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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

ab
=
18 Aortic andPulmonic Regurgitation
Fig. 18.11 Color ow
Doppler (CFD) of severe
pulmonary regurgitation
(PR). (Figure courtesy
of Department of
Anesthesiology and
Critical Care at Baylor
St. Luke’s Medical
Center—Texas Heart
Institute. Permission to
use obtained)
253
Fig. 18.12 (a) Pulse wave (PW) Doppler of the RVOT.
(b) RVOT diameter measured from the parasternal short
axis aortic view focused on the pulmonary valve. (Figure
LVOT and subtract them [2] (Fig. 18.12). The
RVOT diameter can be measured in the parasternal short-axis inow-outow view and the pulse
wave Doppler at the RVOT will provide VTI
courtesy of Department of Anesthesiology and Critical
Care at Baylor St. Luke’s Medical Center—Texas Heart
Institute. Permission to use obtained)
RF less than 20% is mild PR and greater than
40% is considered a severe PR [2]. Unfortunately,
the cut-off values for regurgitant volume and RF
are not well validated.
measurement. This method is challenging due to
the difculties of obtaining an adequate view and
measuring the RVOT diameter [2].
RVOT stroke volumeRVOT area
RVOT VTI
×
The RF can also be calculated using the regurgitant volume and the RVOT stroke volume. The
Continuous Wave Doppler: Jet
Density, Pressure Half-Time, PR Index
Similar to the AR, the density of the PR jet is
proportional to the number of red blood cells
through the PV.This can be evaluated with CW

254
PR
= AB
Fig. 18.13 Continuous
wave (CW) Doppler of
the pulmonary valve
showing severe
PR.Note the density of
the regurgitant ow and
the equalization of both
inow and outow
Doppler, which is very
classic for severe PR.
(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
Doppler in the parasternal short-axis view and
the subcostal short-axis view (Fig. 18.13).
Shortened deceleration rate can be measured
with the PHT can also be calculated using the
CW Doppler and <100ms is considered accurate
(high sensitivity and specicity) for severe PR
[2]. Severe PR can be suspected if there is cessation of ow before end diastole. One of the limitations of this measurement is the poor
visualization and alignment of Doppler.
Furthermore, RV and PA pressure differences
especially due to the RV diastolic dysfunction
can affect the PHT.
Lastly, the PR index can be calculated using
the CW Doppler and it has a high diagnostic
accuracy. This needs complete forward and
regurgitant ow on CW Doppler, which can be
challenging to obtain depending on the available window. However, this is a more advantageous measurement since it uses both PR
duration and duration of diastole and accounts
for the pressure differences between PA and RV
[2] The disadvantage is that it does not distinguish between moderate and severe PR.The PR
index less than 0.77 is considered moderate-tosevere PR [2].
Index
/
include the size of the regurgitant orice, the
hydraulic impedance/afterload, and the right ven-
tricular diastolic compliance, and the right ven-
tricular diastolic lling time. Indeed, the degree
of regurgitant volume depends proportionally
upon the RV size and stroke volume [5]. Thus,
the evaluation of RV systolic and diastolic func-
tion should be included in the PR assessment.
• Chronic aortic regurgitation is more prevalent
in older male patients, but rarely is the admission diagnosis to the intensive care unit.
• Acute aortic regurgitation is life-threatening
and caused by systemic or specic structural
valve disease that requires urgent surgical
intervention.
• Pulmonary regurgitation is more recognized
following surgical repair of congenital heart
disease.
• A methodic echocardiographic approach to
aortic and pulmonary regurgitations includes
initial two-dimensional assessment (i.e., lack
of leaets coaptation, recognition of mobile
masses) followed by CFD (regurgitant ow in
diastole), PWD, and CWD to determine quantitation of regurgitant volume.

18 Aortic andPulmonic Regurgitation
1. Which of the following echocardiographic
ndings is consistent with severe acute aortic
regurgitation:
A. Globular, spherical shape of the left
ventricle
B. Fluttering of the anterior mitral leaet
C. Late opening of the aortic valve
D. Left atrial dilation
E. Eccentric left ventricular hypertrophy
Answer: B.Although uttering of the anterior mitral leaet has a sensitivity of 41%, yet
its specicity is up to 81%, especially in grade
3 to 4+ AR.The positive predictive value is
92%. The following echocardiography ndings (globular, spherical shape of the left ventricle, eccentric left ventricular hypertrophy,
left atrial dilation) are ndings commonly
seen in chronic aortic regurgitation. Early
rather than late opening of the aortic valve is
seen in aortic regurgitation.
2. The following biplane TEE clip (Fig.18.14)
was obtained in a patient with suspected aortic regurgitation admitted to the ICU with
acute respiratory failure. The
echocardiographic nding in the mid-esophageal long-axis view is the most suggestive of:
A. Thickened bicuspid aortic valve
B. Rheumatic aortic valve
255
C. Tricuspid aortic valve with abnormal
coaptation
D. Degenerative bicuspid aortic valve
E. Nonbacterial thrombotic endocarditis of
the aortic valve
Answer: C.In this mid-esophageal longand short-axis echocardiographic view, the
utilization of biplane modality facilitates
the recognition of lack of coaptation (short
axis). A subsequent utilization of CFD in
this specific area can reveal the regurgitant
jet [6].
3. Which of the following echocardiographic
ndings is associated with severe PR and
increased pulmonary vascular resistance with
Spectral Doppler in a patient with repaired
tetralogy of Fallot:
A. PHT of 90ms
B. Narrow and short regurgitant ow with
CFD
C. Lack of late-systolic notching in RVOT
PWD evaluation
D. Lack of mid-systolic notching in RVOT
PWD evaluation
E. Atrial contraction does not induce an
anterograde forward ow
Answer: A.The pressure half-time represents the time needed for the maximum transvalvular gradient (from PA to RV in this case)
Fig. 18.14 Question 2.
(Figure courtesy of
Department of
Anesthesiology and
Critical Care at Baylor
St. Luke’s Medical
Center—Texas Heart
Institute. Permission to
use obtained)

256
J. Sohn and J. L. Diaz-Gomez
to decrease to its half value or the time interval for the peak velocity to reach 0.707 of the
peak velocity value in milliseconds. The cutoff to determine signicant PR has been suggested to be <100ms [7].
References
1. Lancellotti P, Tribouilloy C, Hagendorff A, Moura
L, etal. 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(3):223–44.
2. Zoghbi WA, Adams D, Bonow RO, EnriquezSarano M, et al. Recommendations for noninvasive
evaluation of native valvular regurgitation. J Am
Soc Echocardiogr. 2017;30(4):303–71. https://doi.
org/10.1016/j.echo.2017.01.007.
3. Walpot J, Vermeiren G, Al Mafragi A, Malbrain
MLNG. Comprehensive assessment of the aor-
tic valve in critically ill patients for the noncardiologist. Part II: chronic aortic regurgitation
of the native valve. Anaesthesiol Intensive Ther.
2021;53(1):55–68. https://doi.org/10.5114/
ait.2021.104892.
4. Maciel BC, Simpson IA, Valdes-Crus LM, etal. Color
ow Doppler mapping studies of “physiologic” pulmonary and tricuspid regurgitation: evidence for true
regurgitation as opposed to a valve closing volume. J
Am Soc Echocardiogr. 1991;4:589–97.
5. Redington A.Determinants and assessment of pulmonary regurgitation in tetralogy of Fallot: practice and
pitfalls. Cardiol Clin. 2006;24:631–9.
6. Grayburn PA, Smith MD, Handshoe R, Friedman BJ,
DeMaria AN. Detection of aortic insufciency by
standard echocardiography, pulsed Doppler echocardiography, and auscultation. A comparison of accuracies. Ann Intern Med. 1986;104(5):599–605.
7. Silversides CK, Veldtman GR, Crossin J, Merchant
N, Webb GD, McCrindle BW, et al. Pressure halftime predicts hemodynamically signicant pulmonary regurgitation in adult patients with repaired
tetralogy of Fallot. J Am Soc Echocardiogr.
2003;16(10):1057–62.

Mitral andTricuspid Stenosis
NicholasLevin andChristopherKelly
19
Learning Objectives
1. Understand the multiple ways to obtain an
estimated mitral valve area and be able to
grade the severity of mitral stenosis
2. Know the consequences of long-standing
mitral stenosis
3. Explain how to calculate a tricuspid valve
area and know the cutoff for severe stenosis
4. Review the other echocardiographic ndings
indicative of hemodynamically signicant tricuspid stenosis
Mitral Stenosis
The normal mitral valve area (MVA) is
4.0–5.0 cm2. Symptoms from mitral stenosis
(MS) usually occur when the valvular area is less
than 2.5 cm
symptoms prior to this cutoff during states of
need for increased cardiac output such as exer-
Supplementary Information The online version contains supplementary material available at https://doi.
org/10.1007/978- 3- 031- 80038- 2_19.
N. Levin (*)
Stanford University, Stanford, CA, USA
e-mail: nmlevin@stanford.edu
C. Kelly
University of Utah, Salt Lake City, UT, USA
e-mail: christopher.kelly@hsc.utah.edu
2
; however, patients may develop
cise or pregnancy. Mitral valve stenosis usually
becomes clinically signicant at rest when the
MVA is less than 1.5cm
elevated transvalvular pressure gradients with
subsequent left atrial pressure elevation and
eventual enlargement. A further discussion
regarding consequences of mitral stenosis is
below. Table19.1 lists the American Society of
Echocardiography cutoffs for severity based on
several criteria [1].
2
. This stenosis leads to
Etiologies
Globally, the primary etiology of mitral stenosis
is rheumatic valvular disease. This predominance
is largely due to the signicant burden that rheumatic heart disease (RHD) continues to have in
developing countries where current estimates
nd that it accounts for approximately >85% of
the identied mitral stenosis [2]. Mitral stenosis
caused by RHD has a classic appearance of the
anterior leaet of the mitral valve that is often
described as a “hockey stick” as seen in Video
19.1. In developed countries, RHD carries a substantially smaller burden of disease. Other nonrheumatic causes include mitral annular
calcication (MAC), radiation valvulitis, and
systemic inammatory processes such as rheumatoid arthritis and lupus. Congenital MS is
exceedingly rare and accounts for approximately
1% of mitral stenosis etiologies. Congenital
© 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_19
257

258
S
32
()=()
×
()
SVS
12
=
LV
IV
×=×
M
I
M
()
=
()
N. Levin and C. Kelly
Table 19.1
mean gradient, and pulmonary artery pressure
Valve area (cm
Mean gradient (mmHg) <5 5–10 >10
Pulmonary artery pressure
(mmHg)
a
60–80beats/min in sinus rhythm (Circulation Volume 129, Number 23, March 3, 2014)
abnormalities include cor triatriatum, supravalvular mitral ring, double-orice mitral valve, and
parachute mitral valve. Additional functional
causes of MS include cardiac masses such as
myxomas or valvular vegetations such as endocarditis [3, 4].
American Society of Echocardiography guideline cutoffs for degree of mitral stenosis based on valve area,
2
) >1.5 1.0–1.5 <1.0
Mild Moderate Severe
<30 30–50 >50
surements acquired from the LVOT. A basic
formula derivation is provided below. The needed
variables include the cross-sectional area and
velocity time integral (VTI) of the LVOT as well
as the VTI of the diastolic mitral valve inow. An
example of obtaining and measuring the mitral
valve VTI is demonstrated in Fig.19.3.
Quantication ofMitral Valve Area
Planimetry
Direct planimetry can be utilized with 2D or 3D
VcmAreacmVTI cm
OT LVOT MVAMV
AREA VT
echocardiography imaging to calculate the anatomic mitral valve area. A short-axis view of the
mitral valve during mid-diastole is obtained and
the smallest orice is then traced using the inner
contours (Fig.19.1). To optimize this measurement, biplane imaging can be used to nd the
optimal location and it is recommended to use the
lowest gain possible to dene the orice area. In
several studies, these measurements have been
equation to solve for the MVA is when there is
concurrent aortic or mitral regurgitation.
Additionally, in patients with underlying atrial
brillation, the continuity equation should not be
utilized as the primary MVA assessment [1, 6].
VA LVOT
=×
AREA
An important caveat to using the continuity
well validated to surgical and cardiac catheter
determined areas. Calculations based on 3D
echocardiography images have also been found
to be more accurate than those based on 2D
images as it can be difcult to ensure measurement at the true tips of the leaets (Fig.19.2) [5].
Pressure Half-Time
A quantitative approach using doppler measurements for MVA calculation is that of pressure
half-time (PHT). This approach utilizes the concept that the rate of pressure decline across a valve
is related to the cross-sectional area of the valve,
Continuity Equation
The continuity equation, as previously described
in Chap. 17, assumes a conservation of stroke
volume (SV) throughout the various chambers
and valves of the heart. Diastolic stroke volume
across the mitral valve is assumed to equal systolic stroke volume across the left ventricular
outow tract (LVOT). We can use this assumption to then determine the MVA utilizing mea-
i.e., the smaller the cross-sectional area, the slower
the decline in pressure [7]. Pressure half-time is
dened as the length of time in milliseconds for
the maximal early diastolic trans- mitral pressure
gradient to reach one-half its value as demonstrated in Fig.19.4. An equation was derived for
calculating the MVA from the PHT [8]:
VA cm PHTms
2
220
V
LVOTVT
MVVTI
/
TI

19 Mitral andTricuspid Stenosis
Fig. 19.1 2D
parasternal short-axis
view with tracing of
mitral valve orice area.
(Image courtesy of
University of Utah
Division of
Echocardiography and
Perioperative Ultrasound
database)
Fig. 19.2 3D
parasternal short-axis
view with tracing of
mitral valve orice area.
Accompanying Video
19.2. (Image courtesy of
University of Utah
Division of
Echocardiography and
Perioperative Ultrasound
database)
259
Important Considerations and
Caveats [6]
Atrial brillation: In patients with atrial brillation, an average PHT should be calculated by
averaging at least ve cardiac cycles.
Co-existing aortic regurgitation: In patients
with concomitant aortic regurgitation, trans-
mitral lling may be affected due to retrograde
lling from the aortic regurgitation or via direct
impairment of mitral valve opening secondary to
the retrograde aortic regurgitant jet. Special
attention should be made to the aortic valve in
patients with mitral stenosis in order to accurately assess the degree of mitral stenosis.

260
Fig. 19.3 Continuous
wave Doppler through
the mitral valve. Two
mitral valve velocity
time integral
measurements are
traced. (Image courtesy
of University of Utah
Division of
Echocardiography and
Perioperative Ultrasound
database)
N. Levin and C. Kelly
Fig. 19.4 Mitral inow waveform demonstrating measurement location for pressure half-time (PHT) and deceleration time (DT). The mitral valve area using PHT is
calculated by the formula MVA=220/PHT which in this
example would be 220/103 (in ms) = 2.14 cm
2
Alternatively, if one used the DT of 351ms and applied it
to the formula MVA = 759/DT, one would calculate the
MVA as 2.16cm
2
which is congruent with the PHT calculation. (Image courtesy of University of Utah Division of
Echocardiography and Perioperative Ultrasound
database)
.

M
()
=
()
PH
sD
()
=×
()
19 Mitral andTricuspid Stenosis
261
Left ventricular Diastolic Dysfunction: Due to
abnormal LV relaxation in patients with diastolic
dysfunction, the PHT may be affected in either
direction.
Deceleration Time
An alternative and complimentary approach for
MVA using the same mitral inow waveform as
PHT is that of deceleration time (DT). DT is
dened as the time, in milliseconds, from peak
mitral inow E-wave velocity to the end of ow
(i.e., when mitral inow velocity= 0 cm/s) as
shown in Fig. 19.5. A formula was derived to
convert DT to MVA:
VA cm DT ms
2
759
/
The relationship between PHT and DT is
demonstrated in the conversion formula:
Tm
029.
Tms
Often times if mitral inow waveform denition allows, both PHT and DT are obtained.
Figure19.4 demonstrates an example of obtaining both measurements.
Qualication ofMitral Valve Stenosis
Severity
There are three categories of assessment to determine mitral valve stenosis severity as dened by
the American Society of Echocardiography and
shown in Table 19.1. This chapter has already
covered the several ways for obtaining a mitral
valve area, and additional chapters have shown
how to obtain an estimated pulmonary artery
pressure. We will therefore focus on the third and
nal severity assessment, that of mean transmitral pressure gradient.
Mean Pressure Gradient
A pressure gradient is the difference in pressure of
two chambers at any one time across a valve and
can be expressed as both the maximum pressure
gradient and the mean pressure gradient. For qualication of mitral valve stenosis severity, the mean
pressure gradient is utilized. The more stenotic the
mitral valve is, the higher the mean pressure gradient will be. Pulsed or continuous wave doppler
through the mitral valve can be utilized. A parallel
Fig. 19.5 Mitral inow
waveform demonstrating
how to obtain a
deceleration time. Using
this value, the estimated
MVA for this patient
would be 759 divided by
521ms resulting in a
MVA of 1.46cm
(Image courtesy of
University of Utah
Division of
Echocardiography and
Perioperative Ultrasound
database)
2
.

262
N. Levin and C. Kelly
intercept angle with regard to direction of blood
ow is needed to ensure accurate velocity measurements and subsequently accurate pressure gradient calculations. It is therefore possible to have
eccentric jets that makes obtaining true parallel
ow assessment difcult. An example of obtaining
the maximum and mean mitral valve pressure gradients is shown in Figure19.3[1, 4, 9].
Consequences ofLong-Standing
Mitral Stenosis
The consequences of mitral stenosis follow a predictable pattern of increasing left atrial pressure.
Due to decreased left ventricular lling, left atrial
pressure increases over time causing enlargement
of the left atrium. This in turn comes with increased
risk of atrial brillation secondary to increased
atrium distension which has inherent risks with
relation to thromboembolic disease due to left atrial
thrombi. The increased left atrial pressure over
time leads to an increase in pulmonary pressures.
This in turn may lead to the cascade of right ventricular dilation, resultant tricuspid insufciency,
and ultimately right ventricular failure [1, 3].
Tricuspid Stenosis
A normal tricuspid is composed of three leaets,
the septal, anterior, and posterior. Normal tricuspid valve area (TVA) is 7–9cm
dient across the valve of less than 2 mmHg.
Hemodynamically signicant tricuspid stenosis
typically occurs with the valve area is less than
1 cm2. As the valve becomes increasingly stenosed, patients often present with sequela of
increased venous congestion including fatigue,
edema, and congestive hepatopathy. Without
other valve involvement, patients rarely present
with symptoms of dyspnea [1].
2
with a mean gra-
extremely rare. Primary etiologies are rheumatic
heart disease (RHD), carcinoid syndrome, autoimmune, metastatic processes, and complications
from valvular prosthesis. Most often, tricuspid
stenosis is combined with another valvular
pathology. This can involve another valve (e.g.,
RHD will almost always have concurrent mitral
stenosis) or a combined pathology with the tricuspid valve (e.g., in carcinoid syndrome there is
almost always concurrent tricuspid regurgitation). Additionally, large valvular vegetations
such as myxomas on the tricuspid valve can cause
a relative valvular stenosis [1, 10].
Planimetry
Quantication of the tricuspid valve area can be
measured by direct visualization by utilizing 3D
echocardiography but the practice is neither validated nor widely utilized [1].
Continuity Equation
The continuity equation can be utilized to estimate the tricuspid valve area. Similar to the
approach in mitral stenosis assessment, continuous wave doppler can be used to calculate the VTI
across the tricuspid inow. Pulmonic or aortic
valve cross-sectional area and VTI measurements
can then be used to complete the continuity equation where the tricuspid valve area can be calculated. Greater than mild concurrent tricuspid
regurgitation presents a signicant caveat to using
the continuity equation and can cause underestimation of the calculated valve area. Tricuspid
valve stenosis is considered severe when the valve
area is less than 1cm
acquisition of measurements, an inow VTI
>60cm is indicative of hemodynamically signicant tricuspid stenosis (Table19.2) [1].
2
. Additionally, during this
Etiology
Among all of the valvular stenosis, tricuspid
valve stenosis is the least common and is overall
Pressure Gradients
From a low parasternal right ventricular inow
view or from a RV-focused apical 4-chamber view,
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