial depression in patients with septic shock. Crit Care Med.
1990;18:1055-1060.
15. Brown SM, Pittman JE, Hirshberg EL, et al. Diastolic dysfunction and mortality in early severe sepsis and septic shock: a prospective,
observational echocardiography study. Crit Ultrasound J. 2012;4:8.
16. Ueti OM, Camargo EE, Ueti AA, et al. Assessment of right ventricular function with Doppler echocardiographic indices derived from
tricuspid annular motion: comparison with radionuclide angiography. Heart. 2002;88:244-248.
17. Etchecopar-Chevreuil C, François B, Clavel M, et al. Cardiac morphological and functional changes during early septic shock: a
transesophageal echocardiographic study. Intensive Care Med. 2008;34:250-256.
18. Lawrence R, Lai WW, Afialo J, et al. Guidelines for the echocardiographic assessment of the right heart in adults: a report from the
American Society of Echocardiography. J Am Soc Echocardiogr. 2010;23:685-713.
19. Peake SL, Delaney A, Bailey M, et al. Goal-directed resuscitation for patients with early septic shock. N Engl J Med. 2014;371:1496-1506.
20. Yealy D, Kellum J, Huang D, et al. A randomized trial of protocol-based care for early septic shock. N Engl J Med. 370;18:1683-1693.
21. Mouncey P, Osborn T, Power S, et al. Trial of early, goal-direct resuscitation for septic shock. N Engl J Med. 2015;372:1301-1311.
22. Benes J, Mariateresa G, Brienza N, et al. The effects of goal-directed fluid therapy based on dynamic parameters on post-surgical
outcome: a meta-analysis of randomized control trials. Crit Care. 2014;18:584.
23. Kanji H, McCallum J, Sirounis D, et al. Limited echocardiography-guided therapy in subacute shock is associated with change in
management and improved outcomes. J Crit Care. 2014;29:700-705.
24. Via G, Price S, Storti E. Echocardiography in the sepsis syndrome. Crit Ultrasound J. 2011;3:71-85.
Chapter 22
Vascular Injuries
Daniel Theodoro, MD, MSCI
OBJECTIVES
Recognize how ultrasound technology can identify vascular abnormalities responsible for critical illness
Describe the technique for performing ultrasound assessment of the aorta and large vascular structures of the
limbs
Recognize vascular irregularities associated with aneurysms and dissection of vascular structures
Recognize clinical scenarios in which ultrasound evaluation of vascular structures aids in the diagnosis of life-
and limb-threatening pathology
INTRODUCTION
Ultrasound allows noninvasive evaluation of large vascular structures for aneurysmal dilatation,
intraluminal dissection, and abnormal flow patterns. Of additional benefit, ultrasound uses no ionizing
radiation. These features make ultrasound ideal for bedside evaluation of critical pathologies encountered
in practice. Practitioners will find that having the capacity to identify vascular abnormalities in general
will translate to various systems of the body. One can expect great uses for noninvasive bedside
technology when occult diagnoses lurk behind subtle presentations of pathology. Practitioners greatly
expand their diagnostic capabilities by learning to identify patterns of vascular injury.
The 3 most common relevant abnormalities on vascular ultrasound are a luminal flap, aneurysmal (or
pseudoaneurysmal) dilatation of a vascular structure, and abnormal flow characteristics documented on
color and spectral Doppler. Luminal flaps frequently undulate with each beat of the heart. Vascular
dilatations appear like bulbous enlargements surrounding blood vessels. Although color and spectral
Doppler may seem difficult to execute, operators will benefit from knowing that turbulent flow appears
like contrasting colors in a blood vessel. A triphasic or biphasic waveform on spectral ultrasound should
be limited to arteries, and when noted in a venous structure, is cause for concern. Although there are
certainly more nuanced findings, critical care sonologists should become familiar with these signs of
potentially serious diagnoses.
Acute aortic syndrome refers to a range of pathologies related to the aortic root, thoracic aorta, and
abdominal aorta. More specifically, it refers to aortic dissection, aortic aneurysms, intramural hematoma,
and symptomatic aortic ulcer. The main pathologies discussed herein will include thoracic aortic
aneurysm, aortic dissection, abdominal aortic dissection, and injuries to vascular structures.
CASE STUDY
A 47-year-old man with a history of hypertension is admitted to the coronary critical care unit for a
myocardial infarction. Upon presentation, his blood pressure readings were 220/146 mm Hg, pulse rate
was 98 beats/min, respirations 22 breaths/min, and pulse oxygenation was 98%. He was afebrile and
complained of severe chest pain radiating down his left arm. Initial cardiac troponin was elevated, and he
was treated with aspirin, heparin, nitroglycerin, oxygen, and morphine. He was accepted to the ICU for
further control of blood pressure and potential cardiac intervention. Bedside echocardiography is
performed.
How Did Bedside Echocardiography Change Therapy?

A transthoracic echocardiogram (TTE) is performed on the patient. In the parasternal long-axis view, an
intimal flap is noted. On abdominal examination of the aorta, a flap is also noted. Type A thoracic
dissection is diagnosed, anticoagulation is promptly discontinued, and the cardiothoracic surgery service
plans for surgical repair (Figure 22-1).
Figure 22-1. Heart and Proximal Aorta, Transthoracic Parasternal Long View
The left ventricle (LV) and aorta (Ao) are visualized. The arrows point to an intraluminal flap, suggesting an ascending aortic dissection.
Courtesy of Srikar Adhikari, MD.
AORTIC DISSECTION
An aortic dissection occurs when the intima and media of the aorta tear apart, resulting in a false lumen or
channel. An acute dissection is the most common of the acute aortic syndromes and occurs with annual
incidence of 3 to 4 per 100,000 people per year in the western hemisphere. Some regional variation
appears to be present, likely dependent on genetic backgrounds as well as lifestyle. The prognosis
depends on the anatomic classification of the disease, which in turn depends on the position of the
opening tear. Dissections are classified as either type A, which involves the ascending aorta, arch, or
both; or type B, which involves the descending aorta distal to the subclavian artery. Because the 30-day
mortality of medically managed type A dissections is more than 50%, most cases are dealt with
operatively.1 The 30-day mortality of type A dissections after repair has decreased in the last decade to
20%, and 1-year mortality of patients discharged from the hospital after repair has decreased from
approximately 40% to 32% between 2000 and 2011.2 The 30-day mortality of type B dissections is 7%.
The 1-year mortality of type B dissections is 10%, and the 3-year mortality has been estimated at 23%.3
Although most type B dissections are commonly managed medically, in 20% of cases uncontrolled blood
pressure or a threat of end-organ perfusion may necessitate surgical or endovascular repair. However,
surgical or endovascular therapy does not appear to alter 1-year survival rates. The incidence of
diagnosed aortic dissection is rising. Whether this is because of increased rates of discovering previously
unknown disease on imaging or an acceleration of etiologic risk factors is debatable.4
Epidemiology
The most commonly accepted risk factors for aortic dissections include Marfan disease, Ehlers-Danlos
syndrome, bicuspid aortic valve, vasculitic disease, and pregnancy.5 However, hypertension and
atherosclerosis are the most common comorbidities associated with the disease.2 Other cohorts have
identified smoking history as a significant risk factor.6 In general, younger patients with dissections tend
to have underlying genetic or congenital disease. The disease is more common in men than women, and
women are diagnosed later in life.2
Clinical Presentation
Clinical presentation will vary by anatomic location of the disease. Both are commonly characterized by
sharp tearing chest pain. Ascending aortic dissection will radiate to the neck whereas descending will
radiate to the back and scapula. Interrupted perfusion may cause neurologic and vascular abnormalities
resulting in limb and intestinal ischemia and loss of conscioiusness.5 However, it is abundantly clear from
missed presentations, often with catastrophic outcomes, that presenting symptoms may be vague and
include no pain radiation and sometimes no pain complaints at all.
E X P E RT T I P
Preparation for ultrasound scanning requires a dimly lit setting and properly positioned patient.
Optimize preparation even in challenging settings.
Diagnostic Strategy
The first and most important diagnostic step is simply having dissection on the proposed differential.
Many diagnostic failures start with this key element, such as when anchoring bias constrains the clinician
from including dissection in a possible diagnosis list. The most common diagnostic strategy for making
the definitive diagnosis is computed tomography, magnetic resonance imaging, or transesophageal
echocardiography. Each imaging modality has benefits and constraints. For example, patients with dye
allergies or those who are hemodynamically unstable may have contraindications to computed
tomography and magnetic resonance imaging, and transesophageal echocardiography may be immediately
unavailable. In these circumstances, TTE can play an important role in the initial management of a patient
suspected of having an aortic dissection. In one cohort, TTE had a sensitivity in the range of 67% (95%
confidence interval [CI], 62%-82%) to 87% (95% CI, 75%-93%) and a specificity of 91% (95% CI,
85%-95%).7,8 It is important to note that the majority of these studies were performed by experienced
sonographers or reviewed by sonographers with extensive experience. However, a critical portion of the
aorta, the proximal aortic root, can often be assessed with TTE. This allows the clinician to identify and
potentially rule out a proximal dissection that is about to threaten coronary artery perfusion, aortic valve
function, and pericardial effusion with tamponade. Examining these 3 or 4 cm of the aorta does little to
rule out aortic dissection, but it can be critical clinically while further diagnostic efforts are undertaken.
Ultrasound Technique
Ascending Aorta and Aortic Arch
To view the ascending aortic arch, most sonographers use a phased-array probe in the cardiac setting. The
most widely reported position to visualize aortic pathology is the parasternal long view. In this view, the
operator can visualize proximal structures of the aortic root and portions of the ascending aorta. The
probe is held approximately at the second or third intercostal space just lateral to the sternum. The probe
indicator should be facing the patient’s right shoulder and the machine setting should be in “cardiac”
mode.
E X P E RT T I P S
Position the patient in the left lateral decubitus position for optimal cardiac views.
Ensure settings on the ultrasound machine are correct for visualizing the aorta (cardiac settings
in the thorax and abdominal setting in the abdomen)
Operators may also choose to perform a suprasternal window. In this view, the patient must slightly
extend the neck and the probe is placed at the suprasternal notch aiming at the aortic arch. Using pillows
to extend the neck can bring the arch into view nicely if body habitus and patient flexibility allow. The
aortic arch will pass under the probe, resulting in a “longitudinal” view of the aortic arch. The indicator
typically faces the patient’s right but can be rotated to optimize the image. Rotation and posterior
angulation also allows viewing of the ascending and descending portions of the aorta (in this case, the
indicator typically points to the patient’s left and is rotated slightly posteriorly). In some cases, it is
possible to see down to the aortic valve (Figure 22-2). Other vascular branches of the aorta may also be
visualized on rotation and angulation, including the innominate, the left common carotid, and the left
subclavian. Finally, with the descending aorta in view, the right pulmonary artery may also be visualized
in cross-section.
Figure 22-2. Ascending Aorta, Suprasternal Window

Abbreviations: BCV, brachiocephalic vein; AA, ascending aorta; AV, aortic valve; LVOT, left ventricular outflow tract; RPA, right pulmonary
artery.
The ascending aorta is well visualized. The aortic valve could be seen moving in real time. In addition, this image shows the brachiocephalic
vein, a portion of the left ventricular outflow tract, and right pulmonary artery.
Courtesy of Peter Croft, MD.
Descending Aorta
The descending aorta is most readily seen in the abdomen using an abdominal probe in the abdominal
setting. The abdominal aorta may be visualized with a cross-sectional view of the proximal, mid, and
distal aorta to the iliac bifurcation. An additional view of the thoracic descending aorta may sometimes
come into view inferior to the heart with a parasternal long view. In this window, the aorta is visualized
in cross-section as it descends through the thorax and into the abdomen.
Ultrasound Findings
The sine qua non finding of a vascular dissection is a thin white strand flapping, often in rhythmic motion,
in the vessel. One may see a flap in various locations depending on the window. In a type A dissection
involving the ascending aorta, a cardiac TTE in the parasternal long position can reveal a flap that
originates near the aortic root (Figure 22-3). The flap will move with each heart beat from surrounding
blood flow through the true and false lumen.
Figure 22-3. Heart and Aorta, Parasternal Long-Axis View

Abbreviations: LA, left atrium; LVOT, left ventricular outflow tract; Ao, aorta.
Solid arrows point to an intraluminal flap, suggesting a dissection of the ascending aorta.
Figure 22-4. Aortic Arch, Suprasternal View

The arrow points to a subtle intimal flap in the ascending aortic lumen.
In a suprasternal view, the aortic arch may be visualized as it ascends toward the probe then curves away.
In this view, the operator is again searching for a thin white band frequently waving in the midportion of
the vessel (Figure 22-4). In the parasternal long axis view, a window of the descending aorta may also be
obtained posterior to the left atrium. In this case, the descending aorta is seen in the short axis and a
dissection again may appear as a thin white flap (Figure 22-5). Lastly, the aorta may be viewed in
crosssection as it courses through the abdomen (Figure 22-6).
Figure 22-5. Heart, Parasternal Long-Axis View

Abbreviations: DAo, descending aorta; LA, left atrium; LV, left ventricle; RV, right ventricle; AAo, ascending aorta.
Solid arrow points to a flap suggestive of a descending aortic dissection.
Courtesy of Srikar Adhikari, MD.
Figure 22-6. Descending Abdominal Aorta, Cross-Sectional View

The arrow points to a flap, suggesting dissection of the descending aorta.
Understand how color Doppler may help to identify a dissection flap by showing flow in 1
portion of the vessel but not the other.
THORACIC ANEURYSM
Aneurysmal dilatation of the thoracic aorta is a risk factor for dissection and rupture. The incidence is
estimated at 10 per 100,000 person-years. Risk factors include Marfan syndrome; bicuspid aortic valve
aortopathy; familial thoracic aortic aneurysm; Loeys-Dietz syndrome; Ehlers-Danlos syndrome; mitral
valve prolapse associated with dilated aortic root diameter, stretch marks of the skin, and skeletal
conditions; Beals-Hech syndrome; and atherosclerosis. 9 Most aneurysms follow an indolent course and
require annual assessment with echocardiography. Decisions regarding surgical or medical management
depend on the etiology. The incidence of aortic rupture after aortic dilatation is approximately 3.5 per
100,000 person-years.10
Most aneurysms are clinically asymptomatic or found on incidental testing. Aneurysms may present with
acute congestive heart failure resulting from acute aortic regurgitation, myocardial ischemia caused by
mass effect on cardiac vascular structures, or embolic sequelae caused by the disintegration of a large
mural thrombus at the aneurysm site. Other symptoms may result from the mechanical compression of
thoracic structure and can include hoarseness, Horner syndrome, wheezing, dysphagia, and stridor.11
Ultrasound Technique
Symptomatic thoracic aortic aneurysms are time critical. In 1 study, more than 20% of admitted patients
died within 6 hours of hospitalization.12 Although the diagnosis of symptomatic aneurysms is likely
multimodal, point-of-care ultrasound has the distinct advantage of portability. Transthoracic ultrasound
images are typically obtained in the parasternal long window. In this window, the aorta may be visualized
at distinct points. As mentioned previously, the first 3 or 4 cm of the proximal aortic root may be seen in
many patients with appropriate transducer and patient manipulation, allowing for detection of luminal
irregularities and dilation.
Ultrasound Findings
Typically measurements are obtained at the sinuses of Valsalva, the sinotubular junction, and the
visualized portions of the ascending aorta (Figure 22-7). There is a paucity of data to support guidelines
for when surgical intervention is necessary and, although widely implemented, aneurysmal size may be
insufficient to guide therapeutic pathways.13 However, most ascending aneurysms greater than 60 mm
carry an increased risk of rupture, dissection, and death nearing 14%. At this size, wall tension
approaches tensile limits of the tissue.14 Symptomatic aneurysms and those greater than 55 mm will
require intervention, whereas those associated with Marfan syndrome, bicuspid aortic valve, or family
history of aneurysms may require intervention at 50 mm or less, depending on other clinical factors
(Figure 22-8). There is no consensus as to whether the aortic wall should be measured or not when
obtaining the aortic diameter irrespective of the imaging modality. The tortuous nature of the ascending
aorta presents geometric challenges to all modes of imaging, including ultrasound. For example,
asymmetric dilatation of the sinus can lead to slight increases in measurement of the diameter. In a cohort
of patients suspected of aortic pathology, the sensitivity of TTE for aortic aneurysms greater than 45 mm
was 64% (95% CI, 35%-86%) and the specificity was 99% (95% CI, 90%-100%).15
Figure 22-7. Measurement of Aortic Root at Sinotubular Junction
Abbreviations: RV, right ventricle; LA, left atrium; LVOT, left ventricular outflow tract.
The hatched line represents the measurement of the aortic root at the sinotubular junction. The solid arrow points to the leaf of the aortic
valve.
Courtesy of Mathew Nelson, DO.
Figure 22-8. Sinuses of Valsalva, Parasternal Long View of Heart

Abbreviations: SV, sinus of Valsalva; LVOT, left ventricular outflow tract; RV, right ventricle.
This parasternal long view of the heart demonstrates the sinuses of Valsalva.

Adjust depth settings to avoid dead scanning space and maximize the size of the vessel of interest.
ILIAC AND POPLITEAL ANEURYSM

Epidemiology
Isolated iliac and popliteal aneurysms are rare. Isolated iliac aneurysms occur in 2% of cases but can
reach up to 10% in cases associated with abdominal aortic aneurysms. Autopsy data suggest a prevalence
of 0.03%. They are diagnosed more often in men than women, and the median age is 72 years, with a
range of 47 to 89 years. The common identified risk factor for isolated iliac artery aneurysms is
atherosclerosis, though they have been associated with genetic connective tissue disorders, pelvic trauma,
and following birth in cases of forceps delivery and caesarian section. Isolated popliteal aneurysms are
more common than isolated iliac artery aneurysms. They are associated with atherosclerotic disease and
are bilateral in 50% to 70% of cases.
Clinical Presentation
There is a lack of data characterizing typical presenting signs and symptoms of iliac aneurysms. However,
because the iliac vessels are in proximity to the genitourinary and nervous systems of the pelvis, hip, and
urinary symptoms are common. Approximately 10% present without any symptoms. When rupture occurs,
mortality approaches 50%. Rupture is associated with lower abdominal, groin, and back pain. Pelvic
masses associated with hydronephrosis are another reported presenting pattern. Popliteal aneurysms may
present as a mass or painful lump in the popliteal fossa.
Ultrasound Technique and Findings

Typically iliac artery evaluation may occur concomitantly with aortic evaluation because the technique
and equipment are similar. Operators may continue to scan distally toward the patient’s feet. By
definition, an aneurysm is a vessel 1.5 times its native size.16 Native size refers to the undilated portion
typically measured proximally to the area in question. Aneurysms 3 cm in size can rupture, though the
median size of ruptured aneurysms is 7 cm (range, 5-13 cm).17 Placing a linear probe in the popliteal
fossa is generally all that is necessary to image the popliteal vessels. Normal popliteal arteries will
measure between 7 and 10 mm. Vessels larger than 10 mm are considered for further diagnostic testing
(Figure 22-9).18
Figure 22-9. Popliteal Aneurysm Measuring Over 20 mm

Abbreviations: T, thrombus; PA, popliteal artery.
A thrombus is noted. White arrows point to the walls of the popliteal artery.
VASCULAR INJURY
Vascular injury can occur as the result of trauma as well as iatrogenic complications of procedures. At
most institutions, cases with a high likelihood of vascular injury will rely on computed tomography
angiography for the diagnosis. However, in occult cases, ultrasound offers a portable and rapidly
accessible testing modality. In injuries caused by penetrating and blunt trauma, the reported sensitivity of
ultrasound will range from 66% to 95% and specificity will range from 95% to 100%, depending on
factors such as technical expertise, location, and nature of the injury.19-21 In suspected cases, various
imaging modalities may be used to confirm the diagnosis and orchestrate treatment.
Ultrasound Technique and Findings

Techniques to identify vascular injury will vary depending on mechanism. Common findings will include
anatomic variations noted in brightness mode coupled with variations of blood flow noted on spectral
Doppler analysis of waveforms. Hence the term “duplex ultrasound” has been adopted to describe the
process whereby both modes of ultrasound technology are used to arrive at the ultrasound diagnosis.
Because most injuries occur in the extremities, duplex ultrasound is performed at or near the injury site,
with the intention of visualizing abnormalities as well as analyzing the quality of blood flow through the
vessel.
PSEUDOANEURYSM
Pseudoaneurysm and hematoma are common findings in vascular trauma in the extremities. These injuries
may commonly follow patients who have undergone procedures requiring arterial vascular access, most
commonly in the groin. Although commonly cited to occur in 2 in 1,000 cases, prospective studies have
suggested that injuries occur in as many as 4 in 100 cases.22,23 Multiple blind femoral vein cannulation
attempts during cardiac resuscitation can result in pseudoaneurysm development if resuscitation efforts
are successful. Injury to a blood vessel will cause blood to extravasate. If the contained blood has no
connection to the flowing blood vessel, an anechoic collection adjacent to the vessel will be noted and a
hematoma is the likely diagnosis (Figure 22-10). If blood flow communicates with the fluid collection,
swirling may be noted and a pseudoaneurysm is likely to exist (Figure 22-11). Further querying with color
Doppler will frequently highlight active rotational flow in the space. If noted, the spectral Doppler tracing
will confirm bidirectional flow through the communicating channel, and is often referred to as the “ying-
yang” sign.
Figure 22-10. Hematoma Following Blunt Trauma to Leg

Abbreviation: PA, popliteal artery.
The white arrow points to an anechoic area suggesting vasculature dilatation or pseudoaneurysm, but color Doppler demonstrates no flow,
suggesting a hematoma. White arrow heads indicate the walls of the popliteal artery (PA).
Figure 22-11. Injury to Popliteal Artery Resulting in Pseudoaneurysm
Abbreviations: PsA, pseudoaneurysm; PA, popliteal artery.
The lumen of a PsA is noted adjacent to the PA. Doppler signal demonstrates flow in the PA communicating with the PsA. The white arrow
points to flow through the communicating channel. Note the varying Doppler signals (different colors) indicating turbulent flow through the
channel.
ARTERIOVENOUS FISTULA
An arteriovenous fistula can develop when a channel communicating between the vein and artery is
established. This can result from trauma to any vascular site, but ultrasound can be helpful in the neck and
extremity areas following central or peripheral venous access. Arteriovenous fistulas may also potentially
occur after blind femoral vein cannulation attempts during cardiac resuscitation efforts. Ultrasound
findings of an arteriovenous fistula include a visualized communicating channel noted on B-scale imaging
and evidence of high-velocity, turbulent flow through the communicating channel on color Doppler.
Spectral Doppler will demonstrate arterial waveforms through the communicating channel as well as an
arterialized waveform in the venous system next to the fistula.24,25

Optimize the image in B-mode before setting color and spectral Doppler controls.
Figure 22-12. Thrombosis of Popliteal Artery
Abbreviations: ST, soft tissue; T, thrombus.
A) The red arrow points to the directional flow of the popliteal artery. The blue arrow points to the directional flow of the popliteal vein. An
echogenic thrombus is noted obstructing the entire lumen of the popliteal artery. No color Doppler signal is noted. B) The red arrow points in
the directional flow of the popliteal artery. The blue arrow points to the directional flow of the popliteal vein. The white arrow points to the
spectral Doppler signal. Note that no spectral Doppler signal is observed when the gate is placed in the lumen of the vessel, indicating
complete vascular obstruction.
THROMOBOSIS
Penetrating trauma or endovascular procedures involving the arterial system can result in thrombosis of
an arterial structure. Endovascular procedures carry an inherent risk of arterial thrombosis based on
where access is obtained. Procedures through the femoral artery carry a 1 in 1,000 risk of thrombosis
compared with a 1 to 2 in 100 risk when the brachial artery is used for access.26 Thrombosis may be often
visualized in B-mode as an echogenic signal in the lumen of the suspected artery. Color and spectral
Doppler signals are often absent or dampened distal to the suspected occlusion (Figure 22-12).
DISSECTION/FLAP
Vascular dissection can occur in any branch of the vascular system following penetrating trauma or from
progression of disease. Dissection may also occur following iatrogenic complications of vascular
procedures. As with aortic dissections, the principal findings will include an intraluminal flap. Color
flow may highlight flow on either side of the flap or may demonstrate turbulent flow in the false lumen
and true directional flow in the true lumen (Figure 22-13).
Figure 22-13. Carotid Artery, Long-Axis View

Abbreviations: CA, carotid artery; SC, sternocleidomastoid.
The sternocleidomastoid is noted here. The red arrows point to the normal carotid artery vessel wall. The white arrows point to an intraluminal
flap suggesting dissection.
KEY POINTS
An intraluminal flap represents a dissection of the vascular wall.
Focal dilatations suggest either pathologic aneurysms or pseudoaneurysms.
Color and spectral Doppler are key adjuncts to determining flow patterns through suspected
pathologic vascular injuries.
REFERENCES
1. Hagan PG, Nienaber CA, Isselbacher EM, et al. The international registry of acute aortic dissection (IRAD): new insights into an old
disease. JAMA. 2000;283:897-903.
2. Mody PS, Wang Y, Geirsson A, et al. Trends in aortic dissection hospitalizations, interventions, and outcomes among Medicare beneficiaries
in the United States, 2000- 2011. Circ Cardiovasc Qual Outcomes. 2014;7:920-928.
3. Tsai TT, Fattori R, Trimarchi S, et al. Long-term survival in patients presenting with type B acute aortic dissection: insights from the
International Registry of Acute Aortic Dissection. Circulation. 2006;114:2226-2231.
4. Walker KL, Shuster JJ, Martin TD, et al. Practice patterns for thoracic aneurysms in the stent graft era: health care system implications.
Ann Thorac Surg. 2010;90:1833- 1839.
5. Collins JS, Evangelista A, Nienaber CA, et al. Differences in clinical presentation, management, and outcomes of acute type A aortic
dissection in patients with and without previous cardiac surgery. Circulation. 2004;110(suppl 1):II237-242.
6. Howard DP, Sideso E, Handa A, et al. Incidence, risk factors, outcome and projected future burden of acute aortic dissection. Ann
Cardiothorac Surg. 2014;3:278-284.
7. Cecconi M, Chirillo F, Costantini C, et al. The role of transthoracic echocardiography in the diagnosis and management of acute type A
aortic syndrome. Am Heart J. 2012;163:112- 118.
8. Khandheria BK, Tajik AJ, Taylor CL, et al. Aortic dissection: review of value and limitations of two-dimensional echocardiography in a six-
year experience. J Am Soc Echocardiogr. 1989;2:17-24.
9. Paterick TE, Humphries JA, Ammar KA, et al. Aortopathies: etiologies, genetics, differential diagnosis, prognosis and management. Am J
Med. 2013;126:670-678.
10. Clouse WD, Hallett JW Jr, Schaff HV, et al. Acute aortic dissection: population-based incidence compared with degenerative aortic
aneurysm rupture. Mayo Clin Proc. 2004;79:176-180.
11. Pressler V, McNamara JJ. Aneurysm of the thoracic aorta: review of 260 cases. J Thorac Cardiovasc Surg. 1985;89: 50-54.
12. Meszaros I, Morocz J, Szlavi J, et al. Epidemiology and clinicopathology of aortic dissection. Chest. 2000;117:1271- 1278.
13. Pape LA, Tsai TT, Isselbacher EM, et al. Aortic diameter >or = 5.5 cm is not a good predictor of type A aortic dissection: observations
from the International Registry of Acute Aortic Dissection (IRAD). Circulation. 2007;116:1120-1127.
14. Elefteriades JA. Thoracic aortic aneurysm: reading the enemy’s playbook. World J Surg. 2008;32:366-374.
15. Taylor RA, Oliva I, Van Tonder R, et al. Point-of-care focused cardiac ultrasound for the assessment of thoracic aortic dimensions, dilation,
and aneurysmal disease. Acad Emerg Med. 2012;19:244-247.
16. Freel KA, Nutley WK. Internal iliac artery aneurysm detected by sonography. J Diagnos Med Sonogr. 2013;29:234-237.
17. Dix FP, Titi M, Al-Khaffaf H. The isolated internal iliac artery aneurysm: a review. Eur J Vasc Endovasc Surg. 2005;30: 119-129.
18. Wolf YG, Kobzantsev Z, Zelmanovich L. Size of normal and aneurysmal popliteal arteries: a duplex ultrasound study. J Vasc Surg.
2006;43:488-492.
19. Bynoe RP, Miles WS, Bell RM, et al. Noninvasive diagnosis of vascular trauma by duplex ultrasonography. J Vasc Surg. 1991;14:346-352.
20. Meissner M, Paun M, Johansen K. Duplex scanning for arterial trauma. Am J Surg. 1991;161:552-555.
21. Pezeshki Rad M, Mohammadifard M, Ravari H, et al. Comparing color Doppler ultrasonography and angiography to assess traumatic
arterial injuries of the extremities. Iran J Radiol. 2015;12:e14258.
22. Moll R, Habscheid W, Landwehr P. HÃ¤ufigkeit des Aneurysma spurium der Arteria femoralis nach Herzkatheteruntersuchung und PTA.
Fortschr RÃ¶ntgenstr. 1991;154:23-27.
23. Standard for diagnostic arteriography in adults. Standards of Practice Committee of the Society of Cardiovascular and Interventional
Radiology. J Vasc Interv Radiol. 1993;4:385- 395.
24. Roubidoux MA, Hertzberg BS, Carroll BA, et al. Color flow and image-directed Doppler ultrasound evaluation of iatrogenic arteriovenous
fistulas in the groin. J Clin Ultrasound. 1990;18:463-469.
25. Lopez-Quinones M, Bargallo X, Blasco J, et al. Iatrogenic carotid-jugular arteriovenous fistula: color Doppler sonographic findings and
treatment with covered stent. J Clin Ultrasound. 2006;34:301-305.
26. Tonnessen BH. Iatrogenic injury from vascular access and endovascular procedures. Perspect Vasc Surg Endovasc Ther. 2011;23:128-
135.
Chapter 23
Ultrasound Quality Improvement,
Documentation, and Billing
Chapter 24
Credentialing in Ultrasound for
Critical Care Medicine Providers
Chapter 23
Ultrasound Quality Improvement,
Documentation, and Billing
OBJECTIVES
Describe the structure of, need for, and benefit of an ongoing quality improvement program
Provide plausible mechanisms for internal review and discuss commonly encountered pitfalls
Discuss billing requirements and mechanics as well as commonly used billing codes in critical care ultrasound
Discuss documentation options, image archiving, and utilization of picture archiving and communication
systems and their variant
INTRODUCTION
On a quick review of the table of contents of an ultrasound textbook, a chapter on logistics may not seem
an inherently exciting and interesting chapter; however, it can prove to be every bit as critical as the
ultrasound techniques described in other chapters. Logistics means: “The detailed coordination of a
complex operation involving many people, facilities, or supplies.” Many ultrasound program directors,
both in academic centers and in private practice, eventually find that they have embarked on utilization of
a technology that is different from anything most clinicians have decided to add to their clinical skill set in
the past. Unlike learning to place a central venous line from a supraclavicular approach to broaden one’s
skill set or intubate with a video laryngoscope, ultrasound spans a great breadth of applications and is by
itself a diagnostic and interventional imaging modality. Although few critical care physicians will
perform the type and number of in-depth, comprehensive examinations as a radiology, cardiology, or
vascular laboratory, this great new technology requires that the clinician make special logistic
considerations.
Forgoing the establishment of policies and a healthy concern for quality improvement (QI), internal
review, billing, and documentation can result in quick closure of a critical care ultrasound program. An
exhaustive review of billing nuances and medical coding is beyond the scope of this chapter; however, the
information provided will suffice to allow providers to bill and collaborate with their coders to optimize
reimbursement for their effort.
ULTRASOUND DIRECTION AND QI REQUIREMENT

Quality improvement, or quality assurance as it is sometimes known, is an important component of a
critical care ultrasound program, perhaps on par with education. QI is potentially an all-encompassing
phrase, but always has 1 central goal: to improve the quality of services provided. The basic premise is
that the quality of ultrasound examinations being performed requires continual monitoring and
improvement. There is a somewhat automatic contrarian belief that arises among ultrasound practitioners
that once they have reached competency and are credentialed by the hospital, mistakes will rarely, if ever,
be made and specific reviews are not required. However, because ultrasound differs so much from other
new skills, critical care providers learn throughout their career that a special and separate QI program is
required and mandatory as the number of users and applications used grows.
To enable a QI program, a mechanism is required by which ultrasound procedures or studies can be
reviewed. This review should occur by the most qualified person in the department or section, who is
likely to be the ultrasound program director. As the program grows in size, assistants may take over part
of or this entire role. As mentioned before, each reviewer requires some documentation of the ultrasound
procedure and its results to perform the QI job. Optimal methods of documentation will be discussed later
in this chapter.
A key component to any ultrasound program is an ultrasound director. This director should be a board-
eligible or board-certified critical care provider with adequate ultrasound training and experience. This
person is assigned the administrative task of oversight for all aspects of the ultrasound program as well as
education. Many of these tasks may need to be delegated as the program grows in size. However, in
general, the ultrasound director is responsible for coordinating and carrying out machine maintenance and
acquisition; ultrasound education for all levels in the critical care unit or program; and developing,
implementing, and updating the QI process.
DOCUMENTATION
Point-of-care ultrasound is inherently different from traditional imaging that is performed on a
consultative basis involving multiple imaging modalities, including ultrasound. Rather than an ultrasound
examination performed by a technologist, interpreted by a radiologist or cardiologists at a remote location
and time, and then later reported to the treating clinician who now incorporates it into his or her medical
decision hours to days later, critical care ultrasound combines all these steps, cutting out the significant
time delay of the “middlemen” involved. Scanning and interpretation occur simultaneously and the results
are contemporaneously integrated into medical decision making. It is tempting and even appears more
efficient at first glance to not document the ultrasound examination, decision making, or examination
findings. However, documentation is critical for a number of reasons, including later review of findings,
proper documentation of medical decision making, and support of the decisions made as well as potential
regulatory requirements.
Critical care ultrasound documentation should be as expansive as required by the situation, and include
the examination performed, findings, and decisions made. Typically these are focused and goal oriented,
such as documentation of the absence of a pericardial effusion during a cardiac arrest. However, it may
be longer if ultrasound is used to guide resuscitation and management of fluid and inotropes used to treat
the patient over the period of an hour. It is important to realize that billing and regulatory documentation
requirements may go beyond a simple note in the chart and will typically include a reason for the
examination, technique used, examination findings, and the scanning clinician’s impressions. Although
documentation may be handwritten, most physicians will opt for dictation. Documentation done using a
template and computerized is becoming more common, and as electronic medical records (EMRs) evolve
to their full potential, may be the most efficient method for documentation. During focused examinations, it
is not rare to encounter incidental findings such as gallstones during a RUSH (rapid ultrasound in shock
examination) or E-FAST (extended focused assessment with sonography in trauma) examination. Such
incidental findings should be relayed to the patient and ideally to a follow-up physician/provider. When
discharging a patient from the service, critical care ultrasound findings should be documented in the
discharge summary just like any other diagnostic examination result. As will be discussed later,
ultrasound images should be saved in the medical record or hospital archival systems. These can include
digital still images or video as part of an EMR. Hard copy image reports are discouraged, unless
scanned, because of their inaccessibility and wear over time.
QI PROCESS
Quality improvement systems are a key part of any ultrasound program being considered. The goal of an
ultrasound QI system is to evaluate saved images or video for accuracy of interpretation as well as
technical quality. Such a program would ideally sample 100% of studies performed by clinicians who
have yet to attain hospital credentialing and a portion of studies for those who are credentialed. The QI
system provides feedback to clinicians to allow improvement in performance and functions as a key
component of the ultrasound credentialing process as well as ultrasound education. In traditional imaging
in laboratory settings, technologists may not enter a QI process unless particular errors are noted by the
reading radiologist, whose interpretations, in turn, are rarely reviewed unless a problem case arises. In
contrast, a critical care ultrasound study has multiple aspects that should be evaluated. These aspects
include basics such as gain; image depth; focus zone location; proper image orientation and preset
selection; proper use of adjunct imaging such as color, pulsed-wave, and continuous-wave Doppler;
definition of anatomic details and key structures; and overall image quality or resolution. Not only should
saved videos or images be reviewed for each study going through the QI process, follow-up studies such
as radiology or cardiology ultrasound examinations, other imaging studies, surgical results, and patient
outcome should also be evaluated and compared with the study being reviewed. The QI process, by
necessity, must be undertaken by an experienced and credentialed critical care physician who is able to
review and interpret all required materials and evaluate the ultrasound study for accuracy.
Timely feedback is important, especially for clinicians in training, without sacrificing quality of review.
The ideal method of ultrasound review is for the ultrasound director to critique a recorded video of the
ultrasound study. These may take the form of short ultrasound cine loops to entire ultrasound studies
recorded on digital media lasting several minutes. The latter would be the most time consuming because
of the potential length of a trainee’s ultrasound examination, if recorded in entirety. Review of still images
is least time consuming, but like many traditional imaging practices, if any questions arise about missed
pathology or anatomic accuracy, gleaning additional supportive information from several still images may
be all but impossible. A video clip of adequate length (typically 10-30 seconds) will allow the clinician
to sweep through an entire organ of interest or capture physiologic findings. It is up to an individual
program to decide on the percentage of cases to undergo the QI process outside specific issues raised for
credentialed ultrasound providers. Established programs range from 10% to 100%, and many point-of-
care experts suggest 25% as a minimum. Review of credentialed providers’ studies can also be used to
train newer providers and accumulate cases for education. The general flow process for QI is depicted in
Figure 23-1.
Figure 23-1. Quality Improvement Process
Abbreviations: PACS, picture archiving and communication system; EMR, electronic medical record; QA, quality assurance; QI, quality
improvement.
BILLING
Billing for ultrasound examinations and ultrasound guidance of procedures by nontraditional imagers is
not a new concept. Billing by clinicians in office and emergency department settings goes back to the
early 1990s and earlier. However, while billing is not a requirement, providing potentially reimbursable
expert procedures and ignoring available appropriate compensation is ill advised, given the current
financial state of medicine. Billing, in this chapter, refers to issuing a bill for the ultrasound component of
one’s work. This may be ultrasound guidance for the vascular access in a central line placement; needle
direction to a pleural effusion; or an evaluation of the heart, lungs, and other structures. An alternate
method used by some critical care providers is to include time spent performing and interpreting
ultrasound into their critical care time, which thereby encompasses the time the provider spends
performing the ultrasound examination. Such an approach may have potential drawbacks, and depends on
national and local regulatory environments, which cannot be fully addressed in this chapter. Critical care
physicians should consult with their local billing and compliance offices to ensure that their billing
practices are appropriate. Billing codes for a multitude of ultrasound-guided procedures and focused
diagnostic ultrasound examinations exist for a reason, and are the appropriate pathway to obtaining
reimbursement for this additional component of patient care.
There are several components to ultrasound billing that will be discussed to help the critical care
provider understand how they may be reimbursed for the ultrasound studies being performed. In this
chapter we outline procedure-specific billing strategies.
Coding
The Current Procedural Terminology (CPT) system is the effective lexicon of terminology for identifying
particular codes used in reporting diagnostic, surgical, and medical services rendered to patients. The
CPT system includes utilization review, claims processing by insurers and government, and
documentation of medical care provided. Existing CPT codes describe many of the ultrasound
applications used by critical care ultrasound providers. Table 23-1, although not an exhaustive inventory,
lists some codes used in critical care ultrasound. It is important to note that this list is not all-inclusive,
and also that periodic updates from the Centers for Medicare and Medicaid Services (CMS) require
changes to be made in the CPT codes used. In addition, several CPT codes may be used for the same
patient in some instances. However, CPT codes are not specialty specific and the critical care provider
may use the same code as the family practitioner or general internist.
Focused Studies and Limited Codes

The CPT code system was created to reflect complete or comprehensive studies unless otherwise
specified, and the same is true for ultrasound codes. A complete study is one that evaluates and visualizes
all the major structures within the anatomic description provided by the CPT code. However, there also
exists a concept of the limited study, which is specifically differentiated from a complete ultrasound study.
For a complete study, the report should address all components of the examination specified by the CPT
code, even if portions of the region of interest could not be visualized, such as a surgically removed
gallbladder noted on right upper quadrant examination. Another example is when significant bowel gas
obscures a key portion of the kidney or other structure. A common applicable example may be a critical
care clinician who is scanning a patient with new-onset renal failure and evaluates the kidneys for
hydronephrosis and the bladder for size/volume. This would be a limited scan. However, the radiology
department would likely perform a complete examination of the same region covering the bladder, both
kidneys, liver, gallbladder, common bile duct, pancreas, spleen, aorta, and inferior vena cava and
describe any abnormality discovered. This would be billed under CPT code 76700. Because in such a
case, the critical care clinicians’ study addresses only a single diagnostic problem, this is a limited study.
The same reasoning is applied to a single quadrant such as the right upper quadrant or when a follow-up
study is performed. Another way to look at a limited examination is an ultrasound study meeting less than
the required elements for a complete examination described in a CPT code. The limited examination
performed by the critical care clinician should be billed as a limited examination, or CPT code 76705
(Table 23-1).
Table 23-1. 2015 ICU Ultrasound CPT Codes and RVU Values
CPT Code RVU Value
Ultrasound Study Performed CPT Description from CMS No. 2015 from CMS
T EE Echocardiography, transesophageal, real time with image documentation (2D) (with or without M-mode 93312 2.55
recording); includes probe placement, image acquisition, interpretation, and report
Ultrasound-guided pericardiocentesis Requires image of site to be localized but does not require image of needle in site 76930 0.67
Limited cardiac Echocardiography, transthoracic, real-time with image documentation (2D), with or without M-mode 93308 0.53
recording; follow-up or limited
FAST: Checking for pericardial effusion, Echocardiography, transthoracic, real-time with image documentation (2D), with or without M-mode 93308 0.53
abdominal fluid, and potentially PT X recording; follow-up or limited
Echography, abdominal, B-scan, and/or real time with image documentation, limited (eg, single organ, 76705 0.59
quadrant, follow-up)
Ultrasound, chest, B-scan (includes mediastinum), and/or real time with image documentation 76604 0.55
AAA Echography, retroperitoneal (eg, renal, aorta, nodes), B-scan, and/or real time with image documentation; 76775 0.58
limited
Biliary Echography, abdominal, B-scan, and/or real time with image documentation; limited (eg, single organ, 76705 0.59
quadrant, follow-up)
Urinary tract/renal Echography, retroperitoneal (eg, renal, aorta, nodes), B-scan, and/or real time with image documentation; 76775 0.58
limited
Bladder imaging Imaging of bladder 76857 0.5
Focused DVT study Duplex scan of extremity veins including responses to compression and other maneuvers; unilateral or 93971 0.45
limited study
Lower extremity Ultrasound, extremity, nonvascular, B-scan, and/or real time with image documentation 76882 0.49
Ultrasound-guided lumbar puncture Ultrasound localization of lumbar puncture site 76942 0.67
Ultrasound-guided paracentesis Requires image of site to be localized but does not require image of needle in site 49083 2
Ultrasound-guided thoracentesis with T horacentesis and catheter placement; requires image of site to be localized but does not require image of 32557 3.12
catheter placement the needle in site
Ultrasound-guided thoracentesis Ultrasound localization of drainage site; does not require image of needle 32555 2.27
Ultrasound-guided vascular access placement Real-time ultrasound guidance; requires written documentation and image of fluid; does not require image of 76937 0.3
needle
Musculoskeletal (extremity, nonvascular) Ultrasound, extremity, nonvascular, B-scan, and/or real time with image documentation 76882 0.49
T horacic Ultrasound, chest, B-scan (includes mediastinum), and/or real time with image documentation 76604 0.55
Ocular Ophthalmic ultrasound, diagnostic, B-scan (with or without superimposed nonquantitative A-scan) 76512 0.94
Ocular FB Ophthalmic ultrasonic FB localization 76529 0.57
Abbreviations: CPT, Current Procedural Terminology; TEE, transesophageal echocardiography; RVU, relative value unit; CMS, Centers for
Medicare and Medicaid Services; 2D, 2-dimensional; FAST, focused assessment with sonography in trauma; PTX, pneumothorax; AAA,
abdominal aortic aneurysm; DVT, deep vein thrombosis; FB, foreign body.
Code Modifiers
Providers can modify CPT codes to provide additional information useful to payers about the
examination. In fact, using modifier codes in addition to a CPT code may be mandatory to avoid denial of
payment or overpayment in some cases. Many different modifiers exist, and a complete discussion of them
or their use is beyond the scope of this chapter. However, a basic understanding of relevant modifiers and
their use will allow the reader to communicate and cooperate with their local facility coders and billers
more efficiently and effectively. Medicare carriers regularly publish CPT code updates such as
clarifications, changes, and explanations. Some regional variability may exist based on local or regional
specific bulletins. Such bulletins are referred to as “local coverage determinations,” but the precise
terminology can change.
Repeat Procedure by Another Clinician

This is a modifier designed to specify a repeat procedure by another physician during a single patient
encounter. The modifier is 77 and should be used when another clinician performs a repeat ultrasound
examination. An example for the critical care provider is evaluation of an inferior vena cava or perhaps
lung ultrasound scan for assessment of B-lines indicating increased lung water while resuscitating a
patient with intravenous fluids. A process that began earlier on the floor with an ultrasound study by the
internist then continues in the ICU and requires a repeat ultrasound examination by the intensivist. The
intensivist’s group Medicare provider number differs from that of the internist and calls for the 77
modifier. As with every ultrasound examination, the chart should appropriately document the necessity,
findings, images, and interpretation of the examination.
Repeat Procedure by Same Clinician

This CPT modifier applies to a repeat procedure by the same physician on the same date of service or
same patient encounter. The modifier not only applies to the same individual, but also to the members of
the same critical care group. In fact, clinicians in the same specialty during the same encounter are
viewed as the same physician. The group’s Medicare provider number is what determines payment, rather
than a physician’s unique identifier number. Therefore, as mentioned before, in a case in which an
intensivist resuscitating a patient moves the patient from the floor to the ICU and performs a second
ultrasound in the ICU to evaluate the inferior vena cava or lung to measure volume status, the modifier
code 76 is used for a repeat examination by the same physician. Again, proper documentation should
include the need for repeating the examination, along with findings and any abnormalities encountered.
Professional Component in Billing

A bill received by CMS or a third-party payer for an ultrasound examination theoretically has 2
components to it: a professional and a technical component. The CPT codes for ultrasound are effectively
global or combined codes, combining the 2 components of billing. In an ICU or hospital setting, clinicians
bill with a code of 26, or a professional component modifier. The hospital or facility will bill for the
technical component, or the “TC modifier,” which will be discussed later in this chapter. In hospital
settings, physicians should not use the TC modifier. Strictly speaking, the code 26, or professional
component modifier, is used to report the physician’s services for interpreting diagnostic studies and
requires the preparation of a distinct report from anything noted by an ultrasound or radiology technician.
This is the only direct billing a physician can make for an ultrasound examination he/she performs in the
ICU. The modifier code 26 is simply attached to the end of the limited examination code, such as 76705-
26 in the aforementioned example. A bill issued without the 26 modifier, only 76705 for instance, would
be a global service code accounting for both the professional and technical components. Again, it is
important for the reader to check the latest bulletins and changes in CPT codes as they are updated
periodically.
Technical Charges in Ultrasound

As mentioned before, the TC of the ultrasound bill (TC modifier) is reported by the hospital in the ICU
setting and is designed to cover the hospital’s overhead for the cost of equipment, ultrasound-related
supplies, and salary of the ultrasound technician who performed the examination. For the hospital to
charge for a TC modifier, an ultrasound image must be placed in the patient’s medical record. It is
important to note that the TC charge is often larger than the physician’s component and the difference may
be significant. Although not directly related to this discussion, intensivists are wise to keep track of
hospital TC billing, especially when proving to a facility that ultrasound-related work should be
reimbursed and equipment should be maintained and updated as needed.
Reduced Services Charges

In some cases, a clinician may want to bill a partially reduced charge, and modifier code 52 is used to
indicate that the typical procedure was not performed as described for the particular CPT code. For
example, in the case of a scrotal ultrasound, a critical care physician may include a more comprehensive
examination to search for an infectious source such as an abscess, but may not perform the complete
examination including Doppler measurements.
Distinct Procedural Service

The modifier code 59 is used to report multiple distinct procedures that are covered by the same CPT
code. One example might be a code used for a trauma patient in the ICU with multiple foreign bodies from
a shotgun blast who receives an upper and lower extremity evaluation. Such an evaluation would be
billed using a 76882-59 code with modifiers reflecting an ultrasound evaluation of a nonvascular
extremity and indicating that it was used more than once.
DOCUMENTATION AND IMAGE ARCHIVING

As mentioned before, to some degree the documentation required for ICU ultrasound studies is dictated by
payer requirements as well as regulatory ones. In addition, ultrasound providers have a standard-of-care
pressure for proper and complete documentation. When submitting a bill, more extensive documentation
will be required, such as describing the study indication, findings, and details about the technique and the
impression of the intensivist performing the study. Documentation is permitted via a transcribed report,
handwritten report, and template-generated or computerized report. Digital images and video should be
saved and stored or archived. The required written report that goes into the patient’s medical record, even
if generated by a template, may be a separate procedure note, much like a central line placement or
thoracentesis note. A separate note may be used to append the medical record and is the pathway taken by
most consultative imaging services such as the department of radiology. Along with medical necessity
documentation or test indication, the ultrasound study report must also list who performed and interpreted
the study. The written summary should describe the test performed and findings, and also specify whether
a limited or complete examination was performed. An example of such a report could be the following:
“I performed a limited examination of the bladder and kidneys to evaluate for bladder outlet and ureteral obstruction.
Indication: New onset renal failure.
Findings: Moderate hydronephrosis noted bilaterally. The bladder volume is 1,400 mL by volume calculations. Discomfort noted when
scanning over the bladder. Images and video are archived and attached to the EMR.
Impression: Bladder outlet obstruction and bilateral hydronephrosis.”
The number of images stored is typically not described in the CPT code, with exceptions such as needle
placement into a vessel. However, the intensivist should seek to adequately describe and document his or
her examination findings and allow the report (with images and video) to stand up to later scrutiny and
support the impression given. In the aforementioned example, a midsagittal long-axis image of each
kidney as well as an image of the bladder with the volume calculation estimate on it would suffice. Video
sweeps, even relatively short ones, would also be helpful in documenting a lack of other gross
abnormalities, such as large renal cysts not seen in the midsagittal view or free fluid in the pelvis.
Image archiving goes hand in hand with documentation. Although this is a path well established by
traditional imagers such as radiologists and cardiologists, a new frontier is being charted by more robust
EMR systems, often combined with a picture archiving and communication system (PACS) system
substitutes for reasons that will become obvious. Most ultrasound images are stored using an existing
format that is found on all but the most rudimentary ultrasound machines — Digital Imaging and
Communications in Medicine (DICOM). This is a standard format used throughout medicine which stores
images along with embedded data such as the patient’s identifiers and study information. The system on
which such images are stored in many hospitals is the PACS. This system is typically, but not always,
controlled by a radiology or cardiology department for computerized storage and retrieval of ultrasound
images and video. Images and videos can be uploaded to a PACS and placed in an archive. The archive
or database may be searched, and studies as well as radiology and other reports stored on the PACS can
be retrieved from work stations. PACS also interfaces with EMRs and typically has special work stations
at which studies can be accessed and viewed at higher resolutions. PACS is not designed for the ICU
ultrasound workflow, nor can most intensivists gain access to such systems easily. It is important to note
that, especially as more of these systems fall under the control of the hospital information technology
departments, fewer roadblocks are appearing for clinicians wishing to use PACS for storing ultrasound
examination findings.
The PACS storage model, however, is not ideal; especially given that there is a need for image storage
and QI review during the hospital credentialing process for intensivists who are not trained in
fellowships and are building a portfolio of ultrasound scans in pursuit of hospital credentialing.
Educational studies for fellows and others may not be optimally stored on PACS as well, unless a clear
delineation can be provided between credentialed study results and educational ones; the latter should not
be used for decision making and not relied upon by other services and physicians. Currently for many
point-of-care ultrasound programs, a workflow solution by a third party works well. This is a rapidly
evolving area of critical care ultrasound, and it behooves the reader to check for the most up-to-date
vendors and options available.
The goal of a third-party workflow solution is to optimize a potentially complex and time-consuming
process. They allow for efficient completion of ultrasound scan upload, image archiving, interpretation of
studies, QI review of studies, portfolio building for hospital credentialing, feedback to trainees and others
for education, interfacing with and creation of EMR reports, and billing. Performed individually without a
workflow solution of some sort, all of these steps can be extremely time consuming when large volumes
of scans are involved in a busy ICU with multiple providers scanning.
Ideally wireless transfer or upload of ultrasound images, video, and patient information can be performed
from the ultrasound machine using a secure Wi-Fi system. Manual upload to the machine through a direct
cable connection or transfer of studies to some sort of digital medium such as a flash drive is much less
efficient, but also possible. A barcode scanner, available on many but not all point-of-care ultrasound
machines, helps enter the patient information into the work list on the system. Entering the information
manually on the ultrasound machine for each scan is an alternative that will consume more time and may
lead to a greater number of entry errors. Most workflow solution systems allow for the creation of
customizable interpretation sheets so that intensivists can check a box to indicate their interpretation, thus
adequately relaying the findings on each examination.
Once the ultrasound examination is completed and patient information is entered as well as the
examination interpretation selected, still images and videos can be stored on a local or cloud server. All
workflow solution providers are keenly cognizant of the Health Insurance Portability and Accountability
Act (HIPAA) and security requirements and adapt to changing regulations and security challenges. Studies
consisting of videos and images may be reviewed for accuracy as part of a QI or credentialing process.
This allows the ultrasound director to give rapid feedback to providers. If a credentialed provider has
completed the study, the report can be saved to the EMR and images transferred to PACS or linked to
another server but still available through the EMR. If a noncredentialed provider completed the study, it
can remain hidden from the EMR except for any needed notation of an educational or initial study and then
reviewed by a credentialed intensivist or the ultrasound director. The 2 most popular workflow solution
vendors allow emails to be sent to providers, often with images and notes showing potential errors and
suggestions for improvement. At the end of a credentialing process, providers will have a folder or
portfolio with all of their required studies that have been reviewed to present to a hospital credential
board for potential review before credentialing.
KEY POINTS
QI is a critical component of critical care ultrasound program building and survival.
Billing is appropriately and easily accomplished with existing CPT codes for ultrasound
procedures.
Knowledge of CPT codes and their modifiers is important for accurate billing, which is more likely
to be reimbursed.
Image archiving is an essential component of any critical care ultrasound program, allowing for QI,
reporting, and enabling hospital credentialing.
ADDITIONAL SOURCES
Centers for Medicare and Medicaid Services. http://www.cms.hhs.gov/mcd/search.asp?clickon=search. Latest bulletins and coding updates
from CMS.
American Medical Association. http://www.ama-assn.org/ama/pub/physician-resources/solutions-managing-your-practice/coding-billing-
insurance/cpt.page. Information on billing and coding management.
American College of Emergency Physicians. www.acep.org. Information on point-of-care ultrasound practice, billing, and coding.
American Institute of Ultrasound in Medicine. www.aium.org. Information on ultrasound-related policies.
Chapter 24
Credentialing in Ultrasound for Critical Care
Medicine Providers
Aliaksei Pustavoitau, MD, MHS; Ranjit Deshpande,
MD
OBJECTIVES
Review currently available resources in ultrasound credentialing for critical care providers
Define different terms when addressing training in ultrasound for critical care providers
Formulate a plan for intensivists for initial credentialing and maintenance of credentialing in ultrasound
Provide examples of critical care provider evaluations for the purpose of credentialing in ultrasound
INTRODUCTION
Establishing an ultrasound program requires a systematic approach to ensuring quality and consistency
across critical care providers. In this chapter, we outline an approach to credentialing and certification
based on available literature on the use of ultrasound in critical care medicine.
GUIDING DOCUMENTS
The American Medical Association’s (AMA) resolution 802 on privileging in ultrasound imaging1
provided the grounds for expanding ultrasound beyond the “classical” specialties of radiology and
cardiology. In resolution 802, the AMA stated that (1) ultrasound imaging is within the scope of practice
of appropriately trained physicians; (2) multiple applications of ultrasound imaging exist; (3) privileging
in ultrasound imaging in the hospital setting is a function of medical staffs and should be delineated in the
departmental Delineation of Privileges form; and (4) hospital staffs base their criteria for ultrasound
privileges on education and training of the providers and that these criteria are guided by standards
established by each physician’s respective specialty.
Ultrasound in critical care medicine evolved consistent with AMA resolution 802, and credentialing is
guided by standards established by critical care medicine societies, as we specify below. The bulk of
knowledge on ultrasound in critical care medicine was outlined in 2 supplemental issues to Critical Care
Medicine in 2007.2,3 Since then, several major documents were published, which guided the development
of credentialing for critical care providers:
1. The World Interactive Network Focused on Critical Ultrasound (WINFOCUS) provided guidance to
the practice of critical care echocardiography,4 with recommendations focusing on building an
echocardiography program in a critical care setting, defining aspects of echocardiography for critical
care providers, and describing pathways for critical care providers to achieve competence in
echocardiography.
2. The American College of Chest Physicians and the Société de Réanimation de Langue Française
published a statement on competence in critical care ultrasonography.5 This statement described the
knowledge and skills required for achieving competence in critical care ultrasonography and
echocardiography, based on the consensus opinion of ultrasound experts in critical care medicine.
3. A group of experts representing 12 critical care societies worldwide6 described the minimal training
requirements for each area of competence in critical care ultrasonography and echocardiography.
4. In a statement expanding on training requirements for advanced critical care echocardiography,7
experts from 9 critical care societies provided answers to what could be considered standard
echocardiographic views, cognitive base in cardiovascular physiology and echocardiography, methods
of training, and assessment of competence.
5. The Ultrasound Certification Task Force, on behalf of the Society of Critical Care Medicine (SCCM),
developed recommendations for achieving and maintaining competence and credentialing in critical
care ultrasound.8 These recommendations are all-inclusive for providers of critical care medicine,
suggesting that the practice of ultrasound extends beyond physicians.
The aforementioned documents use various terms, and for the purpose of this chapter, we adopted the
terms included in the SCCM recommendations,8 because they best reflect our approach to credentialing
and are in line with other documents5,6:
Critical care ultrasound (CCUS) includes noncardiac ultrasound applications as well as focused
cardiac ultrasound.
Advanced critical care echocardiography (ACCE) includes advanced applications of

echocardiography.
Focused cardiac ultrasound as part of CCUS and ACCE may include transthoracic echocardiography
(TTE) and transesophageal echocardiography (TEE) applications, depending on clinical needs.
Ultrasound core applications are specified in Table 24-1. Although other applications may become
universally relevant as the field evolves, we included only widely accepted applications.
Table 24-1. Core Applications of Ultrasound in Critical Care Medicine
Categories Applications
CCUS
Diagnostic ultrasound Focused cardiac ultrasound
Pleural/pulmonary ultrasound
Focused abdominal ultrasound
Vascular ultrasound
Procedural ultrasound Vascular access guidance
Other procedures requiring needle guidance (eg, thoracentesis, paracentesis, etc)
ACCE Advanced applications of echocardiography
Abbreviations: CCUS, critical care ultrasound; ACCE, advanced critical care echocardiography.
COMMONLY USED TERMS

Before describing the requirements for credentialing, we would like to clarify definitions of commonly
used terms related to competence and credentialing as applied specifically to CCUS and ACCE.
Proficiency involves both technical skills of acquisition and real-time interpretation of ultrasound images,
with imaging information incorporated into clinical decision-making in caring for critically ill patients.
These skills are measurable objectives during the training process.
Competence9 involves a system-based approach to the practice of CCUS and ACCE in the critical care
environment. Competence in CCUS and ACCE encompasses proficiency, as well as the ability to manage
ultrasound equipment on a day-to-day basis, document ultrasound examinations, and archive images, as
well as participation in continuous quality improvement (CQI), education, and the peer-review process.
The most efficient way to achieve competence is through habitual participation in an established
ultrasound program.
Credentialing is a process by which the hospital establishes whether the provider has achieved the
competence to be appointed to the hospital medical staff. Through this process the hospital defines which
clinical services a given caregiver can provide, and establishes whether these services fall within the
privileges granted. Credentialing is regulated by rules and policies of the department within which the
provider plans to practice.
Privileges are permissions granted to individual critical care providers to perform certain clinical
services as defined by rules and policies set forth by the department where the provider intends to
practice. Privileging is the goal of the credentialing process.
Certification is a process by which an external agency recognizes competence. The external agency is
usually a specialty medical board. Certification commonly involves an examination of special
competence. For example, for echocardiography applications in the United States, the National Board of
Echocardiography is the certifying agency. Certification in special competence may be required by
hospitals as part of the credentialing process.
Accreditation is a voluntary peer-review process by which an external agency recognizes that the
ultrasound practice meets or exceeds nationally recognized standards in the performance and
interpretation of diagnostic ultrasound examinations. To be accredited, the practice must demonstrate
competence in all aspects of ultrasound operations. The American Institute of Ultrasound in Medicine is
the accreditation agency for many ultrasound practices in the United States, and the Intersocietal
Accreditation Commission is the accreditation agency for echocardiography practices in the United
States. Currently ultrasound practices in critical care medicine are not being accredited by the American
Institute of Ultrasound in Medicine or the Intersocietal Accreditation Commission.
CREDENTIALING PROCESS
The SCCM recommendations8 outline the principles behind credentialing in CCUS and ACCE for critical
care medicine providers. These principles are outlined below with modifications, and can be divided
based on the responsibilities of departments and individual providers. We also provided our comments
wherever needed to further clarify the subject. The departmental responsibilities are as follows:
1. Departments should follow the specialty-specific guidelines for the credentialing and privileging
process in ultrasound.
Comment: This recommendation is in accordance with AMA resolution 802,1 with guidance provided
by critical care medicine specialty–based documents.5-8
2. Departments should grant CCUS and ACCE privileges separately.

Comment: This recommendation is based on different approaches to credentialing for CCUS and
ACCE, whereby CCUS credentialing does not require certification, but for ACCE credentialing
purposes, certification is recommended.
3. Each department should choose which core critical care ultrasound applications are relevant to its
critical care environment.
Comment: These applications need to be incorporated into the departmental Delineation of Privileges
form. Although SCCM recommendations8 do not provide specific guidance in this respect, we think
that, for the sake of simplicity, each application should be checked separately. This will give providers
substantial flexibility to focus on applications relevant to their clinical area.
4. Each department should track critical care providers in the use of these applications by following a
CQI process.
The responsibilities of individual providers are as follows:
1. Providers applying for initial privileges in CCUS and/or ACCE should complete the necessary
training outlined in relevant documents.5-8
Comment: The necessary training is discussed later in this chapter, and includes education
requirements in critical care medicine, ultrasound, and performance of ultrasound examinations.
2. Privileges in ACCE should require testamur or certification status in adult echocardiography

(Examination of Special Competence in Adult Echocardiography [ASCeXAM]), basic or advanced
perioperative TEE (Examination of Special Competence in Perioperative Transesophageal
Echocardiography [PTEeXAM]), or ACCE-specific certification once one becomes available.
Comment: The National Board of Echocardiography administers the ASCeXAM and PTEeXAM.
3. Credentialed providers should demonstrate clinical competence during each reappointment and
actively participate in the CQI process as part of maintaining privileges in ultrasound.
CREDENTIALING PATHWAYS
Critical care providers have 2 pathways to achieve competence in CCUS and ACCE: the fellowship-
based pathway and the practice-based pathway.8 This differentiation recognizes that ultrasound is a
relatively new technology in the critical care environment, and providers currently in training and in
practice should have an opportunity to incorporate ultrasound into their practice. SCCM
recommendations8 define the precise requirements for credentialing in CCUS and ACCE. Credentialing in
CCUS and ACCE will require successful fulfillment of the following requirements:
License to practice medicine independently

Primary specialty board certification
Critical care medicine training
Ultrasound education, including didactics and exposure to clinical pathology
Minimum number of ultrasound examinations
Examination of special competence (applicable to ACCE only)
Fellowship-Based Pathway
The requirements for both CCUS and ACCE are provided in Table 24-2 and are based on SCCM
recommendations.8 The minimum number of ultrasound examinations in each major application is
provided in Table 24-3, which was adapted from SCCM recommendations.8 The major difference
between CCUS and ACCE is the level of knowledge and skills required to achieve competence in these
categories of ultrasound in critical care medicine.
Unlike credentialing in CCUS, credentialing in ACCE via the fellowship pathway requires primary
specialty board certification, in line with previously reported requirements for certification in adult
echocardiography10 or basic or advanced perioperative TEE.11,12
Postgraduate trainees should receive 40 hours of instruction for ACCE, compared with 20 hours for
CCUS.
Finally, credentialing in ACCE requires successfully passing the ASCeXAM or basic or advanced
PTEeXAM.
The existing documents all recognize that competence cannot be achieved by purely performing a
certain number of ultrasound examinations.5-8 While understanding these limitations, the experts in
ultrasound6,7 and the SCCM Ultrasound Certification Task Force8 attempted to provide guidance as to
the minimal number of examinations needed for a critical care provider to achieve competence in the
application of CCUS and ACCE, in line with previous literature in emergency medicine,13
anesthesiology,14 and cardiology.15
Table 24-2. Credentialing Requirements for Applicants Pursuing the Fellowship-based Pathway
Requirements CCUS ACCE
Current license to practice medicine Required
Primary specialty board certification Eligible or certified Certified

status
Critical care medicine training Postgraduate training in critical care medicine
Didactics in ultrasound Curriculum during fellowship training; ≥20 hours Curriculum during fellowship training; ≥40 hours
Spectrum of pathology Broad spectrum, including main diagnoses within each Full spectrum
application
Minimum numbers of ultrasound Specified in Table 24-3

examinations
Examination of special competence Not required Required, currently ASCeXAM, or basic or advanced PT EeXAM through
NBE
Abbreviations: CCUS, critical care ultrasound; ACCE, advanced critical care echocardiography; ASCeXAM, Examination of Special
Competence in Adult Echocardiography; PTEeXAM, Examination of Special Competence in Perioperative Transesophageal
Echocardiography; NBE, National Board of Echocardiography.
Pustavoitau A, Blaivas M, Brown S, et al. Recommendations for achieving and maintaining competence and credentialing in critical care
ultrasound with focused cardiac ultrasound and advanced critical care echocardiography. Published in Crit Care Med. 2014;42(5).
Table 24-3. Minimum Number of Ultrasound Examinations to Achieve Competence in Different Applications of Ultrasound in Critical Care
Medicine
Minimum Number of Ultrasound Examinations Minimum Number of Ultrasound
Categories Application Individually Performed Examinations Interpreted
CCUS
Diagnostic Focused cardiac ultrasound 30 50

ultrasound
Pleural/pulmonary ultrasound 20 30
Focused abdominal ultrasound 20 30
Vascular ultrasound 20 30
Procedural ultrasound Vascular access guidance 10 10
Other procedures requiring needle guidance (eg, 5 for each additional application 5 for each additional application
thoracentesis, paracentesis, etc)
ACCE Advanced* applications of echocardiography 200 400
T EE† 50 of 200 total required 100 of 400 total required
Abbreviations: CCUS, critical care ultrasound; ACCE, advanced critical care echocardiography; TEE, transesophageal echocardiography.
* Only numbers based on SCCM recommendations8 are provided here.
† Competence in TEE is optional, and involves only providers working in environments of high TEE use.
Practice-Based Pathway
The requirements for both CCUS and ACCE are provided in Table 24-4, and are based on SCCM
recommendations.8 The minimum number of ultrasound examinations in each major application are the
same as for the fellowship-based pathway (Table 24-3).
Table 24-4. Credentialing Requirements for Applicants Pursuing the Practice-based Pathway
Requirements CCUS ACCE
Current license to Required

practice medicine
Primary specialty Eligible or certified Certified

board certification
status
Critical care Fellowship in critical care medicine or 24 months of clinical experience in critical care medicine, with at least 25% of clinical time dedicated to care of
medicine training critically ill patients for the last 2 years of practice
Didactics in 20 hours of continuing medical education, AMA PRA category 1 credits or 40 hours of continuing medical education, AMA PRA category 1 credits or
ultrasound their equivalents; credits should be obtained while acquiring practical their equivalents; credits should be obtained while acquiring practical
experience in CCUS experience in ACCE
Spectrum of Broad spectrum, including main diagnoses within each application Full spectrum
pathology
Minimum numbers Specified in Table 24-3

of ultrasound
examinations
Examination of Not required Required, currently ASCeXAM, or basic or advanced PT EeXAM through
special competence NBE
Abbreviations: CCUS, critical care ultrasound; ACCE, advanced critical care echocardiography; ASCeXAM, Examination of Special
Competence in Adult Echocardiography; PTEeXAM, Examination of Special Competence in Perioperative Transesophageal
Echocardiography; NBE, National Board of Echocardiography.
The requirements largely mirror those for applicants pursuing the fellowship-based pathway, with the
exception that ultrasound education and training are obtained while the applicant remains at his/her
current practice. The main differences between the practice-based and fellowship-based pathways are as
follows:
Critical care medicine training can be achieved not only through postgraduate training, but also through
practice-based training (eg, hospitalists moving into critical care medicine). Thus, minimal clinical
practice requirements are incorporated into definitions of critical care training.
Ultrasound education is acquired through the infrastructure of continuing medical education.
CCUS and ACCE examinations are commonly expected to be performed within 2 years, but no longer
than 4 years since initiation of the process. These examinations are performed while the provider is
learning the didactic aspects of CCUS and/or ACCE.8
ADVANCED CRITICAL CARE ECHOCARDIOGRAPHY

The 3 documents that describe training requirements in ACCE provide different minimal ACCE
examination numbers.6-8 These numbers are summarized in Table 24-5.
The disagreements center on the number of examinations and on whether TEE training is a mandatory
component to achieve competence in ACCE. We believe that the numbers based on SCCM
recommendations and provided in Table 24-3 more closely reflect the requirements established by
anesthesiology14 and cardiology,15 the specialties with the longest track record in developing a
certification process for echocardiography applications. Advanced perioperative TEE14 and level 1
training in adult echocardiography15 require 150 individually performed examinations and 300 interpreted
examinations. Although the numbers provided by the experts6 and SCCM recommendations8 are higher,
they take into account the fact that providers can receive TEE training in addition to TTE training. Finally,
SCCM recommendations acknowledge that TEE utilization is unit-specific, and not all units purchase
TEE probes because of their high cost. However, ultrasound experts in those ICUs are still able to
achieve competence in ACCE. Ultimately, further consensus on the subject as well as future development
of ACCE certification will clarify the issue.
Table 24-5. Minimum Number of Examinations to Achieve Competence in ACCE
Expert Statement on T raining in
Minimum Number of ACCE Examinations Ultrasound in Critical Care6 Expert Statement on T raining in ACCE7 SCCM Recommendations8
All (T T E and T EE) individually performed 200 135 200
All (T T E and T EE) interpreted by the 200 135 400

trainee, including individually performed
T EE training Mandatory Mandatory Optional
T EE examinations individually performed 50 35 50
T EE examinations interpreted by the 50 35 100

trainee, including individually performed
Abbreviations: ACCE, advanced critical care echocardiography; SCCM, Society of Critical Care Medicine; TTE, transthoracic
echocardiography; TEE, transesophageal echocardiography.
ASSESSING QUALITY OF EDUCATION PROGRAMS IN CCUS AND ACCE

Part of evaluating the competence of the critical care provider during the credentialing process is to
understand how education and training of the applicant was structured. A proper education program
should have the following components:
1. Training objectives in both knowledge and skills in CCUS and ACCE. These are beyond the scope of
this chapter and are well-described in existing documents.5,8
2. Educational programs in CCUS and ACCE applications. The format of an educational program should
target the needs of learners, and can involve any combination of live and electronic-based activities in
the form of simulation, lectures, case studies, and hands-on workshops.6,8
3. Proctored ultrasound examinations under the mentorship of a CCUS- and/or ACCE-credentialed
provider. This is a very important component of ultrasound training, and depends on the quality of
mentorship, availability of qualified mentor(s), and involvement in the CQI process.
4. Assessment of knowledge and skills of the applicant. This may involve direct observation, testing of
skills, reviewing documentation, and image archives.
5. Training environment. This involves access to ultrasound machines capable of 2-dimensional imaging
and all Doppler applications at all times, as well as the ability to care for patients who present with a
broad variety of critical illnesses.
6. Participation in a CQI program.
Applicants should be able to provide information on all components of the program in which they trained,
so that they can be evaluated according to current rules and policies.
MAINTAINING CREDENTIALING
The only document that provides guidance on maintaining credentialing in both CCUS and ACCE is the
SCCM recommendations.8 A successful credentialing and recredentialing program is based on a
systematic approach to education, training, image archiving, documentation, and CQI. To maintain
competence, the program would require providers to:
Maintain licensure and certification in primary medical specialty.
Demonstrate continuing proficiency in applications of CCUS and ACCE.
Participate in ongoing education in CCUS and ACCE. The education consists of at least 10 hours of
continuing medical education in each CCUS and ACCE, which may include AMA PRA category 1
activities, online educational activities, simulation, teaching, preceptorship, research, image review,
textbook and journal reading, manuscript preparation, morbidity and mortality conferences specifically
discussing ultrasound-related cases, and other activities related to CCUS and ACCE.
Perform the minimum number of ultrasound examinations. These include 50 CCUS examinations and/or
50 ACCE examinations (with 20 of those being in TEE if privileges in TEE are desired).
Participate in CQI. The purpose is to maintain quality, facilitate education, and satisfy credentialing
requirements. Participation involves systematic collection and archiving of ultrasound images, timely
and comprehensive documentation of CCUS and ACCE examinations. Part of the CQI process is to
review images for technical competence, analyze interpretations for clinical accuracy, and provide
feedback to improve performance. In addition, CQI aims to evaluate technical aspects of image
acquisition, with the gold standard being direct supervision of the trainees’ performance.
ROLE OF SPECIALISTS IN ULTRASOUND EDUCATION

In places with no CCUS or ACCE specialists, arrangements can be made to train critical care providers
in ultrasound. In this situation, collaboration with other specialists with expertise in ultrasound
applications (eg, emergency medicine, cardiology, and radiology) is required. One collaborative
approach is by joining established programs in ultrasound and echocardiography, and holding
multidisciplinary review sessions where different types of images are discussed. Working together will
make us understand the limitations of focused bedside ultrasound.
CASE STUDIES
We present several case scenarios to help navigate credentialing requirements.
Case 1
A critical care–certified licensed physician, who finished a fellowship in critical care 5 years ago and
has no previous exposure to ultrasound, now would like to apply for privileges in CCUS.
In this situation, the credentialing process will find out that the provider still has to take several steps
toward obtaining privileges in CCUS.
License requirements have been fulfilled.
Board certification in critical care has been obtained.
Medical education in critical care medicine has been obtained through fellowship.
The provider will have to obtain 20 continuing medical education credits in CCUS. Various training
methods can be used to achieve this goal.
The provider will have to perform a minimum number of CCUS examinations in applications for
which he/she would like to apply for privileges (Table 24-3).
The provider should document all CCUS examinations in a logbook, save the images, and provide
interpretations.
The provider should perform the CCUS examinations within 2 years.
The provider should practice in a critical care environment that has a diverse patient population with a
full spectrum of pathology.
A supervisor will attest to the provider’s successful completion of the education program.
Case 2
A licensed board-eligible anesthesiologist, who just completed training in anesthesiology and did
rotations in the ICU with an ACCE program, would like to apply for privileges in ACCE, including TEE.
While some requirements are fulfilled, the anesthesiologist still has to complete additional training. We
propose a fellowship-based pathway as the only achievable pathway at this point.
License requirements have been fulfilled.
The anesthesiologist will have to complete fellowship in critical care medicine.
The anesthesiologist will have to obtain certification in anesthesiology.
The anesthesiologist will either need to train in ACCE during his/her critical care fellowship, or enter
a practice-based pathway once he/she finishes the fellowship.
The anesthesiologist will be required to obtain 40 hours of education in ACCE.
The anesthesiologist will have to perform 150 TTE examinations and 50 TEE examinations
independently while under supervision, and interpret a total of 300 TTE and 100 TEE examinations.
The anesthesiologist should perform the ACCE examinations within 2 years, with maximum 4 years
(minimum 50 examinations per year individually performed).
The anesthesiologist should document all CCUS examinations in a logbook, save the images, and
provide interpretations.
The anesthesiologist should practice in a critical care environment that has a diverse patient
population with a full spectrum of pathology.
A supervisor will attest to the anesthesiologist’s successful completion of the education program.
Certification in adult echocardiography or basic perioperative TEE has to be considered as the most
feasible option.
KEY POINTS
Ultrasound in critical care medicine is appropriately guided by specialty-based documents on
various aspects of ultrasound.
Credentialing in CCUS and ACCE necessitates fulfilling requirements in licensure, specialty board
certification, ultrasound education and performance of ultrasound examinations, and passing
examination of special competence (ACCE only).
The credentialing process differs for CCUS and ACCE. Applicants requesting privileges in ACCE
should hold testamur or certification status in adult echocardiography or advanced or basic
perioperative TEE until a specific ACCE board certification process exists.
The 2 pathways to achieve competence in CCUS and ACCE are fellowship-based and practice-
based pathways, depending on when training in ultrasound occurs in relationship to postgraduate
training.
Maintaining privileges in CCUS and ACCE involves ongoing education, performing ultrasound
examinations, and participation in a robust CQI process.
REFERENCES
1. American Medical Association. H-230.960: Privileging for ultrasound imaging. Res. 802, I-99; Reaffirmed: Sub. Res. 108, A-00;
Reaffirmed: CMS Rep. 6, A-10. Available at: https://www.ama-assn.org/ssl3/ecomm/PolicyFinderForm. pl?site=www.ama-
assn.org&uri=/resources/html/Policy- Finder/policyfiles/HnE/H-230.960.HTM. Accessed March 4, 2015.
2. Critical care medicine: Focused applications of ultrasound in critical care medicine. Crit Care Med. 2007;35(suppl 5).
3. Critical care medicine: echocardiography in intensive care medicine. Crit Care Med. 2007;35(suppl 8).
4. Price S, Via G, Sloth E, et al. Echocardiography practice, training and accreditation in the intensive care: document for the World
Interactive Network focused on critical ultrasound (WINFOCUS). Cardiovasc Ultrasound. 2008;6:49.
5. Mayo PH, Beaulieu Y, Doelken P, et al. American College of Chest Physicians/La Societe de Reanimation de Langue Francaise statement
on competence in critical care ultrasonography. Chest. 2009;135:1050-1060.
6. Expert Round Table on Ultrasound in ICU. International expert statement on training standards for critical care ultrasonography. Intensive
Care Med. 2011;37:1077-1083.
7. Expert Round Table on Echocardiography in ICU. International consensus statement on training standards for advanced critical care
echocardiography. Intensive Care Med. 2014;20:654-666.
8. Pustavoitau A, Blaivas M, Brown SM, et al. Recommendations for achieving and maintaining competence and credentialing in critical care
ultrasound with focused cardiac ultrasound and advanced critical care echocardiography. Available at
http://journals.lww.com/ccmjournal/Documents/Critical%20Care%20Ultrasound.pdf Accessed February 15, 2015. Published in Crit Care
Med. 2014;42(5).
9. Epstein RM, Hundert EM. Defining and assessing professional competence. JAMA. 2002;287:226-235.
10. National Board of Echocardiography. Adult echocardiography (ASCeXAM): certification requirements and application. Available at
http://echoboards.org/sites/default/files/ASCE%20Cert%20App%20%282%29%20Revised.pdf. Accessed March 7, 2015.
11. National Board of Echocardiography. Basic perioperative transesophageal echocardiography (basic PTEeXAM): certification requirements
and application. Available at http:// echoboards.org/sites/default/files/BasicPTE%20Cert%20 App%20Revised%2093014.pdf. Accessed
March 7, 2015.
12. National Board of Echocardiography. Advanced perioperative transesophageal echocardiography (advanced PTEeXAM): certification
requirements and application. Available at http://echoboards.org/sites/default/files/ AdvPTE%20Cert%20App.pdf. Accessed March 7,
2015.
13. American College of Emergency Physicians. Emergency ultrasound guidelines. Ann Emerg Med. 2009;53:550-570.
14. Cahalan MK, Stewart W, Pearlman A, et al. American Society of Echocardiography and Society of Cardiovascular Anesthesiologists Task
Force Guidelines for training in perioperative echocardiography. J Am Soc Echocardiogr. 2002;15:647-652.
15. Ryan T, Armstrong WF, Khandheria BK, American Society of Echocardiography. Task force 4: training in echocardiography endorsed by
the American Society of Echocardiography. J Am Coll Cardiol. 2008;51:361-367.
Chapter 25
Basic Evaluation of the
Pediatric Patient
Chapter 26
Pediatric Ultrasound Procedures:
Central Venous Access
and Arterial Access
Chapter 25
Basic Evaluation of the Pediatric Patient
Thomas Conlon, MD; Erik Su, MD;
Akira Nishisaki, MD, MSCE
OBJECTIVES
Discuss facets of pediatric physiology and anatomy important in implementing bedside ultrasound for the care
of critically ill children
Discuss performance of procedural applications specific to pediatric critical care with the assistance of
ultrasound
Discuss modalities in critical care diagnostic ultrasound applied to the critically ill pediatric patient
Discuss training and implementation of pediatric critical care ultrasound at the bedside and institutional level
INTRODUCTION
Pediatric acute care specialties are increasingly using ultrasound in clinical practice to augment
procedural safety, diagnostic accuracy, and therapeutic guidance. Pediatric patients have unique
characteristics that may both facilitate and hinder ultrasound examination compared with adults.
However, multiple ultrasound applications used in adult critical care medicine are useful in the care of
pediatric patients, especially when pediatric imaging characteristics are considered. Providers should
recognize differences in anatomy, pathology, and physiology in children necessary for acquiring
ultrasound images, interpreting results, and applying those findings to managing critically ill children. As
critical care ultrasound in the pediatric ICU (PICU) evolves, providers must define scope of practice and
competence, generate pediatric-specific training, and implement institutional programs that incorporate
provider credentialing.
In 2011, more than 70% of surveyed pediatric critical care providers were using bedside ultrasound for
central venous catheter (CVC) placement.1 Ultrasound technology is present in most PICUs across the
United States. Familiarity with using ultrasound during CVC placement has expanded the use of
ultrasound in other procedural techniques. Diagnostic critical care ultrasound applications are an
emerging area of interest among pediatric critical care providers. This chapter will identify unique
aspects of pediatric bedside ultrasound as well as caveats in translating applications previously
implemented in adult ICUs. Though the literature on bedside ultrasound in the pediatric acute care setting
is still limited, there are a number of important studies this chapter will discuss.
CASE STUDY
A 7-month-old unvaccinated infant presented to the emergency department with respiratory distress after
completing a course of antibiotics as an outpatient. He was initially admitted to an inpatient pediatrics
unit for pneumonia and started on broad-spectrum antibiotics. Shortly after admission, he was transferred
to the PICU because of increased work of breathing. In the PICU, the patient was intubated for respiratory
failure, and his shock progressively worsened as characterized by delayed capillary refill, decreased
urine output, and elevated heart rate.
An ultrasound examination was performed by a pediatric critical care provider. This revealed that the
patient had a distended inferior vena cava (IVC) (Figure 25-1) without respiratory variation as well as a
dilated and poorly contractile right ventricle (RV) with preserved left ventricular (LV) function (Figures
25-2 and 25-3). Continuous-wave Doppler measurement across the coaptation of the tricuspid valve
leaflets revealed a significant tricuspid regurgitant jet, confirming elevated RV systolic pressure (Figure
25-4).
Figure 25-1. Transverse View of the Abdominal IVC and Aorta

Abbreviations: IVC, inferior vena cava; AO, aorta.
Note the IVC is round and approximately 2:1 in anterior-posterior diameter ratio.
Figure 25-2. Parasternal Long-Axis Views of RV Dilation
Abbreviations: RV, right ventricle; LV, left ventricle; AO, aorta; LA, left atrium.
Parasternal long-axis view of patient with pertussis demonstrating RV dilation.
Figure 25-3. Parasternal Short-Axis View of RV Dilation

Abbreviations: RV, right ventricle; PA, pulmonary artery; RA, right atrium; AO, aorta.
Parasternal short-axis view of patient with pertussis demonstrating RV dilation.
Figure 25-4. Continuous-Wave Doppler Across Tricuspid Valve

Continuous-wave Doppler across the tricuspid valve measuring regurgitant jet velocity to estimate right ventricular systolic pressure.
How Did the Use of Point-of-Care Ultrasound Influence the Treatment of This Patient?
Shock physiology is the common pathway of many pediatric disease states, and the specific hemodynamic
disturbance must be identified for both supportive and definitive care. Bedside ultrasound performance
identified elevated RV pressure consistent with a diagnosis of critical pertussis and secondary pulmonary
hypertension. The ultrasound findings facilitated an immediate transition to inhaled nitric oxide and
placement of a catheter for leukopheresis. After a 24-day course of venovenous extracorporeal membrane
oxygenation and 3-month hospital stay, the patient was discharged home. Early bedside ultrasound
performance in critically ill children can rapidly identify clinically important, and sometimes previously
unknown, pathophysiology, thus facilitating targeted therapies.
PEDIATRIC ANATOMY: IMPACT ON CRITICAL CARE ULTRASOUND APPLICATIONS

Children are not just small adults, and this notion applies in pediatric critical care ultrasound. Transducer
frequency, footprint, and crystal orientation all play important roles in optimal imaging of pediatric
patients. Imaging with higher-frequency transducers facilitates high-resolution images of developmentally
smaller structures. Sacrificing depth of penetration for improved resolution is less concerning given the
smaller patient size and proximity of organs to the skin surface. Transducer selection is also affected by
patient size; large curvilinear probes are seldom useful in pediatrics because of the size of the probe
relative to available windows on the patient. A microconvex curvilinear or phased-array probe is useful
for a multitude of applications, including cardiac assessment and abdominal evaluation, as well as the
capability to fit into intercostal spaces for visualizing the thorax (Figure 25-5). Conversely, a small
pediatric phased-array probe that can accommodate infant cardiac views may not penetrate the abdomen
of an obese adolescent because of its higher frequency range. Similarly, a small linear array transducer
useful for vascular access in an infant may not penetrate deep enough for visualization of femoral vessels
in an older child with contractures. Consequently, an array of transducers is often helpful in imaging
patients of different sizes.
Figure 25-5. Transthoracic Coronal Chest View of Adolescent with Pneumonia

Pleural effusion is marked with #. Lung consolidation is marked with *. Probe is positioned at the left lower intercostal space.
Factors that improve image quality in young children include:
Less penetration needed to visualize structures
Higher body water content
Incomplete ossification
Factors that limit image quality in young children include:

Small size of target structures
Patient intolerance of procedure due to agitation or environmental factors
Probe-to-patient size discordance
Faster heart rates
Pediatric physical development is also relevant in ultrasound performance and interpretation. Bone
ossification is an ongoing process from birth through early adulthood. In the very young, incomplete
ossification of ribs allows for ultrasound wave transduction and visualization of underlying structures.
With less rib shadowing, ultrasonographers may image the pleural line in continuity as well as lung and
pleural pathology (Figure 25-6). Ultrasound of the spine in infants often reveals the dural space, spinal
cord, and cauda equina (Figure 25-7). Open fontanelles in the cranial vault permit assessment of
intracranial pathology until their closure in late infancy.
Figure 25-6. Linear Probe Evaluation of Infant Thorax

Note the visualization of the pleural line below incompletely ossified ribs.
Figure 25-7. Conus Medularis and Cauda Equina in Infant
Visualization of the conus medularis and cauda equina in preparation for lumbar puncture in an infant.
Anatomic and physiologic differences between pediatric and adult patients can also limit measurement
accuracy, precision, and validity. Imaging the left ventricular outflow tract (LVOT) in the apical 5-
chamber view is difficult in an infant both because of size and shape of the chest and rapid translation of
myocardium at higher resting heart rates than in adults. This often precludes precise placement of a
pulsed-wave Doppler cursor for aortic velocity measurements, thereby limiting acquisition of reliable
information. Foreshortening the pediatric IVC by missing the central axis of the vessel in a longitudinal
view can dramatically alter its absolute measured diameter (cross-sectional, or transverse, images are
also recommended [Figure 25-1]) and percentage collapsibility through the respiratory cycle.
Time-dependent measurements require adequate frame rate, an important consideration in pediatric

cardiac assessment because baseline heart rates are higher in children than in adults. Faster frame rates in
children permit improved temporal resolution, which is the ability of the machine to correctly represent
small movements over time. Frame rate is improved by narrowing the image sector in height and width, if
possible, or turning on multifocus, if it is available. Turning on color or power Doppler also consumes
machine processing power, and limiting the Doppler scan area to a small window also increases frame
rate. In time-dependent modalities such as M-mode and pulsed-wave Doppler, if a patient has tachycardia
and too many cardiac contractions are occurring in 1 screen, increasing sweep speed may improve
visualization of features.
Environmental effects are important considerations in imaging infants or other temperature-sensitive

patients. Exposure of skin and application of gel increase radiative, conductive, and evaporative heat
losses, which can lower the temperature of small children over the course of a single examination.2
Sonographers should pay careful attention to avoid displacement and kinking of tubes, drains, and
monitoring equipment during scanning. Activating audible pulse oximetry tones for patient monitoring to
prevent unrecognized desaturations is advisable for noncommunicative patients, especially if the
sonographer is alone with the patient during the study.
E X P E RT T I P
Determine the depth of structure of interest, examine the surface window available, and choose
the appropriate transducer based on transducer footprint, ability to fit between anatomic bony
structures, and frequency.
Critical illness presents challenges for ultrasound performance, whether in an adult or child, at the
extremes of physiology. Positive pressure ventilation can limit cardiac windows by increasing
ultrasound-obstructing lung expansion in between the heart and chest wall. Ileus with gas-filled bowel
loops, body wall edema, and monitoring equipment or dressings can also restrict available windows for
insonation. Awake and interactive critically ill children can also be difficult patients for scanning. A
calm, quiet environment with distractions such as parents, toys, or child life specialists can help facilitate
an examination. Frequently children will enjoy looking at the images on the screen and hearing basic
descriptions of what you are looking at. Older, cooperative adolescents may find imaging themselves with
the probe enthralling. When possible, a sonographer should describe what she or he is doing and ask for
permission before starting an examination to foster the trust of patients and their parents.
ULTRASOUND USE IN PEDIATRIC PROCEDURAL APPLICATIONS
Vascular Access
There is a paucity of prospective data evaluating CVC insertion in children, though meta-analyses and
individual studies support ultrasound use for increasing first-pass success and improving safety.3,4 In
pediatrics, vascular access sites can be restricted by patient size and require smaller probes. In certain
sites, such as the internal jugular vein in small children, access is more difficult using the long-axis
approach. A guideline statement based on author consensus recommends that the diameter of a CVC not
exceed one-third the diameter of the target vessel.5 Anatomic considerations, including identification of
the carotid bifurcation in the neck, are important before insertion of a needle, given the risk of arterial
puncture without recognition of a second arterial vessel in an ultrasound image (Figure 25-8).
Investigators have reported alternative approaches for CVC placement facilitated by ultrasound guidance,
and highlighted its use for identifying anatomic variations.6,7 Increased skill with ultrasound can maximize
procedural safety and success by facilitating safe site selection.
Figure 25-8. Carotid Bifurcation
Note the position of the internal jugular vein in relation to the internal carotid.
Central venous access is only one aspect of pediatric vascular access. Ultrasound-guided peripheral
venous access is becoming increasingly common for intravenous catheter insertion in difficult-to-access
pediatric patients. The technique is now embedded in difficult-access algorithms at various pediatric
institutions.8 In children, the procedure for ultrasound-guided peripheral access is approached from either
the long or short axis, similar to adult patients.
Ultrasound-guided peripheral arterial access in adults increases first-pass success rates.9 Similar findings
are described in the pediatric anesthesiology literature, with trainees demonstrating a first-pass success
rate of 14% using a palpation technique without ultrasound.10 A recent study demonstrated that ultrasound-
guided arterial catheterization in children undergoing cardiac surgery doubles the first-pass success rate;
after 3 attempts, this cumulatively increases to a 95% success rate compared with 51% using palpation.11
Umbilical Catheter Placement

Ultrasound-assisted placement of umbilical catheters has also been described in neonatal patients. In a
prospective randomized trial of 31 newborns admitted to a neonatal ICU, ultrasound reduced the time to
confirmation of line placement by an average of 64 minutes by reducing manipulations while also limiting
exposure to radiography.12 In this manner, ultrasound likely improves procedural safety in neonates.
Reduction of potential critical care morbidity is particularly important in this patient population given
their long projected average lifespan after discharge.
Ultrasound facilitates umbilical venous catheter insertion and reduces the use of abdominal radiography
for confirming catheter position. When the catheter is at or near the estimated depth of correct insertion,
obtain a longitudinal view of the IVC using a phased-array or microconvex sector probe. With the view
aligned along the long axis of the IVC, the walls of the umbilical venous catheter should appear echogenic
as it approaches the diaphragm and resides in the IVC ( Figure 25-9). Utilizing this view, the umbilical
venous catheter can be adjusted under ultrasound guidance if it is in the IVC but not yet at the level of the
diaphragm. If the tip is not in the IVC, it can also be visualized in the liver.13 The tip position of an
umbilical artery catheter is also visualized using this same technique.14
Figure 25-9. Umbilical Arterial Catheter in Descending Aorta

The umbilical arterial catheter in the descending aorta is marked with *. (Note the radiology convention – the indicator is on the left side of the
screen.)
Effusion Drainage
As with vascular access, complications during needle insertion for the drainage of effusions are largely
composed of inadvertent puncture of neighboring structures. Ultrasound improves the recognition of fluid
quality and quantity in abnormal collections compared with radiographs both in the thorax and
abdomen.15,16 In performing thoracentesis or thoracostomy, identification of the proximity of the insertion
site to the diaphragm in a patient’s midaxillary line improves procedural safety in adults, though studies
have not been performed in children.17 Notably, one study found that 10% of sites selected using
landmarks for thoracentesis by both inexperienced and experienced physicians lay over a solid organ.18
Paracentesis is another common procedure in the pediatric critical care setting. Though complication
rates with this procedure are low, blind insertion of a needle into patients with coagulopathy can have
catastrophic consequences if an epigastric artery is injured. In preparation for the procedure, localization
of the largest pockets of fluid can assist in sampling and drainage. Further, ultrasound identification of the
epigastric artery is possible in even small pediatric patients ( Figure 25-10) and helps avoid arterial
injury. Real-time procedural guidance for thoracentesis and paracentesis allows the needle to be
visualized during the entire procedure. Again, although the literature suggests improved success with
adjunct use of ultrasound in adult populations, there are no pediatric studies.19
Figure 25-10. Transverse View of Epigastric Vessels in Infant with Ascites

The epigastric artery (red) and vein (blue) can be found using a linear probe before insertion of the needle for paracentesis, thereby optimizing
procedure success and minimizing complications.
Lumbar Puncture
As discussed before in the section on pediatric anatomy, the pediatric spinal cord and dural space are
readily visualized in infants (Figures 25-11 and 25-12) and the success rate with first-pass lumbar
puncture in children has been described at 67%.20 Providers report increased procedure confidence after
identifying an appropriate insertion point for lumbar puncture in children using ultrasound.21 In adults,
data suggest ultrasound guidance in lumbar puncture reduces failed or traumatic needle insertions and
decreases the number of attempts and redirections. However, these studies have not been performed in
pediatric populations.22
To perform static ultrasound-assisted lumbar puncture:
1. Position the patient as for a landmark-based lumbar puncture.

2. Identify the estimated landmark for procedure.
3. Align a linear array transducer transversely across the spine with the indicator toward the patient’s
head. Identify the top of the spinous process on the ultrasound image (Figure 25-11) and center it under
the middle of the linear array. Mark the patient at the midline on both sides of the probe.
4. Rotate the probe 90 degrees counterclockwise so the probe is aligned parallel to the orientation of the
spine. Identify the lateral profile of the spinous processes and center the middle of the probe over an
interspinous space between processes. Mark the patient at the midline of both sides of the probe and
continue these lines for several inches lateral to the spine (perpendicular to previously drawn lines)
(Figure 25-12).
5. The angle of entry can be estimated in the orientation parallel to the spine by looking at the angle of the
gap between the spinous processes. The estimated depth of insertion can be measured with machine
calipers in patients where the dural space is visible. It will look like a dark anechoic space
surrounding horizontally bright cauda equina fibers. The conus medullaris should not be visible
underlying the targeted interspinous space.
C AVE AT
When performing an ultrasound-guided lumbar puncture, the dural space will appear as a dark
anechoic space surrounding horizontal bright fibers. Once the area is marked, remember not to
reposition the child to avoid disrupting the underlying anatomy.
Figure 25-11. Longitudinal View of Spinous Process

A) Probe placed in longitudinal plane over spinous process. B) Spinous process in longitudinal view marked with *.
Figure 25-12. Transverse View of Spinous Process

A) Probe placed in transverse plane over spinous process. B) Spinous process in transverse view marked with *.
Intubation and Endotracheal Tube Position

Although the position of the endotracheal tube (ETT) is commonly confirmed with exhaled end-tidal
carbon dioxide (ETCO2) capnography, in situations involving poor pulmonary blood flow (ie, cardiac
arrest), providers may encounter low detected ETCO2 despite endotracheal intubation. In these scenarios,
other methods of confirming ETT placement, such as urgent chest radiography, may be impractical in the
critical period immediately after ETT placement.
A prospective randomized trial of 50 pediatric patients in a PICU and emergency department (ages 0-17
years) using ultrasound to confirm tracheal vs. esophageal intubation reported that ultrasound identified
the ETT location in all patients. Ultrasound notably detected 2 cases of proper ETT placement despite
absent ETCO2 using qualitative capnography, as well as one case of esophageal intubation despite
detection of ETCO2 using qualitative capnography. 23 Several previously published studies used tracheal
ultrasound with a transverse approach, resulting in high sensitivity and specificity in detecting esophageal
intubation. 24 Detection of bilateral diaphragm movement also facilitates rapid detection of mainstem
intubation (Figure 25-13).25 Despite the varied methods available, all ultrasound approaches perform
excellently in assessing the success of tracheal intubation, and the accuracy of the method is not
significantly limited by the setting or experience of providers.26
E X P E RT T I P
To assess the diaphragm after endotracheal intubation, tilt a phased-array transducer in the
subcostal window so that it is aimed roughly 30 degrees cephalad.
The right and left leaflets of the diaphragm are visible lateral to the spine. Manual ventilations should be
cued and the bilateral motion of the diaphragm noted as both leaflets move down simultaneously. If one
moves and the other does not, there is likely an obstruction of the mainstem bronchus on the side of the
static diaphragm.
Figure 25-13. Bilateral Diaphragms from Subcostal View

Bilateral diaphragms visualized from the subcostal view using a phased-array probe on a child. (Note the radiology convention – the indicator is
on the left side of the screen.)
PEDIATRIC DIAGNOSTIC ULTRASOUND APPLICATIONS

Cardiac/Hemodynamic Ultrasound
Pediatric critical care physicians are limited in their abilities to accurately assess hemodynamic condition
based on physical examination and laboratory data alone at the extremes of critical illness.27 Ultrasound
provides the means for a rapid, accurate, and noninvasive assessment of hemodynamic variables in
critically ill children.
Figure 25-14. Pediatric Cardiology Versus Critical Care Ultrasound Orientation

A) Pediatric cardiology orientation of the apical 4-chamber view compared with (B) critical care ultrasound orientation in a patient with normal
anatomy and function. Note that the indicator is on the right, and the left-sided structures remain on the right side of the screen in both views
despite inversion of the image.
The cardiac views for critical care evaluation of the pediatric patient are the same as those for an adult
patient (as discussed in Chapter 3): (1) subcostal long-axis view, (2) parasternal long-axis view, (3)
parasternal short-axis view, (4) apical 4-chamber view. A smaller, higher-frequency phased-array probe
may help optimize image quality in children. Note that cardiac conventions in this text differ from those
used by other pediatric imaging specialties. Pediatric cardiology echocardiographers view apical and
subcostal images with the probe and LV apex at the bottom of the screen. This is in contrast to adult
cardiology or critical care practitioners (Figure 25-14). Individual imaging protocols differ between
institutions as well and contribute to variability in comparing imaging between providers and centers.
Pediatric cardiac convention views the apical and subcostal windows with the face of the probe (tip of
the triangle) at the bottom of the screen. The transducer indicator remains on the right side of the screen in
both pediatric cardiology and critical care imaging convention.
E X P E RT T I P
Pediatric cardiac convention views the apical and subcostal windows with the face of the
probe (tip of the triangle) at the bottom of the screen. The transducer indicator remains on the
right side of the screen in both pediatric cardiology and critical care imaging conventions.
E X P E RT T I P S
Factors that improve image quality in young children include:
Subcostal: Both longitudinal and transverse views of the IVC and aorta are recommended as the
aorta and spine are easily visualized.
Apical 4-chamber: Palpation for the apex of the heart is recommended because the heart is often
displaced due to changing lung compliance.
Parasternal short-axis: Moving up a rib space between second and third rib can allow for
visualization of the pulmonary valve and the pulmonary trunk with bifurcation. In smaller children,
the thymus is often seen in front of this cardiac/vessel structure.
Patient diagnoses as well as management decisions may dramatically change when echocardiographic
data are considered in both adult and pediatric populations.28-30 Furthermore, pediatric acute care
providers with minimal training can acquire adequate images with correct interpretations, especially
when assessing specific clinical questions.31-33 Focusing clinical questions and translating them to
specific diagnostic tests is a fundamental skill of the intensivist. In assessing the hemodynamically
unstable child, the following questions may be considered by pediatric intensivists as encompassing the
majority of hemodynamic disturbances experienced in the PICU:
Is the patient hypovolemic and potentially volume responsive?

What is the function of the LV and RV, respectively?
Is the RV larger than the LV?
Is there a hemodynamically significant pericardial effusion present?
Volume Assessment
Measuring the IVC in children was first reported in the evaluation of fluid status in dialysis patients.34
Absolute IVC size measurements for assessing volume status in pediatrics are not practical given changes
in IVC diameter with age. The IVC-to-aorta ratio (IVC-Ao) as a parameter for IVC assessment recognizes
differences in pediatric size, with the aorta being an age-independent reference value for the IVC (Figure
25-15). To obtain the IVC and aorta transverse view, place a phased-array or curvilinear transducer in the
subcostal region with the indicator pointing at the 3 o’clock position using the Society of Critical Care
Medicine cardiology convention and the transducer face perpendicular to the skin, pointed toward the
spine. Kosiak et al35 found that patients presenting to the emergency department with illnesses
characterized by hypervolemia had a high IVC-Ao ratio, whereas patients with illnesses characterized by
hypovolemia had a low IVC-Ao ratio. After hospitalization and treatment with presumed restoration of
euvolemia, all children had an IVC-Ao ratio of approximately 1.0 to 1.2:1. Use of the IVC-Ao ratio is
useful in evaluating the degree of dehydration in spontaneously breathing patients. Chen and colleagues36
found that an IVC-Ao cutoff of 0.8:1 in pediatric emergency department gastroenteritis patients
demonstrated a sensitivity of 86% and specificity of 56% for identifying severe dehydration. Levine et
al37 found that an IVC-Ao cutoff of 0.8:1 was 93% sensitive and 59% specific for severe dehydration in
rural Rwandan children. Though the IVC-Ao ratio may be useful in spontaneously breathing patients, it is
likely that positive pressure ventilation and elevated right atrial pressures from pulmonary, cardiac, or
pericardial disease may increase IVC anteroposterior diameter irrespective of intravascular volume
status. Conversely, abdominal compartment syndrome may decrease IVC anteroposterior diameter.38
Despite the limitations to conclusions derived from IVC measurements, it is a simple measurement to
perform. When placed in the context of the complete hemodynamic ultrasound examination, and alongside
other clinical information, IVC measurements can be useful for real-time management.
Figure 25-15. Inferior Vena Cava and Aorta Above Vertebral Body, Transverse Abdominal View
Abbreviations: IVC, inferior vena cava; Ao, aorta.
IVC and Ao above the vertebral body on transverse abdominal view in the subcostal position.
E X P E RT T I P
Technique for measuring the IVC:aorta ratio: The IVC is a circular structure in cross section
anterior to the spine, located in the liver and to the right of midline. The Ao is outside the liver
anterior to the spine and to the left of midline. In a spontaneously breathing patient, the IVC
should be measured at end expiration and the Ao should be measured at end systole. In the intubated
patient, the IVC should be measured at end inspiration.
In pediatrics, as in adults, static markers of intravascular volume (such as central venous pressure or IVC-
Ao ratio) are not strongly associated with fluid responsiveness.39 Fluid responsiveness, that is, a
measurable increase in cardiac output after receiving an intravenous fluid bolus, is a metric of
intravascular status. Dynamic markers of volume status are changes in physiologic variables over time,
usually derived over several cardiac and respiratory cycles. Aortic peak velocity variation during
inspiratory and expiratory phases of respiration measured via Doppler interrogation of the LVOT is an
example. It appears to be superior to static markers in predicting fluid responsiveness in pediatric
patients.40
C AVE AT
In pediatric patients, as in adults, static parameters like central venous pressure are not
predictive of volume responsiveness.
Qualitative Ventricular Assessment

Qualitative biventricular function can be assessed from basic parasternal, apical, and subcostal cardiac
views. The American Society of Echocardiography supports the use of quantitative measures of LV and
RV function but also cautions that comparisons to normal values are complicated by the effects of
development and conditioning.41 LV and RV function changes are not subtle at the extremes of physiology
in the critical care setting. Intensivists and emergency medicine providers can detect LV functional
changes with more than 93% concordance with expert echocardiographers with short amounts of
training.32,34,42 Quantitative measures of cardiac function like cardiac output have been used by clinician
sonographers in adult critical care, and their role in pediatric critical care ultrasonography remains
undetermined.
Table 25-1. Causes of Right Ventricular Failure with Dilation in Pediatric Patients
Increased Afterload
Left ventricular dysfunction
Pulmonary arterial hypertension
Acute respiratory distress syndrome/hypoxic pulmonary vasoconstriction
Acute chest syndrome in sickle cell disease
Hyperleukocytosis
Leukemia
Critical pertussis
Mechanical ventilation
Pulmonary embolism
Pulmonary stenosis
Right ventricular outflow tract obstruction
Structural Heart Disease Leading to Volume Overload
Ebstein anomaly
Tetralogy of Fallot with pulmonary regurgitation
Atrial septal defect
Anomalous pulmonary venous return
T ricuspid regurgitation
Cardiomyopathy
Dilated/genetic
Infectious/inflammatory
Ischemic
Metabolic
Arrhythmogenic
Endocrine
Toxin
Figure 25-16. Apical 4-Chamber View of Patient with Dilated Right Ventricle
Abbreviations: RV, right ventricle; LV, left ventricle; RA, right atrium; LA, left atrium.
Apical 4-chamber view of a patient with a dilated RV. Care must be taken to ensure correct transducer orientation, with the indicator on the
right side of the screen and pointed toward the left side of the patient.
RV Morphologic Assessment
Multiple conditions predispose a critically ill pediatric patient to having a dilated RV (Table 25-1). The
RV:LV end-systolic diameter ratio is typically 0.6. At any age, a ratio of 1 or more is indicative of
moderate to severe dilation. As with all findings on cardiac ultrasound, placement of the plane of the
ultrasound beam off-axis can foreshorten cardiac views such that the RV appears larger than the LV.
Therefore, confirming findings with different views is essential. In the apical 4-chamber view, providers
must understand probe and image orientation on the screen such that the RV and LV are in standard
positions (Figure 25-16). Identification of RV dilation may not only suggest RV dysfunction requiring
pulmonary vasodilators, but could also cue practitioners to take additional precautions when intubating or
titrating positive pressure ventilation.
Presence of Pericardial Fluid

Pericardial effusion can be seen in a number of views but is most commonly visualized in the subcostal
view because effusions layer inferiorly to the heart. As in adults, it is normal for children to have a trace
amount of fluid in the pericardium. Of note for sonographers, subcostal and apical views are typically
less tolerated in children and may provoke some agitation.2 Echocardiographic findings of tamponade
physiology are similar in children and adults.43 Tamponade physiology in children may develop because
of acute or chronic accumulation of fluid in the pericardium, and symptom onset is dependent on
pericardial compliance as pressure around the heart increases. Although tamponade remains largely a
clinical diagnosis, echocardiographic findings like systolic collapse of the right atrium can be informative
particularly for children who may not necessarily manifest clinical signs of hemodynamic instability as
early as adults. Consequently, tamponade physiology in children is not solely an echocardiographic
diagnosis; cardiac ultrasound can identify effusion size, measure tricuspid valve inflow velocity
variation, and delineate cardiac morphology.
C AVE AT
Measurement of cardiac output in critically ill pediatric patients is more challenging because of
the changing diameter of the LVOT with age and rapid heart rates. Therefore, the role of
hemodynamic measurements in pediatric critical care is unclear.
Lung/Pleural Ultrasound
Pulmonary ultrasound artifacts identified in adults are also seen in children and are associated with
similar diagnoses (ie, B-lines: pulmonary edema; hepatization: consolidation; lung point: pneumothorax;
etc).44 The pediatric intrathoracic space can be easily visualized in infants. However, as pediatric ribs
ossify, narrow rib spaces may restrict views of the pleural line. A sonographer can remedy this by
rotating the transducer in plane with the intercostal space, and pleural motion oblique to the plane of the
transducer view can still be seen (Figure 25-17). Pneumonia in pediatric populations has been
characterized by ultrasound and found to have high specificity compared with chest radiography.45 In a
cohort of pediatric emergency department patients, ultrasound findings in bronchiolitis have been
described as an increase in B-line patterns in the affected lung.46
Figure 25-17. Pleural Line with Linear Array

A) Sagittal orientation. B) Intercostal orientation.
In diagnostic radiology, ultrasound is the primary imaging modality for evaluating pediatric pleural
effusions, and can identify the quantity and quality of pleural effusions.47 Direct transthoracic views for
assessing pleural effusion in adults with linear and phased-array probes can be performed in children, as
well as a transverse view of the diaphragmatic gutters performed from the subcostal position. Loculations
and organized empyema will appear as echogenic, space-filling septations, and debris in the pleural
space (Figure 25-18). Hemothorax in evolution may reveal both anechoic flowing blood and echogenic
“smoke” or debris (Figure 25-19). In the subcostal view, the pleural spaces at the base of the lungs are
visualized through the liver using a phased-array or curvilinear transducer (Figure 25-20). This places the
area of interest (the pleural space) in the far field of the imaging sector and permits a wider view of
effusion geometry, facilitates identification of loculation, and helps identify anterior or posterior
thoracostomy tube trajectory. Bedside ultrasound can share timely information with surgeons and guide
patient management within institutional algorithms.
Figure 25-18. Complex Pleural Effusion in Child
Sagittal image from anterior midclavicular line. (Note the radiology convention – the indicator is on the left side of the screen.).
Figure 25-19. Hemothorax in Postoperative Patient with Complex Congenital Heart Disease
Note the subtle echogenicity to the pleural effusion.
Figure 25-20. Subcostal View of Costophrenic Recess
Subcostal view of costophrenic recess for the evaluation of pleural effusion. Pleural effusion within the costophrenic recess is marked with *.
(Note the radiology convention – the indicator is on the left side of the screen.)
Abdominal Ultrasound
Blunt pediatric abdominal trauma is different from adult trauma because fewer children present with
hemodynamic instability, and the management of solid organ injury tends to be conservative. The focused
assessment with sonography in trauma (FAST) examination has been evaluated in the pediatric setting and
is used, as in adults, for detecting fluid collections from ruptured viscera or bleeding. However, FAST is
poorly sensitive in pediatric populations, with some series reporting values as low as 20%. This test
does not obviate the need for computed tomography in most pediatric blunt abdominal trauma
algorithms.48,49 The reasons may include operator variability and smaller pathological fluid collections.
Despite this limitation, ultrasound minimizes radiation exposure from computed tomography and remains
readily available. Moreover, identification of fluid is indicative of pathology and could alter decision
making. In pediatric blunt abdominal trauma, fluid is most frequently visualized in the pelvis.50
Furthermore, abdominal ascites is easily visualized as a sequelae of other abdominal pathology. As
described previously, drainage can be accomplished with ultrasound-guided paracentesis.
Visualization of the diaphragmatic gutter from the subcostal position: In the subcostal position and
angle, the transducer is 30 degrees cephalad, with the indicator oriented to the 3 o’clock position.
The spine should be visible beneath the probe, the right diaphragmatic gutter should be visible on
the left side of the screen as a thin bright arc overlying the liver. A dark anechoic space distal to the
diaphragm is suggestive of effusion. Simple effusions will appear to divide the 2 arcs with an anechoic,
dark space.
Renal and bladder ultrasound are useful for assessing anuria in critically ill children. Interpretation of
hydronephrosis in children varies among radiologists, though it is commonly based on pelvic and calyceal
dilation.51 Hydronephrosis is not a specific disease, but rather an indicator of obstructed urinary drainage
and, if suspected, warrants further evaluation by diagnostic sonographers. Bladder volume in a pediatric
patient, as in adults, is calculated by multiplying bladder length, width, and height, the result of which is
then multiplied by a correction factor unique to the ultrasound machine calculation package. In
comparison, the equation (2 × age in years) + 2 = capacity (in ounces) for patients less than 2 years of age
and (age/2) + 6 = capacity (in ounces) for patients 2 years or older should provide approximate average
bladder capacity.52 In the anuric patient with a urinary catheter, it is important to note whether the bladder
is distended or empty as well as the location of the catheter cuff visible on ultrasound, which will appear
as an echogenic sphere enclosing dark anechoic water with the central bright catheter. A distended
bladder without evidence of urinary catheter in the bladder likely represents malposition of the catheter,
whereas a distended bladder with evidence of the catheter cuff in the bladder likely represents urinary
catheter obstruction. Visualization of only the urinary catheter balloon with no dark anechoic space
around it usually does not confirm that the catheter is in the bladder, because it is difficult to distinguish
from surrounding tissue. In this circumstance, anuria likely has prerenal or intrarenal causes.
Abdominal assessment of appendicitis and intussusception have been reported in the literature by
clinicians using ultrasound, though even in the hands of radiology subspecialists, views are at times
difficult to obtain because of variability in bowel position and shadowing from overlying air-filled
spaces.53 Therefore, a negative or indeterminate study is not reassuring. Although a positive study is
potentially meaningful, questions persist as to whether intensivists can identify enough positive results for
maintaining proficiency. In contrast, pyloric stenosis imaging has been described in the bedside
ultrasound literature.54 It is readily performed in infants because of the proximity of the pylorus to the skin
and relatively consistent anatomic location. In a cohort of 67 patients, emergency medicine providers
identified 10 patients with hypertrophic pyloric stenosis with a sensitivity and specificity of 100%.
Larger studies are necessary to determine its screening usefulness in acute care settings.
Neurologic Ultrasound
Head ultrasound is frequently used in neonatal populations for assessment of intraventricular hemorrhage.
However, its application is limited in the detection of parietal cortical surface pathology such as subdural
hematoma and cortical stroke, because of limited imaging windows and subtle parenchymal changes
associated with ischemia. Literature on successful training or performance of head ultrasound by pediatric
intensivists in older infants is nonexistent at the time of this writing.
Transcranial Doppler measuring blood flow velocity of the intracranial arteries is an established
neurophysiologic monitoring modality potentially useful to pediatric intensivists. It is, however, also one
of the most difficult modalities because of difficulties imaging through bone and restrictive windows for
cranial insonation. In children, transcranial Doppler was found to have a sensitivity of 94% and
specificity of 41% for predicting intracranial pressure of 20 mm Hg or more, and flow reversal was
associated with brain death in children with severe traumatic brain injury.55,56
In adults, increased intracranial pressure has been associated with increased optic nerve diameter on
ultrasound, but the data in pediatrics are conflicting and no reliable standard for a threshold optic nerve
sheath diameter is accepted for children across ages.57 Ophthalmologic ultrasound use for evaluating
retinal hemorrhages in pediatric patients with suspected abuse and retinal detachment in trauma victims
are among many other potential uses of ultrasound in the pediatric critical care setting.
NEXT STEPS: 4 “Cs” OF IMPLEMENTATION (COMPETENCE, CERTIFICATION,

CREDENTIALING, and COLLABORATION)
The practice of critical care medicine at the bedside yields questions every day as to a patient’s status and
response to therapy. As ultrasound evolves in pediatric critical care, the discipline must identify core
questions and objectives for bedside ultrasound use, and teach providers methods for reliably answering
those questions. In incorporating basic ultrasound into pediatric critical care training and practice, one
must recognize that institutional needs, capabilities, and provider experience will vary.
Regardless of location of practice, the 3 Cs of programmatic implementation58 are important. Competence

is the implicit, internalized knowledge of critical care ultrasound for clinical benefit. Training develops
competence. Thus, with defined clinical questions and objectives, reliable training should follow.
Courses oriented toward pediatric critical care providers are readily available internationally. However,
while the training exists, literature about how pediatric critical care ultrasound education translates to
performance at the bedside does not. Such data are needed for definitions of competence and guide
implementation.
Certification is the process by which competence is recognized by an external agency. This usually
incorporates a test of individual competence. There is no universally accepted process of certification
specific to pediatric critical care ultrasonography in North America at the time of this writing. One
example of a successful certification process is an education and evaluation mechanism for use of
transesophageal echocardiography (TEE) in adult cardiovascular anesthesiology.59 After
anesthesiologists in the 1980s recognized the usefulness of continuous TEE in the cardiac operating room,
collaboration among the Society of Cardiovascular Anesthesiologists, the American Society of
Anesthesiologists, and the American Society of Echocardiography resulted in a certification process for
anesthesiologists in TEE through the National Board of Echocardiography. Relationships across
specialties strengthened program implementation and improved patient care.
Credentialing is institution dependent and recognizes a provider as having met a set of educational or
occupational criteria for a specialized task. Credentialing is not dependent on certification, but there is a
presumed level of competence with required ongoing evaluation that remains institutionally defined.
The bedside credentialing experience of a critical care division in a tertiary level children’s hospital was
published recently, and describes education and experience-based criteria modeled from the American
College of Emergency Physicians emergency ultrasound guidelines policy statement.60,61 Core
applications were specifically defined for the pediatric critical care setting: procedural,
cardiac/hemodynamic, thoracic, and abdominal. Paramount to implementation was the communication and
cooperation among critical care, cardiology, and radiology departments as well as hospital
administration. Furthermore, experts in bedside ultrasound, particularly adult emergency medicine
providers, were used for training and guidance in developing programmatic framework. This
accomplishment underscores a critical fourth “C”: collaboration. Collaboration is essential in pediatric
ultrasound practice, whether individual, institutional, national, or international.
In conclusion, ultrasound has multiple practical applications in the hands of pediatric intensivists for
augmenting procedure success and bedside assessment. Many applications described in adult patients are
translatable to the pediatric patient, with some notable caveats described in this chapter. As ultrasound
applications evolve in pediatric critical care with innovation and thoughtful implementation, the
technology will establish itself as a mainstay in the intensivist’s armamentarium.
KEY POINTS
Ultrasound benefits procedural guidance in children by providing additional landmarks, and can
improve safety in a number of procedures.
Ultrasound assists the pediatric clinician with bedside real-time imaging that augments bedside
diagnostic capacity.
A number of diagnostic bedside ultrasound modalities have a higher false-negative rate in children
than in adults, an important factor when ultrasound findings are used for time-sensitive decisions in
therapy.
Bedside ultrasound is best performed in concert with other imaging specialties both during imaging
and in the larger scope of managing an ultrasound program.
REFERENCES
1. Lambert RL, Boker JR, Maffei FA. National survey of bedside ultrasound use in pediatric critical care. Pediatr Crit Care Med.
2011;12:655-659.
2. Kluckow M. Use of ultrasound in the haemodynamic assessment of the sick neonate. Arch Dis Child Fetal Neonatal Ed. 2014;99:F332-
337.
3. Wu S, Ling Q, Cao L, et al. Real-time two-dimensional ultrasound guidance for central venous cannulation. Anesthesiology. 2013;118:361-
375.
4. Sigaut S, Skhiri A, Stany I, et al. Ultrasound guided internal jugular vein access in children and infant: a meta-analysis of published studies.
Paediatr Anaesth. 2009; 19:1199-1206.
5. Lamperti M, Bodenham AR, Pittiruti M, et al. International evidence-based recommendations on ultrasound-guided vascular access.
6. Guilbert AS, Xavier L, Ammouche C, et al. Supraclavicular ultrasound-guided catheterization of the subclavian vein in pediatric and
neonatal ICUs: a feasibility study. Pediatr Crit Care Med. 2013;14:351-355.
7. P Souza Neto E, Grousson S, Duflo F, et al. Ultrasonographic anatomic variations of the major veins in paediatric patients. Br J Anaesth.
2014;112:879-884.
8. Doniger SJ, Ishimine P, Fox JC, et al. Randomized controlled trial of ultrasound-guided peripheral intravenous catheter placement versus
traditional techniques in difficult-access pediatric patients. Pediatr Emerg Care. 2009;25:154-159.
9. Shiloh AL, Eisen LA. Ultrasound-guided arterial catheterization: a narrative review. Intensive Care Med. 2010;36:214-221
10. Ganesh A, Kaye R, Stern W, et al. Evaluation of ultrasound-guided radial artery cannulation in children. Pediatr Crit Care Med.
2009;10:45-48.
11. Ishii S, Shime N, Sawa T, et al. Ultrasound-guided radial artery catheterization in infants and small children. Pediatr Crit Care Med.
2013;14:471-473.
12. Fleming SE, Kim JH. Ultrasound-guided umbilical catheter insertion in neonates. J Perinatol. 2011;31:344-349.
13. Pulickal AS, Charlagorla PK, Tume SC, et al. Superiority of targeted neonatal echocardiography for umbilical venous catheter tip location:
accuracy of a clinician performance model. J Perinatol. 2013;33:950-953.
14. Garg AK, Houston AB, Laing JM, et al. Positioning of umbilical arterial catheters with ultrasound. Arch Dis Child. 1983;58:1017-1018.
15. Froudarakis ME. Diagnostic work-up of pleural effusions. Respiration. 2008;75:4-13.
16. Rothlin MA, Naf R, Amgwerd M, et al. Ultrasound in blunt abdominal and thoracic trauma. J Trauma. 1993; 34:488-495.
17. Barnes TW, Morgenthaler TI, Olson EJ, et al. Sonographically guided thoracentesis and rate of pneumothorax. J Clin Ultrasound.
2005;33:442-446.
18. Diacon AH, Brutsche MH, Soler M. Accuracy of pleural puncture sites: a prospective comparison of clinical examination with ultrasound.
Chest. 2003;123:436-441.
19. Nazeer SR, Dewbre H, Miller AH. Ultrasound-assisted paracentesis performed by emergency physicians vs the traditional technique: a
prospective, randomized study. Am J Emerg Med. 2005;23:363-367.
20. Nigrovic LE, McQueen AA, Neuman MI. Lumbar puncture success rate is not influenced by family-member presence. Pediatrics.
2007;120:e777-e782.
21. Kim S, Adler DK. Ultrasound-assisted lumbar puncture in pediatric emergency medicine. J Emerg Med. 2014; 47:59-64.
22. Shaikh F, Brzezinski J, Alexander S, et al. Ultrasound imaging for lumbar punctures and epidural catheterisations: systematic review and
meta-analysis. BMJ. 2013;346:f1720.
23. Grmec S. Comparison of three different methods to confirm tracheal tube placement in emergency intubation. Intensive Care Med.
2002;28:701-704.
24. Chou EH, Dickman E, Tsou PY, et al. Ultrasonography for confirmation of endotracheal tube placement: a systematic review and meta-
analysis. Resuscitation. 2015;90:97-103.
25. Galicinao J, Bush AJ, Godambe SA. Use of bedside ultrasonography for endotracheal tube placement in pediatric patients: a feasibility
study. Pediatrics. 2007; 120:1297-1303.
26. Hosseini JS, Talebian MT, Ghafari MH. Secondary confirmation of endotracheal tube position by diaphragm motion in right subcostal
ultrasound view. Int J Crit Illn Inj Sci. 2013;3:113-117.
27. Tibby SM, Hatherill M, Marsh MJ, et al. Clinicians’ abilities to estimate cardiac index in ventilated children and infants. Arch Dis Child.
1997;77:516-518.
28. Stanko LK, Jacobsohn E, Tam JW, et al. Transthoracic echocardiography: Impact on diagnosis and management in tertiary care intensive
care units. Anaesth Intensive Care. 2005;33:492-496.
29. Kutty S, Attebery JE, Yeager EM, et al. Transthoracic echocardiography in pediatric intensive care: impact on medical and surgical
management. Pediatr Crit Care Med. 2014;15:329-335.
30. Ranjit S, Aram G, Kissoon N, et al. Multimodal monitoring for hemodynamic categorization and management of pediatric septic shock: a
pilot observational study. Pediatr Crit Care Med. 2014;15:e17-26.
31. Pershad J, Myers S, Plouman C, et al. Bedside limited echocardiography by the emergency physician is accurate during evaluation of the
critically ill patient. Pediatrics. 2004;114:e667-e671.
32. Longjohn M, Wan J, Joshi V, et al. Point-of-care echocardiography by pediatric emergency physicians. Pediatr Emerg Care. 2011;27:693-
696.
33. Spurney CF, Sable CA, Berger JT, et al. Use of hand-carried ultrasound device by critical care physicians for the diagnosis of pericardial
effusions, decreased cardiac function, and LV enlargement in pediatric patients. J Am Soc Echocardiogr. 2005;18:313-319.
34. Cheriex EC, Leunissen KM, Janssen JH, et al. Echography of the inferior vena cava is a simple and reliable tool for the estimation of dry
weight in haemodialysis patients. Nephrol Dial Transplant. 1989;4:563-566.
35. Kosiak W, Swieton D, Piskunowicz M. Sonographic inferior vena cava/aorta diameter index, a new approach to the body fluid status
assessment in children and young adults in emergency ultrasound- preliminary study. Am J Emerg Med. 2008;26:320-325.
36. Chen L, Hsiao A, Langhan M, et al. Use of bedside ultrasound to assess degree of dehydration in children with gastroenteritis. Acad
Emerg Med. 2010;27:1042-1047.
37. Levine AC, Shah SP, Umulisa I, et al. Ultrasound assessment of severe dehydration in children with diarrhea and vomiting. Acad Emerg
Med. 2010;17:1035-1041.
38. Cavaliere F, Cina A, Biasucci D, et al. Sonographic assessment of abdominal vein dimensional and hemodynamic changes induced in
human volunteers by a model of abdominal hypertension. Crit Care Med. 2011;39:344-348.
39. Marik PE, Baram M, Vahid B. Does central venous pressure predict fluid responsiveness? A systematic review of the literature and the
tale of seven mares. Chest. 2008; 134:172-178.
40. Gan H, Cannesson M, Chandler JR, et al. Predicting fluid responsiveness in children: a systematic review. Anesth Analg. 2013;117:1380-
1392.
41. Lopez L, Colan SD, Frommelt PC, et al. Recommendations for quantification methods during the performance of a pediatric
echocardiogram: a report from the pediatric measurements writing group of the American Society of Echocardiography Pediatric and
Congenital Heart Disease Council. J Am Soc Echocardiogr. 2010;23:465-495.
42. Gaspar HA, Morhy SS, Lianza AC, et al. Focused cardiac ultrasound: a training course for pediatric intensivists and emergency physicians.
BMC Med Educ. 2014;14:25.
43. Guntheroth WG. Sensitivity and specificity of echocardiographic evidence of tamponade: implications for ventricular interdependence and
pulsus paradoxus. Pediatr Cardiol. 2007;28:358-362.
44. Lichtenstein DA, Mauriat P. Lung ultrasound in the critically ill neonate. Curr Pediatr Rev. 2012;8:217-223.
45. Shah VP, Tunik MG, Tsung JW. Prospective evaluation of point-of-care ultrasonography for the diagnosis of pneumonia in children and
young adults. JAMA Pediatr. 2013;167:119-125.
46. Caiulo VA, Gargani L, Caiulo S, et al. Lung ultrasound in bronchiolitis: comparison with chest X-ray. Eur J Pediatr. 2011;170:1427-1433.
47. Islam S, Calkins CM, Goldin AB, et al. The diagnosis and management of empyema in children: a comprehensive review from the APSA
outcomes and clinical trials committee. J Pediatr Surg. 2012;47:2101-2110.
48. Fox JC, Boysen M, Gharahbaghian L, et al. Test characteristics of focused assessment of sonography for trauma (FAST) for clinically
significant abdominal free fluid in pediatric blunt abdominal trauma. Acad Emerg Med. 2011;18:477-482.
49. Scaife ER, Rollins MD, Barnhart DC, et al. The role of focused abdominal sonography for trauma (FAST) in pediatric trauma evaluation. J
Pediatr Surg. 2013;48:1377-1383.
50. Nance ML, Mahboubi S, Wickstrom M, et al. Pattern of abdominal free fluid following isolated blunt spleen or liver injury in the pediatric
patient. J Trauma. 2002;52:85-87.
51. Swenson DW, Darge K, Ziniel SI, et al. Characterizing upper urinary tract dilation on ultrasound: a survey of North American pediatric
radiologists’ practices. Pediatr Radiol. 2015;45:686-694.
52. Kaefer M, Zurakowski D, Bauer SB, et al. Estimating normal bladder capacity in children. J Urol. 1997;158:2261-2264.
53. Ross MJ, Liu H, Netherton SJ, et al. Outcomes of children with suspected appendicitis and incompletely visualized appendix of ultrasound.
Acad Emerg Med. 2014;21:538-542.
54. Sivitz AB, Tejani C, Cohen SG. Evaluation of hypertrophic pyloric stenosis by pediatric emergency physician sonography. Acad Emerg
Med. 2013;20:646-651.
55. Melo JR, DiRocco F, Blanot S, et al. Transcranial Doppler can predict intracranial hypertension in children with severe traumatic brain
injuries. Childs Nerv Syst. 2011; 27:979-984.
56. Hindy-Francois C, Orliaquet G, Meyer P, et al. Pediatric brain death diagnosis in the view of organ donation in France. Transplantation.
2009;87:616-617.
57. Le A, Hoehn ME, Smith ME, et al. Bedside sonographic measurement of optic nerve sheath diameter as a predictor of increased
intracranial pressure in children. Ann Emerg Med. 2009;53:785-791.
58. Levitov A, Mayo PH, Slonim AD. Training of the critical care physician as sonographer. In: Levitov A, Mayo PH, Slonim AD, eds. Critical
Care Ultrasonography. New York, NY: McGraw-Hill; 2009:45-57.
59. Reeves ST, Finley AC, Skubas NJ, et al. Basic perioperative transesophageal echocardiography examination: A consensus statement of the
American Society of Echocardiography and the Society of Cardiovascular Anesthesiologists. J Am Soc Echocardiogr. 2013;26:443-456.
60. Conlon TW, Himebauch AS, Fitzgerald JC, et al. Implementation of a pediatric critical care focused bedside ultrasound training program in
a large academic PICU. Pediatr Crit Care Med. 2015;16:219-226.
61. American College of Emergency Physicians. ACEP emergency ultrasound guidelines. Ann Emerg Med. 2009;53:550-570.
Chapter 26
Pediatric Ultrasound Procedures: Central
Venous Access and Arterial Access
Jeff Burzynski, MD, FRCPC; David Kirschner, MD,
FRCPC;
OBJECTIVES
Describe the basic technique of using ultrasound for arterial and central venous cannulation in children of all
sizes
Recognize the optimal mechanics for ultrasound-guided arterial and venous access
Determine the common approaches and ultrasound views for arterial and venous access
Describe in detail common ultrasound-guided techniques for the 3 sites of central venous cannulation
Incorporate expert tips and tricks for cannulation and procedural success
INTRODUCTION
Obtaining central venous access in critically ill infants and children is one of the most common
procedures in the pediatric ICU. The indications for placement vary widely but commonly include
hemodynamic monitoring, blood sampling, and administration of vasoactive medications, among others. In
infants and children, cannulation has a number of challenges, and is relatively more difficult than in adults
because of the smaller vessel size and the child’s inability to cooperate with the procedure. Ultrasound
guidance results in fewer complications than the classic landmark technique. Ultrasound-guided vascular
access has become the standard of care in a number of jurisdictions and healthcare organizations across
the world.
CASE STUDY
An 8-month-old girl presents with progressive respiratory distress necessitating endotracheal intubation.
Her physiologic and hemodynamic profile worsens, requiring more invasive monitoring. The decision is
made to place a percutaneous central venous line. The infant has a significant medical history of repaired
complex congenital heart disease (2 ventricles), all performed at a different institution. Her past surgical
course was complicated by extracorporeal support on 2 occasions. The parents report multiple thrombi in
the patient’s venous system, but the formal images are not available.
Where Is the Best Location to Obtain Central Venous Access in This Child?
Children with complicated conditions and multiple previous admissions have become common in many
pediatric critical care units. Children who have undergone instrumentation on previous admissions with
or without multiple thrombi are also frequently seen. Central venous cannulation in this situation is fraught
with difficulty and potential complications. Blind attempts using the landmark method will almost
certainly lead to multiple punctures and increased risk of complications, such as arterial puncture and
pneumothorax. Ultrasound clarifies the patient’s anatomy and can identify the presence of thrombi to
enhance procedural safety. It can also be used to confirm placement of the catheter in the vessel, thereby
decreasing the time required for therapy while awaiting radiographs in an emergency situation.
ULTRASOUND CANNULATION MECHANICS AND TECHNIQUES
For vessel catheterization, ultrasound can be performed as a 1- or 2-person procedure, with both
techniques reported to be equally effective.1,2 If performed as a 2-person procedure, the first person is
responsible for keeping the vessel of interest centered on the screen, and the second person is responsible
for keeping the needle tip in view at all times during the catheterization. This method works best when the
needle tip is in plane, as it can be too easily lost in an out-of-plane approach. Alternatively, a sole
provider can focus on both tasks, keeping the vessel in view with the ultrasound transducer in one hand
and catheterizing with the other. The sole provider method, though more difficult to learn, allows the
clinician to autocorrect for motion and more readily adjust a maneuver if difficulties are encountered. The
single provider method can be readily mastered with simulation and practice. Roughly 50 attempts (15
minutes) on a simulated vessel can quickly refine the skills of fanning the probe and keeping the needle tip
in plane and in view.
In this chapter, we will first describe optimal ultrasound-guided ergonomics and review different
ultrasound techniques. We will then discuss the most common sites for central venous and arterial access.
The remainder of the chapter focuses on expert techniques for a given vessel of interest. The basic steps
involved in appropriate sterile, full-barrier, and Seldinger techniques are only described once. All
appropriate steps for your particular institutional procedural standards should be followed. For simplicity
and brevity, we will not repeat basic procedural standards.
Ergonomics
Correct positioning of both the patient and the clinician is essential for procedural success. It is important
to ensure that the clinician and patient are as comfortable as possible, and that the setup of equipment
maximizes efficiency and minimizes excessive movements.
Clinicians should avoid positions in which they are leaning over the bed and patient, with their knees
locked or overextended. Holding such a position for more than a short period leads to undue stress and
fatigue that can translate into loss of focus on the procedure at hand. The clinician should stand or sit with
the patient directly in front of him or her and ideally have the ultrasound machine in plane with the line of
vision. Equipment required for the procedure and for sterile imaging with the probe should be within easy
reach. The patient should be placed near enough to the edge of the bed that there is not too much extension
at the elbows.
The ultrasound machine should be positioned so minimal eye movement is required to look between the
site of the procedure and the ultrasound screen. This often requires placing the machine at the side of the
patient’s bed opposite the procedure. However, this requires a second operator to save images, angle the
screen, and manipulate the ultrasound functions. The machine is preferably positioned opposite the
clinician, such that a quick glance up at the screen is possible with minimal risk of moving the hands off
the axis.
Techniques
Static vs. Dynamic Ultrasound Guidance
Identifying the desired vessel is of utmost importance. Significant variability in the relational position
between arteries and veins exists in children,3 and ultrasound can help identify anatomic variations. It can
allow direct measurement of the vessel diameter via M-mode, which can help in choosing the correctly
sized catheter. Consensus suggests that the catheter be no larger than one-third the diameter of the vessel.4
Other features that can be used in vessel identification include pulsed-wave and color flow Doppler. The
flow pattern and difference in scale are helpful in differentiating arterial from venous flow (Figure 26-1).
The static approach is used every time a clinician does a prescan of the vessel of interest. If the clinician
were to set the ultrasound probe down at this point and attempt to catheterize the vessel based on what
was just viewed, this would be considered a static approach. It entails a basic visual of the vessel,
“marking” the spot, and then attempting to cannulate without direct visualization. Although this approach
may reduce the risk of complications compared with the landmark technique, it does not offer the same
benefits as a dynamic approach. Hence, we recommend the dynamic approach.
The dynamic approach involves real-time visualization of the needle and wire during insertion into the
vessel. The dynamic approach is superior because it gives the clinician the ability to troubleshoot an
attempt that is not initially successful: Am I off axis? Am I too shallow in my approach or depth? Has the
anatomy changed due to a slight change in patient position? The dynamic approach also prevents off-angle
punctures of the vessel and subsequent hematoma because the insertion can be aborted if direct
visualization is not occurring.
Figure 26-1. Central Artery vs. Central Vein

Pulsed-wave Doppler showing the difference in flow pattern between a central artery (A) and a central vein (B). Note the difference in scale
that is associated with the different vessels. This holds true for any of the 3 areas of central venous catheterization.
Out-of-Plane vs. In-Plane Approach

Two sets of terms are commonly used to describe the relationship between the vessel of interest and
needle tip visualization. The vessel is visualized either along its long axis or across its short axis,
depending on the ultrasound probe’s orientation to the vessel. The needle tip is described as being in
plane with the ultrasound beam or out of plane. In the out-of-plane approach, a hyperechoic dot with
distal artifact is often all that is visualized on the screen (Figure 26-2).
Two common methods using the short-axis out-of-plane approach are as follows:
1. The clinician inserts the needle just ahead of the transducer, and then advances it continuously until the
needle tip is visualized. Following visualization, the transducer is either slid or fanned distally, and
the needle tip is then advanced toward it. This method is often described as the needle constantly
trying to “catch up” to the transducer beam. If done in small increments (or degrees, if fanning the
transducer), this can be very effective.
2. A clinician may use simple math and knowledge of angles to plan the initial approach. First, the
clinician measures the distance from the skin surface to the vessel lumen on the ultrasound screen.
Using an angle of approach of 45°, the clinician can calculate the distance that the needle should be
from the transducer as it enters the skin. If the angle of entry is indeed 45°, and if there are no
dangerous structures near the vessel of interest, this technique is successful. The downside is that the
needle tip is not visualized until it enters the vessel. Potential dangers with this method are obvious
and are magnified the deeper the vessel is from the skin surface.
An oblique orientation has also been discussed in the literature. This involves visualizing the vessels in
an oblique orientation and inserting the needle in plane to the ultrasound beam.5,6 Two approaches–
cephalomedial to caudolateral and cephalolateral to caudomedial–are described and suggested as
superior.7 Although this method is frequently used for catheterization of the internal jugular vein, it can be
applied to any vessel. Regardless of the approach taken, a firm understanding of the underlying anatomy
and potential complications must be kept in mind with any procedure.
Figure 26-2. Possible Approaches During Needle-guided Procedures

A) Long-axis in-plane approach. B) Short-axis in-plane approach. C) Short-axis out-of-plane approach.
No angle of approach will work sufficiently for every clinician, in every situation; however, some key
concepts need to be kept in mind when deciding on the angle of approach (Table 26-1).
Table 26-1. Comparison of Long- and Short-Axis Approaches
Long Axis Short Axis
Benefits Drawbacks Benefits Drawbacks
Ability to visualize posterior wall of vessel, Longer learning curve, requires Shorter learning curve, ability to visualize relevant Provider may lose track of needle tip if
less likely to puncture posterior wall more space in the long axis anatomy surrounding vessel of interest using out-of-plane technique
Transducer Selection
The linear transducer typically is recommended for vascular access. It uses a higher frequency, allowing
for better resolution of more superficial structures.
In pediatrics, 2 linear transducers are commonly used: a rectangular linear transducer and a hockey stick,
or epicardial, transducer. The microconvex or curvilinear transducer can also be applied for vascular
access because it has a frequency that is high enough to adequately visualize central vessels and a small
footprint, thereby taking up less skin surface. The clinician should note the depth of the vessel of interest
and the footprint of the available transducers when deciding which probe to use.
Needle Tip Visualization

Ultrasound waves are best able to be reflected back to the transducer when the area of interest is at 90° to
the ultrasound beam. If the needle angle of approach is too steep, it may be difficult to follow its path. A
shallow angle of approach maximizes needle tip visualization, but takes up more room and requires the
clinician to follow the needle for a longer distance under the skin.
Steering the angle of the sound beam as it leaves the ultrasound machine improves visualization of a
needle. This feature is best used with the long-axis approach.
If a large respiratory variation is visualized in the central vein of choice or the vessel does not appear
circular in transverse view, consider giving a 10- to 15-mL/kg bolus before beginning the procedure.
ARTERIAL AND VENOUS PROCEDURAL GUIDANCE WITH ULTRASOUND
Arterial Cannulation
Arterial cannulation is a common procedure for arterial blood analysis and continuous hemodynamic
monitoring in the pediatric ICU. The most common cannulation sites include the radial and femoral
arteries. The brachial and axillary arteries are also used but have more complications; the specifics will
not be discussed here.
Radial Artery Cannulation

Anatomically, the radial artery runs along the anterolateral aspect of the distal forearm and is commonly
found with paired radial veins but no associated peripheral nerve.
Although both the short-axis and long-axis approaches can be attempted, the limited data available on
pediatric patients suggest that the long-axis approach is more likely to result in success at the first
attempt.8,9 In pediatric patients, there may be an ideal depth (2-4 mm) for successful catheterization, and
infiltrating with subcutaneous saline may improve the view by placing the vessel at this depth.10
Using sterile technique, the steps for ultrasound-guided radial artery catheterization include the following:
1. Prescan both distal radial arteries near the wrists for diameter, depth from skin, and course.
2. Confirm ulnar artery flow with
(a) the Allen test, and
(b) ultrasound-confirmed color flow (Figure 26-3).
3. Select right/left radial artery based on steps 1 and 2.
4. (a) Identify the radial artery in short axis using a combination of anatomic location, compressibiity,
and flow pattern in the vessel (using pulsed-wave or color Doppler).
(b) If using the long-axis approach, rotate the transducer 90° to obtain the long-axis view of the radial
artery (Figure 26-4).
5. Optimize image depth/gain, so that the radial artery is in the center of the screen and as large as it can
be. Note the distance from the skin to the center of the vessel. Grasp the ultrasound probe between the
tips of the fingers and resting on the medial palmar aspect of the hand. Orient the indicator of the
ultrasound probe to align with the correct anatomy of the patient.
6. Clean the area with your institution’s recommended antiseptic solution (eg, chlorhexidine, povidone,
alcohol swabs, etc).
7. Anesthetize the area with 0.1 to 0.3 mL of local anesthetic (optional).
8. Using either the long- or short-axis approach, insert the catheter at an angle of 30° to 45° with the skin
just proximal to the ultrasound transducer. In the short-axis approach, place the needle tip in the
centerline of the transducer as it is centered over the vessel (Figure 26-5).
9. Watch for the needle tip on the screen, as well as tenting of the anterior vessel wall just before
catheterizing the vessel.
10. Observe for blood flash in the arterial line setup.
11. Lower the needle, and advance 1 to 2 mm, confirming that there is still flow in the needle.
12. For the 1-provider technique, place the probe down and advance the guidewire. The provider may
have an assistant advance the guidewire while continuing to watch on the ultrasound screen
13. Secure in place and connect to the arterial line transducer kit according to institutional standards.
The same technique can be used to cannulate the ulnar or brachial arteries.
E X P E RT T I P
The radial artery should be palpated with varying levels of pressure before scanning to help
mentally visualize the anticipated course of the artery.
Femoral Artery Cannulation

The femoral artery catheterization follows the same basic steps as in the radial artery, but a few key
differences must be kept in mind.
1. The femoral artery is bound intimately to both the common femoral vein (medially) and the femoral
nerve (laterally). The femoral vein can be identified by its thin walls, relative ease of collapsibility
compared with the artery, and anteromedial insertion of the greater saphenous vein if it is followed
more distally. Color flow or Doppler flow can be added to differentiate the artery and vein if in doubt.
The femoral nerve often is not well visualized and does not commonly have the rounded “honeycomb”
appearance of many peripheral nerves at this point, which can make identification more difficult
(Figure 26-6).
2. Although the femoral artery is relatively larger than the radial artery, it remains important to choose an
appropriately sized catheter. There is little reliable collateral flow distal to the common insertion
point of the femoral artery catheter, and complications could arise at this point should the lumen
become completely occluded.
Figure 26-3. Palpation of the Radial Artery as Part of the Prescan
Figure 26-4. Anatomy of the Distal Wrist
Anatomy of the distal wrist, including the radial artery and paired radial veins, and the median nerve, which is located medially on the volar
aspect of the distal forearm.
Figure 26-5. Long-Axis and Short-Axis Orientations for Radial Artery Catheterization
A) Long-axis orientation. B) Short-axis orientation. Although not shown, sterile technique should be observed for this procedure.
Figure 26-6. Anatomy of Femoral Neuromuscular Bundle

Abbreviations: FN, femoral nerve; FA, femoral artery; FV, femoral vein.
Relative anatomy of the femoral neuromuscular bundle in the right leg of a patient, seen in a transverse orientation as though the provider were
standing at the foot of the bed.
The key steps to follow for ultrasound-guided femoral artery catheterization include:
1. Prescan both right and left femoral arteries in the short and long axes, assessing for thrombus, location
compared with surrounding structures, and other patient factors. Scan from just below the inguinal
ligament to the bifurcation of the femoral artery into its superficial and deep branches.
2. Select the right or left femoral artery based on your findings.
3. Introduce the needle under the skin, right next to the transducer, then watch the screen for the needle in
its short axis or long axis, depending on the in-plane or out-of-plane approach. Using continuous
negative pressure, advance the needle until it is visualized puncturing the anterior wall of the femoral
artery and a flash of blood is obtained.
Central Venous Cannulation

Vessel Selection Specific to Central Vein Catheterization
When selecting a central vessel to catheterize, a clinician chooses a site or approach based on 2 groups of
factors: patient factors and clinician factors. Patient factors include any factor related to the patient’s
position, pathology, or stabilization that may make catheterization at a site difficult or impossible. Factors
common to all sites include overlying soft tissue damage (eg, lacerations, burns) and anatomic constraints
(eg, contractures). Clinicians are usually more comfortable with a single site for central venous
catheterization based on their experience and training. While one site may be more ideal than the others, if
the clinician is not comfortable with that site (eg, little training/experience, lack of skilled assistant, time
restraints), he or she may opt for the more familiar approach (Table 26-2).
Table 26-2. Contraindications to Central Venous Access by Sites
Internal jugular vein Short neck, cervical collar in place
Subclavian vein Clavicle fracture, contralateral pneumothorax, or other lung pathology that is not yet stabilized
Femoral vein Ipsilateral femur fracture, pelvic fracture
Patient Factors
The clinician may be faced with limited locations for central venous access (eg, burn victims, cervical
collar in place, short neck). The size and footprint of the ultrasound transducer can also be a limiting
factor because the probe may be too long to enable a shallow approach with the needle, based on the
patient’s size. In such cases, it may be necessary to modify the angle of approach.
Vessel Size
In contrast to peripheral vessels, the vessels of interest with central cannulation tend to be larger.
However, in the young infant, this may still only be a few millimeters. Any time a small vessel is being
cannulated, it is prudent to make the angle of approach as shallow as possible to avoid going through the
posterior wall. This complication is reduced by using a long-axis in-plane approach, but the angle must
still be kept in mind.1,2
Potential Complications
The complications related to vascular access include infection, thrombosis, phlebitis, vasospasm,
hemorrhage, and infiltration (also known as extravasation). Although the data on phlebitis, vasospasm,
and infiltration are sparse in the adult central access literature and all but nonexistent in the pediatric
literature, case reports and experience suggest that it is important to keep potential complications in mind.
Ultrasound can assist in early identification and avoidance of these complications.
Hemorrhage can take a number of forms, with the most concerning being hemorrhage from an improperly
dilated vein or from an arterial puncture. The in-plane and out-of-plane approaches attempt to reduce
these risks, but small risks are inherent to the views they obtain.
Although the risk of infection has historically deterred providers from inserting femoral lines, more recent
data suggest that the risks of infection from femoral vein catheterization do not differ significantly from the
risks of the other 2 sites.11
A Cochrane review on central venous line cannulations reported a small increased risk of thrombosis
with femoral vein cannulation compared with the subclavian approach, as well as a small increased risk
of catheter colonization.12 The authors ultimately concluded that femoral and internal jugular vein
approaches had a similar rate of catheter-related complications despite a small increase in mechanical
complications with internal jugular vein insertion. 12 It should be noted that this work studied adult
populations, a significant portion of which were patients with cancer. Therefore, not all of these data may
be transferable to the pediatric population, and more research is necessary in this area.
Internal Jugular Vein

In the pediatric population, ultrasound-guided internal jugular vein catheterization has been found to be
superior to the landmark technique by increasing first-pass success rates and improving patient safety.13,14
The best approach and clear benefits of the long-axis in-plane versus the short-axis out-of-plane approach
are less well studied. Patient size alone may limit the ability to successfully insert an internal jugular
catheter via the long-axis technique. To date, the only randomized study involved experienced
anesthesiologists and concluded that the short-axis out-of-plane approach led to fewer complications and
more rapid vessel catheterization.15 Differing conclusions from the literature on the optimal head position
reinforce the need for clinicians to prescan the neck with the patient in various degrees of neck rotation to
determine the ideal positioning for each patient. Ultrasound can assist in identifying anatomic variations
across the pediatric population.3
Internal jugular vein catheterization steps (single operator, dynamic technique) include:
1. Position the patient in the Trendelenburg position (head down) to increase the diameter of the internal
jugular vein.
2. Prescan both internal jugular veins in their entire length, assessing for diameter, thrombosis,
compressibility, relation to carotid artery, and changes in relative position with neck rotation. Scan
from the clavicle up the neck to the ear. Pick the area where the internal jugular vein is at its largest
diameter. Be sure to note the relative angle required to advance the wire underneath the clavicle
because this can limit success.
3. Select the right or left internal jugular vein accordingly.
4. Clean and prepare the area using standard sterile techniques according to institutional standards and
guidelines.
5. Re-image the selected internal jugular vein, and infiltrate with local anesthetic of your choice
(optional). Use gentle pressure with the ultrasound to prevent venous compression.
6. (a) In the short-axis approach, insert the needle proximal to the ultrasound transducer, while keeping
negative pressure on the syringe, with an eye on the ultrasound screen. Once it is visualized,
advance the ultrasound probe 0.5 to 1 cm, and then advance the needle again until it reappears on
the screen. The clinician should see the needle tip indenting the vessel with insertion pressure,
and care should be taken to ensure this is occurring in the middle of the vessel. Repeat these
steps, so that the needle is continually catching up to the ultrasound probe, until there is a flash of
blood in the syringe, and the needle tip is visualized in the vessel lumen.
(b) In the long-axis approach, visualize the internal jugular vein in its long axis. Insert the needle tip
proximally, keeping negative pressure on the syringe, and follow it on the ultrasound screen.
Advance the needle until it is seen puncturing the anterior wall of the vessel, and a flash of blood
is seen in the syringe. Continue to advance the needle until the tip is in the middle of the vessel
(Figure 26-7).
7. Re-image the vessel in its long axis to confirm that the wire is in the lumen. Institutional standards may
required that an image of this view be saved.
Figure 26-7
By keeping a small color flow box at the side of the image closest to the thorax, regardless of central access site, the provider is able to
continually confirm that he or she is overlying the vessel of interest. If the paired vessels are near the same diameter, the addition of a color
flow box becomes even more valuable.
Femoral Vein
The technique for femoral vein catheterization is similar to that for the internal jugular vein. In pediatrics,
a frog leg position appears to decrease the overlap between the femoral artery and vein, and may also
increase the diameter of the femoral vein.16 This position is best obtained by placing the patient’s heel
against the medial aspect of the opposite knee, and letting the leg fall to the side.
The steps for ultrasound-guided femoral vein catheterization include the following:
1. Place the patient in the frog leg position if possible.

2. Prescan both right and left femoral veins in the short and long axes, assessing for thrombus, location
compared with surrounding structures, and patient factors (eg, fracture location, burns, etc). Scan from
just below the inguinal ligament to where the greater saphenous vein joins the common femoral vein
medially.
3. Select the right or left femoral vein accordingly.
4. Clean and prepare the area using full sterile procedures according to institutional directions and
current guidelines, including sterile probe cover and gel.
5. Identify the femoral vein in short or long axis using a combination of anatomic location, flow pattern,
and compressibility.
6. Decide which approach will be most successful (long vs. short axis); in small infants, the short axis is
likely the only view that is possible.
7. Continue with institutional procedural standards.
Subclavian Vein
Cannulation of the subclavian vein (SCV) using ultrasound guidance can be accomplished in various
ways. Historically, the landmark technique was used to cannulate the SCV underneath the clavicle, or the
infraclavicular approach. The vascular and intrathoracic orientation make this site more prone to
mechanical complications, particularly for the inexperienced clinician. Because of the anatomy and
difficult windows, using ultrasound was not popular until more recently. This is likely because of the
acoustic shadowing from the clavicle that overlies the vessels. A recent clinical trial in adult patients
showed significant benefits to ultrasound-guided SCV cannulation mostly by showing a reduction in
mechanical complications.17 Both the long- and short-axis approaches have been described in the
literature. The long-axis approach has been championed by some because it allows the clinician to
visualize the needle throughout the procedure, thereby minimizing the risks of both pneumothorax and
arterial puncture (Figure 26-8).
Subclavian Vein Approaches

Steps similar to those of the internal jugular vein cannulation are followed for the SCV cannulation.
Figure 26-8. Subclavian Artery/Vein Anatomy Showing Infraclavicular Approach

1. Position the patient in the Trendelenburg position (head down) to increase the diameter of the SCV.
2. Prescan both SCVs in their entire length, assessing for size, diameter, thrombosis, compressibility,
relation to the subclavian artery, and changes in relative position with neck rotation. Scan from the
deltoid groove and along the clavicle, taking special care to tilt the face of the ultrasound probe
underneath the clavicle. Small adjustments of the ultrasound probe will allow for full visualization of
the SCV under the S curve of the clavicle.
3. Select the right or left SCV vein accordingly.
4. Clean and prepare the area using standard sterile techniques according to institutional standards and
guidelines.
5. Place the ultrasound machine on the opposite side of the patient.
6. Re-image the selected SCV, and infiltrate with local anesthetic of your choice.
7. (a) In the infraclavicular short-axis approach, place the probe in the short-axis orientation just under
the clavicle at the deltoid groove and scan about halfway to the sternoclavicular junction.
Depending on the size of the patient, this typically provides a view of the subclavian or axillary
vein in short axis. The vein is the vessel located at the top of the screen or more superficially. The
use of color and/or pulsed-wave Doppler can differentiate the SCV and artery. Stand to the lateral
side of the patient. Be sure to correctly orient the probe anatomically with the intended procedure.
Option 1: At the deltoid groove, or slightly lateral, the vessel is visualized in the center of the
screen. Insert the needle lateral to the ultrasound transducer, while keeping negative pressure on
the syringe, and watch for it on the ultrasound screen. Once it is visualized, the needle is
advanced until the tip of the needle is seen puncturing the vein. The angle of approach is steeper
and typically the vein punctured is the axillary vein. This technique has the advantage of
decreasing proximity of the needle pathway to the pleural interface and the disadvantage of
targeting a smaller-diameter vessel.
Option 2: At the halfway point to the sternoclavicular junction, the SCV is centered in the middle
of the screen. Slide the probe along the clavicle until the first rib is visualized as well. Insert the
needle lateral to the ultrasound transducer, while keeping negative pressure on the syringe, and
watch for it on the ultrasound screen. Once it is visualized, the needle is advanced until the tip of
the needle is seen puncturing the vein. The angle of approach is more shallow and the skin
puncture is closer to the clavicle than in the landmark technique. Centering above the first rib has
the advantage of ensuring the needle will puncture the vein and not the artery. The advantage of
this location is the larger-vessel diameter, and the disadvantage is the proximity of the needle
pathway to the lung pleura. The operator must take special care to keep the needle pathway in
view on the ultrasound screen the entire time.
(b) In the infraclavicular long-axis approach, place the probe in the short-axis orientation just under
the clavicle and at the deltoid groove, and scan about halfway to the sternoclavicular junction.
Identify the vein and center it in the middle of the probe. The vein is located more superficially or
at the top of the ultrasound screen. Rotate the probe keeping the vein in the center of the screen
and visualize the vein in the long axis. Tilt the face of the probe underneath the clavicle and make
fine adjustments, sliding medially or laterally to open up the pathway of the SCV. Next stabilize
the transducer against the clavicle. The use of color and/or pulsed-wave Doppler can confirm
appropriate isolation of the SCV. Stand to the lateral side of the patient. Be sure to correctly
orient the probe anatomically with the appropriate side of SCV cannulation. In the long axis,
puncture the skin lateral and in plane to the ultrasound probe while keeping negative pressure on
the syringe, and watch the ultrasound screen. The needle tip should be seen entering the skin
through the soft tissue and directly into the vessel. The long-axis approach is recommended only
after a clinician is comfortable with the dynamic single-operator technique. Either the
microconvex or the hockey stick probe can be used. The microconvex probe has the advantage of
providing a larger scanning sector so that the SCV, artery, and pleural line can all be visualized at
the same time. The hockey stick probe allows for enhanced magnification of the SCV (Figure 26-
9).
Figure 26-9. Infraclavicular View of the Subclavian Vein
A) Short-axis view indicating relationship between clavicle and subclavian vein. B) Long-axis infraclavicular view with pulsed-wave
Doppler gate, indicating triphasic venous flow. C) Long-axis infraclavicular view of the vein (blue) and the artery (red).
E X P E RT T I P
Always scan both sides of the patient before sterilizing, prepping, and choosing a
cannulation vessel.
(c) In the supraclavicular long-axis approach, locate the internal jugular vein and follow it in short
axis by sliding down the neck from the angle of the jaw toward the clavicle using a high-
frequency linear transducer. Once the probe abuts the clavicle, the tail of the probe is fanned
toward the head to visualize the junction of the internal jugular vein and the SCV (left or right) as
they form the innominate vein. Be sure to correctly identify the innominate or SCV and avoid the
subclavian artery, which lies posterior to the vein. The pulsed-wave Doppler function can be
helpful; place the gate over the vessel to determine arterial vs. venous flow. The pleural line is
easily identified as it is very close to the vessels in this view. Stabilize the transducer against the
superior aspect of the clavicle. Using the long-axis approach, insert the needle lateral to the
ultrasound transducer while keeping negative pressure on the syringe, and watch for the needle on
the ultrasound screen. The needle is advanced under direct and constant view into the confluence
of the internal jugular and subclavian or the innominate vein. Sometimes the cephalad section of
the superior vena cava is seen in this view.
8. Re-image the vessel in its long axis to confirm that the wire is in the lumen. Institutional standards may
require that an image of this view be saved. Procedural standards are not included (Figure 26-10).
Figure 26-10. Supraclavicular Approach

Abbreviations: IJ, internal jugular; SCV, subclavian vein.
A) Junction of SCV and IJ vein. B) Needle entering right IJ vein.
TIPS AND TRICKS

Ultrasound allows the clinician to get a comprehensive understanding of a patient’s volume status.
Significant variation in the size of the central vessel with respiration may indicate the need for a fluid
bolus during the procedure, thereby preventing the vein from collapsing completely during needle
insertion.
With experience, the long-axis in-plane approach improves and clinicians can modify the insertion
technique to reduce the number of hand transfers required to insert the wire. Seeing the tip of the needle in
the middle of the desired vessel negates the need for flashback upon entry into the vein. The wire can be
threaded directly in the needle before skin insertion. Once the needle tip punctures the middle of the
vessel, the clinician advances and visualizes the wire entering the vessel with the ultrasound. This
requires a steady hand and some preplanning, but reduces the number of times the provider moves the
needle and reduces the likelihood of it becoming dislodged (Figure 26-11).
Figure 26-11.
A) With the wire loaded on the needle, the provider can thread the wire directly once the vessel is punctured, using the long-axis in-plane
approach. B) The provider can also remove the wire holder for easier threading of the wire, using the long-axis in-plane approach. The end of
the wire is no longer contained, so care is needed to ensure that it does not become contaminated.

In the long axis, adding color Doppler to a small area at the far end of the vessel where the needle
will be inserted assists the clinician in staying in plane with the vessel. Keeping the color box small
preserves the appropriate frame rate for adequate images.
Line Placement Confirmation

Regardless of initial central venous vessel and approach used, ultrasound confirmation of the wire in the
vessel should occur in both the short-axis and long-axis views.
The first step is direct visualization of the needle tip in the center of the vessel. After the wire is inserted,
the clinician should scan the length of the visible vessel in both the long and short axes and record images
(Figure 26-12). Careful manipulation will allow the experienced ultrasonographer to confirm that the
wire has not gone through the posterior wall of the vessel. Scanning up the neck can also identify a wire
wrapped on itself or that has not reached the vena cava/atrial junction. A second ultrasonographer can use
a nonsterile cardiac phased-array transducer and attempt to visualize the tip of the wire in the right atrium
(Figure 26-12). If measurements are taken carefully, the catheter can be advanced to the tip of the wire,
and the catheter and wire can be pulled back until the wire is no longer seen in the right atrium. Each of
these steps will confirm the appropriate placement of the central venous catheter. Finally, it should
become part of routine practice to scan the pleural line on the side of catheter insertion to rule out
potential pneumothorax. This is particularly desirable when using the supraclavicular approach for SCV
cannulation.
Figure 26-12. Line Confirmation

A) Wire seen in the internal jugular vein. B) Tip of the wire seen in the right atrium from a subcostal 4 window.
E X P E RT T I P
Practice with the dynamic long-axis approach reduces the number of hand transfers required to
insert the wire.
KEY POINTS
Keep the needle tip in view at all times.

Gain proficiency in multiple techniques (ie, short and long axis) to improve success rate in difficult
patients.
Gain proficiency at multiple anatomic sites to improve success rate.
Use color Doppler to help identify vascular anatomy
Remember ergonomics!
REFERENCES
1. Rose J, Norbutas C. A randomized controlled trial comparing one-operator versus two-operator technique in ultrasound-guided basilic vein
cannulation. J Emerg Med. 2008;35:431-435.
2. Milling T, Holden C, Melniker L, Briggs WM, Birkhahn R, Gaeta T. Randomized controlled trial of single-operator vs. two-operator
ultrasound guidance for internal jugular central venous cannulation. Acad Emerg Med. 2006;13:245- 247.
3. Souza Neto EP, Grousson S, Duflo F, Tahon F, Mottolese C, Dailler F. Ultrasonographic anatomic variations of the major veins in paediatric
patients. Br J Anaesth. 2014;112:879- 884.
4. Lamperti M, Bodenham AR, Pittiruti M, et al. International evidence-based recommendations on ultrasound-guided vascular access.
5. Phelan M, Hagerty D. The oblique view: an alternative approach for ultrasound-guided central line placement. J Emerg Med. 2009;37:403-
408.
6. DiLisio R, Mittnacht A. The “medial-oblique” approach to ultrasound-guided central venous cannulation: maximize the view, minimize the
risk. J Cardiothorac Vasc Anesth. 2012;26:982-984.
7. Blaivas M, Adhikari S. An unseen danger: frequency of posterior vessel wall penetration by needles during attempts to place internal
jugular central catheters using ultrasound guidance. Crit Care Med. 2009;37:2345-2349.
8. Vogel J, Haukoos JS, Erickson CL, et al. Is long-axis view superior to short-axis view in ultrasound-guided central venous catheterization?
Crit Care Med. 2015;43:832-839.
9. Berk D, Gurkan Y, Kus A, Ulugol H, Solak M, Toker K. Ultrasound-guided radial artery cannulation: long axis/in-plane versus short
axis/out-of-plane approaches? J Clin Monit Comput. 2013;27:319-324.
10. Nakayama Y, Nakajima Y, Sessler DI, et al. A novel method for ultrasound-guided radial artery catheterization in pediatric patients. Anesth
Analg. 2014;118:1019-1026.
11. Mark P, Flemmer M, Harrison W. The risk of catheter-related bloodstream infection with femoral venous catheters as compared to
subclavian and internal jugular venous catheters: a systematic review of the literature and meta-analysis. Crit Care Med. 2012;40:2479-
2485.
12. Ge X, Cavallazzi R, Li C, Pan SM, Wang YW, Wang FL. Central venous access sites for the prevention of venous thrombosis, stenosis and
infection. Cochrane Database Syst Rev. 2012;3:CD004084.
13. Froehlich CD, Rigby MR, Rosenberg ES, et al. Ultrasound-guided central venous catheter placement decreases complications and
decreases placement attempts compared with the landmark technique in patients in a pediatric intensive care unit. Crit Care Med.
2009;37:1090- 1096.
14. Sigaut S, Skhiri A, Stany I, et al. Ultrasound guided internal jugular vein access in children and infant: a meta-analysis of published studies.
Paediatr Anaesth. 2009;19:1199- 1206.
15. Chittoodan S, Breen D, O’Donnell BD, Iohom G. Long versus short axis ultrasound guided approach for internal jugular vein cannulation: a
prospective randomised controlled trial. Med Ultrason. 2011;13:21-25.
16. Hopkins J, Warkentine F, Gracely E, Kim IK. The anatomic relationship between the common femoral artery and common femoral vein in
frog leg position versus straight leg position in pediatric patients. Acad Emerg Med. 2009;16:579-584.
17. Fragou M, Gravvanis A, Dimitriou V, et al. Real-time ultrasound guided subclavian vein cannulation versus the landmark method in critical
care patients: a prospective randomized study. Crit Care Med. 2011;39:1607-1612.
INDEX
Videos and supplemental images cited in the index
may be accessed at www.sccm.me/ultcomp.
A
Abdominal aortic aneurysm (AAA)
rupture
saccular (berry)
Abdominal examination
A-lines
focused, competence, minimal number to achieve
pediatric patient
positioning
probes
Abdominal wall, blood vessels
Abscess
cutaneous, appearance
Doppler ultrasound
drainage, ultrasound-guided
evaluation
foreign body
incision, ultrasound-guided
mimics
soft tissue, in gluteal region
Absorption, energy
Accreditation, definition
Acoustic shadowing
Acoustic window
location
Acute aortic syndrome
Acute coronary syndrome
Acute respiratory distress syndrome (ARDS),Video 10-6
absence of lung sliding
acute cor pulmonale
BLUE profile
diagnosis
ground glass opacities
lung recruitment
postpartum
right ventricular function
ultrasound and computed tomography findings
volume expansion
Advanced cardiac ultrasound
Advanced critical care echocardiography (ACCE)
competence, minimal number of examinations to achieve
credentialing
pathways
requirements
education programs, assessment
privileges
Afterload
increased, causes in pediatric patient
Air, intraperitoneal free
Air bronchogram
dynamic
static
Akinesia, of heart muscle
ALARA principle
Aliasing
minimizing
A-lines
abdominal ultrasound
BLUE protocol
lung ultrasound
Allen test
Alveolar-interstitial syndrome
diagnosis
American College of Emergency Physicians (ACEP)
core emergency ultrasound applications
curriculum for trauma
guidelines on training
American College of Surgeons, (ACS), support for FAST
American Institute of Ultrasound in Medicine, statement on ultrasound safety
American Medical Association (AMA), resolution 802 on privileging in ultrasound imaging
American Society of Echocardiography (ASE), criteria for wall motion abnormalities
Amniotic fluid embolism,Video 5-1
A-mode ultrasound
Amplitude, ultrasound wave
Amplitude mode
Anechoic structure
Aneurysm(s), See also Aortic aneurys
iliac
left ventricular
popliteal
Anticoagulation
deep venous thrombosis
pulmonary embolism
Aorta
abdominal. See also Abdominal aortic aneurysm (AAA)
diameter, Supplemental image 11-14
distal segment, Supplemental image 11-13
inferior vena cava, distinguishing
Supplemental image 11-10
longitudinal view
middle segment, Supplemental image 11-12
mural thrombus
proximal segment, Supplemental image 11-11
examination
transverse view
apical 5-chamber view
apical long-axis view
ascending, imaging
cross-sectional view
descending, imaging
identification
intramural hematoma
parasternal long-axis view
subcostal long-axis view, pediatric patient
subcostal view
thoracic. See also Aortic aneurysm
imaging, Supplemental images 11-15, 11-16, 11-17
transverse abdominal view, pediatric patient
Aortic aneurysm, See also Abdominal aortic aneurysm (AAA)
thoracic
Aortic arch
imaging, Supplemental image 11-17
suprasternal view
Aortic dissection
Supplemental images 11-15, 11-16, 11-17
associated abnormalities
classification
clinical presentation
diagnostic strategy
epidemiology
imaging
risk factors
type A
type B
Aortic flap, in aortic dissection
Aortic insufficiency
assessment
color flow Doppler
continuous-wave Doppler
Aortic regurgitation
acute, and cardiac arrest
evaluation
Aortic root
aortic dissection
measurement at sinotubular junction
Aortic stenosis
assessment
cardiac arrest
color flow Doppler
evaluation
Aortic ulcer
Aortic valve. See also Aortic regurgitation; Aortic stenosis
aortic dissection
blood velocity
fluid responsiveness
respiratory variation
sepsis
imaging
infective endocarditis
M-mode imaging
parasternal short-axis view
prosthetic
TEE assessment
TTE assessment
velocity time integral, respiratory variation
Appendicitis, pediatric patient
Arterial catheterization/cannulation. See also specific artery
ultrasound-guided
pediatric patients
Arterial puncture
femoral vein access
subclavian vein access
Arteriovenous fistula
Arteriovenous malformation(s)
Artifact(s) See also Acoustic shadowing; Aliasing; Reverberation
comet-tail See also B-lines
edge
lung ultrasound
mirror image, of liver
ring down
reverberation
side lobe
Ascites
evaluation
fluid depth
pediatric patient
vs. pleural effusion
Asthma
BLUE profile
Asystole, Video 20-3
Atelectasis, Videos 10-4, 10-5
complete
compressive
lung imaging
resorptive
Atrial contraction, and diastole
Atrial fibrillation
diastolic function
echocardiographic evaluation of fluid responsiveness
inflow velocity
Atrial septal defect
bidirectional shunt
bubble study
color flow across
coronary sinus
evaluation
signs
sinus venosus
types,
Atrium
left
apical long-axis view
subcostal 4-chamber view
right
subcostal long-axis view
Attenuation
Attenuation coefficient
A´ velocity
A wave
Axillary vein, color Doppler
B
Barcode sign
Baseline, for pulsed-wave Doppler
Bedside lung ultrasound in emergency (BLUE) protocol
Billing
Bioeffects
Bladder
blood clots, Supplemental image 11-5
female
identification
uterus, anatomical relationship
Foley balloon
longitudinal view
pediatric patient
postvoid residual
transverse view
volume, pediatric patient
B+ lines. See Lung rockets
B-lines
after fluid resuscitation
bilateral
BLUE protocol
extravascular lung water
lung imaging Videos 9-6, 9-7, 10-4, 10-5
confluent
diffuse, differential diagnosis
distribution
focal, differential diagnosis
frequency
sepsis
spacing
Blood flow
central artery vs. central vein
color Doppler imaging
continuous-wave Doppler imaging
pulsed-wave Doppler imaging
venous, augmentation
B-mode ultrasound
Bone ossification, pediatric patient
Bowel gas
imaging of abdominal aorta
vs. intraperitoneal free air
Brightness mode
Bronchiolitis, pediatric patient
Bubble study
C
Cardiac apex
pediatric patient
Cardiac arrest
echocardiography
with pulmonary embolism
reversible causes, identification
shockable vs. nonshockable rhythm
transesophageal echocardiography, Video 20-6
Cardiac assessment. See also Echocardiography
pediatric patient
Cardiac consultation
Cardiac injury, in trauma
Cardiac output
calculation
sepsis
volume expansion
Cardiac tamponade (pericardial tamponade)
diagnosis
Doppler echocardiographic findings
echocardiographic limitations
echocardiographic signs
pediatric patient
physiology
signs and symptoms
therapeutic options
transvalvular blood flow velocity
2-dimensional echocardiographic findings
Cardiac ultrasound. See also Echocardiography focused
Cardiomyopathy
catecholamine
hypertrophic obstructive
pediatric patient
septic
right ventricular dysfunction
stress
Takotsubo
Cardiopulmonary resuscitation, and echocardiography
Carotid artery
dissection
flow, pulsed-wave Doppler of
internal jugular vein cannulation
left, aortic dissection, Supplemental image 11-18
puncture, in internal jugular vein cannulation
Catecholamine cardiomyopathy
Cauda equina, pediatric patient
Cavitation
Celiac trunk, Supplemental image 11-11
Cellulitis
Central venous access, ultrasound-guided
advantages
pediatric patients
complications
contraindications
line placement confirmation
patient factors
vessel selection
vessel size
Central venous pressure
Certification
definition
pediatric critical care ultrasound
transesophageal echocardiography
Chamber dimensions, M-mode imaging
Chest examination. See also Thoracic ultrasound
E-FAST,
zones
Chest pain, evaluation
Chest tube(s), placement. See Tube thoracostomy
Chest wall, in thoracic ultrasound, Video 14-2
Cholecystitis
acalculous
acute, Supplemental image 11-3
Cholelithiasis. See also Gallstone(s)
Chronic obstructive pulmonary disease (COPD)
BLUE profile
Circulatory collapse
Circulatory failure
Cobblestoning
Collaboration, and pediatric critical care ultrasound
Color Doppler
abscess
color map
controls,
diagnosis of deep venous thrombosis
differentiation of venous and arterial flow
direction-independent mode
frame rate
resolution
sector width
variance mapping
Color power Doppler
Common bile duct
location, Supplemental image 11-2
obstruction
Common femoral vein. See Femoral vein
Competence
definition
Compression
Compression examination, for deep venous thrombosis
Computed tomography (CT), in trauma
Continuous quality improvement (CQI)
Continuous-wave Doppler
controls
range ambiguity
Contrast, automatic adjustment
Contrast agents
endocardium
power setting
segmental wall motion abnormalities
Contrast-enhanced ultrasound, solid organ injury in blunt trauma
Controls, of ultrasound machine
color Doppler
default settings
pulsed-wave Doppler
Conus medullaris, pediatric patient
Core applications, in critical care medicine
Coronary artery(ies)
circumflex, myocardial areas supplied by
left anterior descending, myocardial areas supplied by
right, myocardial areas supplied by
territorial distribution
Cor pulmonale
acute, in acute respiratory distress syndrome
postpartum
Costophrenic recess, subcostal view, pediatric patient
Credentialing
definition
departmental responsibilities
fellowship-based pathway
guiding documents
individual provider’s responsibilities
maintaining
practice-based pathway
process
study and image review
Critical care ultrasound (CCUS)
competence, minimal number of examinations to achieve,
credentialing
pathways
requirements
education programs, assessment
privileges
Cross-sectional area (CSA), calculation of
Current Procedural Terminology (CPT)
codes, in critical care ultrasound
modifiers
repeat procedure by another physician
repeat procedure by same physician
D
Deceleration time, E wave
Decidual reaction
Decontamination
Deep venous thrombosis (DVT)
epidemiology
examination
methods
probes
lower extremity
prevalence
progression to pulmonary embolism
evaluation
pulmonary embolism,
signs and symptoms
treatment
upper extremity
evaluation
prevalence
progression to pulmonary embolism
risk factors
signs and symptoms
Depth, in imaging
adjustment
M-mode ultrasound
penetration
Diagnostic peritoneal lavage (DPL)
Diaphragm
dynamic respiratory motion
identification in thoracic examination
movement, pediatric patient
thickening
thickness measurement
success of extubation
weakness, evaluation
Diaphragmatic gutter, subcostal view in pediatric patient
Diaphragmatic paralysis
Diaphragmatic ultrasound
assessment of patient-ventilator interactions
postoperative
Diastole
definition
diastasis
E:E´ ratio
isovolumic relaxation
phases
physiology
pressure gradient
Diastolic dysfunction
EA ratio
E:E´ ratio
etiologies
grades
incidence
prognostic significance
S/D ratio
therapeutic implications
Diastolic function
assessment
classification
factors affecting
Diffuse parenchymal lung disease
differential diagnosis
Digital Imaging and Communications in Medicine (DICOM)
Documentation
Doppler effect
Doppler ultrasound. See also Color Doppler; Continuous-wave
Doppler; Pulsed-wave Doppler; Tissue Doppler; Transcranial
Doppler
abscess
modes
physical principles
tuning
Double decidual sign
Double-ring sign
Draping, of patient
Dynamic range
Dyskinesia, interventricular septal
Dyskinesis, of heart muscle
E
Echocardiography. See also Focused assessment of transthoracic
echocardiography (FATE); Transesophageal echocardiography;
Transthoracic echocardiography
3-dimensional (3D)
acute respiratory distress syndrome
advanced
apical window
2-chamber view (A2C)
long-axis view (ALAX)
assessment of volume status, limitations of
cardiac arrest
cardiogenic pulmonary edema
chronic pulmonary hypertension
critical care use
default settings
diagnosis of pulmonary embolism
diffuse parenchymal lung disease
fat embolism
fish mouth view
focused, protocol-driven
frame rate
gas embolism
guidelines
indicator placement
left ventricular systolic function
liberation from mechanical ventilation
and lung ultrasound, in respiratory failure
midpapillary view
myocardial infarction
myocardial ischemia
noncardiogenic pulmonary edema
parasternal long-axis view (PLAX)
pediatric patient
parasternal short-axis view (PSAX)
pediatric patient
pericardial effusion
pericardial tamponade
positioning
protocols
pulmonary embolism
qualitative ventricular assessment, pediatric patients
respiratory illness
right ventricular views
sepsis
septic shock, Video 21-1
stroke volume estimation
subcostal window
4-chamber view
inferior vena cava, in long axis
inferior vena cava/cavoatrial view
temporal resolution
views and windows
Edema
pulmonary. See Pulmonary edema
tissue
Edge artifact
Education and training. See also Credentialing
programs, assessment of
specialists
E/e´ ratio
Ejection fraction
inotropes
left ventricular, measurement
preserved, heart failure with
reduced, heart failure with
right ventricular
Simpson biplane
Teichholz
Elastic recoil
Elastography
Electrocardiography
echocardiography during cardiac arrest
myocardial ischemia
Electromechanical dissociation, Video 20-1
Electronic medical record (EMR)
Embolectomy, pulmonary embolism
Emergency ultrasound
Empyema
End-expiratory occlusion (EEO) test, and fluid responsiveness
Endocarditis, and cardiac arrest
Endocardium, contrast imaging,
Endotracheal tube position, pediatric patient
Epigastric artery identification, pediatric patient
Ergonomics
E´ velocity
E wave
deceleration time
Examination of Special Competence in Adult Echocardiography
(ASCeXAM)
Examination of Special Competence in Perioperative Transesophageal
Echocardiography (PTEeXAM)
Exclamation point view
Extended FAST (E-FAST)
Extravascular lung water, estimation of
F
Far field
Fat embolism, and right ventricular function
Femoral artery
anatomy
catheterization/cannulation, ultrasound guidance
anatomical considerations
double wall puncture
pediatric patient
positioning
procedure
separate guidewire approach
evaluation
locating, transducer placement
Femoral nerve, anatomy
Femoral vein
access/cannulation, ultrasound guidance
complications
contraindications
pediatric patient
positioning
procedure
rationale
anatomy
differentiation from femoral artery
evaluation
thrombosis
Fetal heart rate, Supplemental image 11-20
Fetal pole
First harmonic
Fish mouth view
Fistula, gallbladder-duodenum
Fluid
free (intraperitoneal)
ectopic pregnancy
inferior to right kidney
Morison pouch
pelvis
perisplenic
ruptured abdominal aortic aneurysm
small bowel obstruction, Supplemental image 11-8
intrathoracic
periaortic, with ruptured abdominal aortic aneurysm
pericardial
pericholecystic
retroperitoneal, with ruptured abdominal aortic aneurysm
Fluid administration limited by lung ultrasonography (FALLS)
protocol
Fluid challenge
Fluid-color sign
Fluid responsiveness
assessment
decisional algorithm
dynamic predictors
echocardiographic indices
end-expiratory occlusion test
passive leg raising test
prediction in pediatric patients
respiratory variability in diameter of venae cavae
Fluid therapy, in septic shock, goal-directed
Fluid tolerance, FALLS protocol and
Focal length
Focal zone
adjustment
Focus, adjustment of
Focused assessment of transthoracic echocardiography (FATE)
Focused assessment with sonography in trauma (FAST)
advantages
ascites
cardiac view
drawbacks/limitations
ectopic pregnancy
essential steps
evidence supporting
hepatorenal recess
historical perspective
pediatric patient
pelvic images
perisplenic space
probe
schematic anatomy
skills acquisition
splenic view
subxiphoid images
suprapubic view
technique and training
upper abdominal scans
Focused echocardiographic evaluation in life support (FEEL)
Focused echocardiographic evaluation in resuscitation (FEER)
protocol
Foley catheter, evaluation
Fontanelles, pediatric patient
Foramen ovale, patent
Frame rate
cardiac imaging, pediatric patients
color Doppler
M-mode
Frank-Starling relationship
Freeze
Frequency
adjustment
attenuation
depth of penetration
echocardiography
fundamental
image resolution
G
Gain
adjustment
automatic
image quality
output power
pulsed-wave Doppler
total
Gallbladder
distension
polyps, Supplemental image 11-1
sludge
examination
approaches
indications
patient positioning
wall thickening
Gallstone(s). See also Cholelithiasis
Gallstone ileus
Gas embolism, and right ventricular function
Gel pad, stand-off
General mode
Gestational sac
Great vessels. See also Aorta
identification
H
Harmonic frequencies
Harmonic imaging, for echocardiography
Head examination, pediatric patient,
Heart. See also Atrium; Echocardiography; Left ventricle; Right ventricle
pediatric patient
identification
pediatric patient
Heart failure
acute decompensated
diastolic
preserved ejection fraction
reduced ejection fraction
Heart rate
fetal. See Fetal heart rate
mitral inflow velocity
pediatric patients
Heat generation
Hematocrit sign
Hematoma
pericardiac
sonographic appearance
Hemodynamic assessment. See also Volume status echocardiography guided
Hemoperitoneum, FAST evaluation
Hemorrhage
central venous access
hypovolemic shock
femoral vein access
Hemothorax, Video 14-1
FAST evaluation
pediatric patient
trauma
Hepatic vein, subcostal long-axis view
Hepatization, of lungs
Hepatorenal recess, in FAST
Hernia, abdominal wall
Horizontal xiphisternal line (HXL)
Hydraulic orifice formula
Hydronephrosis, Supplemental image 11-4
pediatric patient
Hyperechoic structure
Hyperemia, in cellulitis
Hypotension
pulmonary embolism
septic shock
Hypovolemia. See also Shock, hypovolemic cardiac arrest
inferior vena cava collapse in, Video 21-2
septic shock
Hypoxic pulmonary vasoconstriction
I
Ileus. See also Gallstone ileus vs. mechanical obstruction
Iliac artery(ies)
aneurysm
diameter, Supplemental image 11-14
Image(s), saving/archiving
Incidental findings
Indicator(s), placement, for echocardiography
Infection(s). See also Sepsis
femoral vein access
necrotizing
prevention
skin evaluation
soft tissue
evaluation
necrotizing
Infective endocarditis
diagnosis
echocardiography in
modified Duke criteria
risk factors
Inferior vena cava
aorta, distinguishing, Supplemental image 11-10
collapse, in hypovolemia, Video 21-2
collapsibility, assessment in sepsis
diameter
hypovolemia
measurement
pediatric patient
respiratory variability
dilated and non-collapsing
distention
cardiac tamponade
pediatric patient
echocardiographic image optimization
imaging in pediatric patient
incompressible, causes
measurement
hypovolemia
intravascular volume status
pediatric patient
M-mode imaging
plethora
respiratory-related variation
pediatric patient
subcostal short-axis view (in M-mode)
transverse abdominal view, pediatric patient
Inotropes, ejection fraction
Instrumentation
Intensity, ultrasound wave
Interatrial septum
artifactual echocardiographic dropout
subcostal view
Internal jugular vein
complications
contraindications
in-plane approach
oblique approach
pediatric patient
positioning
procedure
rationale
short-axis approach
anatomy
Interstitial pneumonitis with septal thickening, findings
Interventricular septum
D-shaping
dyskinesia
flattening
morphology
motion
right ventricular pressure overload
Intubation, assessment in pediatric patient
Intussusception, Supplemental image 11-9
pediatric patient
IVC-to-aorta ratio, pediatric patient
K
Kidney(s)
FAST
examination
trauma, epidemiology
Kidney stones
Knobology
L
LAD. See Coronary artery(ies)
Lawn-mower technique, for small bowel obstruction
Left atrial pressure
diastolic dysfunction
estimation
Left ventricle
apical 2-chamber view (A2C)
apical long-axis view (ALAX)
apical ventricle
blood supply to
cavity size
contractility
measurement
subjective estimation, using TTE
diastole
diastolic function
evaluation
sepsis
dilation
dimensions, measurement
D-shaped
dysfunction
cardiac arrest
sepsis
ejection fraction, measurement
end-diastolic area
fractional area change
fractional shortening
hypertrophy
internal dimensions
motion vectors
regional wall motion abnormalities
segments
akinesia
aneurysmal
dyskinesia
hypokinesia
Simpson biplane ejection fraction
systolic function
assessment
factors affecting
longitudinal, assessment
regional
sepsis
visual estimation
teardrop-shaped, on parasternal short-axis view
Teichholz ejection fraction
wall thickness
Left ventricular outflow tract
cardiac output
cross-sectional area, measurement
diameter, measurement
Doppler imaging
circulatory collapse
flow through, pulsed-wave Doppler
M-mode imaging
obstruction
pediatric patient
pulsed-wave Doppler
velocity, respiratory variation
velocity time integral
Doppler ultrasound
Liver
mirror image artifact
Logistics
critical care ultrasound program
definition
Lumbar puncture, pediatric patient
Lung(s)
aeration patterns
airless, ultrasound
A-lines
anterior predominance
area/zone of apposition
B-lines, Videos 9-6, 9-7, 10-4, 10-5
confluent
diffuse, differential diagnosis
distribution
focal, differential diagnosis
frequency
sepsis
spacing
consolidation, Videos 10-4, 10-5, 10-9
diagnosis
pediatric patient
subpleural
contusion
hepatization
infarction
motionless
parenchyma, on ultrasound
pulsations. See Lung pulse
zones
Lung aeration score
Lung point, Video 14-5
BLUE protocol
pneumothorax
identification
Lung pulse, Videos 9-5, 10-7
Lung re-aeration score
Lung recruitment
Lung rockets
Lung sliding, Videos 9-3, 9-4, 14-3
BLUE protocol
clinical significance
conditions affecting
pneumothorax
Lung ultrasound. See also Bedside lung ultrasound in emergency (BLUE) protocol; Thoracic ultrasound
echocardiography, combined, in respiratory failure
evaluation of lung recruitment
liberation from mechanical ventilation
lung congestion
mechanical ventilation
normal findings
pediatric patient
probes
respiratory failure
scanning protocol
4-zone examination
8-zone examination
12-zone examination
Lusitropy
Lymph node, Doppler imaging
M
McConnell sign
Mechanical ventilation
diaphragmatic dysfunction due to, assessment
liberation
patient-ventilator interactions, diaphragmatic ultrasound
evaluation
weaning
diaphragmatic ultrasound
failure
Methicillin-resistant Staphylococcus aureus (MRSA)
Midpapillary view
Midventricle
parasternal long-axis view, M-mode
Mini fluid challenge
Mitral annular plane systolic excursion (MAPSE)
Mitral annular velocity
diastolic function
measurement
pathology affecting
tissue Doppler imaging
Mitral regurgitation
acute, and cardiac arrest
assessment
color flow Doppler
diastolic function
evaluation
Mitral stenosis
assessment
cardiac arrest
color flow Doppler
diastolic function
evaluation
severity quantification
Mitral valve. See also Mitral regurgitation; Mitral stenosis aortic dissection
early diastolic velocity (E´). See also E´ velocity E/e´ ratio
inflow
atrial fibrillation
diastolic function
Doppler velocity, respiratory-related changes
measurement
physiology
pulsed-wave Doppler
respiratory variation, and cardiac tamponade
tachycardia
late diastolic filling velocity (A)
late diastolic velocity (A´)
lateral annulus, velocity measurement
M-mode ultrasound
peak early filling velocity (E)
prosthetic
diastolic function
pulsed-wave Doppler
septal annulus, velocity measurement
systolic anterior motion
TEE assessment
tissue Doppler
TTE assessment
M-mode ultrasound
depth
frame rate
sweep speed
Modality(ies)
Morison pouch
free fluid
Motion mode
Murphy sign
Myocardial infarction
cardiac arrest caused by
Myocardial ischemia
evaluation
Myocardial stunning
Myocardium. See also Sepsis-induced myocardial dysfunction (SIMD)
coronary artery supply
motion, tissue Doppler
motion vectors
Myometrial mantle, measurement
N
Near field
Necrotizing fasciitis
Nerve(s), normal appearance
Nyquist limit
O
Ophthalmologic ultrasound, pediatric patient
Optic nerve sheath diameter, pediatric patient
Output power
Ovarian cyst
Ovarian mass
P
Paracentesis
complications
contraindications
diagnostic
indications
needle insertion site
pediatric patient
preprocedural ultrasound assessment
therapeutic
ultrasound-guided
procedure
Passive leg raising (PLR) test
technique
Pediatric patient(s)
anatomic differences from adults
anuria
appendicitis
arterial cannulation
arterial catheterization
ascites
blunt abdominal trauma
cardiac assessment
central venous access (ultrasound-guided)
costophrenic recess, subcostal view
critical care ultrasound, 4 Cs
critically ill, examination,
diaphragm movement, assessment
effusion drainage
endotracheal tube position
examination
fluid responsiveness, prediction,
head ultrasound
hemodynamic ultrasound
hemothorax
hydronephrosis
image quality, factors affecting
intracranial pressure
intussusception
IVC-to-aorta ratio
lumbar puncture
lung/pleural ultrasound
neurologic ultrasound
ophthalmologic ultrasound
optic nerve sheath diameter
paracentesis
pericardial effusion
pericardial fluid
peripheral arterial access
peripheral venous access
physiologic differences from adults
pleural effusion
pyloric stenosis
qualitative ventricular assessment
radial artery cannulation
right ventricular failure with dilation, causes
right ventricular morphologic assessment
tamponade physiology
temperature sensitivity
thoracentesis
transcranial Doppler
transducer selection
umbilical catheter placement
vascular access
cephalomedial to caudolateral approach
cephalolateral to caudomedial approach
ergonomics
long-axis approach
needle tip visualization,
oblique orientation
one-person procedure
out-of-plane vs. in-plane approach
positioning
short-axis approach
static vs. dynamic approach
two-person procedure
volume assessment
Pelvic ultrasound
FAST
longitudinal view
transverse view
Penetration mode
Periaortic fluid, with ruptured abdominal aortic aneurysm,
Pericardial effusion
accumulation
causes
speed of, and tamponade
vs. anterior fat pad
drainage
echocardiographic identification
pediatric patient
vs. pleural effusion
pressure-volume relationships with
size
tamponade
trauma
Pericardial fluid
accumulation
causes
speed of, and intrapericardial pressure
pediatric patient
evaluation
Pericardial space
Pericardial tamponade. See Cardiac tamponade
Pericardiocentesis
emergent
ultrasound guidance
Pericarditis, constrictive, and diastolic function
Pericardium
identification, on ultrasound
parietal
visceral
Pericholecystic fluid
Peripheral arterial access, pediatric patients
Peripheral venous access, pediatric patients
Perisplenic space, in FAST
Peritoneum
free air
free fluid, Supplemental image 11-8
ectopic pregnancy
paracentesis
Pertussis
Picture archiving and communications system (PACS)
Piezoelectric effect
Pleura
identification, on ultrasound, Videos 9-1, 9-2, 14-3
nodules
parietal and visceral, anechoic space between
thickening
Pleural access
partial vs. real-time needle guidance
procedural approach
ultrasound-guided, real-time
Pleural adhesions
Pleural effusion
vs. ascites
diagnosis
chest radiography
computed tomography
ultrasound
exudative, ultrasound appearance
malignant
pediatric patient
vs. pericardial effusion
septations
thoracentesis
transudative, ultrasound appearance
trauma
ultrasound evaluation
high-frequency linear probe
patient positioning
probes
technique
volume, ultrasound assessment
Pleural fluid, features, Video 14-4
Pleural line
pediatric patient
Pleural ultrasound, competence, minimal number of examinations to achieve
Pneumatosis, bowel wall
Pneumobilia
Pneumomediastinum
Pneumonia
BLUE profile
diagnosis
chest radiography
ultrasound
features
interstitial
pediatric patient
Pneumothorax
A-lines
BLUE profile
cardiac arrest
diagnosis, Video 20-5
chest radiography
computed tomography
ultrasound
internal jugular vein cannulation
lung point
lung sliding
postthoracentesis
size, ultrasound measurement
trauma
ultrasound
algorithm
anatomic considerations
evidence for use
examination technique
probe orientation, Videos 9-1, 9-2
Popliteal artery
aneurysm
injury, causing pseudoaneurysm
thrombosis
Position/positioning
echocardiography
examiner
femoral artery cannulation, ultrasound-guided
femoral vein access, ultrasound guidance
gallbladder examination
internal jugular vein cannulation, ultrasound guidance
patient
pleural effusion evaluation
radial artery cannulation, ultrasound-guided
subclavian vein cannulation, ultrasound guidance
thoracic ultrasound
erect
lateral
semidecubitus
supine
tube thoracostomy, ultrasound-guided
vascular access in pediatric patient
Positive end-expiratory pressure
lung recruitment
titration, using lung ultrasound
Positive-pressure ventilation, and right ventricular function
Posterior acoustic enhancement
Posterolateral alveolar or pleural syndrome (PLAPS) point
Postextubation distress, prediction
Post-thrombotic syndrome
Postvoid residual (PVR)
Power
contrast agents
Power Doppler
vascular ultrasound
Pregnancy
double-ring sign
ectopic
cornual (interstitial), Supplemental image 11-19
heterotopic
image acquisition
indications
intrauterine (IUP), diagnosis
Preload,
positive-pressure mechanical ventilation
sepsis, assessment
static ultrasound indices
stroke volume
Preload dependence
functional indices
Preload independence
Privileges, definition
Proficiency, definition
Pseudoaneurysm
Pseudo-PEA, Video 20-2
Pulmonary artery occlusion pressure (PAOP)
Pulmonary artery pressure
estimation
mean (mPAP)
systolic
ARDS, with right ventricular dysfunction
Pulmonary capillary wedge pressure (PCWP)
A-line predominance
B-line predominance
Pulmonary edema
BLUE profile
cardiogenic
ground glass opacities in acute
interstitial
interstitial and alveolar patterns, Video10-3
noncardiogenic
Pulmonary embolism (PE), Video 5-1
BLUE profile
cardiac arrest
clot in transit, Video 20-4
deep vein thrombosis
epidemiology
risk
massive
morbidity and mortality
right ventricle-left ventricle end-diastolic dimension ratio
submassive
treatment
ultrasound examination
method
transducer type
views
workup
Pulmonary fibrosis
Pulmonary hypertension
chronic
echocardiography
severe acute presentation
Pulmonary trunk, with bifurcation, parasternal short-axis view,
pediatric patient
Pulmonary valve
parasternal short-axis view, pediatric patient
Pulmonary vascular resistance (PVR)
calculation
Pulmonary vein
inflow pattern
diastolic function
evaluation
pathology affecting
peak diastolic velocity (D)
peak systolic velocity (S)
Pulmonary venous inflow (PVI)
Pulsed echo mode
Pulsed-wave Doppler
baseline,
blood flow velocity
controls
diagnosis of deep venous thrombosis
energy output
gain
left ventricular outflow tract
mitral inflow
sample volume
scale
sweep speed
Pulseless electrical activity (PEA), Video 20-1
Pulse oximetry, pediatric patient
Pulse pressure, and fluid responsiveness
Pulse repetition frequency (PRF)
Pulsus paradoxus
Pyloric stenosis, pediatric patient
Q
Quality improvement (QI). See also Continuous quality improvement (CQI)
image archiving
process
R
Radial artery
anatomy
catheterization/cannulation, ultrasound-guided
anatomical considerations
efficacy
pediatric patient
positioning
procedure
color Doppler
M-mode ultrasound
Range ambiguity, of continuous-wave Doppler
Rectouterine pouch (of Douglas), in FAST
Rectovesical pouch, in FAST
Reflection
Refraction
Regional wall motion abnormalities (RWMA)
diastolic function
evaluation, in shock
nomenclature,
structured evaluation
Reimbursement. See Billing
Reject function
Resolution
axial
color Doppler
depth
lateral
sector size
temporal
Resolution mode
Respiratory failure
BLUE ultrasound diagnosis
combined echocardiography and lung ultrasound
diagnostic protocols
lung ultrasound
Respiratory illness, and right ventricular function
Retroperitoneal fluid, with ruptured abdominal aortic aneurysm
Reverberation
arterial catheterization
lung parenchyma
lung ultrasound
Ribs
ossification, pediatric patient
ultrasound identification, Videos 9-1, 9-2
Right atrial pressure (RAP)
Right atrium, collapse, in cardiac tamponade
Right ventricle
anatomy
apex
pediatric patient
apical long-axis view (ALAX)
apical ventricle
basal diameter
collapse, cardiac tamponade
contractility
diastole
diastolic function, advanced evaluation
dilatation
ARDS
pediatric patient
dimensions
dysfunction
cardiac arrest
prognostic value
pulmonary embolism
sepsis
ejection fraction
elastance
end-diastolic area
fractional area change (FAC)
function
assessment
diseases affecting
sepsis
hypertrophy
infundibulum (conus)
inlet
isovolumetric contraction time
longitudinal dimension
midcavitary diameter
morphologic assessment
pediatric patient
morphology
ARDS
overload
physiology
pressure overload
chronic vs. acute
diastolic, in ARDS
septal morphology
systolic, in ARDS, Video 18-1
reference measurements
regional wall motion abnormalities
segments
size, relative to left ventricle
strain, with pulmonary embolism
systolic function
assessment
estimation
normal
volume overload, Video 5-1
pediatric patient, structural heart disease causing
wall thickness
measurement
Right ventricular outflow tract
Right ventricular systolic pressure (RVSP)
S
Safety
Sample volume, for pulsed-wave Doppler
Scale, for pulsed-wave Doppler
Scatter
Seagull sign, Supplemental image 11-11
Seashore sign
motion artifact appearing as
Sector size
M-mode
Sector width, color Doppler
Sepsis, Video 21-1. See also Septic shock
diastolic dysfunction
reduced systemic vascular resistance
ultrasound findings
ventricular dysfunction,
ventricular performance, assessment
volume expansion
Sepsis-induced myocardial dysfunction
Septic shock
cardiac function
echocardiography, Video 21-1
left ventricular function
treatment, echocardiography directed
ultrasound findings
Septum. See Interatrial septum; Interventricular septum
Seroma, appearance
Shear forces
Shock
cardiogenic
mitral regurgitation
tricuspid regurgitation
tricuspid stenosis
causes
distributive. See also Sepsis left ventricular function
hypovolemic. See also Hypovolemia causes
hemorrhage
trauma-related
neurogenic
obstructive
pediatric patient
pulmonary embolism,
septic. See Septic shock ultrasound
Short abdominal screening
Shred sign
Shunt, with atrial septal defect
bidirectional
flow across, calculation
left-to-right
Side lobe artifact
Simpson biplane ejection fraction
Sine wave sign
Sinuses of Valsalva, parasternal long view
Sinusoid sign
Small bowel
examination
image acquisition
indications
peristaltic activity
ileus
lack
small bowel obstruction
wall
edema
pneumatosis
Small bowel obstruction (SBO)
causes
high-grade, Supplemental image 11-18
lawn-mower (Zamboni) technique
simple vs. ileus
ultrasound diagnosis
Society of Critical Care Medicine (SCCM), recommendations on
credentialing
Soft tissue(s)
infection
necrotizing
normal, appearance
Sound, velocity
air
bone
soft tissue
water
Spatial peak temporal average (ISPTA)
Specialists, in ultrasound education
Speckle tracking
Spectral Doppler
Spine, pediatric patient
ultrasound
Spine sign
Spinous process(es), imaging
Spleen
FAST
Spontaneous bacterial peritonitis (SBP)
Strain
Stratosphere sign
Stroke volume
calculation
cardiac preload
left heart (Qs)
left ventricular, echocardiographic estimation
measurement
passive leg raising (PLR) test
respiratory variability
right heart (Qp)
right ventricle
sepsis
Subclavian vein (SCV)
complications
contraindications
pediatric patient
positioning
procedure
rationale
anatomy
Subxiphoid window, in FAST
Superior mesenteric artery (SMA), Supplemental image 11-12
Superior vena cava, respiratory collapsibility,
Suprasternal notch view, Supplemental image 11-16
Sweep speed
M-mode imaging
pulsed-wave Doppler
Systemic vascular resistance, reduced, in sepsis
Systole
T
Tachycardia
diastolic function
Tamponade. See Cardiac tamponade; Pericardial tamponade
Target sign
Teichholz ejection fraction
Tendon(s), normal appearance
Tension pneumothorax. See also Pneumothorax
cardiac arrest
Thoracentesis
anesthesia
diagnostic
erect position
kit
preparation
therapeutic
ultrasound-guided
Thoracic cage, anatomy
Thoracic ultrasound
advantages
diaphragmatic reflections, Video 9-8
healthy thorax
key anatomic structures, identification
M-mode (motion mode)
pathologic findings
positioning
probe orientation
probe selection
systematic approach
two-dimensional (B-mode), findings
Thromboembolism. See also Deep venous thrombosis (DVT);
Pulmonary embolism (PE)
femoral vein access
Thrombolysis, for pulmonary embolism
Thrombosis
femoral vein access
Tidal volume, and evaluation of fluid responsiveness
Time gain compensation (TGC)
controls
Tissue Doppler
applications
controls
mitral annular velocity
septal and lateral mitral annulus
Tissue harmonic imaging
Trabecula(e)
Transcranial Doppler, pediatric patient
Transducer(s)
cardiac
covering, and infection control
curvilinear
echocardiography, in adults
endocavitary
linear
high-frequency
movements
overhand grip
pediatric patients
phased-array
rock (scan) movement
rotating
selection
clinical indications
slide (pan, translate) movement
sterilization/decontamination
tilt (fan) movement
tripod grip
vascular access, pediatric patient
wave frequency
Transesophageal echocardiography (TEE)
cardiac arrest, Video 20-6
cardiopulmonary resuscitation
certification
mechanically ventilated patients
midesophageal 4-chamber view, Video 20-6
probe temperature
Transthoracic echocardiography (TTE)
aortic dissection
cardiac arrest
focused
Trauma. See also Focused assessment with sonography in trauma(FAST)
blunt abdominal, pediatric patient
computed tomography
epidemiology
hypovolemic shock
ultrasound
Tricuspid annual motion (TAM)
Tricuspid annular plane systolic excursion (TAPSE)
Tricuspid regurgitation
assessment
color Doppler
pediatric patient
pulmonary artery systolic pressure
Tricuspid regurgitation velocity (TRV)
Tricuspid stenosis, assessment,
Tricuspid valve
annulus, M-mode imaging
inflow
Doppler velocity, respiratory-related changes
respiratory variation, and cardiac tamponade
physiology
Tripod grip, for transducer
Tube thoracostomy, ultrasound-guided
contraindications
kit
positioning
preparation
procedure
Two-dimensional ultrasound
energy output
Two-point compression ultrasound, in diagnosis of deep venous thrombosis
U
Umbilical catheter placement
Ureterovesicular junction (UVJ), stone imaging, Supplemental
images 11-6, 11-7
Urinary catheter, pediatric patient
Urosepsis
Uterus
anatomical relationship to bladder
identification
V
Valvular heart disease
severe, assessment
Valvular regurgitation. See also specific valve
color Doppler
continuous-wave Doppler imaging
evaluation
Valvular stenosis. See also specific valve evaluation
Vascular access, ultrasound-guided. See also Arterial catheterization/cannulation
pediatric patients
cephalomedial to caudolateral approach
cephalolateral to caudomedial approach
ergonomics
line placement confirmation
long-axis approach
needle tip visualization
oblique orientation
one-person procedure
out-of-plane vs. in-plane approach
positioning
short-axis approach
static vs. dynamic approach
tips and tricks
two-person procedure
Vascular dissection. See also Aortic dissection
Vascular injury
Vascular intraluminal flap
Vascular ultrasound
common abnormalities
Vasodilation, in sepsis
Vegetation(s), in infective endocarditis
Velocity, of ultrasound wave
Velocity time integral (VTI)
left ventricular outflow tract
Doppler ultrasound
right ventricular outflow tract
Venae cavae. See also Inferior vena cava; Superior vena cava diameter, respiratory variability
Venous blood flow, augmentation
Ventilator weaning, right ventricular function
Ventricle(s), cardiac. See Midventricle; Left ventricle; Right ventricle
Ventricular base, parasternal short-axis view
Ventricular elastance
Ventricular interdependence
Ventricular relaxation, diastole
Vesicouterine pouch, in FAST
Volume expansion
cardiac tamponade
Volume status, determination
limitations of echocardiography
pediatric patient
W
Wall thickness, M-mode imaging
Water bath technique, for scanning distal extremities
Wave, ultrasound
characteristics
production
propagation phenomena
Wave frequency. See Frequency
White lung
Y
Yolk sac
Z
Zamboni technique, for small bowel obstruction
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Critical Care Ultrasound: Comprehensive

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Comprehensive

Critical Care Ultrasound

All rights reserved.

Managing Editor: Katie Brobst

Printed in the United States of America

Society of Critical Care Medicine

International Standard Book Number: 978-1-620750-322

Samuel M. Brown, MD, MS, FASE, FCCM

Michael M. Blaivas, MD, FAIUM

Eliotte L. Hirshberg, MD, MS

Jan Kasal, MD, FCCM

Aliaksei Pustavoitau, MD, MHS

Srikar Adhikari, MD, MS

Samantha K. Brenner, MD, MPH

Jeff Burzynski, MD, FRCPC

Colin K. Grissom, MD, FASE, FCCM

Mark P. Hamlin, MD, MS

Brooke Hensley, MD, RDMS

Beatrice Hoffmann, MD, PhD

Michael J. Lanspa, MD, MS

Xavier Monnet, MD, PhD

Akira Nishisaki, MD, MSCE

Susanna Price, MD, PhD

Julie St-Cyr Bourque, MD, FRCPC

Jean-Louis Teboul, MD, PhD

SECT ION 1: T HE BASICS

CHAPT ER 1 Ultrasound Basics: Physics, Modalities, and Image Acquisition

SECT ION 2: T HE HEART

CHAPT ER 3 Basic Windows and Views

SECT ION 3: T HE LUNGS

CHAPT ER 9 T horacic Ultrasound: Pleural Effusion and Pneumothorax

SECT ION 4: T HE ABDOMEN

CHAPT ER 11 General Diagnostic Abdominal Sonography

SECT ION 5: PROCEDURAL GUIDANCE

CHAPT ER 13 Ultrasound-Guided Vascular Cannulation

SECT ION 6: CLINICAL PROBLEM SOLVING

SECT ION 7: LOGIST ICS

CHAPT ER 23 Ultrasound Quality Improvement, Documentation, and Billing

SECT ION 8: PEDIAT RICS

Samuel M. Brown, MD, MS, FASE, FCCM

Wave Propagation Phenomena

Figure 1-1. Image of Gallbladder with Gallstone

Figure 1-2. M-Mode Ultrasound Across Mitral Valve Leaflet Tips

Figure 1-4. Pulsed-Wave Doppler Image of Mitral Valve Inflow

Figure 1-5. Pulsed-Wave Doppler Image of Carotid Artery Flow

Table 1-1. Tuning the Doppler

1. Start with the best possible B-mode acoustic window.

Figure 1-8. Acoustic Shadowing

ULTRASOUND MACHINE CONTROLS AND IMAGE ACQUISITION

1. Choose the correct transducer type.

ULTRASOUND SYSTEM CONTROLS: KNOBOLOGY AS APPLIED PHYSICS

Figure 2-1. Incorrect Ergonomic Position

Figure 2-3. Ultrasound System Controls

Time Gain Compensation

Figure 2-4. Demonstrating the Importance of Gain on Evaluating Pleural Effusion

PULSED-WAVE DOPPLER CONTROLS

Figure 2-8. Examples of Aliasing

Figure 2-9. Continuous-Wave Doppler