Transcript Valvular Regurgitation - Gvsu - Grand Valley State University

Valvular Regurgitation
Susan A. Raaymakers, MPAS, PA-C, RDCS (AE)(PE)
Assistant Professor of Physician Assistant Studies
Radiologic and Imaging Sciences - Echocardiography
Grand Valley State University, Grand Rapids, Michigan
[email protected]
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Basic Principles
Etiology
Congenital
Acquired abnormalities
Fluid Dynamics of Regurgitation
Characterized
Regurgitant orifice area
High-velocity regurgitant jet
Proximal flow convergence area
Downstream flow disturbance
Increased antegrade flow volume
Fluid Dynamics of Regurgitation
Regurgitant orifice
 characterized by high-velocity laminar
jet
 Related to instantaneous pressure
difference (∆P=4v2)
 Upstream side of regurgitant
acceleration proximal to regurgitant
orifice
 PISA
 Narrowest segment of the regurgitant
jet occurs just distal to the regurgitant
orifice reflects regurgitant orifice area
 Vena Contracta
Fluid Dynamics of Regurgitation
Size, Shape and Direction of Regurgitant Jet
 Size
Affected by physiologic and technical factors
 Regurgitant volume
 Driving pressure
 Size and shape of regurgitant orifice
 Receiving chamber constraint
 Influence of coexisting jets or flowstreams
 Ultrasound system gain
 Depth
 Signal strength
Fluid Dynamics of Regurgitation
Size, Shape and Direction of Regurgitant Jet
 Shape and Directions
Affected by
Anatomy and orientation of regurgitant orifice
Driving force across the valve
Size and compliance of receiving chamber
Volume Overload
 Total Stroke Volume
 Total volume of blood pumped by the ventricle in a single beat
 Forward Stroke Volume
 Amount of blood delivered to the peripheral circulation
 Regurgitant Volume
 Amount of backflow across the abnormal valve
Volume Overload
Chronic valvular regurgitation
 Results in progressive volume overload
of the ventricle
Volume overload in LV results in LV
chamber enlargement with normal wall
thickness (total LV mass is increased)
 Important clinical feature:
• An irreversible decrease in systolic function can occur
in absence of symptoms
Detection of Valvular Regurgitation
 2D imaging
 Indirect evidence
 Chamber dilation and function
 Color flow imaging
 Flow disturbance downstream form regurgitant orifice
 Sensitive (90%) when correct settings are utilized
 Specific (nearly 100%) compared with angiography
 True positives and false positives
 False positives due to mistaken origin or timing
 False negatives due to low signal strength or
inadequate images
Detection of Valvular Regurgitation
 Continuous-wave Doppler ultrasound
Identification of high velocity jet through
regurgitant orifice
Advantage:
 Beam width is broad at the level of the valves
when studied from an apical approach
Valvular Regurgitation in Normal Individuals
 Physiologic
Small degree of regurgitation in normal
individuals
No adverse implications
Typically
 Spatially restricted to area immediately adjacent
to valve closure
 Short in duration
 Represents on a small regurgitant volume
 May be detected in 70 – 80% mitral
 May be detected in 80 – 90% tricuspid
 May be detected in 70 – 80% pulmonary
 May be detected in 5% aortic (increases with
age).
• Clinical significance of AI is unknown
Approaches to Evaluation of the Severity of Regurgitation
 Semi-quantitative measures
Mild, moderate or severe utilizing
 Color jet area
 Vena contracta width
 Pressure half-time (for aortic insufficiency)
 Distal flow reversals
Approaches to Evaluation of the Severity of Regurgitation
 Quantitative measures
Regurgitant volume (RV)
 Retrograde volume flow across the valve
 Expressed either as
• Instantaneous flow rate in ml/sec
• Averaged over the cardiac cycle in ml/beat
 Calculated by
• PISA
• Volume flow rates across the regurgitant and competent
valve (Spectral Doppler Technique)
• 2D total left ventricular stroke volume minus Doppler
forward stroke volume
Regurgitant fraction
 RF = RV/SV total
Regurgitant orifice area
Effective Regurgitant Orifice Area (EROA)
Application of continuity equation
“what flows in must flow out”
Based on theory of conservation of mass
May be calculated utilizing
Spectral Doppler technique
Application of the PISA method
Spectral Doppler Method
Spectral Doppler Technique
 Regurgitant volume through an incompetent valve is
equal to the flow at the regurgitant orifice
 Stroke volume may be calculated from the CSA and the VTI
 RVol = EROA x VTIRJ
 RVol = Regurgitant volume (cc)
 EROA = Effective regurgitant orifice area (EROA)
 VTIRJ = Velocity time integral of the regurgitant jet (cm)
 Rearrange equation
EROA = RVOL/VTIRJ
Non-dynamic
Spectral Doppler Technique
“Step by Step”
1.
2.
3.
4.
5.
Calculate stroke volume (SV) through LVOT
Calculate stroke volume (SV) through MV
Calculate the regurgitant volume (cc)
Measurement of VTI of regurgitant signal
Calculate the effective regurgitant area (cm2)
Non-dynamic
Spectral Doppler Technique
“Step by Step”
1. Calculate stroke volume (SV) through LVOT
 Measure LVOT diameter from PLAX
 Inner edge to inner edge
 CSA = 0.785 x D2
 Measure the LVOT VTI from apical long axis or apical
four chamber anterior tilt
 SV (cc) = CSA (cm2) * VTI (cm)
Spectral Doppler Technique
“Step by Step”
2.
Calculate the stroke volume through the mitral valve

Measure the mitral valve annulus



Measure mitral annulus VTI


Apical four chamber at mid-diastole: inner edge to inner edge
CSA = 0.785 x D2
PW Doppler at the level of the annulus
SV (cc) = CSA (cm2) * VTI (cm)
Spectral Doppler Technique
“Step by Step”
3. Calculate the regurgitant volume

R Vol(MR) = SV (MV) – SV (LVOT)
4. Measurement of VTI of regurgitant signal

Optimize CW Doppler spectrum of regurgitant signal
Spectral Doppler Technique
“Step by Step”
5. Calculate the effective regurgitant orifice area
(EROA in cm2)

EROA = RVol(MR) ÷ VTI(MR)
Spectral Doppler Technique
Limitations
 Accuracy of measurements
 Inadequate spectral Doppler envelope for mitral
regurgitation VTI measurement
 Significant learning curve
 May be considered time consuming and tedious
Spectral Doppler Technique
Clinical Significance of the EROA and Mitral Regurgitation
Color Doppler Imaging
 Jet Area
 Screening for significant flow often based on flow
disturbance in receiving chamber
 Size of flow disturbance evaluated in at least two
views
 Important to evaluate color flow disturbance based on
cardiac cycle timing
 Size of jet relative to receiving chamber provides
qualitative index of regurgitant severity on scale of
0(mild) - 4+(severe)
Color Doppler Imaging
Color Doppler Imaging
 Aortic Regurgitation
 Best evaluated from PLAX approach
 Shorter distance from transducer to flow region
of interest: better signal to noise ratio
 Multiple flow directions within jet
Color Doppler Imaging - Mmode
 Evaluation of exact
timing of flow
 In relation to QRS and
valve opening and
closure
 Higher sampling rate
Vena Contracta




Narrowest diameter of the flow stream
Reflects diameter of regurgitant orifice
Relatively unaffected by instrument settings
Recommended



Perpendicular to jet width
Zoom mode
Narrow sector and depth
Non-dynamic
Proximal Isovelocity Surface Area Method
(PISA)
Proximal Isovelocity Surface Area
Basic Principle
 Based on conservation of energy
 PISA measurement analogous to calculation of
stroke volume proximal to a stenotic valve
 Variation of continuity equation
 Flow rate proximal to a narrowed orifice is
the product of the hemispheric flow
convergent area and the velocity of that
isovelocity shells
 Expressed by Q = 2r2Vr
 Q = flow rate
 2r2 = area of hemispheric shell (cm2)
 Vr = velocity at the radial distance –
r(cm/s)
Non-dynamic
Proximal Isovelocity Surface Area
Basic Principle
 Continuity principle: blood flow
passing through a given
hemisphere must ultimately pass
through he narrowed orifice
Flow rate through any given hemisphere
must equal the flow rate through the
narrowed orifice
 2r2Vr = A0*V0
• A0 = area of the narrowed orifice (cm2)
• V0 = peak velocity through the narrowed
orifice (cm/s)
 Rearrange the equation
• A0 = (2r2Vr )/V0
Non-dynamic
Proximal Isovelocity Surface Area
Basic Principle
 Continuity principle: blood flow passing
through a given hemisphere must ultimately
pass through he narrowed orifice
Flow rate through any given hemisphere must equal
the flow rate through the narrowed orifice
 2r2Vr = A0*V0
• A0 = area of the narrowed orifice (cm2)
• V0 = peak velocity through the narrowed orifice (cm/s)
 Rearrange the equation
• A0 = (2r2Vr )/V0
Proximal Isovelocity Surface Area
(PISA) Application in Calculation of Effective Orifice Area
(EROA)
Regurgitant valve acts as the narrowed orifice
Peak velocity is equivalent to the peak velocity
of the regurgitant jet
Utilizing Doppler colorflow radius and velocity
at the radial distance can be identified
Proximal Isovelocity Surface Area
(PISA) Application in Calculation of Effective Orifice Area (EROA)
 Adjustment of Nyquist limit enlarges size of shell for more accurate
measurement
 Shift baseline to downward typically 20 to 40 cm/sec
 The surface area of a hemisphere is calculated by the formula:
 Surface area = 2πr2
 Multiplication of aliasing velocity with surface area yields regurgitant
volume
Non-dynamic
Proximal Isovelocity Surface Area
Effective Regurgitant Orifice Area (ROA)
 EROA = RVmax /VMR
 RVmax : Regurgitant Volume (cm3)
 VMR : Velocity of mitral regurgitation (cm/sec)
Non-dynamic
Steps for Obtaining PISA Regurgitant Orifice Area
1.
Zoom mitral valve
2.
Decrease color scale to identify surface of hemisphere shell
3.
Note alias velocity – color bar (Valiasing)
4.
Measure alias from orifice to color change (r)
5.
Regurgitant volume

RVmax = 2  r2 x Valiasing
6.
Measure peak mitral regurgitant velocity (VMR)
7.
Effective Regurgitant Orifice Area

EROA = RVmax/VMR
Steps for Obtaining PISA Regurgitant Orifice Area
Surface area = 2r2
2(0.67 cm)2 = 2.80 cm2
Regurgitant Volume Flow Rate
RVmax=Surface Area* Valiasing
2.80 cm2 * 26 cm/sec = 72.8 cm3/sec
Effective Regurgitant Orifice Area
EROA = RVmax/VMR
(72.8 cm3/sec) / (66.2 cm/sec) = 1.1 cm2
0.67cm
Simplified Method for Calculation of the Mitral Regurgitant Volume
 May be employed when appropriate CW jet is
unable to be obtained (i.e. eccentric jet)
 Based on premise:
 Ratio of maximum MR velocity to VTI MR is equal to a
constant of 3.25
 Regurgitant volume = (2r2Valiasing)/3.25

2r2 = area of hemispheric shell derived from the radius [r] (cm2)


Valiasing = aliased velocity identified as the Nyquist limit (cm/s)
3.25 constant
Clinical Significance of the PISA Radius
and Valvular Regurgitation
Proximal Isovelocity Surface Area –
EROA MV Considerations
 Assumption is made that RVmax and VMR occur at the
same position in the cardiac cycle
 PISA is larger in large volume sets and smaller in
smaller volume sets
 Also changes size in accordance with color Doppler scale
 PISA should be recorded in a view parallel to flow
stream typical apical four chamber
 If PISA is hemi-elliptical or if valve is nonplanar,
alternate approach or alternate corrections
PISA Limitations
 Nonoptimal flow convergence
 Phasic changes
 Eccentric jets
 Interobserver variability
 Isovelocity surface not always hemisphere
 PISA model is a sphere. Mitral regurgitant orifice may be irregular
 Multiple regurgitant jets
 May not be able to completely envelope the mitral regurgitation trace
 Mitral flow rate will vary throughout systole
PISA – EROA
Limitations
Nonoptimal flow convergence
Suboptimal Flow Convergence
Suboptimal Flow Convergence
Flow: not symmetric
Perforated mitral leaflet - TEE
Continuous Wave Doppler Approach
Signal intensity
Proportional to number of
blood cells contributing to
regurgitant signal
Compare retrograde to
antegrade flow intensity
Weak signal = mild regurgitation
Strong signal = severe
regurgitation
Intermediate signal = moderate
regurgitation
Continuous Wave Doppler Approach
Antegrade flow velocity
Regurgitation results in increase in antegrade
flow across the incompetent valve
Greater the severity of regurgitation; the greater the
antegrade flow velocity
• Consideration of co-existent stenosis
Continuous Wave Doppler Approach
Time course (shape) of mitral regurgitant
velocity curve
Dependent on time-varying pressure gradient
across regurgitant orifice
Related to pressure gradient
Normal LV systolic pressure = 100 – 140 mmHg
Normal LA systolic pressure = 5 – 15 mmHg
Difference therefore: 85 – 135 mmHg
• MR velocity is typically 5 – 6 m/sec
Continuous Wave Doppler Approach
 Time course (shape) of
mitral regurgitant velocity
curve
 Normal LV systolic function:
• Rapid acceleration to peak
velocity
• Maintenance of high velocity in
systole
• Rapid deceleration prior to
diastolic opening of the mitral
valve
 Increase in left atrial
pressure results in late
systolic decline in the
instantaneous pressure
gradient
Continuous Wave Doppler Approach
 Shape of aortic regurgitant curve
 Dependent on time course of diastolic
pressure difference
 Normal low end-diastolic pressure
 Aortic end-diastolic pressure is
normal (high pressure difference)
 Slow rate of pressure decline
 Acute AI results in more rapid velocity
decline in diastole
Continuous wave Doppler across AV
Decel = 270 cm/sec
Decel >500 cm/sec
With permission, Dunitz 2000
Distal Flow Reversals
Severe atrioventricular valve
regurgitation may result in
Flow reversal of veins entering atrium
Flow reversal in hepatic
vein due to severe tricuspid
regurgitation
Flow reversal in pulmonary
veins on TEE due to
severe mitral regurgitation
Distal Flow Reversals
Severe semilunar valve regurgitation
may result in
Flow reversal of associated vessel
Abdominal flow reversal in diastole due to severe aortic
regurgitation. Note moderate aortic regurgitation is limited to
descending thoracic aorta
Aortic Regurgitation
Aortic Valve
 Diastole: free margins of the cusps coapt
tightly preventing the backflow of blood into
the ventricle.
“Y” shape in PSAX (sometimes referred to as
inverted Mercedes-Benz sign)
 Systole: cusps open widely in a triangular
fashion, with flexion occurring at the base.
 Semi-lunar valve
Aortic Cusps
 Three Cusps named for the corresponding origins of
the coronary arteries.
 Folds of endocardium with a fibrous core attached to
the aortic wall rather than the ventricular wall.
 Base of the cusps is thicker and cusps themselves
are thin and translucent.
 Crescent and pocket shaped.
 Equal in size.
Aortic Cusps
 Free edge of each cusp curves upward from commissure
and form a slight thickening at tip called Arantius nodule.
 When valve closes:
 three nodes meet in center, allowing coaptation to occur
along three lines. “Y” shape in diastole.
 Behind each cusp is its associated Sinus of Valsalva.
Aortic Cusps
Sinotubular junction
Sinus of Valsalva
 Sinuses represent out-pouchings in the aortic root
directly behind each cusps.
 Function to support the cusps during systole and
provide reservoir of blood to augment coronary artery
flow during diastole.
 Sinus and its corresponding cusp share the same
name.
 Noncoronary sinus is posterior and rightward just
above the base of the interatrial septum.
M-mode Normal AV –
Coaptation Point In Center Of Aortic Root
Parasternal Views
Apical views
Aortic valve in the far field
Poor resolution of anatomic details
PARALLEL to flow
Best view for measuring velocities across valve
AR jet
AS jet
Subcostal view
Often the view that “saves” the study
Non-coronary cusp is intersected by the
interatrial septum
Short axis Subcostal view - Non-coronary
cusp intersected by Interatrial septum
TEE views
Anterior root is at the bottom of the screen
(reverse parasternal LAX view)
Leaflet at top of screen usually noncoronary (can be left coronary cusp)
Leaflet at bottom of screen is right
coronary cusp
TEE - 137º
Non-dynamic
Aortic Cusps – Lambl’s Excrescences
Thin, delicate filamentous strands that
arise from ventricular edge of aortic
cusps.
Normal variants.
Seen increasingly with advancing age
and improved image quality.
Aortic Cusps – Lambl’s Excrescences
 Originate as small thrombi on endocardial
surfaces
 Have the potential to embolize to distant organs
10-56 Feigenbaum
21-9 Lambl TEE Feigenbaum
Aortic Insufficiency
 Presence of AI should be assessed by Doppler
 Flail AV leaflet will always produce AI
 Direction of regurgitant jet may or may not
produce MV or septal fluttering
 Use TEE of abscess detection
Aortic Regurgitation
History
 Exertional dyspnea
 Fatigue
 Palpitations
 Chest pain (angina)
 Dizziness
 Syncope (uncommon)
 Congestive Heart Failure (dyspnea on exertion, orthopnea, paroxysmal
nocturnal dyspnea)
 Right heart failure (e.g., jugular venous distention, hepatomegaly,
peripheral edema, ascities, anasarca)
Aortic Insufficiency
Complications
 Chronic AI;
 Initially patients may appear asymptomatic and may later
develop signs of CHF
 Patients with bicuspid valve are at higher risk for
endocarditis
 LV volume overload (similar to MR)
 Diastolic murmur at left sternal border (LSB) and
apex (Austin-Flint murmur- diastolic rumble)
 Acute AI; sudden onset of CHF may occur because
the LA does not have time to enlarge
Aortic Insufficiency
Etiology
• Inflammatory
• Structural
• Genetic
• Stress
Aortic Insufficiency (AI)
Inflammatory
Rheumatic Fever
Ankylosing Spondylitis
Rheumatoid Arthritis
Systemic Lupus Erythematosus
Syphilus
Phen-fen
Aortic Insufficiency (AI)
Structural
 Atherosclerosis
 Bicuspid or unicuspid aortic valve
 Aortic dissection
 Aortic valve prolapse
 Infective endocarditis
 Ventricular septal defect (perimembranous, outlet)
 Sinus of Valvsalva aneurysm
 Trauma
 Catheter balloon valvuloplasty
Dilated root and effacement
sinotubular junction
Non-dynamic
Preserved root - dilated ascending
aorta
Non-dynamic
Aortic Valve Prolapse
Best seen in parasternal long axis
Disruption of commissural support
Dissection
Dilatation
Perimembranous VSD
Myxomatous or congenitally abnormality
Aortic Valve Prolapse Right Coronary Cusp
Non-dynamic
Severe AR filling LVOT
Non-dynamic
Bicuspid Aortic Valve
10-47 Feigenbaum
Quadracusp Aortic Valve
http://video.google.com/videoplay?docid=-1101037639424512577#
Endocarditis
19-32a Feigenbaum
19-32b Feigenbaum
Rupture of Sinus of Valsalva Due to
Endocarditis
13-17 Feigenbaum
Endocarditis
10.33b Feigenbaum
10.33a Feigenbaum
Aortic Dissection
Proximal extent usually 1 cm distal to
sinotubular junction
Flap may extend to root
Rupture into pericardial space
Dissect coronary (right > left)
Disrupt AV architecture
Transthoracic very INSENSITIVE
TEE aortic dissection disrupting commissure
between right and left coronary cusps
Non-dynamic
TEE Long Axis View –
Dissection Flap In Aortic Root
Non-dynamic images
Marfan’s Syndrome
 Connective tissue multisystemic
disorder characterized by
Skeletal changes (arachnodactyly,
long limbs, joint laxity, pectus)
Cardiovascular defects
 Aortic aneurysm which may dissect
 Mitral valve prolapse
Ectopia lentis
Autosomal dominant inheritance,
caused by mutation in the fibrillin-1
gene (FBN1) on chromosome 15q .
Marfan’s Syndrome
 Arachnodactyly in an
8-year-old girl with
Marfan’s syndrome
Marfan Syndrome
20.22b Feigenbaum
20.22a Feigenbaum
Marfan’s Syndrome
10.31b Feigenbaum
Aortic Insufficiency (AI)
Stress
Systemic hypertension (dilated root due
to hypertension is the most common
cause of AI)
Renal failure
Type A Aortic Dissection
20.30b Feigenbaum
20.30a Feigenbaum
“Renal” Heart
22.7 Feigenbaum
Aortic Insufficiency (AI)
M-Mode, 2D Criteria and Doppler Criteria
AI - M-Mode Criteria
 MV fluttering in early diastole
Austin-Flint murmur
Diastolic septal fluttering depends on direction of jet
 Chronic AI
 Increased
LV size with minimal LVH
 Normal or hyperdynamic LV systolic function
 In decompensated state, LV systolic function may be depressed.
 Presence of “B” bump (Increased LV end
diastolic pressure) associated with acute AI.
 Premature AV opening in acute AI
Aortic Insufficiency
2D Criteria
 Valve Anatomy
 Flail, Bicuspid, Endocarditis, Prolapse
 Chronic AI; enlarged LV cavity with minimal LVH – normal or hyperdynamic LV
function unless decompensated
 Ascending aorta size usually increased; identify aortic aneurysms (ascending,
arch, descending)
 Reverse doming of anterior mitral valve leaflets is associated with severe AI
Non-dynamic
Aortic Insufficiency
Doppler Criteria
 Evidence of diastolic turbulence beginning at aortic
valve closure
 Patients with severe aortic insufficiency may
demonstrate a reversed diastolic flow by PW Doppler
in the abdominal or thoracic aorta.
 Color flow mapping of flow disturbance into LV may
disclose severity.
 Color flow may be useful in quantitating severity
based on width of flow disturbance to width of LVOT
in parasternal long-axis view.
Aortic Insufficiency
Doppler Criteria
 Doppler cursor is parallel to flow,
“Normal” peak velocity of an aortic regurgitant jet is
3.0 to 5.0 m/s
 Due to the pressure difference between the aorta and LV
during diastole.
 Spectral Doppler display signal intensity
Should be considered in evaluating the degree of AI.
Compare the forward aortic flow with the signal
strength of the AI jet.
Aortic Insufficiency
10.5 Feigenbaum
Aortic Insufficiency
Aortic Valve Prolapse - 2D Criteria
 Parasternal long-axis view: posterior placement of aortic
leaflet(s) into LVOT during diastole.
 May be noted in association with MV or TV prolapse.
 Right coronary cusp prolapse may occur with membranous
ventricular septal defect.
 M-Mode is not diagnostic; may see echo in LV outflow tract
during diastole.
 Sinus of Valsalva aneurysm
Non-dynamic
Aortic Insufficiency - Flail Aortic Leaflet
2D Criteria
In PLAX, loss of leaflet coaptation and
erratic echoes in LVOT
PSAX-Ao may disclose leaflet(s) involved.
Perforations in leaflets
Aortic ring abscess due to endocarditis
Flail Aortic Leaflets - M-Mode Criteria
 Course flutter of closed aortic leaflets during
diastole.
 Erratic systolic motion of closed aortic
leaflet(s).
 When AI is present, associated diastolic
fluttering of MV and/or septum.
 Enlarged LV chamber with hyperdynamic LV
systolic function.
 Premature closure of AV in acute AI.
Left Ventricular Response
 Chronic volume overload
Progressive dilation and increased sphericity of LV
Initially LV systolic function remains normal
 Stroke volume is ejected across the aortic valve into the
high-impedence systemic vasculature therefore not
hyperdynamic
Long asymptomatic period
Chronic gradual increasing AI
 LV remains compliant in diastole: end-diastolic pressure
remains normal
 Over time LV systolic dysfunction occurs in presence of
significant regurgitation
Diastole
Systole
LV Dysfunction Secondary to AI
10-35 Feigenbaum
Left Ventricular Response
 Acute Aortic Regurgitation
Short interval from set of volume overload to clinical
presentation
Volume overload is poorly tolerated due to the normal
left ventricular size and the constraining effects of the
pericardium.
 Mitral regurgitation
 Left ventricular pressure increases rapidly.
 Premature closing of MV, which can be recorded
using M-mode imaging.
Acute AI
Usually caused by endocarditis

Disruption or destruction of aortic leaflets
and/or aortic dissection

Annular and/or root dilation
Acute AI
Acute AI may also be caused by:
Trauma
Effect of AI on mitral valve
10.030 Feigenbaum
Severity of Aortic
Regurgitation
Severity of Aortic Regurgitation
Semi-quantitative measurement
No gold standard
Invasive measurement is qualitative
Ventricular opacification following aortic root
injection with IV dye
Severity of Aortic Regurgitation
 Size of the color flow jet
Length of jet dependent on ultrasound machine settings
 Gain
 Pulse repetition frequency
 Transmission frequency
Length of jet dependent on ventricular compliance
Severe AR - broad jet extends into LV cavity
Severity of Aortic Regurgitation
Width of jet compared to LVOT diameter
Measured in parasternal long axis view
Or in TEE longitudinal plane
<25% - mild AR
25-40% moderate
>40% severe
Mild AR - jet ratio <25%
Severe AR - jet ratio >60%
Grading Aortic Regurgitation by
Regurgitant Jet Area/LVOT Area (PLAX)
10.44a
Feigenbaum
10.44b
10.44c
≥ 65% Regurgitant Jet Area/LVOT Area
(PLAX)
10.36 Feigenbaum
View Dependent Color Flow Doppler
Evaluation
 Both Images Obtained From Same Patient
10.48b Feigenbaum
10.48a Feigenbaum
Severity of Aortic Regurgitation
Short axis area of regurgitation
Dependent on level of short axis image
Short axis of the LVOT, not aortic sinuses
Color M-mode
Continuous wave Doppler across AV
 Deceleration slope of AR spectral envelope
Pressure gradient = 4 V 2
Fall in velocity during diastole related to
decrease in pressure gradient
Flat slope indicates no change in gradient
during diastole = mild AR
Deceleration Slope
 Grading of AR (AI)
<200 cm2/sec = mild
200 - 350 cm2/sec = moderate
>350 cm2/sec = severe
 Pressure half time also may be used
 Dependent on ventricular compliance
 Eccentric jets may be difficult to assess
Diastolic Reversal of Flow
Sample volume in descending thoracic
aorta from suprasternal notch
Also in abdominal aorta from subcostal
position
Reversal of flow in diastole from abdominal aorta
Indications for Surgery AR
Symptoms
End-systolic internal dimension > 55 mm
May not be applicable in women - use smaller LVIDD
Fall in ejection fraction
Diastolic dimension > 70 mm associated
with sudden death
Mitral Regurgitation
Mitral Valve Apparatus
Left atrial wall
Mitral annulus
Anterior and posterior
leaflets
Chordae
Papillary muscles
Left ventricular myocardium
underlying the papillary
muscles
Mitral Regurgitation
Occurs during systole, which at normal
heart rates constitutes approximately 1/3
of the cardiac cycle.
Mitral Regurgitation
Hemodynamically significant mitral
regurgitation results in volume overload.
Subsequent left ventricular dilation and left
atrial dilation.
Consequentially there is elevation of left atrial
pressure, which is transmitted in pulmonary
congestion.
Mitral Regurgitation
Signs and Symptoms
 Shortness of breath, especially with exertion or
when lying down
 Fatigue, especially during times of increased
activity
 Cough, especially at night or when lying down
 Heart palpitations — sensations of a rapid,
fluttering heartbeat
 Swollen feet or ankles
 Heart murmur
 Excessive urination
Mitral Regurgitation- Acute
 Acute severe mitral regurgitation often results in
acute pulmonary congestion.
 Left atrial size is normal. Left ventricular
sysotolic function is hyperdynamic
 Most common cause of acute MR:
Rupture of chordae tendineae due to mitral valve
prolapse
Acute ischemia
Infarction
Infective endocarditis
Mitral Regurgitation-Chronic
Chronic mitral regurgitation may be
tolrated for decades
Left ventricular size is dilated, left
ventricular function is hyperdynamic early,
may be normal or depressed with longstanding regurgitation, enlarged LA
Etiology
Myxomatous valve disease
Annular dilatation
Mitral Regurgitation
Etiologies













Rheumatic mitral valve disease
Mitral valve prolapse
Myocardial infarction (papillary muscle dysfunction)
Ruptured chordae tendineae
Flail mitral leaflet
Mitral valve vegetations
Dilated cardiomyopathies
Left ventricular outflow tract obstructions
Use of certain appetite suppressants
Calcification of the mitral annulus
Tumors of the mitral valve
Annular Dehiscence
Radiation damage
Rheumatic Heart Disease
Non-dynamic
Mitral Valve Prolapse
Non-dynamic
Mitral Valve Prolapse
11.72a-72b Feigenbaum
Mitral Valve Prolapse
11.80a Feigenbaum
Mitral Valve Prolapse
Ruptured Papillary Muscle
Due to Coronary Artery
Disease
15.44 Feigenbaum
Ruptured Chordae Tendineae
Standard real-time B-scan
Duplex scan: color Doppler superimposed on real-time B-scan
Diagnosis: Severe mitral regurgitation due to flail posterior MV leaflet.
Underlying pathology: Mitral valve prolapse with ruptured chordae tendinae.
Data source : Arizona Society of Echocardiography Image Library
Flail Mitral Leaflet
Rupture of the supporting apparatus of the mitral valve allowing the
tip of the leaflet to project into the left atrium in systole
The most frequent etiologies are :
 Chordal rupture complicating mitral valve prolapse syndrome
 Infective endocarditis
 Papillary rupture caused by acute myocardial infarction.
 Primary degeneration of the chordae is a cause of spontaneous
rupture.
11.81b Feigenbaum
Flail Mitral Leaflet
Yale Atlas of Echo- Flail Mitral Valve
Mitral Valve Vegetations/Infections
Mitral Valve Vegetations/Infections
 Mitral
vegetations
 Found on the
upstream side
of valves such
as the left
atrium in mitral
valvular
vegetation.
Mitral Regurgitation
13.3a & b Feigenbaum
Dilated Cardiomyopathies
Dilated Cardiomyopathy
Hypertrophic Cardiomyopathy
Idiopathic Hypertrophic Subaortic Stenosis (IHSS)
 IHSS
Appetite Suppressants
 Common name: Fen-Phen
(fenfluramine, phentermine, dexfenfluramine)
 Use of Fenfluramine or dexfenfluramine for more
than four months may have an increased risk of
valvular heart disease.
 Fenfluramine and dexfenfluramine are no longer
marketed in the U.S. as of 1997 and have no
current FDA labels.
Calcification of the Mitral Annulus
 Mitral annulus area normally is smaller in systole than in diastole.
 Increased rigidity of the annulus impairs systolic contraction of the annulus leading to
mitral regurgitation.
 Appearance on 2D imaging as area of increased echogenicity on left ventricular side
of annulus immediately adjacent to attachment point of the posterior leaflet.
 Commonly seen in elderly subjects and in younger patients with renal failure or
hypertension.
11.89
Feigenbaum
Tumor of mitral valve/Papillary Fibroelastoma
 Unlike vegetations:
fibroelastomas are
more often found on
the down stream side
of the valve
 Usually of no clinical
significance but may
cause mitral
regurgitation
21.6 Feigenbaum
Annular Dehiscence
 Infrequent sequela of
blunt trauma.
 Presumed mechanism
Sudden dramatic increase in
pressure against a closed
mitral valve resulting in
tearing of the posterior leaflet
from the mitral valve annulus
19.31b Feigenbaum
Radiation Damage
Note
Pathologic echo density of
the anterior mitral leaflet
Reduced mobility of the
portion of the mitral valve
Increased echo densities
in the aortic valve,
 Which is also a consequence
of radiation therapy in these
two relatively young patients.
11.095a Feigenbaum
Mitral Regurgitation
Jets
Central
Bileaflet prolapse
Rheumatic disease
Peripheral
Vegetations
Unicuspid prolapse
Flail
Mitral Regurgitation
Color Doppler is primary tool for detection
and quantification
Recognition of expected timing of
regurgitation is critical.
Mitral Regurgitation
Doppler evaluation of mitral regurgitation
Not all color Doppler signals appearing
within the LA represent mitral regurgitation
Mitral Regurgitation
Normal posterior motion of the blood pool
caused by mitral valve closure.
Pulmonary Vein Flow
11.40 Feigenbaum
Mitral Regurgitation
Reverberation from aortic flow
11.39 Feigenbaum
Mitral Regurgitation
Characteristics of True Mitral Insufficiency/Regurgitation
 Evidence of proximal flow acceleration (proximal
isovelocity surface area (PISA)
 Flow conforms to the appearance of a true “jet” or
ejection flow with a vena contracta
 Downstream (left atrial) appearance is consistent with a
volume of blood being ejected through a relatively
constraining orifice
Mitral Regurgitation
Characteristics of True Mitral
Insufficiency/Regurgitation (cont.)
 Flow signal is appropriately confined to systole
 Color Doppler signals are appropriate in color for
the anticipated direction and/or reveal the
appropriate variance or turbulence encoding
 PW and CW Doppler confirms origin, timing and
direction of blood flow
Mitral Regurgitation
Physiologic
Spacially restricted to the area immediately
adjacent to valve closure
Short in duration
Represents only a small regurgitant volume
When meticulously sought MR can be detected
in 70%-80%.
Determination of Mitral
Regurgitation Severity
Determination of Mitral Regurgitation
 Color Flow Doppler
 Size of the flow disturbance relative to the chamber
receiving the regurgitant jet in at least two views.
 Severity scale of 0(mild) to 4+(severe)
 Limitation: Variation with technical and physiological
factors
 Continuous Wave-Doppler
 Signal intensity
 Shape of velocity curve
 Limitation: Qualitative
 Vena Contract Width
 Width of regurgitant jet at origin
 Limitation: Small values, careful measurement needed
Determination of Mitral Regurgitation
…continued
 PISA
 Calculation of RV (regurgitant volume) and ROA
(regurgitant orifice area)
 Less accurate with eccentric jets
 Volume Flow at Two Sites
 Calculation of RV (regurgitant volume) and ROA
(regurgitant oriface area).
 Limitation: Tedious
 Distal Flow Reversals
 Pulmonary Vein reversal in Doppler
 Limitation: Qualitative, affected by LA pressure
Continuous Wave
 Signal intensity
Proportional to the number of blood cells contributing to
the regurgitant signal
Weak signal reflects mild regurgitation, whereas a signal
equal to intensity to the antegrade (forward) flow reflects
severe regurgitation
 Time course (shape) of the velocity curve
Acute MR: increase in end-systolic left atrial pressure
results in last-systolic decline in the instantaneous
pressure gradient. Waveform appears more early
slanted “V” than an equal “V”.
Vena Contracta
11.42 Feigenbaum
Distal Flow Reversals
 Significant volume of flood is displaced by the
regurgitant resulting in flow reversal seen in the
pulmonary veins entering the left atrium
 Reversal of normal patterns of systolic inflow of
pulmonary veins.
Determination of Mitral Regurgitation
PISA (Proximal Isovelocity Surface Area)
The highest velocity of blood flow occurs
proximal to the valve plane
Series of isovelocity “surfaces” leading to the
high velocity jet in the regurgitant orifice
Decision Making Repair or Replacement
 Most important factor: left ventricular size and function
 Progressive dilatation, an end-systolic dimension of
greater than 45 mm or any reduction of left ventricular
function may prompt surgical intervention regardless of
symptomatic status.
 Posterior leaflet prolapse and annular dilatation are most
amendable to repair, others require more complex
procedures with lower likihood of successful repair.
Intraoperative Evaluation of Mitral Repair
Transesophageal Echo is used during
operations.
Baseline images are obtained in the
operating room to reconfirm regurgitant
severity.
After valve repair, the patient is weaned
from cardiopulmonary bypass and valve
anatomy and regurgitation is re-evaluated.
Intraoperative Evaluation of Mitral Repair
If significant residual mitral regurgitation is
present,
Second bypass pump may be done to allow a
second attempt at repair or mitral valve
replacement.
Complications may include:
Left ventricular outflow tract obstruction
Functional mitral stenosis
Worsening of left ventricular systolic function.
Actually young hairy man. Antibiotics prior to dental cleanings
is no longer indicated in patients with mitral valve prolapse.
Tricuspid Regurgitation
Anatomy of the Tricuspid
Valve
Anatomy of the Tricuspid Valve
Atrioventricular valve that prevents
backflow of blood from the right ventricle
into the right atrium.
Composed of:
tricuspid annulus
leaflet tissue
chordae tendinae
papillary muscles
Tricuspid Annulus
Make-up of the tricuspid valve is similar to
mitral valvular composite but is less strong
Shape is roughly triangular
Largest valvular orifice of the heart
Tricuspid Valve Leaflets
 Three leaflets of the tricuspid valve
 Named based upon the physical location in relation to
the right ventricular walls
 Anterior
 Medial
 Inferior (posterior)
 Leaflets composed of collagenous material surrounded
by endocardium
 Basal zones are thicker than the tips, which possess
indentations or commissures, which attach to chordae
tendinea
Chordae Tendinae
Support the leaflets and prevent them from
prolapsing during systole
Strong, fibrous, collagenous structures
which arise from papillary muscles and
insert on the ventricular side of the valve
leaflets
Primary
Secondary
Tertiary
Papillary Muscles
 Two major papillary muscles
 Less prominent than those of the left ventricle
 Named for their location within the ventricle
 Anterior papillary muscle
 Largest
 Located on the anterolateral wall of the ventricle
 Supplies chordae to the anterior leaflet
 Posterior (sometimes called inferior)
 Located on the inferoseptal wall
 Muscle is smaller and frequently has two or three head
 Supplies chordae to the inferior leaflet
Unique Feature of the Right Ventricle
 Medial or septal leaflet receives its chordae directly from
the ventricular septum, found only in the RV
Normal Valve Area of the Tricuspid Valve
7-9
2
cm
Tricuspid Valve Views
RVIT
Apical 4
PSAX-Ao
Subcostal Long Axis
M-Mode Tricuspid Valve
Transesophageal Echocardiogram 110 degree
view at the base of the heart
12.24 Feigenbaum
M-Mode Tricuspid Valve
Tricuspid Regurgitation
Disorder involving backflow of blood
 From the right ventricle to the right atrium during contraction of the
right ventricle.
May be acute, chronic, or intermittent
The most common cause of tricuspid regurgitation
 Not damage to the valve itself
 Enlargement of the right ventricle, which may be a complication of any disorder that causes right
ventricular failure
Tricuspid Regurgitation
Common abnormality in the adult
population
Caused by two general mechanisms
Functional
Anatomic
Functional (secondary) – Structurally Normal
Tricuspid Valve
Pulmonary hypertension due to left heart
failure
Cor pulmonale
Primary pulmonary hypertension
Right heart pathological conditions
 Pulmonic stenosis, Eisenmenger’s syndrome
Constrictive pericarditis
Anatomic (primary) – Abnormal Tricuspid
Apparatus
















Rheumatic heart disease
Infective endocarditis
Tricuspid valve prolapse
Tricuspid annular dilatation/calcification
Ruptured chordae tendinae
Papillary muscle dysfunction
Carcinoid syndrome
Ebstein’s anomaly
Catheter induced (e.g. pacemaker wire)
Prosthetic heart valve
Systemic lupus erythematosus
Trauma
Tumor
Orthotopic heart transplantation
Endomyocardial fibrosis
Physiologic
Symptoms
Usually well tolerated
Weakness
Fatigue
Congestive heart failure
Dyspnea
Orthopnea
Paroxysmal nocturnal dyspnea
Pulmonary edema
Tricuspid Valve Prolapse
Tricuspid Regurgitation
Complications
Severe right heart failure
Renal failure when severe congestion is
present
Chest X-Ray
 Right atrial enlargement
 Right ventricular enlargement
 Left heart enlargement
http://www.yale.edu/imaging/findings/enlarged_heart/index.html
 Suggests functional tricuspid regurgitation
 Pulmonary congestion
 Suggests functional tricuspid regurgitation
 Pulmonary artery dilatation
 Suggests functional tricuspid regurgitation
 Prominent superior vena cava/right innominate
vein
Cardiac Catheterization
Right ventriculography to determine
presence and severity
Increased right atrial pressure and right
ventricular diastolic pressure
Kussmaul’s sign
Increased right atrial pressure with inspiration
Treatment
 None
Tricuspid regurgitation may be well tolerated for
years
 Endocarditis prophylaxis
 Digitalis/diuretics
 Vasodilators in patients with pulmonary
hypertension
 Anticoagulation
Right heart failure
Treatment
 Tricuspid valve excision
Drug addition with infective endocarditis
 Annuloplasty
Carpentier ring
Kay ring
Dural ring
 Tricuspid valve replacement
Usually with a tissue valve to reduce the risk of
thrombus formation
M-Mode Criteria of Tricuspid Regurgitation
 Right ventricular overload pattern
 Increased D-E amplitude of the anterior tricuspid valve
leaflet
 Increased E-F slope of the anterior leaflet of the tricuspid
valve leaflet
 B “bump” or “notch” of the anterior tricuspid valve leaflet
indicated increased right ventricular end-diastolic
pressure (≥9 mmHg)
 Color M-mode may be useful in determining the
presence, timing and duration of tricuspid regurgitation
when combined with PISA
2D Criteria for Tricuspid Regurgitation
 Anatomic basis for the presence of tricuspid
regurgitation
Tricuspid valve vegetation, ruptured chordae tendinae
 Right atrial dilatation with systolic expansion
 Right ventricular diastolic expansion
 Right ventricular dilatation
 Right ventricular volume overload pattern
2D Criteria for Tricuspid Regurgitation continued
 D-shaped left ventricle during ventricular
diastole indicating a right ventricular diastolic
volume overload
 Globular (spherical)-shaped right ventricle which
may form the cardiac apex
 Dilated tricuspid valve annulus (≥3.0 cm in
systole, ≥3.2 cm in diastole) indicates severe
tricuspid regurgitation
2D Criteria for Tricuspid Regurgitation continued
 Dilated inferior vena cava with lack of inspiratory collapse (normal 1.2 to 2.3
cm)
 Dilated hepatic veins (normal: 05 to 1.1 cm)
 Dilated superior vena cava/innominate vein
 Systolic bowing of the interatrial septum toward the left atrium
 Systolic reflux of saline contrast into the inferior vena cava and hepatic vein
may indicate significant tricuspid regurgitation
 May also be visualized by color flow Doppler
 Determine right atrial dimension, area and volume
 Determine right ventricular end diastolic, end systolic dimensions, volumes
and ejection fraction
PW Doppler - Inflow
 Up to 93% of normal patients appear to have
tricuspid regurgitation; calculate the duration and
length of the regurgitant
 Increased tricuspid E velocity may indicate
significant tricuspid regurgitation
 Laminar tricuspid regurgitation flow may denote
significant regurgitation
Associated with lack of tricuspid valve leaflet coaptation
Important to Note
 Tricuspid regurgitation is a volume overload of the right heart
 Most common etiology of tricuspid regurgitation is pulmonary
hypertension due to left heart pathology
 90% incidence when systolic pulmonary artery pressure is >40 mmHg
 Classic clinical triad of prominent jugular distension, holosystolic
murmur at the lower sternal border increasing with inspiration and a
pulsatile liver is present in only 40% of patients with severe tricuspid
regurgitation
 Myxomatous, redundant appearance of the involved tricuspid valve
leaflet(s)
 Tricuspid annular dilatation (normal 2.2 cm ± 0.3) – apical four
chamber
Important to Note - Continued
Tricuspid regurgitation is the most
common physiologic regurgitation
Normal tricuspid valve apparatus
Normal chamber dimensions
Peak tricuspid regurgitation (2.0 m/s ± 0.2)
Small regurgitant jet area are indicators of
physiologic flow
Significant Tricuspid Regurgitation
Regurgitant jet area ≥0.9 cm2
Right atrial area ›30 cm2
Proximal jet jet width ≥0.8 cm
Systolic flow reversal in the hepatic veins
Paradoxical septal motion
Diastolic septal flattening
Inferior vena cava diameter ≥2.1 cm
Lack of inferior vena cava respiratory
variation
Secondary Effects of TR
Moderately severe
tricuspid
regurgitation.
Dilated right ventricle
and diastolic
flattening of the
ventricular septum
consistent with a
right ventricular
volume overload.
12.33 Feigenbaum
Mild Tricuspid Regurgitation
Apical four-chamber view recorded
in a patient with mild to moderate
tricuspid regurgitation. Note the
color Doppler signal filling
approximately 25% of the right
atrium
Dilated Cardiomyopathy
12.30a Feigenbaum
12.30b Feigenbaum
Flail Tricuspid Leaflet Due to Trauma
(MVA)
12.31a Feigenbaum
12.31b Feigenbaum
Marfan Syndrome
•
Myxomatous changes
• Tricuspid valve with
pronounced bileaflet
prolapse (small
arrows)
•
Incidental note:
• Prominent Eustachian
valve (EV)
12.32 Feigenbaum
Carcinoid Heart Disease
Presence of Carcinoid Tumors
 Found predominantly in the
gastrointestinal tract
 Tumors produce vasoactive substances
that ultimately cause endothelial damage
to the right side of the heart
 Primary tumors can be small, with hepatic
metastases noted in most patient who
demonstrate cardiac involvement
 Involvement of the heart occurs late in the
progression of the disease in nearly half of
those with carcinoid syndrome
Carcinoid heart disease. Insert shows
pulmonary stenosis. The leaflets of the
tricuspid valve are thickened. The valve
is predominantly incompetent and
causes pulmonary regurgitation. Fibrous
plaques are deposited on the lining of
the right ventricle and pulmonary trunk.
Carcinoid Heart Disease
Clinical Symptoms
 Episodes of facial flushing with stimuli
 Abdominal pain
 Diarrhea
 Renal and hepatic failure
 Hepatomegaly is usually associated with later
stages of the disease
 Cardiac signs include
Elevated venous pressure
Systolic and diastolic murmurs
Carcinoid Heart Disease
2D Echocardiographic Signs
 Distinctive and are usually restricted to the right
heart
 Findings include:
Dilation of the right ventricle with abnormal septal
motion, indicative of right ventricular volume overload
Thickened tricuspid valve leaflets that are retracted, with
foreshortened chordae
Tricuspid valve leaflets usually do not coapt completely
and remain open throughout the cardiac cycle
Carcinoid Heart Disease
Tricuspid Doppler Signs
Tricuspid regurgitation, most prevalent
finding
Increased diastolic velocities across the
tricuspid valve
Carcinoid
Complete failure of coaptation of the
leaflets, which results in severe tricuspid
regurgitation, confirmed in an apical fourchamber view with color flow Doppler
imaging
12.41 Feigenbaum
Epstein’s Anomaly
 Congenital Anomaly
 Apical displacement of one or more leaflets
Most often septal leaflet is involved
Degree of displacement is extremely variable
 Epstein’s should be considered when separation between
mitral and tricuspid valve is > 1cm
 Results in atrialization of a portion of the right
ventricle.
Normal
Ebstein’s Anomaly
Note: apical
displacement of the
septal leaflet
Epstein’s Anomaly
• Marked distortion of right ventricular and right
atrial geometry.
• The approximate position of the mitral anulus
is noted by the broad arrow at the lower right.
• Septal leaflet of the tricuspid valve: apically
displaced from the anulus by approx 3 cm
• Lateral leaflet is tethered to the right
ventricular wall along much of its length
(small arrows).
• Also pathologically elongated.
12.43 Feigenbaum
Pacemakers
Stiffer, larger diameter leads used for
implantable defibrillators may interrupt
normal coaptation to a greater degree
Typically does not result in significant TR
Fibrosis combined with pacemakers may
result in more significant regurgitation
Pacemakers
• Pacemaker wire has
restricted motion of the
tricuspid valve
• Moderate tricuspid
regurgitation
Non-dynamic
Bi-Ventricular Pacemaker
Pulmonic Valve
Pulmonic Valve
Similar to aortic valve
Trileaflet
Inserted into pulmonary artery annulus
distal to the right ventricular outflow tract
Pulmonic Valve Views
PSAX-Ao
RVOT
Subcostal Short-Axis
Etiology of Pulmonic Regurgitation
 Pulmonary hypertension
 Causing regurgitation secondary to dilatation of the valve ring
 Most common
 Referred to as high pressure pulmonary disease
 Infective endocarditis
 Second most common cause
 Rheumatic heart disease
 Myxomatous degeneration
Etiology – Cont.
 Idiopathic dilatation of the pulmonary artery
 Connective tissue disorders (e.g. Marfan’s
syndrome)
 Congenital abnormalities
e.g. tetralogy of Fallot, ventricular septal defect, valvular
pulmonic stenosis, congenital agsence of the pulmonic
valve
 Iatrogenic
Post surgical repairs for congenital heart disease
Etiology – Cont.
Pulmonary artery catheter
Carcinoid heart disease
Syphilis
Tuberculosis
Chest trauma
Prosthetic heart valve
Physiologic
History/Physical Examination
 May tolerated for years w/o difficulty
 Severe hemodynamic changed due solely to
pulmonary regurgitation is rare
 Dyspnea
 Fatigue
 Palpable right ventricular impulse along left
sternal border
 Right heart failure
e.g. jugular venous distention, hepatomegaly, peripheral
edema, ascites, anasarca
Complication
Right heart failure
Treatment
Pulmonary regurgitation is generally well
tolerated
Endocarditis prophylaxis
Digitalis (right heart failure)
Valvuloplasty/valve replacement
M-Mode Criteria
 Right ventricular dilatation
 Right ventricular volume overload pattern
 Right ventricular dilatation with paradoxical septal motion
 Fine diastolic flutter of the tricuspid valve
 Diastolic flutter of the pulmonic valve
 Premature opening of the pulmonic valve due to severe acute
pulmonary regurgitation
 Defined as pulmonic valve opening on or before the QRS complex
 Evidence of pulmonary hypertension
2D Criteria
 Anatomic basis for the presence of pulmonary regurgitation
 Evidence of pulmonary hypertension
 Common cause
 Right ventricular dilatation
 Right ventricular volume overload pattern
 Right ventricular dilatation with paradoxical septal motion
 Right ventricular diastolic expansion
 D-shaped left ventricle due to right ventricular volume overload
 Pulmonary valve ring/artery dilatation
 Right atrial dilation
Pulsed Wave Doppler
 Up to 87% of normal patients appear to have
pulmonary regurgitation
Length and duration of the regurgitant jet differentiate
between true and physiologic regurgitation
 <1 cm in length and non-holodiastolic in duration with
normal pulmonary artery pressures implies physiologic
regurgitation
 Peak velocity across the RVOT is increased with
significant pulmonary regurgitation
 Increased RVOT velocity time integral (VTI) with
significant pulmonary regurgitation
Color Flow Doppler
Holodiastolic flow reversal in main
pulmonary artery and its branches may
indicate severe pulmonary regurgitation
Continuous Wave Doppler
Compare the pulmonary regurgitation
Doppler spectral display with the pulmonic
outflow Doppler spectral display strength
Steep slope with cessation of flow at or
before end diastole may indicate severe
pulmonary regurgitation
Shortened pressure half-time
Pulmonary Regurgitation Severity Scales
PW and Color
 Physiologic
 Normal pulmonic valve and pulmonary artery
 Normal chamber dimensions
 Normal pulmonary artery pressures
 <1 cm in length and not holodiastolic in duration
 Borderline
 1 to 2 cm in length and holodiastolic in duration
 Clinically significant
 > 2 cm in length with a peak velocity ≥1.5 m/sec and
holodiastolic in duration
Pulmonary Regurgitation Severity Scale
CW Spectral Strength of Regurgitant Jet
Grade 1+ (mild)
Spectral in tracing stains sufficiently for
detection, but not enough for clear
delineation
Grade 2+ (moderate)
Complete spectral tracing can just be
seen
Grade 3+ (moderate severe)
Distinct darkening of spectral tracing is
visible but density is less than
antegrade flow
Grade 4+ (severe)
Dark-stained spectral training
Important to Note
Significant pulmonary hypertension is a
right heart pressure overload
The velocity of pulmonic regurgitation
varies with respiration
When determining the mean pulmonary artery
pressure and pulmonary artery end diastolic
pressure, 3 to 5 beats should be averaged
Eccentric Jet PI
 Parasternal short-axis view
recorded at the base of the heart
in a patient with minimal
pulmonary valve insufficiency
originating at the lateral aspect of
the cusp commissure.
 Because this jet originates
immediately adjacent to the aorta
(Ao), it could be confused for an
aorta-pulmonary fistula.
 Note, however, the exclusively
diastolic flow, which would not be
expected in the presence of the
true shunt.
12.13 Feigenbaum
Mild Pulmonic Insufficiency/Regurgitation
12.14a Feigenbaum
Moderate Pulmonic
Insufficiency/Regurgitation
12.14b Feigenbaum
Severe Pulmonic
Insufficiency/Regurgitation
12.14c Feigenbaum
Sources
 Azis F, Baciewicz F. (2007). Texas Heart Institute Journal. 34(3)
366-8.
 Feigenbaum H, Armstrong W. (2004). Echocardiography. (6th
Edition). Indianapolis. Lippincott Williams & Wilkins.
 Goldstein S., Harry M., Carney D., Dempsey A., Ehler D., Geiser E.,
Gillam L., Kraft C., Rigling R., McCallister B., Sisk E., Waggoner A.,
Witt S., Gresser C.. (2005). Outline of Sonographer Core Curriculum
in Echocardiography.
 Otto C. (2004). Textbook of Clinical Echocardiography. (3rd Edition).
Elsevier & Saunders.
 Reynolds T. (2000). The Echocardiographer's Pocket Reference.
(2nd Edition). Arizona. Arizona Heart Institute.