Understanding Doppler and its Current Uses in OB Diana M. Strickland, BSBA, RDMS, RDCS.
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Transcript of Valvular Regurgitation Susan A. Raaymakers, MPAS, PA-C, RDCS (AE)(PE) Assistant Professor of...
Valvular Regurgitation
Susan A. Raaymakers, MPAS, PA-C, RDCS (AE)(PE)Assistant Professor of Physician Assistant Studies
Radiologic and Imaging Sciences - EchocardiographyGrand Valley State University, Grand Rapids, Michigan
Basic Principles
EtiologyCongenital Acquired abnormalities
Fluid Dynamics of Regurgitation
CharacterizedRegurgitant orifice areaHigh-velocity regurgitant jetProximal flow convergence areaDownstream flow disturbanceIncreased antegrade flow volume
Fluid Dynamics of RegurgitationRegurgitant orificecharacterized 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 JetSize
Affected by physiologic and technical factorsRegurgitant volumeDriving pressureSize and shape of regurgitant orificeReceiving chamber constraintInfluence of coexisting jets or flowstreamsUltrasound system gainDepth Signal strength
Fluid Dynamics of Regurgitation
Size, Shape and Direction of Regurgitant JetShape and Directions
Affected byAnatomy and orientation of regurgitant orificeDriving force across the valveSize 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 regurgitationResults in progressive volume overload
of the ventricleVolume 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 Regurgitation2D imaging
Indirect evidenceChamber 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 timingFalse negatives due to low signal strength or
inadequate images
Detection of Valvular RegurgitationContinuous-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 IndividualsPhysiologic
Small degree of regurgitation in normal individuals
No adverse implicationsTypically
Spatially restricted to area immediately adjacent to valve closure
Short in durationRepresents on a small regurgitant volumeMay be detected in 70 – 80% mitralMay be detected in 80 – 90% tricuspidMay be detected in 70 – 80% pulmonaryMay be detected in 5% aortic (increases with
age). • Clinical significance of AI is unknown
Approaches to Evaluation of the Severity of Regurgitation
Semi-quantitative measuresMild, moderate or severe utilizing
Color jet areaVena contracta widthPressure half-time (for aortic insufficiency)Distal flow reversals
Approaches to Evaluation of the Severity of Regurgitation
Quantitative measuresRegurgitant volume (RV)
Retrograde volume flow across the valveExpressed 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 fractionRF = 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 techniqueApplication of the PISA method
Spectral Doppler Method
Spectral Doppler TechniqueRegurgitant 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 equationEROA = RVOL/VTIRJ
Non-dynamic
Spectral Doppler Technique“Step by Step”
1. Calculate stroke volume (SV) through LVOT
2. Calculate stroke volume (SV) through MV
3. Calculate the regurgitant volume (cc)
4. Measurement of VTI of regurgitant signal
5. 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
Apical four chamber at mid-diastole: inner edge to inner edge CSA = 0.785 x D2
Measure mitral annulus VTI 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 TechniqueLimitations
Accuracy of measurements Inadequate spectral Doppler envelope for mitral
regurgitation VTI measurement
Significant learning curve May be considered time consuming and tedious
Spectral Doppler TechniqueClinical 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 AreaBasic 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 = 2r2Vr
Q = flow rate2r2 = area of hemispheric shell (cm2)Vr = velocity at the radial distance –
r(cm/s) Non-dynamic
Proximal Isovelocity Surface AreaBasic 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
2r2Vr = A0*V0
• A0 = area of the narrowed orifice (cm2)• V0 = peak velocity through the narrowed
orifice (cm/s)
Rearrange the equation• A0 = (2r2Vr )/V0 Non-dynamic
Proximal Isovelocity Surface AreaBasic 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
2r2Vr = A0*V0
• A0 = area of the narrowed orifice (cm2)• V0 = peak velocity through the narrowed orifice (cm/s)
Rearrange the equation• A0 = (2r2Vr )/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 = 2r2
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 AreaEROA = 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 = (2r2Valiasing)/3.25 2r2 = 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 – EROALimitations
Nonoptimal flow convergence
Suboptimal Flow Convergence
Flow: not symmetric
Suboptimal Flow Convergence
Perforated mitral leaflet - TEE
Continuous Wave Doppler Approach
Signal intensityProportional to number of
blood cells contributing to regurgitant signal
Compare retrograde to antegrade flow intensityWeak signal = mild regurgitationStrong signal = severe
regurgitationIntermediate signal = moderate
regurgitation
Continuous Wave Doppler Approach
Antegrade flow velocityRegurgitation results in increase in antegrade
flow across the incompetent valveGreater 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 curveDependent on time-varying pressure gradient
across regurgitant orificeRelated to pressure gradient
Normal LV systolic pressure = 100 – 140 mmHgNormal LA systolic pressure = 5 – 15 mmHgDifference therefore: 85 – 135 mmHg
• MR velocity is typically 5 – 6 m/sec
Continuous Wave Doppler ApproachTime 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 ApproachShape of aortic regurgitant curve
Dependent on time course of diastolic pressure difference
Normal low end-diastolic pressureAortic end-diastolic pressure is
normal (high pressure difference)Slow rate of pressure declineAcute 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 inFlow 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 ReversalsSevere semilunar valve regurgitation
may result inFlow 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 ValveDiastole: 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 fieldPoor resolution of anatomic details
PARALLEL to flowBest view for measuring velocities across valve
AR jet
AS jet
Subcostal view
Often the view that “saves” the studyNon-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 non-coronary (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 RegurgitationHistory 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 InsufficiencyComplicationsChronic 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 FeverAnkylosing SpondylitisRheumatoid ArthritisSystemic Lupus ErythematosusSyphilusPhen-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 axisDisruption of commissural support
DissectionDilatationPerimembranous VSDMyxomatous 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
10.33a Feigenbaum
10.33b Feigenbaum
Aortic Dissection
Proximal extent usually 1 cm distal to sinotubular junction
Flap may extend to rootRupture into pericardial spaceDissect coronary (right > left)Disrupt AV architecture
Transthoracic very INSENSITIVE
TEE aortic dissection disrupting commissurebetween right and left coronary cusps
Non-dynamic
TEE Long Axis View – Dissection Flap In Aortic Root
Non-dynamic images
Marfan’s SyndromeConnective tissue multisystemic
disorder characterized by Skeletal changes (arachnodactyly,
long limbs, joint laxity, pectus)
Cardiovascular defects Aortic aneurysm which may dissectMitral 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
20.22a Feigenbaum
20.22b 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
20.30a Feigenbaum
20.30b 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 murmurDiastolic 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 Insufficiency2D 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 InsufficiencyDoppler 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 InsufficiencyDoppler Criteria
Doppler cursor is parallel to flow, “Normal” peak velocity of an aortic regurgitant jet is
3.0 to 5.0 m/sDue 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 Leaflet2D Criteria
In PLAX, loss of leaflet coaptation and erratic echoes in LVOT
PSAX-Ao may disclose leaflet(s) involved. Perforations in leafletsAortic 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 overloadProgressive 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 periodChronic 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 RegurgitationShort interval from set of volume overload to clinical
presentationVolume 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 measurementNo gold standard
Invasive measurement is qualitativeVentricular opacification following aortic root
injection with IV dye
Severity of Aortic Regurgitation
Size of the color flow jetLength of jet dependent on ultrasound machine settings
GainPulse repetition frequencyTransmission 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 diameterMeasured in parasternal long axis viewOr in TEE longitudinal plane
<25% - mild AR25-40% 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 10.44b 10.44c
Feigenbaum
≥ 65% Regurgitant Jet Area/LVOT Area (PLAX)
10.36 Feigenbaum
View Dependent Color Flow Doppler EvaluationBoth Images Obtained From Same Patient
10.48a Feigenbaum
10.48b Feigenbaum
Severity of Aortic Regurgitation Short axis area of regurgitation
Dependent on level of short axis imageShort axis of the LVOT, not aortic sinuses
Color M-mode
Continuous wave Doppler across AV
Deceleration slope of AR spectral envelopePressure 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 SlopeGrading of AR (AI)
<200 cm2/sec = mild200 - 350 cm2/sec = moderate>350 cm2/sec = severe
Pressure half time also may be usedDependent on ventricular complianceEccentric 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
SymptomsEnd-systolic internal dimension > 55 mm
May not be applicable in women - use smaller LVIDD
Fall in ejection fractionDiastolic dimension > 70 mm associated
with sudden death
Mitral Regurgitation
Mitral Valve Apparatus
Left atrial wallMitral annulusAnterior and posterior
leafletsChordaePapillary musclesLeft 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 RegurgitationSigns 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
prolapseAcute 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 long-standing regurgitation, enlarged LA
EtiologyMyxomatous valve diseaseAnnular dilatation
Mitral RegurgitationEtiologies
Rheumatic mitral valve diseaseMitral valve prolapseMyocardial infarction (papillary muscle dysfunction)Ruptured chordae tendineaeFlail mitral leafletMitral valve vegetationsDilated cardiomyopathiesLeft ventricular outflow tract obstructions Use of certain appetite suppressantsCalcification of the mitral annulusTumors of the mitral valveAnnular DehiscenceRadiation 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
Data source : Arizona Society of Echocardiography Image Library
Standard real-time B-scan Duplex scan: color Doppler super-imposed on real-time B-scan
Diagnosis: Severe mitral regurgitation due to flail posterior MV leaflet. Underlying pathology: Mitral valve prolapse with ruptured chordae tendinae.
Flail Mitral LeafletRupture 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
JetsCentral
Bileaflet prolapseRheumatic disease
PeripheralVegetationsUnicuspid prolapseFlail
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
PhysiologicSpacially restricted to the area immediately
adjacent to valve closureShort in durationRepresents only a small regurgitant volumeWhen meticulously sought MR can be detected
in 70%-80%.
Determination of Mitral Regurgitation Severity
Determination of Mitral Regurgitation
Color Flow DopplerSize 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-DopplerSignal intensityShape of velocity curveLimitation: Qualitative
Vena Contract WidthWidth of regurgitant jet at originLimitation: Small values, careful measurement needed
Determination of Mitral Regurgitation…continued
PISACalculation of RV (regurgitant volume) and ROA
(regurgitant orifice area)Less accurate with eccentric jets
Volume Flow at Two SitesCalculation of RV (regurgitant volume) and ROA
(regurgitant oriface area).Limitation: Tedious
Distal Flow ReversalsPulmonary Vein reversal in DopplerLimitation: Qualitative, affected by LA pressure
Continuous Wave
Signal intensity Proportional to the number of blood cells contributing to
the regurgitant signalWeak signal reflects mild regurgitation, whereas a
signal equal to intensity to the antegrade (forward) flow reflects severe regurgitation
Time course (shape) of the velocity curveAcute 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 planeSeries 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 obstructionFunctional mitral stenosisWorsening 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 annulusleaflet tissuechordae tendinaepapillary 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 leafletsPrimarySecondaryTertiary
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 VentricleMedial 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 cm2
Tricuspid Valve Views
RVIT PSAX-Ao
Apical 4 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 mechanismsFunctionalAnatomic
Functional (secondary) – Structurally Normal Tricuspid Valve
Pulmonary hypertension due to left heart failure
Cor pulmonalePrimary pulmonary hypertensionRight 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 toleratedWeaknessFatigueCongestive heart failure
DyspneaOrthopneaParoxysmal nocturnal dyspneaPulmonary edema
Tricuspid Valve Prolapse
Tricuspid RegurgitationComplications
Severe right heart failureRenal failure when severe congestion is
present
Chest X-Ray
Right atrial enlargementRight ventricular enlargementLeft heart enlargement
Suggests functional tricuspid regurgitationPulmonary congestion
Suggests functional tricuspid regurgitationPulmonary artery dilatation
Suggests functional tricuspid regurgitationProminent superior vena cava/right innominate
vein
http://www.yale.edu/imaging/findings/enlarged_heart/index.html
Cardiac Catheterization
Right ventriculography to determine presence and severity
Increased right atrial pressure and right ventricular diastolic pressure
Kussmaul’s signIncreased right atrial pressure with inspiration
Treatment
NoneTricuspid regurgitation may be well tolerated for
yearsEndocarditis prophylaxisDigitalis/diureticsVasodilators in patients with pulmonary
hypertensionAnticoagulation
Right heart failure
Treatment
Tricuspid valve excisionDrug addition with infective endocarditis
AnnuloplastyCarpentier ringKay ringDural ring
Tricuspid valve replacementUsually 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 regurgitationTricuspid 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 regurgitationAssociated 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 regurgitationNormal tricuspid valve apparatusNormal chamber dimensionsPeak 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 cm2Right atrial area ›30 cm2Proximal jet jet width ≥0.8 cmSystolic flow reversal in the hepatic veinsParadoxical septal motion Diastolic septal flatteningInferior vena cava diameter ≥2.1 cmLack 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 Apical four-chamber view recorded in a patient with mild recorded in a patient with mild to moderate tricuspid to moderate tricuspid regurgitation. Note the color regurgitation. Note the color Doppler signal filling Doppler signal filling approximately 25% of the right approximately 25% of the right atriumatrium
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 Myxomatous changes
• Tricuspid valve Tricuspid valve withwith pronounced pronounced bileaflet prolapse bileaflet prolapse ((small arrowssmall arrows) )
• Incidental note:Incidental note:• Prominent Prominent
Eustachian valve Eustachian valve ((EVEV))
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 DiseaseClinical Symptoms
Episodes of facial flushing with stimuliAbdominal painDiarrheaRenal and hepatic failureHepatomegaly is usually associated with later
stages of the disease
Cardiac signs include Elevated venous pressureSystolic and diastolic murmurs
Carcinoid Heart Disease2D Echocardiographic SignsDistinctive 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 DiseaseTricuspid 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 four-chamber view with color flow Doppler imaging
12.41 Feigenbaum
Epstein’s Anomaly
Congenital Anomaly
Apical displacement of one or more leafletsMost often septal leaflet is involvedDegree 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 apical displacement of the displacement of the septal leafletseptal 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 valveTrileafletInserted 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 arteryConnective 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
IatrogenicPost surgical repairs for congenital heart disease
Etiology – Cont.
Pulmonary artery catheterCarcinoid heart diseaseSyphilisTuberculosisChest traumaProsthetic heart valvePhysiologic
History/Physical Examination
May tolerated for years w/o difficultySevere hemodynamic changed due solely to
pulmonary regurgitation is rareDyspneaFatiguePalpable right ventricular impulse along left
sternal borderRight heart failure
e.g. jugular venous distention, hepatomegaly, peripheral edema, ascites, anasarca
Complication
Right heart failure
Treatment
Pulmonary regurgitation is generally well tolerated
Endocarditis prophylaxisDigitalis (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 regurgitationLength 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 regurgitationShortened pressure half-time
Pulmonary Regurgitation Severity Scales PW and ColorPhysiologic
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)
Grade 2+ (moderate)
Grade 3+ (moderate severe)
Grade 4+ (severe)
Spectral in tracing stains sufficiently for detection, but not enough for clear delineation
Complete spectral tracing can just be seen
Distinct darkening of spectral tracing is visible but density is less than antegrade flow
Dark-stained spectral training
Important to Note
Significant pulmonary hypertension is a right heart pressure overload
The velocity of pulmonic regurgitation varies with respirationWhen 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.