Right side and pulmonary heart valves
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| 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
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| TRICUSPID STENOSIS .CAUSES | .Rheumatic heart disease (90%)
.Systemic lupus erythmatosus
.Carcinoid heart disease
.Loeffler’s endocarditis
.Metastatic melanoma
.Congenital heart disease
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| RHEUMATIC TV STENOSIS | .Rheumatic MV disease can have associated TV involvement
.Isolated rheumatic TV stenosis almost never occurs
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| 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
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| RHEUMATIC TV STENOSIS .M-MODE |
.Diminished EF slope
.Anterior displacement of posterior leaflet
.Thickening of valve leaflets and apparatus
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| 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
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| 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
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| 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
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| 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
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| TV VELOCITIES | .With TR, TV velocities usually not higher than 0.7 m/sec
.With TV stenosis the velocities are > 1.0 m/sec
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| 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
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| CARCINOID HEART DISEASE | .Results from the presence of carcinoid tumors
.Tumors found mostly in GI tract
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| 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
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| CARCINOID HEART DISEASE | .Heart affect late in disease progression
1/2 of patients with carcinoid syndrome have cardiac involvement
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| CLINICAL SYMPTOMS | .Facial flushing with stimuli
.Abdominal pain
.Diarrhea
.Renal failure
.Hepatic failure
.Hepatomegaly in later stages
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| CARCINOID HEART DISEASE Cardiac signs: | .Elevated venous pressure
.Systolic and diastolic murmurs
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| 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
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| DOPPLER SIGNS | .TR (most prevalent finding)
.Increased diastolic TV velocities
.Increased diastolic PV velocities
.Pulmonary insufficiency
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| ECHO FINDINGS | .Similar to rheumatic TV stenosis
.Rheumatic disease would have left-sided valvular involvement, carcinoid disease will not
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| TRICUSPID REGURGITATION Caused by 2 mechanisms | .Secondary to right heart chamber abnormalities (RAE, RVE, RV infarction)
.Actual tricuspid valve disease
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| ABNORMAL RighT HEART RAE | .Dilatation of tricuspid valve annulus
.Prevents complete leaflet closure
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| 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
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| TR CAUSES | .Pacer wire in the rt heart
.Cardiac transplant
.Tricuspid valve disease
.RV infarction
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| TR CAUSED BY RV DILATATION Caused by : | .Congenital heart disease such as partial anomalous venous return
RVVO which alters TV apparatus
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| TR CAUSED BY RV INFARCTION | .Involves posterior papillary muscle
.This attaches to posterior and septal leaflets of the tricuspid valve
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| 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
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| PHYSICAL FINDINGS W/ TR | .Jugular venous distention with prominent v wave
.Jaundice
.Thrill (lower left sternal border)
.Hyperdynamic RV impulse along left sternal border
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| COLOR ASSESMENT OF TR | .1/3 into RA = mild TR
.2/3 into RA = moderate TR
.Fills RA = severe TR
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| 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
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| SEVERE TR. Color flow doppler shows | .Retrograde flow in hepatic veins and IVC
.Systolic flow reversal
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| 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)
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| PRESSURE GRADIENTS | .Use CW in presence of high velocities or aliasing
.Calculate pressure using Bernoulli equation
4V2
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| 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
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| ESTIMATION OF RA PRESSURE part 1 | .0-5 mmHg
.IVC is small (<1.5cm)
.Change with respiration or “sniff”
.collapse
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| 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%
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| 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%
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| ESTIMATION OF RA PRESSURE part 4 | .15 – 20 mmHg
.IVC is dilated (> 2.5 cm)
.Change with respiration or “sniff”
.Decrease < 50%
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| ESTIMATION OF RA PRESSURE part 5 | .>20 mmHg
.IVC dilated with dilated hepatic veins
.Change with respiration or “sniff”
.No change
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| SYSTOLIC PA PRESSURE | .Alternate calculation method
.(TV PG x 25%) + TR gradient
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| TV PROLAPSE | .Buckles into RA
.Common to see with MVP
.Use RV inflow view or apical four-chamber to visualize
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| TV ENDOCARDITIS | .Rare
.Usually seen with:
.IV drug use
.Alcoholism
.Congenital defects (ie VSD)
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| CLINICAL SBE FINDINGS | .Temperature > 100 degrees
.Murmurs of TR and PI
.Positive blood cultures
.Usually Staphylococcus aureus
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| 2D SBE FINDINGS | .Dense mass
.Highly mobile
.Shaggy appearance of entire valve
.Polypoid structure attached to .single leaflet
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| DIFFERENTIAL DIAGNOSIS | .Myxoma (attach to IAS by stalk)
.Vegetations
.Move with valve during cardiac cycle
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| COMPLICATIONS | .TR
.Flail tricuspid valve
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| PULMONIC VALVE DISEASE. Pulmonic valve is best seen from: | .Left parasternal short-axis view
.Subcostal short-axis view
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| PULMONIC VALVE STENOSIS Three types: | .Valvular
.Supravalvular
.subvalvular
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| PULMONIC VALVE STENOSIS Two major forms: | .Bicuspid pulmonary valves
.Dysplastic pulmonary valve
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| 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
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| DYSPLASTIC PULMONARY VALVE | .Severely thickened valve tissue
.Immobile cusps from thickened myxomatous tissue
.Associated with Noonan’s syndrome which includes dysmorphic features
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| 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
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| 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
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| PULMONIC REGURGITATION | .Turbulent flow into RVOT during diastole
.Clinical significance is not known
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| 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
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| 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
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| CAUSES OF PI | .Pulmonary hypertension
.Bacterial endocarditis
.Pulmonary valvotomy
.Congenital defects
.Carcinoid heart disease
trauma
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| 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
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| 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
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| 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
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| 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
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| 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
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| PI DISTANCE | .>20 mm or 2cm in length with a peak velocity > 1.5m/s and holodiastolic in duration
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| 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
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| GRADING PI W/ CW spectral strength of regurg jet part 2 | .Grade 2+ (moderate)
Complete spectral tracing can just be seen
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| 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
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| GRADING PI W/ CW spectral strength of regurg jet part 4 | Grade 4+ (severe)
Dark stained spectral tracing
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| 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
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| 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
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| 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
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| PULMONARY HTN part 3 | .Can occur as primary disease or secondary to other heart disease
.Primary pulmonary HTN cause is unknown
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| 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…..
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| PULMONARY HTN M-mode appearance | .Midsystolic closure of pulmonic valve
.This is referred to as the “flying W” sign
.RVH
.Paradoxical septal motion
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| PULMONARY HTN GRADING SEVERITY There are several methods: | .AcT/RVET ratio
.SPAP values
.RVOT acceleration time
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| 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
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| 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
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| RVET | THIS IS THE TIME FROM THE ONSET TO THE END OF SYSTOLIC FLOW MEASURED FROM
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| ACT/RVET | .Normal ratio .45
.Significant pulmonary hypertension ratio is reduced to .25
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| RVVO Common causes | .TR
.PI
.ASD
.Partial or total anomalous venous return
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| RVVO Less common causes | .VSD w/ LV-RA shunts
.Ruptured sinus of Valsalva
.Coronary artery fistula w/ communication to RA or ventricle
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| 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
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| 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)
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| RVH | .Normal free wall measurement is 1.9-2.9mm
.May become thickened from .infiltrative disease
.Amyloidosis
.Hypertrophic cardiomyopathy
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| RV PRESSURE OVERLOAD Results from | .Increase in volume to RV
.Obstruction to RV blood flow
.Primarily from pulmonary embolism
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| COURSE OF PRESSURE OVERLOAD | .RV dilatation
.TR
.RV fails
.Resulting in hypokinesis of RV
.RA, IVC, main PA dilate
.RVH may also occur
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| 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
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| RVH or pulmonary HTN | .WITH INCREASING PULMONARY PRESSURE THE TIME REQUIRED FOR RV PRESSURE TO EXCEED PA PRESSURE INCREASES, WHICH ESSENTIALLY DELAYS THE OPENING OF THE PV
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