Valvular regurgitation
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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] du. Basic Principles. Etiology Congenital

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Valvular Regurgitation

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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]

du


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”

  • 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”

  • 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”

  • 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”

  • Calculate the regurgitant volume

    • R Vol(MR) = SV (MV) – SV (LVOT)

  • Measurement of VTI of regurgitant signal

    • Optimize CW Doppler spectrum of regurgitant signal


Spectral Doppler Technique“Step by Step”

  • 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 = 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 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

      • 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 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

      • 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

  • Zoom mitral valve

  • Decrease color scale to identify surface of hemisphere shell

  • Note alias velocity – color bar (Valiasing)

  • Measure alias from orifice to color change (r)

  • Regurgitant volume

    • RVmax = 2 r2 x Valiasing

  • Measure peak mitral regurgitant velocity (VMR)

  • 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 – EROALimitations

  • Nonoptimal flow convergence

Suboptimal Flow Convergence

Flow: not symmetric

Suboptimal Flow Convergence

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 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

21-9 Lambl TEE Feigenbaum

10-56 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 InsufficiencyComplications

  • 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 .


Arachnodactyly in an 8-year-old girl with Marfan’s syndrome

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 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/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 InsufficiencyAortic 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 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


Systole

Diastole


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 10.44b 10.44c

Feigenbaum


≥ 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 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 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 long-standing 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 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.

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 cm2


    Tricuspid Valve Views


    PSAX-Ao

    RVIT

    Subcostal Long Axis

    Apical 4


    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 RegurgitationComplications

    • Severe right heart failure

    • Renal failure when severe congestion is present


    Chest X-Ray

    • Right atrial enlargement

    • Right ventricular enlargement

    • Left heart enlargement

      • Suggests functional tricuspid regurgitation

    • Pulmonary congestion

      • Suggests functional tricuspid regurgitation

    • Pulmonary artery dilatation

      • Suggests functional tricuspid regurgitation

    • Prominent 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 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 DiseaseClinical 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 Disease2D 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 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 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


    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

    Pulmonary Regurgitation Severity Scale CW Spectral Strength of Regurgitant Jet


    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.


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