The document provides guidelines for common cardiac measurements included in an echocardiography report. It discusses measurements for structures like the left ventricle, left atrium, right ventricle, and valves. Specific measurements are outlined for assessing things like ventricular size, wall thickness, function, volumes, shunts, prosthetic valves, and more. Diagrams are included to demonstrate how to take measurements in different echocardiography views.
Recommendations for Cardiac Chamber Quantification by Echocardiography in Adults: An Update from the American Society of Echocardiography and the European Association of Cardiovascular Imaging
Hemodynamic monitoring of critically ill patientsV4Veeru25
Hemodynamic monitoring measures the blood pressure inside the veins, heart, and arteries. It also measures blood flow and oxygen proportion in the blood. Monitoring hemodynamic events provides information about the adequacy of a patient's circulation , perfusion, and oxygenation of the tissues and organ systems. The effectiveness of hemodynamic monitoring depends both on available technology and on physician ability to diagnose and effectively treat the disease
Recommendations for Cardiac Chamber Quantification by Echocardiography in Adults: An Update from the American Society of Echocardiography and the European Association of Cardiovascular Imaging
Hemodynamic monitoring of critically ill patientsV4Veeru25
Hemodynamic monitoring measures the blood pressure inside the veins, heart, and arteries. It also measures blood flow and oxygen proportion in the blood. Monitoring hemodynamic events provides information about the adequacy of a patient's circulation , perfusion, and oxygenation of the tissues and organ systems. The effectiveness of hemodynamic monitoring depends both on available technology and on physician ability to diagnose and effectively treat the disease
Right Ventricle (RV) has been treated as the neglected cardiac chamber for a long time. Advent of cardiac MRI and advancements in echocardiography have facilitated the understanding of RV structure and function and elucidated its role in management and prognosis of various cardiac ailments. Further refinement of three-dimensional (3D) and strain imaging and their application to study of right ventricular structural and functional abnormalities will be helpful in early identification of cardiac pathologies and their timely intervention.
Hemodynamics in echo lab by Dr. Ranjeet S.PalkarRanjeet Palkar
ECHO LAB AND CARDIOVASCULAR HEAMODYNAMICS. A simple cost effective,non invasive approach which when used appropriately can be boon for physicians and cardiologists in diagnosis and prognostication.
Aortic acceleration as a noninvasive index of left ventricular contractility ...Scintica Instrumentation
Key topics covered during this webinar include:
Evaluating cardiac contractility using mean or peak aortic acceleration
Investigating cardiac relaxation using mitral peak early velocity to peak atrial velocity ratio
Interpreting myocardial perfusion capacity through coronary flow reserve at baseline and with disease or other conditions
How Doppler Flow Velocity measurements can be used in translational research from mice to mammals
In a recent ground-breaking publication in Scientific Reports by Nature Research, Perez et al. highlight the use of noninvasive blood flow velocity measurements to quantify cardiac contractility as a surrogate to +dP/dt max. The article titled “Aortic acceleration as a noninvasive index of left ventricular contractility in the mouse” describes an alternate methodology to what is highly considered the gold standard for evaluating cardiac contractility and relaxation in preclinical research. The acute and terminal nature of acquiring +dP/dt using invasive blood pressure catheters is less than ideal, so finding a noninvasive surrogate is of great interest to the scientific research community.
Utilizing a Doppler Flow Velocity System (DFVS) from Indus Instruments, Dr. Reddy and his group show that peak acceleration in the ascending aorta can be used in place of invasive LVP catheters. This novel technique enables serial measurements in the same animal, which reduces animal-to-animal variability, allows for the use of fewer subjects, and decreases data collection time.
Please join us during our upcoming webinar on March 4th, 2021 at 11am EST to hear Dr. Reddy present his findings with a LIVE Q&A session at the end.
References:
Perez, J.E.T., Ortiz-Urbina, J., Heredia, C.P. et al. Aortic acceleration as a noninvasive index of left ventricular contractility in the mouse. Sci Rep 11, 536 (2021)
Right Ventricle (RV) has been treated as the neglected cardiac chamber for a long time. Advent of cardiac MRI and advancements in echocardiography have facilitated the understanding of RV structure and function and elucidated its role in management and prognosis of various cardiac ailments. Further refinement of three-dimensional (3D) and strain imaging and their application to study of right ventricular structural and functional abnormalities will be helpful in early identification of cardiac pathologies and their timely intervention.
Hemodynamics in echo lab by Dr. Ranjeet S.PalkarRanjeet Palkar
ECHO LAB AND CARDIOVASCULAR HEAMODYNAMICS. A simple cost effective,non invasive approach which when used appropriately can be boon for physicians and cardiologists in diagnosis and prognostication.
Aortic acceleration as a noninvasive index of left ventricular contractility ...Scintica Instrumentation
Key topics covered during this webinar include:
Evaluating cardiac contractility using mean or peak aortic acceleration
Investigating cardiac relaxation using mitral peak early velocity to peak atrial velocity ratio
Interpreting myocardial perfusion capacity through coronary flow reserve at baseline and with disease or other conditions
How Doppler Flow Velocity measurements can be used in translational research from mice to mammals
In a recent ground-breaking publication in Scientific Reports by Nature Research, Perez et al. highlight the use of noninvasive blood flow velocity measurements to quantify cardiac contractility as a surrogate to +dP/dt max. The article titled “Aortic acceleration as a noninvasive index of left ventricular contractility in the mouse” describes an alternate methodology to what is highly considered the gold standard for evaluating cardiac contractility and relaxation in preclinical research. The acute and terminal nature of acquiring +dP/dt using invasive blood pressure catheters is less than ideal, so finding a noninvasive surrogate is of great interest to the scientific research community.
Utilizing a Doppler Flow Velocity System (DFVS) from Indus Instruments, Dr. Reddy and his group show that peak acceleration in the ascending aorta can be used in place of invasive LVP catheters. This novel technique enables serial measurements in the same animal, which reduces animal-to-animal variability, allows for the use of fewer subjects, and decreases data collection time.
Please join us during our upcoming webinar on March 4th, 2021 at 11am EST to hear Dr. Reddy present his findings with a LIVE Q&A session at the end.
References:
Perez, J.E.T., Ortiz-Urbina, J., Heredia, C.P. et al. Aortic acceleration as a noninvasive index of left ventricular contractility in the mouse. Sci Rep 11, 536 (2021)
comprehensive presentation on 2D echo use in ICu set up. helpful in finding causes of shock and also in monitoring of fluid status in critically ill patients.
June 3, 2024 Anti-Semitism Letter Sent to MIT President Kornbluth and MIT Cor...Levi Shapiro
Letter from the Congress of the United States regarding Anti-Semitism sent June 3rd to MIT President Sally Kornbluth, MIT Corp Chair, Mark Gorenberg
Dear Dr. Kornbluth and Mr. Gorenberg,
The US House of Representatives is deeply concerned by ongoing and pervasive acts of antisemitic
harassment and intimidation at the Massachusetts Institute of Technology (MIT). Failing to act decisively to ensure a safe learning environment for all students would be a grave dereliction of your responsibilities as President of MIT and Chair of the MIT Corporation.
This Congress will not stand idly by and allow an environment hostile to Jewish students to persist. The House believes that your institution is in violation of Title VI of the Civil Rights Act, and the inability or
unwillingness to rectify this violation through action requires accountability.
Postsecondary education is a unique opportunity for students to learn and have their ideas and beliefs challenged. However, universities receiving hundreds of millions of federal funds annually have denied
students that opportunity and have been hijacked to become venues for the promotion of terrorism, antisemitic harassment and intimidation, unlawful encampments, and in some cases, assaults and riots.
The House of Representatives will not countenance the use of federal funds to indoctrinate students into hateful, antisemitic, anti-American supporters of terrorism. Investigations into campus antisemitism by the Committee on Education and the Workforce and the Committee on Ways and Means have been expanded into a Congress-wide probe across all relevant jurisdictions to address this national crisis. The undersigned Committees will conduct oversight into the use of federal funds at MIT and its learning environment under authorities granted to each Committee.
• The Committee on Education and the Workforce has been investigating your institution since December 7, 2023. The Committee has broad jurisdiction over postsecondary education, including its compliance with Title VI of the Civil Rights Act, campus safety concerns over disruptions to the learning environment, and the awarding of federal student aid under the Higher Education Act.
• The Committee on Oversight and Accountability is investigating the sources of funding and other support flowing to groups espousing pro-Hamas propaganda and engaged in antisemitic harassment and intimidation of students. The Committee on Oversight and Accountability is the principal oversight committee of the US House of Representatives and has broad authority to investigate “any matter” at “any time” under House Rule X.
• The Committee on Ways and Means has been investigating several universities since November 15, 2023, when the Committee held a hearing entitled From Ivory Towers to Dark Corners: Investigating the Nexus Between Antisemitism, Tax-Exempt Universities, and Terror Financing. The Committee followed the hearing with letters to those institutions on January 10, 202
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Read| The latest issue of The Challenger is here! We are thrilled to announce that our school paper has qualified for the NATIONAL SCHOOLS PRESS CONFERENCE (NSPC) 2024. Thank you for your unwavering support and trust. Dive into the stories that made us stand out!
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The Roman Empire A Historical Colossus.pdfkaushalkr1407
The Roman Empire, a vast and enduring power, stands as one of history's most remarkable civilizations, leaving an indelible imprint on the world. It emerged from the Roman Republic, transitioning into an imperial powerhouse under the leadership of Augustus Caesar in 27 BCE. This transformation marked the beginning of an era defined by unprecedented territorial expansion, architectural marvels, and profound cultural influence.
The empire's roots lie in the city of Rome, founded, according to legend, by Romulus in 753 BCE. Over centuries, Rome evolved from a small settlement to a formidable republic, characterized by a complex political system with elected officials and checks on power. However, internal strife, class conflicts, and military ambitions paved the way for the end of the Republic. Julius Caesar’s dictatorship and subsequent assassination in 44 BCE created a power vacuum, leading to a civil war. Octavian, later Augustus, emerged victorious, heralding the Roman Empire’s birth.
Under Augustus, the empire experienced the Pax Romana, a 200-year period of relative peace and stability. Augustus reformed the military, established efficient administrative systems, and initiated grand construction projects. The empire's borders expanded, encompassing territories from Britain to Egypt and from Spain to the Euphrates. Roman legions, renowned for their discipline and engineering prowess, secured and maintained these vast territories, building roads, fortifications, and cities that facilitated control and integration.
The Roman Empire’s society was hierarchical, with a rigid class system. At the top were the patricians, wealthy elites who held significant political power. Below them were the plebeians, free citizens with limited political influence, and the vast numbers of slaves who formed the backbone of the economy. The family unit was central, governed by the paterfamilias, the male head who held absolute authority.
Culturally, the Romans were eclectic, absorbing and adapting elements from the civilizations they encountered, particularly the Greeks. Roman art, literature, and philosophy reflected this synthesis, creating a rich cultural tapestry. Latin, the Roman language, became the lingua franca of the Western world, influencing numerous modern languages.
Roman architecture and engineering achievements were monumental. They perfected the arch, vault, and dome, constructing enduring structures like the Colosseum, Pantheon, and aqueducts. These engineering marvels not only showcased Roman ingenuity but also served practical purposes, from public entertainment to water supply.
How to Make a Field invisible in Odoo 17Celine George
It is possible to hide or invisible some fields in odoo. Commonly using “invisible” attribute in the field definition to invisible the fields. This slide will show how to make a field invisible in odoo 17.
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Synthetic Fiber Construction in lab .pptxPavel ( NSTU)
Synthetic fiber production is a fascinating and complex field that blends chemistry, engineering, and environmental science. By understanding these aspects, students can gain a comprehensive view of synthetic fiber production, its impact on society and the environment, and the potential for future innovations. Synthetic fibers play a crucial role in modern society, impacting various aspects of daily life, industry, and the environment. ynthetic fibers are integral to modern life, offering a range of benefits from cost-effectiveness and versatility to innovative applications and performance characteristics. While they pose environmental challenges, ongoing research and development aim to create more sustainable and eco-friendly alternatives. Understanding the importance of synthetic fibers helps in appreciating their role in the economy, industry, and daily life, while also emphasizing the need for sustainable practices and innovation.
The French Revolution, which began in 1789, was a period of radical social and political upheaval in France. It marked the decline of absolute monarchies, the rise of secular and democratic republics, and the eventual rise of Napoleon Bonaparte. This revolutionary period is crucial in understanding the transition from feudalism to modernity in Europe.
For more information, visit-www.vavaclasses.com
Embracing GenAI - A Strategic ImperativePeter Windle
Artificial Intelligence (AI) technologies such as Generative AI, Image Generators and Large Language Models have had a dramatic impact on teaching, learning and assessment over the past 18 months. The most immediate threat AI posed was to Academic Integrity with Higher Education Institutes (HEIs) focusing their efforts on combating the use of GenAI in assessment. Guidelines were developed for staff and students, policies put in place too. Innovative educators have forged paths in the use of Generative AI for teaching, learning and assessments leading to pockets of transformation springing up across HEIs, often with little or no top-down guidance, support or direction.
This Gasta posits a strategic approach to integrating AI into HEIs to prepare staff, students and the curriculum for an evolving world and workplace. We will highlight the advantages of working with these technologies beyond the realm of teaching, learning and assessment by considering prompt engineering skills, industry impact, curriculum changes, and the need for staff upskilling. In contrast, not engaging strategically with Generative AI poses risks, including falling behind peers, missed opportunities and failing to ensure our graduates remain employable. The rapid evolution of AI technologies necessitates a proactive and strategic approach if we are to remain relevant.
2. The following types of measurements are commonly included in a
comprehensive echocardiography report.
1) Left Ventricle:
a) Size: Dimensions or volumes, at end-systole and end-diastole
b) Wall thickness and/or mass: Ventricular septum and left ventricular posterior wall
thicknesses (at end-systole and end-diastole) and/or mass (at end-diastole)
c) Function: Assessment of systolic function and regional wall motion. Assessment
of diastolic function
2) Left Atrium:
• Size: Area or dimension
3) Aortic Root:
• Dimension
4) Right Ventricle:
a)Size: Dimensions
b)Function: Systolic and diastolic function
c)RV & pulmonary hemodynamics
5) Right Atrium:
a) Size: Dimensions, area
b) RA pressure
3. The following cardiac and vascular structures are generally be evaluated as
part of a
comprehensive adult transthoracic echocardiography report:
1) Left Ventricle (LV)
2) Left Atrium (LA)
3) Right Atrium (RA)
4) Right Ventricle (RV)
5) Aortic Valve (AV)
6) Mitral Valve (MV)
7) Tricuspid Valve (TV)
8) Pulmonic Valve (PV)
9) Pericardium
10) Aorta (Ao)
11) Pulmonary Artery (PA)
12) Inferior Vena Cava (IVC) and Pulmonary Veins
4. 6) Valvular Stenosis:
a) Valvular Stenosis: Assessment of severity, including trans-valvular gradient and area.
b) Subvalvular Stenosis: Assessment of severity, Including subvalvular gradient.
7) Valvular Regurgitation: Assessment of severity with semi-quantitative descriptive
statements and/or quantitative measurements
8) Cardiac Shunts: Assessment of severity. Measurements of QP:QS (pulmonary-to
systemic flow ratio) and/or orifice area or diameter of the defect are often helpful.
9) Prosthetic Valves:
a) Transvalvular gradient and effective orifice area
b) Description of regurgitation, if present
The following types of measurements are commonly included in a
comprehensive echocardiography report.
5. ①
This icon identifies the level 1 measurements according to ASE’s standard
guidelines
②
This icon identifies the level 2 measurements according to ASE
standard Guidelines
Clarification
6. Left Ventricle (LV)
LV Dimensions, wall thickness, LV mass: 2D Mode
Input:
- IVSd - Interventricular septal tickness at end-diastole(green)
- LVEDD - LV End-Diastolic dimension (yellow)
- PWd - PW thickness at End-Diastolic (red)
- LVESD – LV End-Systolic dimension (right image)
Output:
- LVEF %
- LVFS (Fractional Shortening )
- LV Mass
-LVMI - LV Mass Index
-RWT - Relative wall thickness
①
8. The most commonly used 2D methods for
measuring LV mass are based on the area-
length formula and the truncated ellipsoid
model, as described in detail in the 1989 ASE
document on LV quantitation. Both methods
rely on measurements of myocardial area at
the midpapillary muscle level. The epicardium
is traced to obtain the total area (A1) and the
endocardium is traced to obtain the cavity
area (A2). Myocardial area (Am) is
computed as the difference: Am = A1 - A2.
Left Ventricle (LV)
LV Mass: 2D Mode (A-L and Truncated ellipsoid method)
Input:
A1 – Area1 Pericardial border
A2 – Area 2 Endocardial border
A-L : LV length
Output:
LV Mass
LVMI – LV Mass index
①
9. LV Volumes & systolic function: Simpson method
The most commonly used 2D measurement
for volume measurements is the biplane
method of disks (modified Simpson’s rule) and
is the currently recommended method of
choice by consensus of the proper ASE
committee. The total LV volume is calculated
from the summation of a stack of elliptical
disks. The height of each disk is calculated as a
fraction (usually 1/20) of the LV long axis
based on the longer of the two lengths from
the 2- and 4- chambers view. Papillary muscles
should be excluded from the cavity in the
tracing.
Input:
LV EDD – LV End-diastolic dimension (A4C)
LV ESD – LV End-systolic dimension (A4C)
LV EDD – LV End-diastolic dimension (A2C)
LV ESD – LV End-systolic dimension (A2C)
Output:
EDV – End-diastolic volume (mL)
ESV - End-systolic volume (mL)
LVDVI – LV Diastolic volume index (mL/m²)
LVSVI – LV Systolic volume index (mL/m²)
LVEF – LV Ejection fraction %
SV – Stroke Volume (mL)
SI - Stroke Index
Left Ventricle (LV) ①
10. LV Volumes & systolic function (A-L)
As an alternative method to calculate the
LV Vol when apical endocardial definition
precludes accurate tracing is the area-
length where the LV is assumed to be
Bullet-shaped. The mid-LV cross-
sectional area is computed by planimetry
in the parasternal short-axis view and
the length of the ventricle taken from
the midpoint of the annulus to the apex
in A4C view. This measurements are
repeated in end-diastole and end-
systole. The most widely used parameter
for indexing volumes is the Body Surface
Area (BSA) in square meters.
Input:
LV diastolic CSA – Cross sectional area
LV diastolic length – A4C
LV systolic CSA
LV systolic length – A4C
Left Ventricle (LV) ②
Output:
EDV – End-diastolic volume (mL)
ESV - End-systolic volume (mL)
LVDVI – LV Diastolic volume index (mL/m²)
LVSVI – LV Systolic volume index (mL/m²)
LVEF – LV Ejection fraction %
SV – Stroke Volume (mL)
SI - Stroke Index
11. LV Systolic function: Stroke Volume (SV), Cardiac output (CO)
CO (LV) is the volume of blood being pumped by the
left ventricle in the time interval of one minute.
In order to obtain CO we need to measure the LVOT
diameter in PLAX view zoomed image (left) in systole
and the Velocity Time Integral in Pulsed wave mode
of the LVOT in apical 5 chamber view (left down).
Formula:
SV = π x (LVOT / 2)² x VTI₁
CO= (SV x HR) / 1000
Input:
LVOT – LV outflow tract diameter (mm)
LVOT VTI - Subvalvular Velocity Time integral (cm)
R-R interval (HR) (Red doted line)
Output:
SV - Stroke Volume
CO - Cardiac output
SI – Stroke Index
CI - Cardiac Index
Left Ventricle (LV) ①
12. LV Systolic function: MPI LV (Myocardial Performance Index)
Also known as the Tei index. It is an index
that incorporates both systolic and
diastolic time intervals in expressing
global systolic and diastolic ventricular
function. Systolic dysfunction prolongs
prejection (isovolumic contraction time,
IVCT) and a shortening of the ejection
time (ET). Both systolic and diastolic
dysfunction result in abnormality in
myocardial relaxation which prolongs the
relaxation period (isovolumic relaxation
time, IVRT).
Input:
MCOT - Mitral valve closure to opening time (orange)
LVET - LV Ejection time (blue lines)
Output:
LV MPI – LV Myocardial performance index
Formula:
LV MPI= (IVCT + IVRT) / LVET = (MCOT – LVET) / LVET
Left Ventricle (LV) ①
13. LV Systolic function: dP/dt (LV Contractility)
Peak dP/dt is one of the most commonly used
indexes for assessing left ventricular function.
Continuous wave Doppler determination of the
velocities of a mitral insufficiency jet should
allow calculation of instantaneous pressure
gradients between the left ventricle and left
atrium. The rising segment of the mitral
insufficiency velocity curve should reflect left
ventricular pressure elevation. The LV
contractility dP/dt can be estimated by using
time interval between 1 and 3 cm/sec on MR
velocity CW spectrum during isovolumetric
contraction, i.e. before aortic valve opens when
there is no significant change in LA pressure.
Formula:
dP/dt= 32/T
Input:
T - Time between 1 and 3 cm/sec
Output:
dP/dt (mmHg/s)
Left Ventricle (LV) ①
14. Systolic myocardial velocity (S’) at
the lateral mitral annulus is a measure
of longitudinal systolic function and is
correlated with measurements of LV
ejection fraction and peak dP/dt. A
reduction in S’ (Systolic velocity
annulus) velocity can be detected within
15 seconds of the onset of ischemia,
and regional reductions in S’ are
correlated with regional wallmotion
abnormalities. Incorporation of TDI
measures of systolic function in exercise
testing to assess for ischemia, viability,
and contractile reserve has been
suggested because peak S’ velocity
normally increases with dobutamine
infusion and exercise and decreases
with ischemia. *
* A Clinician's Guide to Tissue Doppler Imaging Carolyn Y. Ho and Scott D. Solomon Circulation. 2006;113:e396-e398
LV Systolic function: TDI
Input:
S – Systolic velocity in lateral wall A4C (red)
Left Ventricle (LV) ②
16. LV Diastolic function
- PW mitral inflow
IVRT (Isovolumic relaxation time)
- DTI (e ) (Tissue doppler)′
- PV (Pulmonary vein) flow
- Mitral inflow propagation
- LA volume
- PCWP by E/e’ (mean Pulmonary
Capillary Wedge Pressure by E/e’) (Nagueh)
17. Left Ventricle (LV)
Input:
-E-wave - Peak early filling velocity (Yellow)
-A-wave - Late diastolic filling velocity (green)
-DT - Deceleration time (Blue)
-IVRT – Isovolumic relaxation time (red)
-A duration – (orange)
LV diastolic function: PW mitral inflow
The mitral inflow velocity profile is used to
initially characterize LV filling dynamics. The E
velocity (E) represents the early mitral inflow
velocity and is influenced by the relative
pressures between the LA and LV, which, in turn,
are dependent on multiple variables including LA
pressure, LV compliance, and the rate of LV
relaxation. The A velocity (A) represents the
atrial contractile component of mitral filling and
is primarily influenced by LV compliance and LA
contractility. The deceleration time (DT) of the E
velocity is the interval from peak E to a point of
intersection of the deceleration of flow with the
baseline and it correlates with time of pressure
equalization between the LA and LV.
①
Output:
-E/A ratio
18. The IVRT is the time interval between aortic
valve closure and mitral valve opening. The
transducer is placed in the apical position
with either a pulsed or continuous wave
Doppler sample placed between the aortic
and mitral valves. A normal IVRT is
approximately 70 to 90 ms. The IVRT will
lengthen with impaired LV relaxation and
shorten when LV compliance is decreased
and LV filling pressures are increased.
IVRT - measurement from the Ao valve closure (yellow)
And Mitral valve opening (green)
LV diastolic function: IVRT (Isovolumic relaxation time)
Left Ventricle (LV) ①
19. Currently, the most sensitive and widely
used technique for LVDF is TDI.
Diastolic dysfunction is directly related to
the reduction in early LV relaxation
compromising the effective transfer of the
blood from the atrial reservoir into the LV
cavity. The reduction in LV relaxation may be
characterized through the evaluation of
mitral annular motion, generally with
Doppler tissue imaging, which can resolve
subtle changes in LV relaxation by identifying
a low septal annular early diastolic mitral
annular motion (e’) velocity.
For the assessment of global LV diastolic
function, it is recommended to acquire and
measure tissue Doppler signals at least
at the septal and lateral sides of the mitral
annulus and their average, given the
influence of regional function on these
velocities and time intervals.
Input:
s: Systolic annular velocity (blue)
e’: early diastolic annular velocity (yellow)
a’: late diastolic velocity (green)
Output:
E/e’ ratio
e’/a’ ratio
Left Ventricle (LV)
LV diastolic function: Tissue doppler image
①
20. LV diastolic function: Pulmonary veins
PW Doppler of pulmonary venous flow is
performed in the apical 4-chamber view
and aids in the assessment of LV
diastolic function. If the mitral inflow
velocity
profile indicates a predominant
relaxation abnormality with a low E/e=
ratio (normal mean LA pressure), a
pulmonary vein flow duration greater
than mitral inflow duration at atrial
contraction may indicate an earlier stage
of reduced LV compliance as well as
increased LV end-diastolic pressure.
PV flow is better
Input:
S - Peak systolic vel
D - Peak diastolic vel
Ar - Reverse vel in late diatole
Ar duration
Ar - A - Time difference between Ar duration and
mitral A-wave duration
Left Ventricle (LV) ①
Output:
S/D Ratio
21. LV diastolic function: Mitral Inflow Propagation
Acquisition is performed in the apical 4-chamber
view, using color flow imaging with a narrow color
sector, and gain is adjusted to avoid noise. The M-
mode scan line is placed through the center of the
LV inflow blood column from the mitral valve to
the apex. Then the color flow baseline is shifted to
lower the Nyquist limit so that the central highest
velocity jet is blue. Flow propagation velocity (Vp)
is measured as the slope of the first aliasing
velocity during early filling, measured from the
mitral valve plane to 4 cm distally into the LV
cavity. Alternatively, the slope of the transition
from no color to color is measured. Vp 50 cm/s is
considered normal. During heart failure and during
myocardial ischemia, there is slowing of mitral-to-
apical flow propagation, consistent with a
reduction of apical suction.
Input:
Vp - Flow propagation velocity (doted white
Line) (cm/s)
Left Ventricle (LV) ①
22. LV diastolic function: Left Atrium (LA) Volume
Left atrial volume is regarded as a “barometer”
of the chronicity of diastolic dysfunction; with
the most accurate measurements obtained
using the apical 4-chamber and 2-chamber
views (Biplane areal-length or Simpson). This
assessment is clinically important, because
there is a significant relation between LA
remodeling and echocardiographic indices of
diastolic function. However, Doppler velocities
and time intervals reflect filling pressures at the
time of measurement, whereas LA volume
often reflects the cumulative effects of filling
pressures over time.
Input:
A1 – Max planimetry LA area - A4C
A2 – Max planimetry LA area – A2C
L - Length
Left Ventricle (LV) ①
Output:
LA Volume – Left atrial volume
LAVI – LA volume index
23. Left Ventricle (LV)
LV diastolic function: PCWP (Mean capilary wedge pressure) by E/e’
We can use the average e’ velocity obtained
from the septal and lateral sides of the mitral
annulus for prediction of LV filling pressures.
E/e’ ratio < 8 is usually associated with normal
LV filling pressures (PCWP < 15 mmHg) while a
ratio > 15 is associated with increased filling
pressures (PCWP > 15 mmHg). Between 8 ans
15 there is a gray zone with overlapping of
values for filling pressures.
Input:
E: Mitral inflow E
velocity
e’ (lateral)
e’ (septal)
Output:
e’ (Average) - of the lateral and
septal e’ values (m/s)
E/e’: ratio
PCWP - Mean Pulmonary capillary
wedge pressure (mmHg)
Formulas:
e’ = (e’ lateral + e’ septal) / 2
PCWP = 1.24 * (E/e’) + 1.9
①
24. Left Atrium (LA)
When LA size is measured in clinical practice,
volume determinations are preferred over
linear dimensions because they allow
accurate assessment of the asymmetric
remodeling of the LA chamber. In the
area-length formula the length is measured
in both the 4- and 2-chamber views and the
shortest of these
2 length measurements is used in the
formula.
①
Quantification of the Left Atrial size: LA Volume (Biplane)
Input:
A1 – Max planimetry LA area - A4C
A2 – Max planimetry LA area – A2C
L - Length
Output:
LA Diameter – (cm)
LA diameter index – cm/m²
LA Volume – Left atrial volume (mL)
LAVI – LA volume index (mL/m²)
25. Quantification of the Left Atrial size: M-Mode
The LA size is measured at the end-ventricular
systole when the LA chamber is at its greatest
dimension, care should be taken to avoid
foreshortening of the LA. The base of the LA
should be at its largest size indicating that the
imaging plane passes through the maximal
shortening area. The LA length should be also
maximized ensuring alignment along the true
long axis of the LA. The confluences of the
pulmonary veins, and LA appendage should be
excluded. AP linear dimensions of the LA as
the sole measure of LA size may be misleading
and should be accompanied by LA volume
determination in both clinical practice and
research.
Left Atrium (LA)
Input:
LAD – Left atrium diameter (cm)
②
26. Aortic root
Aortic root dimension
Figure 19 Measurement of aortic root diameter at sinuses
of Valsava from 2-dimensional parasternal long-axis image.
Although leading edge to leading edge technique is shown,
some prefer inner edge to inner edge method.
TTE imaging.
Figure 18 Measurement of aortic root diameters at aortic
valve annulus (AV ann) level, sinuses of Valsalva (Sinus
Val), and sinotubular junction (ST Jxn) from midesophageal
long-axis view of aortic valve, usually at angle of
approximately 110 to 150 degrees. Annulus is measured by
convention at base of aortic leaflets. Although leading edge
to leading edge technique is demonstrated for the Sinus Val
and ST Jxn, some prefer inner edge to inner edge method.
TEE imaging.
①
Input:
AV Ann – Aortic valve annulus (TEE)
Sinus Val – Sinuses of Valsalva (TEE)
ST Jxn – Sinotubular junction (TEE)
Ao – Aortic root diameter (TTE)
27. Right Ventricle (RV)
RV segments & coronary supply
Segmental nomenclature of the right ventricular walls, along with their coronary supply.
Ao, Aorta; CS, coronary sinus; LA, left atrium; LAD, left anterior descending artery;
LV, left ventricle; PA, pulmonary artery; RA, right atrium; RCA, right coronary artery;
RV, right ventricle; RVOT, right ventricular outflow tract.
28. Right Ventricle (RV)
RV Size: RV linear dimension
Using 2D echocardiography, RV size can
be measured from a 4-chamber view
obtained from the apical window at
end-diastole. Although quantitative
validation is lacking, qualitatively, the
right ventricle should appear smaller
than the left ventricle and usually no
more than two thirds the size of the left
ventricle in the standard apical 4-
chamber view. If the right ventricle is
larger than the left ventricle in this
view, it is likely significantly enlarged.
RV dimension is best estimated at end-
diastole from a right ventricle–focused
apical 4-chamber view.Input:
RV Basal - RV Basal diameter (mm)
RV mid - RV Mid diameter (mm)
RV long - RV Longitudinal diameter (mm)
①
29. Right Ventricle (RV)
RV size: RVOT Dimensions
The RVOT is generally considered to include the subpulmonary infundibulum,
or conus, and the pulmonary valve. The RVOT is best viewed from the left parasternal
and subcostal windows. The size of the RVOT should be measured at end-diastole on
the QRS deflection.
A) PLAX view, a portion of the proximal RVOT can be measured
B) PSAX view, proximal RVOT measurement
C) PSAX view, Distal RVOT measurement (preferred site for RVOT linear measurement)
Input:
RVOT proximal (mm)
RVOT Distal (mm)
①
30. Right Ventricle (RV)
RV size: RV Wall thickness
(A) Subcostal 2-dimensional image of right ventricular wall.
(B) Zoom of region outlined in (A) with right ventricular wall thickness indicated by arrows.
(C) M-mode image corresponding to arrows
in (B).
(D) Zoom of region outlined in (C) with arrows indicating wall thickness at end-diastole.
RV wall thickness is a useful measurement for RVH, usually the result of RVSP overload. RV free wall thickness
can be measured at end-diastole by M-mode or 2D echocardiography from the subcostal window, preferably at
the level of the tip of the anterior tricuspid leaflet or left parasternal windows. Excluding RV trabeculations and
papillary muscle from RV endocardial border is critical for accurately measuring the RV wall thickness.When
image quality permits, fundamental imaging should be used to avoid the increased structure thickness seen with
harmonic imaging.
Input:
RV Wall thickness (mm)
①
31. Right Ventricle (RV)
RV systolic function: TAPSE (Tricuspid Annular Plane Systolic Excursion)
The systolic movement of the base
of the RV free wall provides one of
the most visibly obvious movements
on normal echocardiography. TAPSE
or TAM is a method to measure the
distance of systolic excursion of the
RV annular segment along its
longitudinal plane, from a standard
apical 4-chamber window. It is
inferred that the greater the descent
of the base in systole, the better the
RV systolic function. TAPSE is usually
acquired by placing an M-mode
cursor through the tricuspid annulus
and measuring the amount of
longitudinal motion of the
annulus at peak systole
Input:
TAPSE – Tricuspid Annular Plane Excursion mm
①
32. Right Ventricle (RV)
RV systolic function: FAC (Fractional Area Change)
The percentage RV FAC, defined as (end-diastolic
area end-systolic area)/end-diastolic area 100, is
a measure of RV systolic function that has been
shown to correlate with RV EF by magnetic
resonance
imaging (MRI). FAC is obtained by tracing the RV
endocardium both in systole and diastole from
the annulus, along the free wall to the
apex, and then back to the annulus, along the
interventricular septum. Care must be taken to
trace the free wall beneath the
Trabeculations. Two-dimensional Fractional Area
Change is one of the recommended methods of
quantitatively estimating RV function, with a
lower reference value
for normal RV systolic function of 35%.
Input:
ED area - End-diastolic Area
ES area - End-systolic Area
Output:
FAC %
①
33. Right Ventricle (RV)
Input:
S’ – Systolic excursion velocity
RV systolic function: RV S’ (Systolic excursion velocity)
Among the most reliably and reproducibly
imaged regions of the right ventricle are the
tricuspid annulus and the basal free wall
segment. These regions can be assessed by
pulsed tissue Doppler and color-coded tissue
Doppler to measure the longitudinal velocity
of excursion. This velocity has been termed
the RV S’ or systolic excursion velocity. To
perform this measure, an apical 4-chamber
window is used with a tissue Doppler mode
region of interest highlighting the RV free
wall. The pulsed Doppler sample volume is
placed in either the tricuspid annulus or the
middle of the basal segment of the RV free
wall.
+
①
34. Right Ventricle (RV)
RV systolic function: MPI RV - Myocardial Performance Index RV
The MPI, also known as the RIMP or Tei index, is a
global estimate of both systolic and diastolic function of
the right ventricle. It is based on the relationship
between ejection and nonejection work of the heart.
The MPI is defined as the ratio of isovolumic time
divided by ET, or [(IVRT + IVCT)/ET]. The right-sided
MPI can be obtained by two methods: the pulsed
Doppler method and the tissue Doppler method: In the
pulsed Doppler method (A), the ET is measured with
pulsed Doppler of Rv outflow (time from the onset to
the cessation of flow), and the tricuspid (valve) closure-
opening time is measured with either pulsed Doppler of
the tricuspid inflow (time from the end of the
transtricuspid A wave to the beginning of the
transtricuspid E wave) or continuous Doppler
of the TR jet (time from the onset to the cessation of
the jet). In the tissue Doppler method (B), all time
intervals are measured from a single beat by pulsing the
tricuspid annulus (left)
Output:
IVCT (Isovolumic Contraction Time)
IVRT (Isovolumic Relaxation Time)
MPI RV
Input:
ET - Ejection Time
TCO - Tric. Closure-Opening Time)
②
35. Right Ventricle (RV)
RV systolic function: RV dP/dt
RV dP/dt can be accurately estimated from the
ascending limb of the TR continuous-wave Doppler
signal. Is commonly calculated by measuring the time
required for the TR jet to increase in velocity from 1 to
2 m/s. Using the simplified Bernoulli equation, this
represents a 12 mm Hg increase in
pressure. The dP/dt is therefore calculated as 12 mm Hg
divided by this time (in seconds), yielding a value in
millimeters of mercury per second.
Because of the lack of data in normal
subjects, RV dP/dt cannot be recommended for routine uses.
It can be considered in subjects with suspected RV
dysfunction. RV dP/dt < approximately 400 mm Hg/s is likely
abnormal.
Point 1 represents the point at which the tricuspid regurgitation
(TR) signal meets the 1 m/s velocity scale marker,
while point 2 represents the point at which the TR signal meets
the 2 m/s velocity scale marker. Point 3 represents the time required
for the TR jet to increase from 1 to 2 m/s. In this example,
this time is 30 ms, or 0.03 seconds. The dP/dt is therefore 12mm
Hg/0.03 seconds, or 400 mm Hg/s.
②
36. Right Ventricle (RV)
RV systolic function: RV IVA (Myocardial Acceleration During
Isovolumic Contraction)
Isovolumetric acceleration (IVA) is a novel
tissue Doppler parameter for the assessment
of systolic function. Myocardial acceleration
during isovolumic contraction is defined as the
peak isovolumic myocardial velocity divided
by time to peak velocity and is typically
measured for the right ventricle by Doppler
tissue imaging at the lateral tricuspid annulus.
For the calculation
of IVA, the onset of myocardial acceleration is
at the zero crossing point of myocardial
velocity during isovolumic contraction. In
studies in patients with conditions affected by
RV function, RV IVA may be used, and when
used, it should be measured at the lateral
tricuspid annulus. RV IVA is not recommended
as a screening parameter for RV systolic
function in the general echocardiography
laboratory population.
Pulsed wave tissue Doppler imaging of the RV free
wall of a control subject. 1: peak myocardial systolic
velocity (Sm), 2: peak early diastolic velocity (Em), 3: peak
late diastolic velocity (Am) 4: isovolumetric contraction time
(IVCT), 5: ejection time (ET), 6: peak myocardial
isovolumetric contraction velocity (IVV), acceleration time
(AT), isovolumetric acceleration (IVA) (red).
②
37. Right Ventricle (RV)
RV diastolic function: PW Tricuspid inflow
From the apical 4-chamber view, the Doppler
beam should be aligned parallel to the RV inflow.
Proper alignment may be facilitated by displacing
the transducer medially toward the lower
parasternal region.
The sample volume should be placed at the tips of
the tricuspid leaflets. With this technique,
measurement of transtricuspid flow velocities can
be achieved in most patients, with low
interobserver and intraobserver variability. Care
must be taken to measure at held end-expiration
and/or take the average of ≥ 5 consecutive beats.
The presence of moderate to severe TR or atrial
fibrillation could confound diastolic parameters,
and most studies excluded such patients.Input:
Tricuspid Flow Profile (red)
Output:
E wave velocity
A wave velocity
E/A ratio
Tricuspid E/e’
DT - Deceleration time (ms)
E
①
38. Right Ventricle (RV)
RV diastolic function: Tissue doppler imaging
Input:
S’ Systolic velocity
E’ velovity
A’ velocity
Output:
E’/A’ ratio
E/E’ ratio
②
Among the most reliably and reproducibly
imaged regions of the right ventricle are the
tricuspid annulus and the basal free wall
segment. These regions can be assessed by
pulsed tissue Doppler and color-coded tissue
Doppler to measure the longitudinal velocity
of excursion. S’ is systolic velocity, E’ is early
diastolic velocity and A’ is late diastolic
velocity. To perform this measure, an apical
4-chamber window is used with a tissue
Doppler mode region of interest highlighting
the RV free wall. The pulsed Doppler sample
volume is placed in either the tricuspid
annulus or the middle of the basal segment
of the RV free wall.
39. Right Ventricle (RV)
RV hemodynamics: sPAP (Systolic pulmonary artery pressure)
SPAP can be estimated using TR velocity, and
PADP can be estimated from the end-diastolic
pulmonary regurgitation velocity. Mean PA
pressure can be estimated by the PA
acceleration time (AT) or derived from the
systolic and diastolic pressures. RVSP can be
reliably determined from peak TR jet velocity,
using the simplified Bernoulli equation and
combining this value with an estimate of the
RA pressure: RVSP = 4 (V) ² + RA pressure,
where V is the peak velocity (in meters per
second) of the tricuspid valve regurgitant jet,
and RA pressure is estimated from IVC
diameter and respiratory changes. Because
velocity measurements are angle dependent,
it is recommended to gather TR signals from
several windows and to use the signal with the
highest velocity.
Input:
TR Jet velocity
PAP mmHg
(depending on
IVC collapsability on sniff)
Output:
TR velocity
sPAP
RV Systolic pressure
①
40. RV hemodynamics: dPAP (Diastolic Pulmonary artery pressure)
mPAP (mean Pulmonary Artery Pressure)
Right Ventricle (RV)
dPAP can be estimated from the velocity
of the end-diastolic pulmonary
regurgitant jet using the modified
Bernoulli equation: [PADP = 4 (end-
diastolic pulmonary regurgitant velocity)²
+ RA pressure]. Mean PA pressure
correlates with 4 x (early PI velocity) ² +
estimated RAP .
Input:
PR PHT (yellow)
PR Vmax – Pulmonary regurgitation
max velocity (red)
PR end Vmax - Pulmonary
regurgitation end max velocity
(green)
Output:
PA Reg PHT (ms)
PA peak diastolic gradient
dPAP (end diastolic gradient)
mPAP (mean Pulmonary
Artery pressure)
①
41. Right Ventricle (RV)
RV hemodynamics: mPAP (mean Pulmonary artery pressure)
AT method
Once systolic and diastolic pressures
are known, mean pressure may be
estimated by the standard formula
mean PA pressure = 1/3(SPAP) +
2/3(PADP). Mean PA pressure may
also be estimated by using pulmonary
AT measured by pulsed Doppler of the
pulmonary artery in systole, whereby
mean PA pressure = 79 (0.45 AT).
Generally, the shorter the AT
(measured from the onset of the Q
wave on electrocardiography to the
onset of peak pulmonary flow
velocity), the higher the PVR
(Pulmonary Vascular Resistance) and
hence the PA pressure.
Input:
PA TVI - (Time velocity
Integral) (yellow)
Output:
PA AT (acceleration time)
mPAP
mPAP (mean Pulmonary
Artery pressure)
①
42. Right Atrium (RA)
The primary transthoracic window for imaging the
right atrium is the apical 4-chamber view. From this
window, RA area is estimated by planimetry. The
maximal long-axis distance of the right atrium is
from the center of the tricuspid annulus to the
center of the superior RA wall, parallel to the
interatrial septum. A mid-RA minor distance is
defined from the mid level of the RA free wall to
the interatrial septum, perpendicular to the long
axis. RA area is traced at the end of ventricular
systole (largest volume) from the lateral aspect of
the tricuspid annulus to the septal aspect, excluding
the area between the leaflets and annulus,
following the RA endocardium, excluding the IVC
and superior vena cava and RA appendage
Right atrium size
Input:
RA End-Systolic Area (cm ²)
RA Major Dimension (mm)
RA Minor Dimension (mm)
①
43. Right Atrium (RA)
Inferior Vena Cava: RA pressure
The subcostal view is most useful for imaging
the IVC, with the IVC viewed in its long axis.
The measurement of the IVC diameter should
be made at end-expiration and just proximal
to the junction of the hepatic veins that lie
approximately 0.5 to 3.0 cm proximal to the
ostium of the right atrium. To accurately
assess IVC collapse, the change in diameter of
the IVC with a sniff and also with quiet
respiration should be measured, ensuring that
the change in diameter does not reflect a
translation of the IVC into another plane.
The measurements are done at end-diastole.
IVC diameter ≤ 2.1 cm that collapses >50% with a sniff suggests a normal RA pressure of 3 mm Hg (range, 0-5 mmHg)
IVC diameter > 2.1 cm that collapses <50% with a sniff suggests a high RA pressure of 15 mm Hg (range, 10-20 mmHg)
In indeterminate cases in which the IVC diameter and collapse do not fit this paradigm, an intermediate value
of 8 mm Hg (range, 5-10 mm Hg) may be used
①
44. Valvular stenosis
Aortic stenosis: AS jet velocity
AS jet velocity (Antegrade Systolic Velocity) is defined as
the highest velocity signal obtained from any window
after a careful examination; lower values from other
views are not reported.The antegrade systolic velocity
across the narrowed aortic valve, or aortic jet velocity, is
measured using continuous-wave (CW) Doppler (CWD)
ultrasound. A dedicated small dual-crystal CW
transducer is recommended both due to a higher signal-
to-noise ratio and to allow optimal transducer
positioning and angulation, particularly when suprasternal
and right parasternal windows are used. However, when
stenosis is only mild (velocity 3 m/s) and leaflet opening is
well seen, a combined imaging-Doppler transducer may
be adequate.
Input:
AS jet velocity (m/s)
VTI – Velocity Time
integral
Output:
Mean gradient (mmHg)
①
45. Valvular stenosis
Aortic stenosis: AVA (Continuity equation VTI)
Aortic valve area can be calculated by using the
principle of conservation of mass – “What
comes in must go out”.
AVA indexed to BSA should be considered for
the large and small extremes of body surface
area.
Left ventricular outflow tract diameter is
measured in the parasternal long-axis view in
mid-systole from the white–
black interface of the septal endocardium to the
anterior mitral leaflet, parallel to the aortic valve
plane and within 0.5–1.0 cm
of the valve orifice.
Input:
LVOT diameter (mm)
VTI1 (Subvalvular VTI) (cm)
VTI2 (Max VTI across the valve
(cm)
Output:
AVA (cm²)
AVAI (Indexed to BSA)
(cm²/m²)
AVA = (CSALVOT x VTILVOT) / VTIAV
①
46. Valvular stenosis
Aortic stenosis: AVA (Continuity equation Vmax)
②
The simplified continuity equation is based on
the concept that in native aortic valve stenosis
the shape of the velocity curve in the outflow
tract and aorta is similar so that the ratio of
LVOT to aortic jet VTI is nearly identical to the
ratio of the LVOT to aortic jet maximum
velocity (V). This method is less well accepted
because some experts are concerned that
results are more variable than using VTIs in the
equation.
AVA = CSALVOT x VLVOT / VAV
Input:
LVOT diameter (mm)
V1 (Subvalvular Velocity) (m/s)
V2 (Max velocity across the valve)
(m/s)
Output:
AVA (cm²)
AVAI (Indexed to BSA)
(cm²/m²)
47. Valvular stenosis
Aortic stenosis: Velocity ratio
②
Another approach to reducing error related to
LVOT diameter measurements is removing CSA from
the simplified continuity equation. This dimensionless
velocity ratio expresses the size of the valvular effective
area as a proportion of the CSA of the LVOT.
Substitution of the time-velocity integral can also be used
as there was a high correlation between the ratio using
time–velocity integral and
the ratio using peak velocities. In the absence of valve
stenosis, the velocity ratio approaches 1, with smaller
numbers indicating more severe stenosis. Severe stenosis
is present when the velocity ratio is
0.25 or less, corresponding to a valve area 25% of
normal.
Velocity ratio = VLVOT / VAV
Input:
V1 (Subvalvular Velocity) (m/s)
V2 (Max velocity across the valve)
(m/s)
Output:
VR - Velocity Ratio
48. Valvular stenosis
Aortic stenosis: Planimetry of anatomic valve area
②
Multiple studies have evaluated the method of
measuring anatomic (geometric) AVA by direct
visualization of the valvular orifice, either by 2D
or 3D TTE or TEE. Planimetry may be an
acceptable alternative when Doppler estimation
of flow velocities is unreliable. However,
planimetry may be inaccurate when valve
calcification causes shadows or reverberations
limiting identification of the orifice.
Input:
AV planimetry
Output:
AVA (cm²)
49. Valvular stenosis
Mitral stenosis: MVA Planimetry
MV planimetry has been shown to have the best correlation with anatomical valve area as assessed on explanted valves.
For these reasons, planimetry is considered as the reference measurement of MVA. Planimetry measurement is obtained
by direct tracing of the mitral orifice, including opened commissures, if applicable, on a parasternal short-axis view. The
optimal timing of the cardiac cycle to measure planimetry is mid-diastole. This is best performed using the cineloop mode
on a frozen image.
A) Mitral stenosis. Both commissures are fused. Valve area is 1.17 cm2.
B) Unicommissural opening after balloon mitral commissurotomy. The postero-medial commissure is opened. Valve area is 1.82
cm2.
C) Bicommissural opening after balloon mitral commissurotomy. Valve area is 2.13 cm2.
①
50. Valvular stenosis
Mitral stenosis: PHT (Pressure Half-time)
Is the time interval in milliseconds between the
maximum mitral gradient in early diastole and the
time point where the gradient is half the maximum
initial value. The decline of the velocity of diastolic
transmitral blood flow is inversely proportional to
valve area (cm2), and MVA is derived using the
empirical formula: MVA = 220 ⁄ T1⁄2.
T1/2 is obtained by tracing the deceleration slope of
the E-wave on Doppler spectral display of
transmitral flow and valve area is automatically
calculated by the integrated software of currently
used echo machines. The Doppler signal used is the
same as for the measurement of mitral gradient.
Input:
MV PHT
Output:
MV PHT (ms)
MVA (cm ²)
①
51. Valvular stenosis
Mitral stenosis: Pressure gradient
Mitral stenosis is the most frequent valvular
complication of rheumatic fever. Even in
industrialized countries, most cases remain of
rheumatic origin as other causes are rare. The
estimation of the diastolic pressure gradient is
derived from the transmitral velocity flow curve
using the simplified Bernoulli equation ΔP = 4v ².
The use of CWD is preferred to ensure maximal
velocities are recorded. Doppler gradient is
assessed using the apical window in most cases as
it allows for parallel alignment of the ultra sound
beam and mitral inflow.
Input:
MV Flow profile
Output:
MV Peak Velocity
MV Peak GP (mmHg)
MV mean Velocity
MV Mean GP (mmHg)
①
52. Valvular stenosis
Mitral stenosis: Continuity equation
②
As in the estimation of AVA, the continuity
equation is based on the conservation of
mass, stating in this case that the filling
volume of diastolic mitral flow is equal to
aortic SV. The accuracy and reproducibility
of the continuity equation for assessing MVA
are hampered by the number of
measurements increasing the impact of
errors of measurements. The continuity
equation cannot be used in cases of atrial
fibrillation or associated significant MR or
AR.
MVA = (CSALVOT x VTIAortic) / VTIMitral
Input:
LVOT (cm)
VTI Ao (cm)
VTI Mitral (cm)
Output:
MVA (cm²)
53. Valvular stenosis ②
The proximal isovelocity surface area method is based
on the hemispherical shape of the convergence of
diastolic mitral flow on the atrial side of the mitral valve,
as shown by colour Doppler. It enables mitral volume
flow to be assessed and, thus, to determine MVA by
dividing mitral volume flow by the maximum velocity of
diastolic mitral flow as assessed by CWD. This method
can be used in the presence of significant MR.
However, it is technically demanding and requires
multiple measurements. Its accuracy is impacted upon
by uncertainties in the measurement of the radius of the
convergence hemisphere, and the opening angle.
MVA = 2 x π x r² x (Vr / Vmax) x (α⁰ / 180°)
Output:
VFR (Volume flow rate) (cc)
MVA (cm²)
Input:
2 × π × r2
: Proximal isovelocity hemispheric surface area at a radial distance r
from the orifice.
Vr : Aliasing velocity at the radial distance r (cm/s)
Vmax : Peak mitral stenosis velocity by CW (m/s)
α : Angle between two mitral leaflets on the atrial side (degree0
)
Mitral stenosis: PISA method
54. Valvular stenosis
Tricuspid stenosis: CWD hemodynamic evaluation
①
Tricuspid stenosis (TS) is currently the least common of the
valvular stenosis lesions given the low incidence of
rheumatic heart disease. As with all valve lesions, the initial
evaluation starts with an anatomical assessment of the valve
by 2D echocardiography using multiple windows such as
parasternal right ventricular inflow, parasternal short axis,
apical four-chamber and subcostal four-chamber. The
evaluation of stenosis severity is primarily done using the
hemodynamic information provided by CWD. Because
tricuspid inflow velocities are affected by respiration, all
measurements taken must be averaged throughout the
respiratory cycle or recorded at end-expiratory apnea. In
theory, the continuity equation should provide a robust method
for determining the effective valve area as SV divided by the
tricuspid inflow VTI as recorded with CWD. In the absence of
significant TR, one can use the SV obtained from either the left or
right ventricular
outflow; a valve area of 1 cm2 is considered indicative of severe
TS.
However, as severity of TR increases, valve area is progressively
underestimated by this method.Input:
TV Flow profile
Output:
Peak diastolic velocity
Mean gradient (mmHg)
PHT (pressure half-time)
mmHg
55. Valvular stenosis
Pulmonic stenosis: Pressure gradient
Pulmonary stenosis is almost always congenital in origin.
The normal pulmonary valve is trileaflet. The
congenitally stenotic valve may be trileaflet, bicuspid,
unicuspid, or dysplastic. Acquired stenosis of the
pulmonary valve is very uncommon. Quantitative
assessment of pulmonary stenosis severity is based
mainly on the transpulmonary pressure gradient. The
estimation of the systolic pressure gradient is derived
from the transpulmonary velocity flow curve using
the simplified Bernoulli equation P =Δ 4 (V) ². This
estimation is reliable, as shown by the good correlation
with invasive measurement using cardiac
catheterization. Continuous-wave Doppler is used to
assess the severity when even mild stenosis is present.
It is important to line up the Doppler sample volume
parallel to the flow with the aid of colour flow mapping
where appropriate. In adults, this is usually most readily
performed from a parasternal short-axis view.
①
Input:
Peak velocity (m/s)
Output:
Peak Gradient (mmHg)
56. Valvular regurgitation
Aortic regurgitation: Jet diameter/LVOT diameter ratio %
①
Imaging of the regurgitant jet is used in all
patients with AR because of its simplicity and
real time availability.The parasternal views are
preferred over apical views because of better
axial resolution. The recommended
measurements are those of maximal proximal
jet width obtained from the long-axis views
and its ratio to the LV outflow tract diameter.
Similarly, the cross-sectional area of the jet
from the parasternal short-axis view and its
ratio to the LV outflow tract area can also be
used. The criteria to define severe AR are
ratios of ≥ 65% for jet width and ≥ 60% for
jet area.
Is possible to use the CSA instead width for
both Jet and LVOT.
Input:
Jet Width (red)
LVOT Width (yellow)
Output:
Jet width/LVOT Width ratio (%)
57. Valvular regurgitation
Aortic regurgitation: VC (Vena contracta)
The Vena contracta is the narrowest portion of the
regurgitant jet downstream from the regurgitant orifice.
It is sligtly smaller than the anatomic regurgitant orifice
due to boundary effect. For AR, imaging of the VC is
obtained from the PLAX view. To properly identify the
VC the three components of the regurgitant jet should
be visualized (flow convergence zone, vena contracta,
jet turbulence). A narrow colour sector scan coupled
with the zoom mode is recommended to improve
measurement accuracy. It provides thus an estimation of
the size of the EROA (Estimated regurgitant orifice
area) and is smaller that the regurgitant jet width in the
LVOT. Using a Nyquist limit of 50-60 cm/s, a vena
contracta width of < 3mm correlates with mild AR,
whereas a width > 6mm indicates severe AR.
When feasible the measurement of VC width is
recommended to quantify AR severity. Intermediate VC
values (3-6 mm) needs confirmation by a more
quantitative method.
Input:
AR VC width – Aortic regurgitation Vena Contracta width (cm)
①
58. Valvular regurgitation
Aortic regurgitation: PISA (Proximal Isovolumetric Surface Area)
The assessment of the flow convergence zone has been
less extensively performed in AR than in MR. The
colour flow velocity scale is shifted towards the
direction of the jet (downwards or upwards in the left
parasternal view depending on the jet orientation and
upwards in the apical view).
1- Color Doppler settings must be correctly adjusted
for the PISA method. The Nyquist-limit should be
placed around 50-60 cm/s.
2- Afterwards, base line should be shifted in the
direction of the regurgitation jet, until a well-defined
hemisphere appears.
3- To calculate VTI of regurgitation jet, CW-Doppler
profile area should be delineated.
4- By measuring PISA radius it is important to hit
correctly the limit ot the hemisphere. Small errors can
produce important variations.
When feasible, the PISA method is highly
recommended to assess the severity of AR. It can be
used in both central and eccentric jets. The window
recommended is PLAX view for flow convergence.
Input:
PISA Radius
AR VTI
Output:
AR EROA (Effective Regurgitant
Orifice Area) cm ²
AR R Vol (regurgitant volume)
mL/beat
①
59. Valvular regurgitation
Aortic regurgitation: Jet deceleration rate (PHT)
The rate of deceleration of the diastolic regurgitant jet
and the derived pressure half-time reflect the rate of
equalization of aortic and LV diastolic pressures. With
increasing severity of AR, aortic diastolic pressure
decreases more rapidly. Pressure half-time is easily
measured if the peak diastolic velocity is appropriately
recorded. A pressure half-time 500 ms is usually
compatible with mild AR whereas a value 200 ms is
considered consistent with severe AR.
CW Doppler of the AR jet should be routinely
recorded but only utilized if a complete signal is
obtained. The PHT is influenced by chamber compliance
and pressure, for this reason it serves only as a
complementary finding for AR severity assessment.
Input:
AR PHT - Aortic reg Pressure half-time (ms)
①
60. Output:
EROA
R Vol.
RF (Regurgitant Fraction ) %
Aortic regurgitation: Flow quantitation - PW
Valvular regurgitation
Quantitation of flow with pulsed Doppler for the
assessment of AR is based on comparison of
measurement of aortic stroke volume at the LVOT
with mitral or pulmonic stroke volume. Total stroke
volume (aortic stroke volume) can also be derived
from quantitative 2D measurements of LV end-
diastolic and end-systolic volumes. EROA can be
calculated from the regurgitant stroke volume and
the regurgitant jet velocity time integral by CW
Doppler. As with the PISA method, a regurgitant
volume ≥60 ml and EROA ≥0.30 cm2
are consistent
with severe AR. The quantitative Doppler method
cannot be used if there is more than mild mitral
regurgitation, unless the pulmonic site is used for
systemic flow calculation. In general, a RF > 50 %
indicates severe AR. Volumetric measurements with
PW are Time consuming, and requires multiple
measurements, so the source of errors are higher.
Input:
LVOT PW profile (A5C)
LVOT diameter (PLAX)
Mitral inflow profile PW (A4C)
Mitral annulus diameter (max
opening MV (A4C)
②
61. Valvular regurgitation
Aortic regurgitation: Aortic diastolic flow reversal PW
It is normal to observe a brief diastolic flow reversal in
the aorta. The flow reversal is best recorded in the upper
descending aorta at the aortic isthmus level using a
suprasternal view, or in the lower descending aorta using
a longitudinal subcostal view. With increasing aortic
regurgitation both the duration and the velocity of the
reversal increase. Therefore, a holodiastolic reversal is
usually a sign of at least moderate aortic regurgitation. A
prominent holodiastolic reversal with a diastolic time
integral similar to the systolic time integral is a reliable
qualitative sign of severe AR. However, reduced
compliance of the aorta seen with advancing age may also
prolong the normal diastolic reversal in the absence of
significant AR. In general, an end-diastolic flow velocity >
20 cm/s is indicative of severe AR.
①
Input:
End-diastolic velocity (cm/s)
62. Valvular regurgitation
Mitral regurgitation: Vena Contracta (VC)
The vena contracta should be imaged in high-resolution,
zoom views for the largest obtainable proximal jet size
for measurements. The examiner must search in multiple
planes perpendicular to the commissural line (such as the
parasternal long-axis view), whenever possible. The width
of the neck or narrowest portion of the jet is then
measured. The regurgitant orifice in MR may not be
circular, and is often elongated along the mitral
coaptation line. The two-chamber view, which is oriented
parallel to the line of leaflet coaptation, The width of the
vena contracta in long-axis views and its cross-sectional
area in short-axis views can be standardized from the
parasternal view.s A vena contracta 0.3 cm
usually denotes mild MR where as the cut-off for
severe MR has ranged between 0.6 to 0.8 cm.
Input:
MR VC width (cm)
①
63. Valvular regurgitation
Mitral regurgitation: PISA
Most of the experience with the PISA method for
quantitation of regurgitation is with MR. Qualitatively, the
presence of PISA on a routine examination (at Nyquist
limit of 50-60 cm/s) should alert to the presence of
significant MR. Several clinical studies have validated PISA
measurements of regurgitant flow rate and EROA. This
methodology is more accurate for central regurgitant jets
than eccentric jets, and for a circular orifice than a
noncircular orifice. Flow convergence should be
optimized from the apical view, usually the fourchamber
view, using a zoom mode. For determination of EROA, it
is essential that the CW Doppler signal be well aligned
with the regurgitant jet. Poor alignment with an eccentric
jet will lead to an underestimation of velocity and an
overestimation of the EROA. Generally, an EROA 0.4
cm2 is consistent with severe MR, 0.20-0.39 cm²
moderate, and 0.20 cm² mild MR.
Input:
PISA Radius
MR VTI
Output:
MR EROA (Effective Regurgitant
Orifice Area) cm²
MR R Vol (regurgitant volume)
mL/beat
①
64. In most patients, maximum MR velocity is 4 to 6 m/s due
to the high systolic pressure gradient between the LV and
LA.
The velocity itself does not provide useful information
about the severity of MR. However, the contour
of the velocity profile and its density are useful. A
truncated, triangular jet contour with early peaking
of the maximal velocity indicates elevated LA pressure or
a prominent regurgitant pressure wave in the LA. The
density of the CW Doppler signal is a qualitative index of
MR severity. A dense signal that
approaches the density of antegrade flow suggests
significant MR, whereas a faint signal, with or without
an incomplete envelope represents mild or trace
MR. Using CW Doppler, the tricuspid regurgitation jet
should be interrogated in order to estimate pulmonary
artery systolic pressure. The presence of pulmonary
hypertension provides another indirect clue as to MR
severity and compensation to the volume overload.
Valvular regurgitation
Mitral regurgitation: Continuous wave doppler
Input:
MR VTI
Output:
MR Peak velocity (m/s)
①
65. Valvular regurgitation
Mitral regurgitation: Mitral to Aortic TVI ratio
In the absence on mitral stenosis, the increase in
transmitral flow that occurs with increasing MR severity
can be detected as higher flow velocities during early
sistolic filling (increased E velocity). In the absence of
mitral stenosis, peak E velocity > 1.5 m/s suggest severe
MR. Conversely, a dominant A wave (Atrial contraction)
basically excludes severe MR. The PW doppler mitral to
aortic TVI ratio is also used as an easily measured index
for the quantification of the isolated pure organic MR.
Mitral inflow doppler tracings are obtaines at the mitral
leaflet tips and aortic flow at the annulus level in the
apical four-chamber view. A TVI ratio > 1.4 strongly
suggest severe MR whereas a TVI ratio < 1 is in favor of
mild MR.
Both the pulsed Doppler mitral to aortic TVI ratio and the
systolic pulmonary flow reversal are specific for severe MR.
They represent the strongest additional parameters for
evaluating MR severity.
Input:
Mitral VTI
Aortic VTI
Output:
Mitral to Aortic VTI ratio
②
66. Valvular regurgitation
Mitral regurgitation: Pulmonary venous flow
Pulsed Doppler evaluation of pulmonary venous flow
pattern is another aid for grading the severity of MR. In
normal individuals, a positive systolic wave (S) followed by
a smaller diastolic wave (D) is classically seen in the
absence of diastolic dysfunction. With increasing severity
of MR, there is a decrease of the S wave velocity. In
severe MR, the S wave becomes frankly reversed if the jet
is directed into the sampled vein. As unilateral pulmonary
flow reversal can occur at the site of eccentric MR jets,
sampling through all pulmonary veins is recommended,
especially during transoesophageal echocardiography.
Although, evaluation of right upper pulmonary flow can
often be obtained using TTE, evaluation is best using TEE
with the pulse Doppler sample placed about 1 cm deep
into the pulmonary vein.
Both the pulsed Doppler mitral to aortic TVI ratio and the
systolic pulmonary flow reversal are specific for severe MR.
They represent the strongest additional parameters for
evaluating MR severity.
②
Pulmonary venous flow is a qualitative
parameter, no measurements have to be
done.
67. Output:
MR EROA
MR R Vol.
MR RF (Regurgitant Fraction ) %
Valvular regurgitation
Input:
LVOT PW profile (A5C)
LVOT diameter (PLAX)
Mitral inflow profile PW (A4C)
Mitral annulus diameter (max
opening MV (A4C)
②
Mitral regurgitation: Flow quantitation - PW
Pulsed Doppler tracings at the mitral leaflet tips are
commonly used to evaluate LV diastolic function.
Patients with severe MR often demonstrate a
mitral inflow pattern with a dominant early filling
(increased E velocity) due to increased diastolic
flow across the mitral valve, with or without an
increase in left atrial pressure. In severe mitral
regurgitation without stenosis, the mitral E velocity
is higher than the velocity during atrial contraction
(A velocity), and usually greater than 1.2 m/sec. For
these reasons, a mitral inflow pattern with an A-
wave dominance virtually excludes severe MR.
Volumetric measurements with PW are Time
consuming and not recommended as first level method
to quantify MR severity.
68. Valvular regurgitation
Tricuspid regurgitation: Vena contracta (VC)
The vena contracta of the TR is typically imaged
in the apical four-chamber view using the same
settings as for MR. Averaging measurements
over at least two to three beats is
recommended. A vena contracta ≥7 mm is in
favour of severe TR although a diameter <6 mm
is a strong argument in favour of mild or
moderate TR. Intermediate values are not
accurate at distinguishing moderate from mild
TR. As for MR, the regurgitant orifice geometry
is complex and not necessarily circular. When
feasible, the measurement of the vena contracta is
recommended to quantify TR.
Input:
TR VC width (cm)
①
69. Valvular regurgitation
Tricuspid regurgitation: Flow convergence (PISA)
Although providing quantitative assessment, clinical
practice reveals that the flow convergence method is
rarely applied in TR. This approach has been validated in
small studies. The apical four-chamber view and the
parasternal long and short axis views are classically
recommended for optimal visualization of the PISA. The
area of interest is optimized by lowering imaging depth
and the Nyquist limit to 15–40 cm/s. The radius of the∼
PISA is measured at mid-systole using the first aliasing.
Qualitatively, a TR PISA radius >9 mm at a Nyquist limit
of 28 cm/s alerts to the presence of significant TR
whereas a radius <5 mm suggests mild TR. An EROA ≥
40 mm2
or a R Vol of ≥45 mL indicates severe TR.
When feasible, the PISA method is reasonable to quantify the
TR severity. An EROA ≥ 40 mm2
or a R Vol ≥ 45 mL indicates
severe TR.
Input:
TR PISA Radius
TR VTI
Output:
TR EROA (Effective Regurgitant
Orifice Area) cm²
TR R Vol (regurgitant volume)
mL/beat
①
70. ②Valvular regurgitation
Tricuspid regurgitation: CW jet velocity
Recording of TR jet velocity provides a
useful method for noninvasive measurement
of RV or pulmonary artery systolic pressure.
It is important to note that TR jet velocity,
similar to velocity of other regurgitant
lesions, is not related to the volume of
regurgitant flow. In fact, massive TR is often
associated with a low jet velocity ( 2m/s), as
there is near equalization of RV and right
atrial pressures, conversely, mild
regurgitation may have a very high jet
velocity, when pulmonary hypertension is
present.
Similar to MR, the features of the TR jet by
CW Doppler that help in evaluating severity
of regurgitation, are the signal intensity and
the contour of the
velocity curve.
Input:
TR flow profile
71. Valvular regurgitation
Tricuspid regurgitation: Anterograde velocity of tricuspid inflow
A small degree of tricuspid regurgitation
(TR) is present in about 70% of normal
individuals. Pathologic regurgitation is often
due to right ventricular (RV) and tricuspid
annular dilation secondary to
pulmonary hypertension or RV dysfunction.
Primary causes of TR include endocarditis,
carcinoid heart
disease, Ebstein’s anomaly, and rheumatic
disease.
Similar to MR, the severity of TR will affect
the early tricuspid diastolic filling (E velocity).
In the absence of tricuspid stenosis, the peak
E velocity increases in proportion to the
degree of TR. Tricuspid inflow Doppler tracings
are obtained at the tricuspid leaflet tips. A peak
E velocity ≥1 m/s suggests severe TR
Input:
E wave velocity
②
72. Valvular regurgitation
Pulmonary regurgitation: Jet width - CFM
Minor degrees of pulmonary regurgitation
(PR) have been reported in 40-78% of
patients with morphologically normal
pulmonary valves and no other evidence of
structural heart disease Pathologic
regurgitation is infrequent, and should be
diagnosed mainly in the presence of
significant structural abnormalities of the
right heart. Color Doppler flow mapping
is the most widely used method to identify
PR. A diastolic jet in the RV outflow tract,
beginning at the line of leaflet coaptation and
directed toward the
right ventricle is diagnostic of PR.
Although this measurement suffers from a
high inter-observer variability, a jet width
that occupies >65% of the RV outflow tract
width measured in the same frame is in
favour of severe PR.
Input:
Color Jet width (white)
RVOT width (yellow)
Output:
Jet to RVOT width ratio (%)
①
73. Valvular regurgitation
Pulmonary regurgitation: Vena contracta (VC)
Although the vena contracta width is
probably a more accurate method than the
jet width to evaluate PR severity by colour
Doppler, it lacks validation studies. As for
other regurgitations, the same limitations are
applicable. The shape of the vena contracta is
complex in most cases.
Input:
PR VC width (cm)
①
74. Valvular regurgitation
Pulmonary regurgitation: Jet density and deceleration rate
CW Doppler is frequently used to measure
the end-diastolic velocity of PR and thus
estimate pulmonary artery end-diastolic
pressure. However, there is no clinically
accepted method of quantifying pulmonary
regurgitation using CW Doppler. Similar to
AR, the density of the CW signal provides a
qualitative measure of regurgitation. A rapid
deceleration rate, while consistent with more
severe regurgitation, is influenced by several
factors including RV diastolic properties and
filling pressures.
A pressure half-time < 200 ms is consistent with
severe PR.
②
Input:
PR PHT
Output:
Deceleration rate (ms)
75. Cardiac shunts
Qp/Qs can be estimated by using 2D echo
and spectral doppler measurements in
patients who have intra- or extra- cardiac
shunts, e.g. atrial or ventricular septal
defects.
This formula only works in cases where there is
pure left to right shunting.
Qp = RVOT VTI x π x (RVOT / 2)²
Qs = LVOT VTI x π x (LVOT / 2)²
Qp/Qs ratio = Qp/Qs
Qp/Qs: Pulmonary-systemic flow ratio
Input:
LVOT (mm)
LVOT VTI (cm)
RVOT (mm)
RVOT VTI (cm)
Output:
Qp/Qs
76. Prosthetic valves
Prosthetic aortic valves: doppler investigation (formulas previously described)
Doppler echocardiography of
the valve
- Peak velocity gradient
- Mean gradient
-Contour of the jet velocity, AT
(acceleration time)
-DVI (doppler velocity index) *
-EOA (Effective orifice area)
- Presence, location, and
severity of regurgitation
Pertinent cardiac chambers - LV size, function, and Hypertrophy
* DVI = VLVO / VPrAV . DVI is the Ratio of respective VTIs, and can
be approximated as the ratio of the respective
peak velocities. (simplified continuity equation)
DVI = Doppler Velocity Index
VLVO = Subvalvular (LVOT) velocity
VPRAV = Max velocity across the valve
77. Prosthetic valves
Doppler echocardiography of
the valve
- Peak early velocity
- Mean gradient
- Heart rate at the time of Doppler
- Pressure half-time
-DVI*: (Doppler velocity index)
-EOA (Effective oriffice area)
- Presence, location, and severity
of regurgitation†
Other pertinent
echocardiographic and doppler
parameters
- LV size and function
- RV size and function
- Estimation of pulmonary artery
pressure
* DVI = VPrMV / VLVO DVI is the Ratio of respective VTIs, and can
be approximated as the ratio of the respective
peak velocities. (simplified continuity equation)
Prosthetic mitral valves: doppler investigation (formulas previously described)
VPRMV = Max velocity across the prosthetic mitral valve
78. Prosthetic valves
Doppler echocardiography of
the valve
- Peak velocity/peak gradient
- Mean gradient
- DVI *
- EOA*
- Presence, location, and severity
of regurgitation
Related cardiac chambers - RV size, function, and hypertrophy
- RV systolic pressure
* Theoretically possible to measure. Few data exist.
Prosthetic pulmonary valves: doppler investigation (formulas previously described)
79. Prosthetic valves
Doppler echocardiography of
the valve
- Peak early velocity
- Mean gradient
- Heart rate at time of Doppler
assessment
- Pressure half-time
- VTIPRTV / VTILVO *
- EOA
- Presence, location, and severity of TR
Related cardiac chambers, inferior
vena cava and hepatic veins
- RV size and function
- Right atrial size
- Size of inferior vena cava and
response to inspiration
- Hepatic vein flow pattern
Prosthetic tricuspid valves: doppler investigation (formulas previously described)
* Feasible measurements of valve function, similar to mitral prostheses,
but no large series to date.
VTIPRTV: Velocity Time Integral Prosthetic Tricuspid Valve
VTILVO: Velocity Time Integral LVOT
80. AT = Acceleration time
EF = Ejection fraction
ET = Ejection time
FAC = Fractional area change
IVA = Isovolumic acceleration
IVC = Inferior vena cava
IVCT = Isovolumic contraction time
IVRT = Isovolumic relaxation time
MPI = Myocardial performance index
MRI = Magnetic resonance imaging
LV = Left ventricle
PA = Pulmonary artery
PADP = Pulmonary artery diastolic pressure
PH = Pulmonary hypertension
PLAX = Parasternal long-axis
PSAX = Parasternal short-axis
PVR = Pulmonary vascular resistance
RA = Right atrium
RIMP = Right ventricular index of myocardial performance (MPI
RV)
RV = Right ventricle
RVH = Right ventricular hypertrophy
RVOT = Right ventricular outflow tract
RVSP = Right ventricular systolic pressure
SD = Standard deviation
SPAP = Systolic pulmonary artery pressure
TAM = Tricuspid annular motion
TAPSE = Tricuspid annular plane systolic excursion
3D = Three-dimensional
TR = Tricuspid regurgitation
2D = Two-dimensional
Other abreviations