Ch 3 TV + PV Stenosis Flashcards by Sarah Anderson

What causes TV stenosis?

-Due to rheumatic heart disease in association with rheumatic MV involvement!!
-Acquired TS is m/c due to rheumatic valve disease
-Carcinoid heart disease
-Rare congenital malformations (of leaflets, chords, pap muscles, or a combo of these)
-RA tumors, large vegetations or atrial thrombus (this obstructs RV inflow + can mimic TS)

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Which valve is the l/c to have stenosis?

TV (b/c of the low incidence of rheumatic heart disease)

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Is TS often an isolated disorder?

No! M/c is accompanied by MV stenosis (this contributes to a greater RAP)

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What is carcinoid heart disease?

-Rare malignant neuroendocrine tumor
-A cardiac manifestation occurring in pt’s with advanced neuroendocrine tumors

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What is rheumatic heart disease?

-A condition in which the heart valves have been permanently damaged by rheumatic fever

-Usually occurs 10-20 years after the initial illness (such as strep throat or scarlet fever), but not everyone with rheumatic fever will develop this heart disease

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What is the pathophysiology of TS?

-Causes obstruction to RA filling during diastole
-RAP increases to maintain forward flow across the stenotic valve
-The increased RAP leads to dilatation of the RA + affects the venous return into the RA, which then causes systemic venous congestion, jugular venous distension, ascites + peripheral edema

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What are the clinical manifestations/symptoms of TS?

-Fatigue (due to low CO)
-Abdominal discomfort (due to systemic venous congestion)
-Dyspnea (SOB due to concurrent MV stenosis)

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What are the symptoms when rheumatic TS occurs with rheumatic MS?

-Pulmonary venous congestion
-Low CO
-AFIB
-Right heart failure

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What is the role of echo with TS?

-Must determine cause of lesion
-Assess RA size
-Assess RV size + systolic function
-Estimate severity of stenosis
-Estimate RVSP (4V^2 + RAP, V = TR velocity)
-Identify associated valve lesions

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How does carcinoid heart disease affect the heart?

-M/c involves the right sided heart valves + eventually leads to right heart failure
-White, fibrous plaque on endocardial surfaces of TV leaflets
-Leads to thickened, retracted + rigid leaflets
-Affects TV m/c first, then PV
-Leads to combination of TS + TR

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Symptoms of pt’s with carcinoid heart disease?

-Murmur
-Symptoms of right heart failure

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Which side of the heart is m/c affected by carcinoid heart disease?

Right side

(note carcinoid tumors metastasize to the heart rarely + also can occur w/o valvular involvement)

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List carcinoid heart disease 2D echo findings?

-Thickening of ventricular aspect of TV, leading to shortened/fused chordae
-Retraction + impaired coaptation of leaflets, causing severe immobility (causing more TR than TS)
-RA + RV enlargement
-Doppler shows a “dagger-wave form” TR jet (early peak pressure + rapid decline)
-Prolonged pressure half time with TS

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Carcinoid heart disease m/c causes more TR or TS?

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List 2D echo findings of TS?

-Thickening + shortening of TV leaflets
-Calcification
-Restricted mobility of leaflets
-Commissural fusion + diastolic bowing (rheumatic disease)
-RA enlargement

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Which windows are used to assess for TS?

-RVIT
-PSAX
-AP4 (best view)
-SUB 4CH

(3D echoes can provide better anatomical detail of the 3 leaflets + better assess the orifice area)

How do we assess RA size?

Best measured in AP4, using RA major + minor

-RA length (major) is from the center of the TV annulus to the superior RA wall
-RA width/diameter (minor) is at the midlevel of the RA wall, from the RA free wall to the IAS

What are the upper limits of normal RA major + minor measurements?

Major: 5.3cm
Minor: 4.4 cm

What are 3 CD findings with TS?

-Narrowing of diastolic inflow jet
-Mosaic color dispersion
-Associated valve regurg

What are 3 quantification methods we use for assessing TS severity?

-Calculation of the mean gradient (> 5 mmHg)
-Pressure half time area (> 190 ms)
-Hallmark of TS is an increase in velocity by CW doppler (> 1 m/s)

How do we calculate the mean gradient with TS?

-By using transvalvular flow velocity through CW
-Best done through RVIT or AP4
-Best measurements acquired when the HR is less than 100 bpm, to appreciate the pressure half time measurement

(remember with AFIB we must average 3 cardiac cycles)

What pressure half-time area (T 1/2) represents significant or critical TS?

> 190 ms

(longer PHTs imply a greater TS severity)

What mean pressure gradient indicates TS?

> 5 mmHg

What velocity by CW must the TV reach to have stenosis?

> 1 m/s

List 2 SF's that are supportive findings indicating TS?

-Enlarged RA -Dilated IVC

What are the measurements for mild, moderate + severe TS?

There are none!

What are the 2 primary consequences of TS?

-Elevated RAP -Development of right sided congestion (b/c of frequent presence of TR, the transvalvular gradient is clinically more relevant for assessing the severity than the actual TS)

What causes PV stenosis?

-M/c due to congenital disease (valve may be trileaflet, bicuspid, unicuspid or dysplastic) -M/c acquired PV disease is from carcinoid disease (occurs with combined stenosis + regurg) -Rheumatic PS is rare -Can occur from more complex congenital lesions (such as tetralogy of fallot, double outlet RV, univentricular heart + AV canal)

Does carcinoid disease more commonly cause TV or PV stenosis?

Role of echo with PS?

-Determine size of obstruction (valvular, subvalvular, supravalvular, branches) -Assess valve morphology (unicuspid, bicuspid, doming of PV) -Assess RV size + systolic function -Estimate severity of stenosis -Measure pulmonary annulus in systole, prox to valve from inner to inner edge (done in zoomed RVOT or PSAX AoV level)

List 2D echo findings with PS?

Valves: -Thickened leaflets with systolic bowing -Calcification of valve is relatively rare Associated lesions: -Severe PS associated with RV hypertrophy, RV + RA enlargement -Dilatation of the pulmonary artery beyond the valve, due to weakness in the arterial wall (bicuspid PV)

Which views are best to assess for RV hypertrophy?

PLAX + SUB 4CH (> 5mm is abnormal for RV wall thickness)

How can we differentiate PS from subvalvular or supravalvular obstruction

Use CD + PW doppler

What is a quantification method for PS severity?

-Calculation of the systolic pressure gradient, derived from the transpulmonary velocity flow curve using CW doppler -Always must multiple views for assessment -Use the highest velocity obtained to determine PS gradient Achieved in: -PSAX with the CW cursor parallel to flow -SUB short axis -Mod AP5 (probe angled anteriorly to bring in RVOT, PV + PA)

Can we use planimetry to calculate the PV area?

No! B/c imaging planes are difficult to obtain

List the peak velocity + peak gradient for mild, moderate and severe PS?

Velocity: Mild <3 Moderate 3-4 Severe >4 Gradient: Mild <36 Moderate 36-64 Severe >64