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Right Heart valves

Right side and pulmonary heart valves

Views for Tri-cuspid Valve 1. RV Inflow view 2. Parasternal short-axis at the base 3. Apical four-chamber 4. Subcostal four-chamber 5. CW Find mitral flow and angle posteriorly
TRICUSPID STENOSIS .CAUSES .Rheumatic heart disease (90%) .Systemic lupus erythmatosus .Carcinoid heart disease .Loeffler’s endocarditis .Metastatic melanoma .Congenital heart disease
RHEUMATIC TV STENOSIS .Rheumatic MV disease can have associated TV involvement .Isolated rheumatic TV stenosis almost never occurs
TV STENOSIS If undetected it can cause: . Increased operative morbidity and mortality in patients having left heart valve disease. .Chronic elevation of RA pressure .Low cardiac output even if left heart valves are repaired
RHEUMATIC TV STENOSIS .M-MODE .Diminished EF slope .Anterior displacement of posterior leaflet .Thickening of valve leaflets and apparatus
ASSOCIATED FINDINGS with TV .RAE .IAS bows to the left from high RA pressure .Dilated IVC .Pulmonary hypertension .Right ventricular hypertrophy .Both of the above can cause diminished EF slope
2D CRITERIA TV STENOSIS .2D criteria is more reliable .Doming of TV leaflets in diastole,more toward the tips of leaflets .Thickening and reduced excursion of the posterior or septal leaflets, or both .Reduced tricuspid orifice diameter relative to annulus diameter in same pl
TRICUSPID STENOSIS The following can obstruct RV inflow and mimic TV stenosis .RA tumors .Large vegetations .Large atrial thrombus .This can be a result of embolization from venous bed
DOPPLER OF TS .Higher diastolic velocity than normal .Decreased EF slope .Turbulent flow .Prolonged reduction in velocity throughout diastole .Increased “a” wave on hepatic vein flow
TV VELOCITIES .With TR, TV velocities usually not higher than 0.7 m/sec .With TV stenosis the velocities are > 1.0 m/sec
GRADING TV STENOSIS .Can’t get planimetry .PHT number validity has not been proven .Would be TVA = 190/PHT .Quantifiable data .Peak velocities .Peak gradient .Mean gradient
CARCINOID HEART DISEASE .Results from the presence of carcinoid tumors .Tumors found mostly in GI tract
CARCINOID TUMORS .Produce vasoactive substance that causes endothelial damage to right side of heart .Primary tumors can be small Can involve heart and cause liver mets
CARCINOID HEART DISEASE .Heart affect late in disease progression 1/2 of patients with carcinoid syndrome have cardiac involvement
CLINICAL SYMPTOMS .Facial flushing with stimuli .Abdominal pain .Diarrhea .Renal failure .Hepatic failure .Hepatomegaly in later stages
CARCINOID HEART DISEASE Cardiac signs: .Elevated venous pressure .Systolic and diastolic murmurs
2D APPEARANCE .RVE .Abnormal septal motion Indicating .RVVO .Thickened TV leaflets that are retracted .Foreshortened chordae .Thickened retracted PV cusps .TV leaflets don’t coapt completely and remain open throughout cardiac cycle
DOPPLER SIGNS .TR (most prevalent finding) .Increased diastolic TV velocities .Increased diastolic PV velocities .Pulmonary insufficiency
ECHO FINDINGS .Similar to rheumatic TV stenosis .Rheumatic disease would have left-sided valvular involvement, carcinoid disease will not
TRICUSPID REGURGITATION Caused by 2 mechanisms .Secondary to right heart chamber abnormalities (RAE, RVE, RV infarction) .Actual tricuspid valve disease
ABNORMAL RighT HEART RAE .Dilatation of tricuspid valve annulus .Prevents complete leaflet closure
RVE Associated with conditions that cause RV volume or pressure overload : .Aortic valve disease .Mitral valve disease .Especially MV stenosis because it causes lt-sided pressure increase resulting in pulmonary hypertension
TR CAUSES .Pacer wire in the rt heart .Cardiac transplant .Tricuspid valve disease .RV infarction
TR CAUSED BY RV DILATATION Caused by : .Congenital heart disease such as partial anomalous venous return RVVO which alters TV apparatus
TR CAUSED BY RV INFARCTION .Involves posterior papillary muscle .This attaches to posterior and septal leaflets of the tricuspid valve
TRICUSPID VALVE DISEASE .Rheumatic tricuspid valve disease .TV prolapse .Endocarditis .Ruptured papillary muscles or chordae .Carcinoid heart disease .Trauma .Congenital defects of TV .TV dysplasia or Ebstein’s anomaly
PHYSICAL FINDINGS W/ TR .Jugular venous distention with prominent v wave .Jaundice .Thrill (lower left sternal border) .Hyperdynamic RV impulse along left sternal border
COLOR ASSESMENT OF TR .1/3 into RA = mild TR .2/3 into RA = moderate TR .Fills RA = severe TR
COLOR ASSESSMENT OF TR .Ratio of RA area to jet area .Hepatic vein and IVC flow .Flows into RA during systole .Pressure falls with atrial relaxation
SEVERE TR. Color flow doppler shows .Retrograde flow in hepatic veins and IVC .Systolic flow reversal
TR SEVERITY The reasons for determining severity: .Deciding to repair or replace TV in patients having other cardiac surgeries .Determining systolic pulmonary pressures (this is the most common reason)
PRESSURE GRADIENTS .Use CW in presence of high velocities or aliasing .Calculate pressure using Bernoulli equation 4V2
SYSTOLIC PA PRESSURES or RIGHT VENTRICULAR SYSTOLIC PRESSURES .Add RA pressure (which is equal to jugular venous pressure) to peak TR gradient .Normal RA pressures range from 10-14 mmHg .Usually just add 10 mmHg
ESTIMATION OF RA PRESSURE part 1 .0-5 mmHg .IVC is small (<1.5cm) .Change with respiration or “sniff” .collapse
ESTIMATION OF RA PRESSURE part 2 .5-10 mmHg .IVC is normal (1.5 – 2.5 cm) .Change with respiration or “sniff” .Decrease by > 50%
ESTIMATION OF RA PRESSURE part 3 .10-15 mmHg .IVC is normal (1.5 – 2.5 cm) .Change with respiration or “sniff” .Decrease by < 50%
ESTIMATION OF RA PRESSURE part 4 .15 – 20 mmHg .IVC is dilated (> 2.5 cm) .Change with respiration or “sniff” .Decrease < 50%
ESTIMATION OF RA PRESSURE part 5 .>20 mmHg .IVC dilated with dilated hepatic veins .Change with respiration or “sniff” .No change
SYSTOLIC PA PRESSURE .Alternate calculation method .(TV PG x 25%) + TR gradient
TV PROLAPSE .Buckles into RA .Common to see with MVP .Use RV inflow view or apical four-chamber to visualize
TV ENDOCARDITIS .Rare .Usually seen with: .IV drug use .Alcoholism .Congenital defects (ie VSD)
CLINICAL SBE FINDINGS .Temperature > 100 degrees .Murmurs of TR and PI .Positive blood cultures .Usually Staphylococcus aureus
2D SBE FINDINGS .Dense mass .Highly mobile .Shaggy appearance of entire valve .Polypoid structure attached to .single leaflet
DIFFERENTIAL DIAGNOSIS .Myxoma (attach to IAS by stalk) .Vegetations .Move with valve during cardiac cycle
COMPLICATIONS .TR .Flail tricuspid valve
PULMONIC VALVE DISEASE. Pulmonic valve is best seen from: .Left parasternal short-axis view .Subcostal short-axis view
PULMONIC VALVE STENOSIS Three types: .Valvular .Supravalvular .subvalvular
PULMONIC VALVE STENOSIS Two major forms: .Bicuspid pulmonary valves .Dysplastic pulmonary valve
CONGENITAL PV STENOSIS Bicuspid valve .Doming of the valve in systole .Fusion of the raphe .There is usually post stenotic dilatation of the PA .Balloon valvuloplasty can correct
DYSPLASTIC PULMONARY VALVE .Severely thickened valve tissue .Immobile cusps from thickened myxomatous tissue .Associated with Noonan’s syndrome which includes dysmorphic features
SUPRAVALVULAR STENOSIS .Occur in any part of the PA Stenotic segment may be localized or diffuse and may involve multiple areas .Can be difficult to diagnose with TTE if peripheral arteries are involved
SUBVALVULAR PULMONARY STENOSIS .Occurs at infundibular level .Usually part of a more complex congenital disease .Isolated subvalvular stenosis may occur from obstruction of a windsock VSD bulging into RVOT
PULMONIC REGURGITATION .Turbulent flow into RVOT during diastole .Clinical significance is not known
PI PI in a normal patient may be from valve characteristics: .PV cusps are thinner than AO valve .PV has a less fibrous ring .PV has shallower sinuses .Retrograde pressure from PA may not be enough to close valve tight
PI CHARACTERISTICS .Long duration in diastole .Centrally located jet .Originates from valve coaptation point into RVOT .Flow velocities are nearly the same as transpulmonary pressure difference
CAUSES OF PI .Pulmonary hypertension .Bacterial endocarditis .Pulmonary valvotomy .Congenital defects .Carcinoid heart disease trauma
PI JET .It is possible to differentiate between PI from physiologic causes and PI from pathology .The velocity of PI jet reflects the transpulmonary pressure difference during diastole
PHYSIOLOGIC PI .In a normal patient transpulmonary gradient is small .Gradient approx 9 mmHg .Velocity approx 1.5 m/sec In pt w. normal PA pressures <18mmHg, PW shows PI that peaks in early diastole and slows in late diastole
HIGHER PA PRESSURES .Pulmonary HTN pts have higher gradient .Higher PA pressure >25 mmHg the PW velocity profile shows wideband spectrum that is sustained throughout diastole
PI DISTANCE .Maximum distance traveled by PI using PW and color flow Doppler .Pts with no significant cardiac abnormalities or a physiologic PI .Normal PV and PA .Normal chamber dimensions
PI DISTANCE .normal PA pressures..<10mm or 1cm in length and not holodiastolic in duration .Patients with borderline PI 1-2 cm in length and holodiastolic in duration .Patients with clinically significant PI or with underlying cardiac pathology ie pulmonary HTN .>20 mm or 2cm in length with a peak velocity > 1.5m/s and holodiastolic in dura
PI DISTANCE .>20 mm or 2cm in length with a peak velocity > 1.5m/s and holodiastolic in duration
GRADING PI W/ CW spectral strength of regurg jet part 1 .Grade 1+ (mild) Spectral tracing stains sufficiently for detection, but not enough for clear delineation
GRADING PI W/ CW spectral strength of regurg jet part 2 .Grade 2+ (moderate) Complete spectral tracing can just be seen
Grade 2+ (moderate) Complete spectral tracing can just be seen part 3 Distinct darkening of spectral tracing is visible, but density is less than antegrade flow
GRADING PI W/ CW spectral strength of regurg jet part 4 Grade 4+ (severe) Dark stained spectral tracing
PI MEASUREMENT .Can also use regurgitant index and regurgitant fraction just like in grading AI .You would have to measure TV and pulmonic valve VTI’s .Measurements have not been validated
PULMONARY HTN part 1 Increased pulmonary pressure due to: .Reduction in the caliber of the pulmonary vasculature .An increase in pulmonary blood flow .Sometimes due to both
PULMONARY HTN part 2 .PHTN is an increase in pulmonary arterial pressure >30mmHg systolic .This causes pressure overload of rt heart .RV responds first w/ hypertrophy followed by RVE, TR, PI, and RAE
PULMONARY HTN part 3 .Can occur as primary disease or secondary to other heart disease .Primary pulmonary HTN cause is unknown
SECONDARY PULMONARY HTN Found in patients with elevated LA pressures from: .Mitral stenosis .Heart failure w/ elevated LV end diastolic pressures .Cor pulmonale (right heart failure due to pulmonary disease) .Thrombolic emboli to lungs .Congenital heart disease w/ a lt-rt shunt .And the list goes on…..
PULMONARY HTN M-mode appearance .Midsystolic closure of pulmonic valve .This is referred to as the “flying W” sign .RVH .Paradoxical septal motion
PULMONARY HTN GRADING SEVERITY There are several methods: .AcT/RVET ratio .SPAP values .RVOT acceleration time
PULMONARY DOPPLER FLOW VELOCITY INDICES .Place sample volume just proximal to PV in the center of RVOT .Measure acceleration time (AcT) .Measure right ventricular ejection time (RVET) .AcT/RVET
ACCELERATION TIME .Measured from onset of systolic flow to the peak of the velocity .Normal > 120msec .Mild PHTN 80-100 msec .Moderate PHTN 60-80 msec .Severe PHTN < 60 msec
ACT/RVET .Normal ratio .45 .Significant pulmonary hypertension ratio is reduced to .25
RVVO Common causes .TR .PI .ASD .Partial or total anomalous venous return
RVVO Less common causes .VSD w/ LV-RA shunts .Ruptured sinus of Valsalva .Coronary artery fistula w/ communication to RA or ventricle
RVVO ECHO SIGNS .Dilated RV .Flatttened septum or “D” sign on 2D .RV appears more oval than usual crescent shape .RV apex may extend past LV apex
RVH Occurs with .PV stenosis or obstruction of infundibular or supravalvular regions .Tetralogy of Fallot .Chronic pulmonary hypertension .Mitral stenosis .Pulmonary emboli .Eisenmenger’s physiology (reversal of congenital shunt from lt-rt to rt-lt)
RVH .Normal free wall measurement is 1.9-2.9mm .May become thickened from .infiltrative disease .Amyloidosis .Hypertrophic cardiomyopathy
RV PRESSURE OVERLOAD Results from .Increase in volume to RV .Obstruction to RV blood flow .Primarily from pulmonary embolism
COURSE OF PRESSURE OVERLOAD .RV dilatation .TR .RV fails .Resulting in hypokinesis of RV .RA, IVC, main PA dilate .RVH may also occur
RV PRESSURE OVERLOAD Echo appearance of septum .IVS becomes erratic or paradoxical as septum flattens in systole and diastole .Can also see this pattern in patients post cardiac surgery
Created by: 100001592513232