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- •Preface
- •Contents
- •Contributors
- •Resolution
- •Axial Resolution
- •Lateral Resolution
- •Elevational Resolution
- •Temporal Resolution
- •The Resolution—Penetration Interplay
- •Sound Waves
- •Ultrasound
- •Pulsed Ultrasound
- •The Range Equation
- •Ultrasound Image Formation
- •Time Gain Compensation
- •M-Mode Imaging
- •The Doppler Principle
- •Doppler Imaging
- •Continuous Wave (CW) Doppler
- •Pulsed Wave (PW) Doppler
- •Color Flow (CF) Doppler
- •Tissue Doppler Imaging (TDI)
- •Pulsed Wave TDI
- •Color TDI
- •Tissue Harmonics Imaging (THI)
- •Probe Selection
- •Curved Linear Array Transducers
- •Linear Array Transducers
- •Phased Array Transducers
- •Ultrasound Artifacts (See Chap. 3)
- •Space/Time Artifacts
- •Refraction
- •Mirror Image
- •Reverberation
- •Bayonet
- •Edge
- •Attenuation Artifacts
- •Shadowing
- •Enhancement
- •Doppler Artifacts
- •Aliasing
- •References
- •Probe Selection
- •Harmonic Imaging
- •Imaging Modes
- •Color Doppler
- •Spectral Doppler
- •Tissue Doppler
- •References
- •3: Ultrasound Artifacts
- •Reverberation Artifacts
- •Comet-Tail Artifact
- •Ring-Down Artifact
- •Mirror Image Artifacts
- •Shadowing Artifact
- •Enhancement Artifact
- •Side-Lobe Artifacts
- •Refraction Artifacts
- •References
- •References
- •Parasternal Long Axis (PLAX)
- •External Surface Anatomy
- •Sonographic Anatomy
- •Imaging Tips
- •External Surface Anatomy
- •Sonographic Anatomy
- •Imaging Tips
- •External Anatomy
- •Sonographic Anatomy
- •Imaging Tip
- •Parasternal Short Axis (PSAX)
- •External Anatomy
- •Sonographic Anatomy
- •Scanning Tips
- •Suprasternal/Supraclavicular View
- •External Anatomy
- •Sonographic Anatomy
- •Imaging Tips
- •6: Transthoracic M-Mode Echocardiography
- •Imaging Tips
- •Apical: A4C, A5C, A2C, A3C
- •Apical Four-Chamber View (A4C)
- •External Anatomy
- •Sonographic Anatomy
- •Scanning Tips
- •Apical Five-Chamber View (A5C)
- •External Anatomy
- •Sonographic Anatomy
- •Scanning Tips
- •Apical Two-Chamber View (A2C)
- •External Anatomy
- •Sonographic Anatomy
- •Scanning Tips
- •Apical Three-Chamber View (A3C)
- •External Anatomy
- •Sonographic Anatomy
- •Scanning Tips
- •Subcostal: SC4, SC Long Access, IVC
- •Subcostal Four-Chamber View (SC4)
- •External Anatomy
- •Sonographic Anatomy
- •Scanning Tips
- •Subcostal Long Axis IVC
- •External Anatomy
- •Sonographic Anatomy
- •M-Mode Echocardiography
- •Left Ventricular (LV) Function
- •Right Ventricular (RV) Systolic Function
- •Cardiac Valves
- •Pericardial Tamponade
- •Inferior Vena Cava (IVC) Collapsibility
- •References
- •7: Transthoracic Doppler Echocardiography
- •General Approach
- •Spectral Broadening
- •Pulse Repetition Frequency
- •Pulmonary Venous Flow (Diastolic Function)
- •Hepatic Vein Flow
- •Pulse-Wave/CW Doppler (Aorta Flows)
- •References
- •8: Transesophageal Echocardiography: Insertion, Manipulation, Risks, Complications
- •Indications
- •Post Cardiac Surgery
- •Acute Cardiopulmonary Disease
- •Hypovolemia, Fluid Responsiveness
- •Endocarditis
- •Aortic Pathology
- •Insertion
- •Manipulation
- •References
- •2D Transesophageal Imaging
- •References
- •Ultrasound Assumptions
- •Reverberation Artifact
- •Side-Lobe Artifact
- •Intravascular Devices
- •3D Ultrasound
- •Stitch Artifact
- •Right Atrium: Crista Terminalis, Eustachian Valve, Chiari Network
- •Right Ventricle-Moderator Band
- •Left Ventricle: Fibroelastoma Versus Lambl’s Excrescence
- •References
- •11: LV Systolic Function
- •Structural Anatomy
- •Left Ventricular Hypertrophy
- •LV Function: Linear Measurements
- •EPSS Method
- •Caution
- •LV Function: Ejection Fraction
- •EF (Simpson’s Biplane) Method
- •Cautions
- •LV Function: Cardiac Output
- •Regional Wall Motion Abnormalities
- •Methods
- •Strain
- •Strain Methods
- •Cautions
- •References
- •Ultrasonic Enhancement Agents (UEAs)
- •M-Mode
- •Mitral Annular Plane Systolic Excursion
- •dP/dt
- •Tissue Doppler Imaging (TDI)
- •Systolic Mitral Annular Velocity (s′)
- •References
- •13: The Right Ventricle
- •The Right Ventricle
- •Right Ventricular-Focused View
- •Semi-Quantitative Right Ventricular Assessment
- •Interventricular Septum
- •Right Ventricular Dimensions
- •Right Ventricular Wall Thickness
- •Right Ventricular Area/Volume
- •Regional Systolic Functional Assessment
- •TAPSE (Tricuspid Annulus Plane Systolic Excursion)
- •Tricuspid Annular Systolic Velocity (Right Ventricular S′)
- •Global Systolic Functional Assessment
- •Right Ventricular Fractional Area Change
- •Right-Sided Hemodynamics
- •Right Ventricular-Pulmonary Artery Coupling
- •Right Ventricular Diastolic Function
- •Right Ventricular Strain
- •Conclusion
- •References
- •Left Atrium
- •Technical Considerations
- •Left Atrial Function
- •Atrial Septum
- •Right Atrium
- •References
- •15: Left Ventricular Diastolic Function
- •Introduction
- •Diastole
- •Isovolumic Relaxation
- •Early Diastolic Filling
- •Diastasis
- •Late Diastolic Filling
- •Diastolic Function Assessment
- •Normal Pattern (Grade 0)
- •LV Relaxation Abnormality Pattern (Grade 1)
- •Pseudonormalization Pattern (Grade 2)
- •Restrictive Pattern (Grade 3)
- •Mitral Annular Motion Velocity
- •Left Atrial Volume Index (LAVI)
- •Tricuspid Regurgitation (TR) Jet Peak Velocity
- •Pulmonary Vein Flow
- •ASE Recommendation 2009
- •ASE Recommendation 2016
- •References
- •16: Cardiomyopathies
- •Dilated Cardiomyopathy
- •Hypertrophic Cardiomyopathy
- •Restrictive Cardiomyopathies
- •Arrhythmogenic Right Ventricular Cardiomyopathy/Dysplasia (ARVC/D)
- •Stress-Induced Cardiomyopathy
- •Takotsubo Cardiomyopathy
- •Neurogenic Stress Cardiomyopathy
- •Cirrhotic Cardiomyopathy
- •Noncompaction Cardiomyopathy
- •Septic Cardiomyopathy
- •References
- •17: Aortic Stenosis
- •Introduction
- •Anatomic Evaluation
- •Hemodynamic Evaluation
- •References
- •Aortic Regurgitation
- •Doppler Findings
- •Vena Contracta (VC)
- •Jet Width/Area
- •Proximal Flow Convergence
- •Pressure Half-Time (PHT)
- •Pulmonary Regurgitation
- •Color Flow Doppler Findings: Jet Width, Jet Area, Jet Length, Vena Contracta
- •References
- •Mitral Stenosis
- •Etiologies
- •Planimetry
- •Continuity Equation
- •Pressure Half-Time
- •Deceleration Time
- •Mean Pressure Gradient
- •Tricuspid Stenosis
- •Etiology
- •Planimetry
- •Continuity Equation
- •Pressure Gradients
- •Pressure Half-Time
- •Consequences
- •References
- •Causes
- •Primary Causes
- •Secondary Causes
- •Jet Area
- •Vena Contracta
- •Jet Density
- •Pressure Half-Time
- •References
- •The Bernoulli Equation
- •Intracardiac Pressures
- •Left Atrial Pressure
- •Left Ventricular End-Diastolic Pressure
- •Right Ventricular Systolic Pressure
- •Case
- •References
- •22: Prosthetic Valves
- •General Imaging Principles
- •2D Imaging
- •3D Imaging
- •Doppler Evaluation
- •Case 1
- •2D Evaluation
- •Doppler Evaluation
- •Prosthetic Aortic Valve Dysfunction: Stenosis
- •Case 2
- •Prosthetic Aortic Valve Dysfunction: Regurgitation
- •Case 3
- •Case 4
- •Prosthetic Mitral Valve Dysfunction: Stenosis
- •Case 5
- •Prosthetic Mitral Valve Dysfunction: Regurgitation
- •Case 6
- •Prosthetic Valve Endocarditis
- •Case 7
- •Prosthetic Valve Thrombosis
- •Mechanical Valve Thrombosis
- •Case 8
- •Bioprosthetic Valve Thrombosis
- •Case 9
- •References
- •23: Infective Endocarditis
- •Introduction
- •Diagnosis
- •Echocardiographic Assessment
- •Left-Sided Endocarditis
- •Right-Sided Endocarditis
- •Prosthetic Valve Endocarditis
- •References
- •24: Cardiac Tamponade
- •Clinical Criteria
- •Cardiac Chamber Collapse
- •Inferior Vena Cava Plethora
- •Spectral Doppler Flow Variation
- •References
- •25: Ultrasound-Guided Pericardiocentesis
- •Background
- •Transthoracic Echocardiogram
- •Inferior Vena Cava Plethora
- •Right Heart Chamber Systolic/Diastolic Collapse
- •Doppler Flow Velocity Changes
- •Complications
- •References
- •Pathophysiology
- •Echocardiographic Diagnosis
- •Evolving Evidence
- •Two-Dimensional Evaluation
- •Septal Motion
- •Other 2D Findings
- •Doppler Evaluation
- •Hepatic Vein Pulse-Wave Doppler
- •References
- •Introduction
- •Normal Anatomical Variants
- •Right Atrium
- •Crista Terminalis
- •Eustachian Valve
- •Thebesian Valve
- •Chiari Network
- •Coronary Sinus
- •Persistent Left Superior Vena Cava (PLSVC)
- •Patent Foramen Ovale (PFO)
- •Atrial Septal Aneurysm
- •Left Atrium
- •Left Atrial Appendage
- •Atrial Suture Line After Cardiac Transplant
- •Right Ventricle
- •Moderator Band
- •Left Ventricle
- •False Tendons
- •Extracardiac Spaces
- •Pericardial Space
- •Sinuses
- •Exogenous Devices
- •Benign Masses
- •Myxoma
- •Fibroelastomas
- •Lambl’s Excrescences
- •Reverberations
- •Mirror Image
- •Side Lobe
- •Acoustic Shadowing
- •Conclusion
- •References
- •28: Left Ventricular Thrombus Part 1
- •Introduction
- •Etiology
- •Diagnosis
- •Echocardiography Technique
- •Contrast-Enhanced Echocardiography
- •Clinical Implications
- •References
- •29: Left Ventricular Thrombus Part 2
- •LV Thrombus Recognition: Sonographic Features
- •References
- •30: Left Atrial Thrombus
- •Etiology
- •Diagnosis
- •Clinical Implications
- •References
- •31: Right-Sided Thrombus
- •Introduction
- •Etiology
- •Diagnosis
- •Clinical Implications
- •Evolving Evidence
- •References
- •Introduction
- •Aortic Dissection
- •Abdominal Aortic Aneurysm
- •Aortic Thrombus
- •Image Acquisition
- •Pitfalls
- •References
- •33: Adult Congenital Heart Disease
- •Problems Causing Increased Pulmonary Blood Flow
- •Patent Ductus Arteriosus (PDA)
- •Atrial Septal Defect (ASD)/Patent Foramen Ovale (PFO) (Unrepaired/Repaired)
- •Problems Causing Decreased Pulmonary Blood Flow
- •Ebstein’s Malformation (Unrepaired)
- •Bicuspid Aortic Valve
- •Summary
- •References
- •Further Reading
- •Scanning Technique
- •Transudative Versus Exudative Fluid
- •Malignant Fluid
- •Empyema
- •References
- •Introduction
- •Background
- •Technique
- •Conclusion
- •References
- •36: Pulmonary Edema
- •Cardiogenic Vs. Noncardiogenic
- •Lung Zones/Locations
- •References
- •References
- •38: Diaphragm
- •Introduction
- •Measurement
- •Caveats
- •Diaphragm Thickening
- •Measurement
- •Caveats
- •Diaphragm Excursion
- •Measurement
- •Caveats
- •Measurement
- •Caveats
- •References
- •Introduction
- •Thoracentesis Technique
- •Tube Thoracostomy Technique
- •Manometry
- •Procedural Complications
- •Subpleural Mass Biopsy
- •Conclusion
- •References
- •40: Ultrasound During Intubation
- •Evidence
- •Limitations
- •References
- •41: Transcutaneous Laryngeal Ultrasonography: Vocal Fold Ultrasound
- •Introduction
- •Vocal Fold Motion Abnormalities
- •Paradoxical Vocal Cord Motion Disorder
- •References
- •Concept
- •Indications
- •Limitations
- •Views
- •The Hepatorenal Recess (Morrison’s Pouch)
- •The Splenorenal Recess
- •The Pericardial Space
- •The Pelvis
- •Pathologic Findings
- •References
- •Indications
- •Limitations
- •Bladder Ultrasound
- •Bladder Volume
- •Urinary Catheters
- •Hydronephrosis
- •Pitfalls
- •Renal Blood Flow
- •References
- •Stomach
- •Liver
- •Biliary System
- •Diagnostic Applications
- •Stomach
- •Liver
- •Biliary System
- •Paracentesis
- •Technique
- •Blakemore/Minnesota Tubes
- •Gastrostomy Tube
- •References

Aortic andPulmonic Regurgitation
JacquelineSohn andJoseL.Diaz-Gomez
1. Describe the clinical signicance of aortic
regurgitation
2. Describe how the echocardiography assessment of aortic regurgitation can help characterize its severity, chronicity, and associated
cardiac or aortic pathology
3. Review two-dimensional, color ow (CF),
pulse wave (PW), and continuous wave (CW)
Doppler techniques for the comprehensive
assessment of patients with suspected aortic
regurgitation and pulmonic regurgitation
Aortic Regurgitation
The aortic valve is a tri-leaet valve composed
of three semilunar cusps. The etiology of aortic
causes: either processes affecting the valve leaflets (40%) or processes affecting the aortic root
(60%) (Table 18.1). AR is classied using the
tains supplementary material available at https://doi.
org/10.1007/978- 3- 031- 80038- 2_18.
18
adapted Carpentier classication where type I
(A)-(C) is due to aortic root causes, type I (D) is
due to aortic cusp perforation, type II is due to
cusp prolapse, and type III is due to cusp restriction (Fig.18.1) [1]. It is also important to differentiate acute versus chronic AR because there
are chronological left ventricular (LV) changes
noticeable in chronic AR.In severe acute AR,
the LV is not dilated, but an early mitral valve
(MV) closure may be seen due to the sudden
increase in LV end-diastolic pressure [2]. This
can be visualized by assessing MV in M-mode.
In chronic AR, LV is dilated with eccentric
hypertrophy and periodic TTE helps to monitor
worsening LV function and size.
AR can be quantied using various measurements. This chapter will include the Doppler ndings, vena contracta (VC), jet width and area, the
density of regurgitant jet, pressure half-time, and
ow reversal in the aorta. An initial practical diagnostic approach is to recognize the anatomic basis
for the presence of AR with 2D echocardiography,
which includes bicuspid aortic valve (Fig. 18.2),
incomplete closure of aortic valve cusps (>2mm),
aortic valve vegetation, or ascending aortic aneurysm. A summary of the echocardiographic criteria
J. Sohn
Department of Anesthesiology and Critical Care
Medicine, Texas Heart Institute at Baylor St. Luke’s
Medical Center, Houston, TX, USA
e-mail: Jacqueline.Sohn@bcm.edu
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2025
M. J. Lanspa, A. T. Levinson (eds.), Echocardiography and Ultrasonography in the ICU,
Respiratory Medicine, https://doi.org/10.1007/978-3-031-80038-2_18
J. L. Diaz-Gomez (*)
Department of Anesthesiology and Critical Care
Medicine, Baylor College of Medicine, Texas Heart
Institute at Baylor St. Luke’s Medical Center,
Houston, TX, USA
e-mail: Jose.Diaz-Gomez@bcm.edu
243

244
J. Sohn and J. L. Diaz-Gomez
Table 18.1
Etiologies of aortic regurgitation (modied from Zoghbi etal.)
Congenital Acquired
Leaet (type II) Bicuspid, unicuspid, quadricuspid Calcication, infective endocarditis, rheumatic
Ventricular septal defect
disease, radiation-induced
Aortic root (type I) Annuloaortic ectasia Idiopathic, systemic hypertension, autoimmune
Connective tissue diseases
diseases, aortitis (syphilitic, Takayasu’s arteritis),
aortic dissection, trauma
Type II Type III
Normal valves with aortic dilation
Type I
Cusp perforation Cusp prolapse Cusp restriction
abcd
Fig. 18.1 The adaptation of the Carpentier classification for aortic regurgitation (AR). (Figure courtesy of
Jacqueline Sohn, DO, Department of Anesthesiology
and Critical Care at Baylor St. Luke’s Medical
Center—Texas Heart Institute. Permission to use
obtained)
Fig. 18.2 2D-TTE image of bicuspid aortic valve.
The bicuspid aortic valve must be assessed in parasternal short-axis view during systole because it may
appear tricuspid when closed during diastole. The
characteristic appearance of oval-shaped valve open-
ing can be seen during systole in bicuspid aortic
valve. (Figure courtesy of Department of
Anesthesiology and Critical Care at Baylor St.
Luke’s Medical Center—Texas Heart Institute.
Permission to use obtained)

18 Aortic andPulmonic Regurgitation
245
Table 18.2
for a severe aortic regurgitation (AR) [2, 3]
Vena Contracta>0.6cm
Jet width/LVOT width≥65%
Jet area/LVOT area≥60%
Regurgitant volume≥60mL
Regurgitant fraction≥50%
EROA≥0.3cm
Pressure half-time<200ms
Holodiastolic ow reversal in the abdominal aorta
Holodiastolic ow reversal in descending thoracic aorta
Abnormal or ail or wide coaptation defect
Summary of the echocardiographic criteria
2
for a severe AR can be found at the end of the section (Table18.2).
Doppler Findings
Doppler ndings are essential in the evaluation of
AR.For the evaluation of AR, color ow Doppler
(CFD), pulsed wave (PW), and continuous wave
(CW) Doppler are used. The PW Doppler can be
used to assess the regurgitant ow in the aorta
and CFD can be used to assess the signal density
and the pressure half-time, which all will be discussed later in the chapter. In addition, PW
Doppler can be helpful to determine increased
left ventricular outow tract (LVOT) velocity
(>1.5m/s) and velocity-time integral (>40cm),
which indicate signicant AR.Furthermore, PW
Doppler can determine shortened deceleration of
the mitral inow (<140ms), increased E/A ratio,
and diastolic mitral regurgitation in severe AR.In
this section, we will discuss the use of the CFD.
The AR is seen in diastole with the CFD originating from the aortic valve. It is evaluated in all
three views apical, parasternal long, and short
axis with the apical view being the most sensitive
for detection of AR (Fig.18.3/Video 18.1) [2].
However, the parasternal views are preferred due
to the better axial resolution [1]. There are three
components to the color jet: ow convergence,
VC, and jet area. The jet length of AR is not a
reliable parameter because it is variable depending on the diastolic blood pressure. The AR jet
usually lasts throughout diastole, but it can be
brief and lower in velocity in acute AR.
Vena Contracta (VC)
portion of the regurgitant jet measured from the
regurgitant orice [1]. For AR, VC is measured in
the parasternal long-axis zoomed-in view and
measured where it is perpendicular to the color
ow to obtain the most accurate VC measurement. Furthermore, to properly identify the VC,
the plane should show all three components of
the regurgitant jet: ow convergence, VC, and
resolution is also maximized by reducing the
color sector size and imaging depth as narrow as
possible. If the VC is measured less than 3mm,
then it is considered mild, and if it is greater than
6 mm, then it is considered severe [2]. For
intermediate values (3–6mm), more quantitative
methods are recommended. The VC is relatively
independent of ow rate and driving pressure, but
it is limited by the lateral resolution of color
Doppler, dynamic orice, multiple jets, bicuspid
valve, and non-circular orice [1, 2].
it is less dependent on technical factors.
Jet Width/Area
The jet width is used to assess the severity of
AR. The ratio of the color jet diameter in the
LVOT and the diameter of the LVOT is calculated
using the parasternal long-axis view and ideally
zoomed to the aortic valve. The LVOT diameter
and the jet width within 1cm of the vena contracta are measured (Fig. 18.5). If the ratio is
≤25%, it is considered a mild AR, and if the ratio
is ≥65%, then it is considered a severe AR.
Although this is an easy and fast measurement to
quantify AR, it can underestimate AR in eccentric jets and overestimate it in central jets. It is
also affected by the size and the measurement of
the LVOT [2].
The jet area can be also used similarly to the
jet width. The ratio of the jet area and the LVOT
area can be used to assess the severity of AR.Both
variables are obtained using the short-axis aortic

246
ab
cd
J. Sohn and J. L. Diaz-Gomez
Fig. 18.3 (Video 18.1) Assessment of Aortic regurgitation in various TTE views. (a) Parasternal long-axis
view, (b) parasternal short-axis view, (c) apical threechamber view, (d) apical ve-chamber view. (Figure
Fig. 18.4 An example
of jet area, vena
contracta (VC), and ow
convergence. This can
be also obtained in
parasternal long-axis
view. (Figure courtesy
of Department of
Anesthesiology and
Critical Care at Baylor
St. Luke’s Medical
Center—Texas Heart
Institute. Permission to
use obtained)
courtesy of Department of Anesthesiology and Critical
Care at Baylor St. Luke’s Medical Center—Texas Heart
Institute. Permission to use obtained)

18 Aortic andPulmonic Regurgitation
Fig. 18.5 Measurement
of LVOT diameter
(LVOTd) and aortic
regurgitation jet width
(pink) in TEE midesophageal long-axis
view. This can also be
measured in TTE
parasternal long axis and
apical three-chamber
view. (Figure courtesy
of Department of
Anesthesiology and
Critical Care at Baylor
St. Luke’s Medical
Center—Texas Heart
Institute. Permission to
use obtained)
view and zoomed to the aortic valve. Trace the
area of the aortic valve and the jet area at the narrowest point (Fig.18.6). If the ratio is <5%, then
it is considered a mild AR, and if the ratio is
≥60%, then it is considered severe. The pitfall of
using jet area and LVOT area for quantifying AR
is that the direction and shape of the AR jet can
overestimate or underestimate the actual jet area
since it is a 2D image of a 3-D structure [2].
247
estimate AR in eccentric and central jets, respectively. The direction of the jet may overestimate
or underestimate the jet area.
Proximal Flow Convergence
The proximal ow convergence can be obtained
in both apical ve-chamber and parasternal longaxis views. The aortic valve is zoomed into the
view and the Nyquist limit baseline is adjusted in
the direction of ow to make a better hemisphere
view (Fig.18.7) [2]. Proximal isovelocity surface
area (PISA) represents the aliasing region surface
area. Using the continuity equation, it is assumed
that the ow through the aliasing region, PISA
shell, is equal to the ow through the orice area.
Fig. 18.6 The parasternal short-axis aortic view is
obtained and trace the area of the aortic valve and the jet
area at the narrowest point to measure the jet area. (Figure
courtesy of Department of Anesthesiology and Critical
Care at Baylor St. Luke’s Medical Center—Texas Heart
Institute. Permission to use obtained)
It is a rapid qualitative assessment of the aortic
regurgitant jet and is used for estimated regurgitant orice area (EROA) calculation.

248
2
π
rV V
=×
()
EROA
π
rV
V
=
=
()
=
Fig. 18.7 The Proximal
isovelocity surface area
(PISA) can be obtained
in both apical vechamber and parasternal
long-axis views. The
Nyquist limit must be
adjusted to obtain the
hemisphere view.
(Figure courtesy of
Department of
Anesthesiology and
Critical Care at Baylor
St. Luke’s Medical
Center—Texas Heart
Institute. Permission to
use obtained)
if non-hemispheric shape.
Regurgitant Orice Area by PISA
Using the proximal ow convergence method,
the regurgitant ow rate is calculated using the
PISA radius and Nyquist limit. The equation for
the regurgitant ow rate at the PISA ring is
2πr2Vn, where the r is the PISA radius and Vn is
the Nyquist limit. Then, using the continuity
equation, the EROA can be calculated.
2
EROA at the orifice
n
The peak AR velocity (cm/s) is obtained using
CW Doppler at the AV on the apical ve-chamber
view. The regurgitant orice area (ROA, cm2)
less than 0.1 cm2 is considered mild AR, and
greater than or equal to 0.3 cm2 is considered
severe AR.
max
2
2
2
cm
=
()
max
n
J. Sohn and J. L. Diaz-Gomez
multiplied by VTI to calculate the regurgitant volume. The VTI is obtained using CW Doppler of
the regurgitant jet (Fig.18.10). Mild AR is considered regurgitant volume less than 30 mL and
severe AR is considered as regurgitant volume
greater than or equal to 60mL. Another way to
calculate regurgitant volume is to subtract volume
across the mitral valve from the volume across the
LVOT assuming that there is no mitral
regurgitation.
LVOT stroke volumeLVOT area
LVOT VTI
×
MV stroke volumeMVarea
MV VTIatannulus
×
Regurgitant volumeLVOT volume
-MVvolume
measurement of the mitral annulus can be challenging; if there is concomitant MR, the pulmonic stroke volume (using the right ventricle
outow tract diameter and PR VTI) is used for
forward stroke volume.
can result in substantial errors in EROA
The regurgitant volume can be also calculated
using the stroke volume method. EROA can be
Lastly, the regurgitant fraction (RF) is another
quantitative parameter that can be calculated
using the regurgitant volume. RF less than 30% is

RF
=∗100
18 Aortic andPulmonic Regurgitation
Fig. 18.8 Aortic
regurgitation (AR)
viewed using continuous
wave (CW) Doppler.
The density of the CW
Doppler signal
correlates with the AR
volume. It suggests
severe AR, if the density
of the regurgitant ow is
similar to the antegrade
ow as shown in the
gure. (Figure courtesy
of Department of
Anesthesiology and
Critical Care at Baylor
St. Luke’s Medical
Center—Texas Heart
Institute. Permission to
use obtained)
considered mild, and RF greater than or equal to
50% is considered severe AR.
249
Pressure Half-Time (PHT)
Regurgitant Volume
%
()
LVOT Stroke Volume
The Density ofRegurgitant Jet
A qualitative assessment of the AR jet can be
performed using CFD. The CFD can be
imaged in various standard views including
apical five- chamber (A5CH), apical threechamber (A3CH) or apical long-axis, and
parasternal long-axis view (Fig. 18.3/Video
18.1). The signal intensity correlates to the
number of red blood cells contributing to the
regurgitant flow [2, 3]. The denser the CW
Doppler signal, the greater the AR volume. If
the density of the regurgitant flow is similar
to the antegrade flow, this suggests severe AR
(Fig.18.8).
Another semi-quantitative method to assess AR
jet is the measurement of the jet deceleration rate
or pressure half-time (PHT). It is measured using
the CW Doppler at the apical window. Eccentric
jet can be also measured from the parasternal window [2]. There should be a complete spectral
envelop to measure the PHT. PHT is the time it
takes for the peak pressure to drop to half of its
value [3] (Fig.18.9). It is a sign of pressure relation between the aorta and the left ventricle. The
PHT is more accurate in acute AR than chronic
AR because LV remodeling and change in diastolic pressure will affect the pressure half-time
and will not reliably reect the severity of AR.As
the severity of AR increases, the aortic diastolic
pressure decreases, and the LV end-diastolic pressure increases. Thus, in acute AR where the
remodeling has not occurred yet, the late diastolic
jet velocity is reduced and the PHT is shortened.

250
Fig. 18.9 Pressure
half-time (PHT)
measured using the CW
Doppler. If
PHT<200ms, it
suggests severe AR.
(Figure courtesy of
Department of
Anesthesiology and
Critical Care at Baylor
St. Luke’s Medical
Center—Texas Heart
Institute. Permission to
use obtained)
Fig. 18.10 Holodiastolic reversal seen in
the descending aorta
suggesting severe AR.
(Figure courtesy of
Department of
Anesthesiology and
Critical Care at Baylor
St. Luke’s Medical
Center—Texas Heart
Institute. Permission to
use obtained)
J. Sohn and J. L. Diaz-Gomez
On the other hand, chronic LV adaptation to AR
will normalize the PHT [1, 3]. PHT greater than
500 ms is considered mild AR and less than
200ms meets the criteria for severe AR [3].
Flow Reversal intheAorta
Recognition of Holodiastolic ow reversal with
PW in the descending aorta (an initial velocity > 0.6 m/s, VTI > 15 cm, and end-diastolic
velocity>20cm/s) and abdominal aorta indicate
severe AR [2, 3]. The abdominal aorta can be
visualized in the subcostal view and the holodiastolic ow reversal in the abdominal aorta has
100% sensitivity and 97% specicity [3]
(Fig.18.10). The aortic arch can be visualized in
the suprasternal view and although not as sensitive and specic as the abdominal aorta, holodiastolic ow reversal in the descending aorta
suggests severe AR.Both color Doppler and PW
Doppler can be used to assess the holodiastolic

18 Aortic andPulmonic Regurgitation
251
Table 18.3
A left-to-right shunt across a patent ductus arteriosus
Reduced compliance of the aorta in the elderly
An upper extremity arteriovenous stula
A ruptured sinus of Valsalva
Aortic dissection with the diastolic ow into the false lumen
Table 18.4
PR
Anatomic structure of interest TTE view TEE view
Pulmonic valve/RVOT Parasternal long-axis view Mid-esophageal RV inow-outow
Pulmonic valve/RVOT
inow-outow
ow reversal. This has to be assessed with caution, however, because other etiologies can cause
holodiastolic ow reversal in the absence of AR
(Table18.3). Furthermore, in an acute severe AR
or bradycardia, there may be a ow reversal that
Other conditions that can cause holodiastolic ow reversal in the absence of AR [2]
TTE and TEE views for an integrated multiparametric assessment ensuring a comprehensive approach to
view
Upper esophageal aortic arch
short-axis view
Parasternal short-axis view Trans-gastric RVOT and pulmonary
Subcostal view—short axis
artery views
echocardiography (TEE) usually is performed
when additional structural and functional details
is needed (Table18.4).
Trace to mild PR is a common nding
reported in about 75% of the population. The
is NOT holodiastolic due to the pressure equalization in the aorta and the LV before the end
diastole [2].
with three cusps that are thinner than the aortic
valve cusps. Primary PR is commonly due to
congenital disease or after balloon valvulo-
plasty for pulmonic stenosis. Acquired PR is
mal descending aorta is less reliable in older
patients given their lower aortic compliance.
Also, it may be seen in other conditions—cerebral arteriovenous stula, upper extremity dialysis stula, ruptured sinus of Valsalva aneurysm,
and congenital heart disease (patent ductus arteriosus) without severe AR.
rare but can be seen in patients with rheumatic
heart disease, endocarditis, carcinoid valve dis-
ease, or pergolide-induced disease [2].
Secondary PR is seen in patients with elevated
pulmonary artery (PA) pressure with dilated
pulmonary artery and normal structured PV [1,
2]. Chronic severe PR can lead to right ventri-
cle (RV) dilation and dysfunction. Primary PR
can lead to RV dysfunction similar to the vol-
Pulmonary Regurgitation
ume overload pattern of the septum [2].
However, there are many other etiologies for
Initial echocardiographic assessment of pulmonary regurgitation (PR) should include information on cusp morphology anomalies (i.e., bicuspid
or quadricuspid valves, hypoplasia, or even
absence of pulmonary valve) and motion (doming
or prolapse) with the utilization of transthoracic
echocardiography. Moreover, transesophageal
RV dilation and dysfunction, and therefore, it is
not a specic sign of severe PR.Dilation may
be localized to the RV outow tract (RVOT),
which can be seen in the Tetralogy of Fallot
(TOF) repair. A summary of the echocardio-
graphic criteria for a severe PR can be found at
the end of the section (Table18.5).

252
J. Sohn and J. L. Diaz-Gomez
Table 18.5
for a severe pulmonary regurgitation (PR)
VCW/pulmonary artery annulus>0.7
Color jet width occupies>65% of the RVOT
Regurgitant volume≥115mL
Regurgitant fraction≥40%
EROA≥115mm
Pressure half-time<100ms
PR index<0.77
Summary of the echocardiographic criteria
2
graphic assessment techniques for other valvular
heart disease, the specic PR severity criteria are
less validated due to the limited number of
patients studied with signicant pulmonary
regurgitation [1]. Only two pulmonic valve cusps
can be visualized simultaneously unless a biplane
(X-plane) modality is used.
Color Flow Doppler Findings: Jet Width, Jet Area, Jet Length, Vena Contracta
Width (VCW) and PV annular diameter ratio is
another quantitative measurement for PR sever-
ity. However, it can underestimate PR in eccen-
tric jets and overestimate in central jets. The
ratio>0.7 is considered a severe PR.Vena con-
tracta relies on an assumption of a circular/ellip-
tical regurgitant ow and only the TEE modality
can modestly increase the reliability of PR esti-
mation in those cases without circular/elliptical
regurgitant ow.
should include increasing frame rate, reducing
the color sector size and image depth, and opti-
mizing of color/gain scale including a Nyquist
limit of 60 s/min. Of note, estimation of PR
severity only based on CFD can be misleading
because it is the pressure gradient between the
PA and the RV, which determines the PR jet.
Thus, whenever equalization between diastolic
pulmonary and RV pressures occurs rapidly, the
color jet can be brief and PR will be underesti-
mated [5].
There is a paucity of validation studies for quantifying PR possibly due to difculty visualizing
PR.However, many of the qualitative and quantitative measuring methods for AR can be applied
to PR.PR can be visualized using the color ow
Doppler (CFD) with a diastolic jet toward the RV
in the parasternal short-axis or the subcostal
short-axis view (Fig.18.11). If the color jet width
occupies >65% of the RVOT, then it suggests
severe PR.Furthermore, a holodiastolic jet in the
main pulmonary artery and its branches, or a jet
with wide origin, and longer (>10mm), indicates
pathologic PR [4].
VC is the most widely used semi-qualitative
assessment of PR, but the data lack validation. It
is measured in parasternal short axis or subcostal
views by visualizing the ow convergence. The
narrowest portion on the jet is measured in diastole immediately below the PV.Vena Contracta
Pulse Wave Doppler: Regurgitant
Volume, Regurgitant Fraction,
Reverse Flow inPulmonary
Artery(PA)
The EROA can also be calculated using the same
method as the AR.The EROA less than 20mm2
is considered mild, and greater than 115mm
considered severe PR. The regurgitant volume
for PV can be calculated by multiplying the 3D
measured VC with the VTI of the PR jet [1]. The
regurgitant volume less than 15mL is considered
mild PR and greater than 115mL is considered
severe PR [2]. The peak velocity and VTI across
the RVOT increase with moderate-to-severe
PR.Indeed, the pulmonic systolic ow is signicantly increased compared to the systemic ow.
Another way to measure the regurgitant volume
is to calculate the stroke volumes of RVOT and
2
is
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