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Normal tricuspid valve anatomy
3 leaflets
1. Anterior
longest, largest and greatest motion
2. Posterior
usually smallest, multiple scallops
3. Septal
least mobile
open during diastole
biggest valve (6-7cm2)
separates RA from RV

Tricuspid annulus characteristics
little fibrous support
very different from mitral annulus
very pre/afterload dependent
saddle-shaped, but flattens as it dilates
dilates in the unsupported lateral and posterior directions (very flexible)
large valve orifice
sits lower in the heart than MV (closer to apex)

Standard echocardiographic views used to evaluate the tricuspid valve
PLAX RVIT
PSAX
A4C RV focus
Apical reverse 4C
SUBX 4C

Primary Tricuspid Regurgitation
Primary
Rheumatic
Carcinoid
Traumatic (acute) TV rupture - due to its anterior location
TV prolapse – isolated is rare, usually found with MVP
TVP best diagnosed from the PLAX view at the level of the aorta
Iatrogenic (caused by accident)
device leads
endocarditis
Ebstein’s Anomaly
Rare congenital malformation
Failure of the developing RV leaflets to split from the inlet portion of the ventricle
Exaggerated apical displacement of septal leaflet
Small functional RV
May be associated with ASD/PFO
displacement of leaflet is > 8mm
Functional Tricuspid Regurgitation
Functional
secondary (annular dilation)
Left heart disease
LV dysfunction
RV dysfunction
RV ischemia/volume overload/cardiomyopathy
Dilation
Pulmonary hypertension
Chronic lung disease
Pulmonary thromboembolism, L to R shunt
Right atrial abnormalities
Afib
Common causes of Tricuspid Regurgitation
most common = annular dilation (secondary)
structurally normal TV leaflets
results in incomplete coaptation of the TV

Causes of Tricuspid Stenosis
Congenital:
Rare, usually associated with other congenital cardiac defects
Ex: maldeveloped leaflets, shortened or malformed chords, annular hypoplasia, papillary muscle abnormalities
Acquired:
Rheumatic
most common cause of TS
TS almost never isolated, occurs with MS/AS
Features resemble MS (commissures fused)
Carcinoid - valve looks stuck open
Caused by rare, malignant neuroendocrine tumor
Secretes excessive amounts of serotonin which damages TV and PV
Plaque-like deposits on leaflets cause the valve to become thickened, retracted and rigid
Creates stenosis and regurgitation
most common valvular issue is TR
Other:
Cor triatriatum dexter
Large masses (TV vegetations, right heart thrombus or tumors)
Hemodynamic consequences of Tricuspid Regurgitation
backward flow of blood from RV → RA
volume backup into the venous system
flow reversal in hepatic veins & IVC
volume overload into RV (regular + regurgitant blood volume)
RV pressure increases

Hemodynamic consequences of Tricuspid Stenosis
obstructed blood flow from RA → RV
increased pressure in RA
systemic venous congestion
jugular vein distension
ascites (fluid buildup)
peripheral edema

Expected chamber remodeling with pressure overload vs. volume overload
RV volume overload
flattening of septum during diastole
RV pressure overload
flattening of septum during systole

Clinical findings associated with right-sided valve disease
systemic venous congestion
ascites
peripheral edema
enlarged, tender liver (congestion backup)
jugular vein distension
RA dilation
RV dilation with LV septal shift
Dilation of inferior vena cava
heart murmur that increases with inspiration
How Tricuspid Regurgitation is used to estimate right ventricular systolic pressure (RVSP)
RVSP = Tricuspid Regurgitation Pressure Gradient + RA pressure

Components needed to calculate RVSP
RVSP = Tricuspid Regurgitation Pressure Gradient + RA pressure
RAP = IVC size & collapsibility

Basic interpretation of calculated pulmonary pressures
normal is less than 35
severe is greater than 60

Clinical situations that may affect Doppler interrogation & alternate imaging windows (Pulmonary Hypertension & RVSP)
The peak TR velocity does not reflect the severity of TR
It reflects the pressure difference between the RV and RA during systole
Ex. there can be mild TR and very high TR velocities or severe TR with very low TR velocities
In Severe TR cases, this cannot accurately be estimated by using the TR velocity technique
PLAX RVOT
PSAX
high PSAX
SUBX short axis
anterior tilt A5C
PSAX PV
Normal pulmonic valve anatomy
3 components
annulus, cusps, commissures
3 cusps
anterior, left, right
not supported by IVS
separates RVOT from PA
most anterior & superior valve
separated from the TV by a muscular fold

Congenital causes of Pulmonic Stenosis
most common cause
valvular
1) Typical dome-shaped PV
Most common type of congenital PS
Preserved valve mobility, narrowed central opening, raphes
2) Dysplastic (abnormally developed) PV
Trileaflet with deformed and thickened leaflets, poor mobility
Frequently associated with Noonan syndrome
3) Unicuspid/Bicuspid PV
Fusion between commissures of leaflets
Bicuspid are frequently found with tetralogy of Fallot
subvalvular (infundibular)
Often associated with Tetralogy of Fallot
May be associated with other complex congenital heart lesions
supravalvular
Can be isolated or in association with tetralogy of Fallot or other syndromes such as Noonan’s
May result secondary to residual scarring of the MPA following removal of a PA band
branch PA Stenosis
May be diffuse or single lesion
Often associated with other syndromes

Acquired causes of Pulmonic Stenosis
rare – usually carcinoid or rheumatic cases
other causes:
HOCM
Masses
Tumors/thrombus
Common causes of Pulmonic Insufficiency (regurg)
Primary
Carcinoid
Congenital
Endocarditis
Rheumatic (rare)
Trauma (rare)
Secondary (functional) – most common cause
PA dilatation
RV cardiomyopathy
RV infarct
PHTN
Hemodynamic effects of Pulmonic Stenosis
RV pressure increase
RVH & dilation
RVEDP increases
increased afterload
RV failure
pulmonary artery systolic pressure increase

Hemodynamic effects of Pulmonic Insufficiency
backflow from PA → RV
RV volume overload
TV annulus dilated → TR
RVEDP increases
right heart failure
peripheral edema
diastolic flow reversal in pulmonary branches

Expected right ventricular remodeling associated with chronic disease
PI
RV volume overload
RV/RA dilation
right heart failure
PA dilation
PS
RVH
RV dilates
decrease in contractility
RV failure
Pulmonary Artery Systolic Pressure
In the absence of RVOT/PV obstruction:
PASP = RVSP
In the presence of RVOT obstruction (PS) use:
PASP = RVSP – peak PS gradient

Risk factors for infective endocarditis
Pre-existing heart conditions
Acquired heart disease (ex. Rheumatic)
Degenerative heart disease (ex. Prolapse)
Congenital Heart disease (ex. Bicuspid)
Prosthetic Valves
Intracardiac Devices
Pacemaker/ICD wires
LVAD
Catheters
Patient Factors
Age >60 yrs
Male
IV drug use
Dental procedures
Common causative organisms
staph
strep
enterococci

Role of transthoracic echocardiography (TTE) in diagnosis
first step
aids in diagnosis of IE
assess the functional abnormalities of the valve(s) affected
assess the secondary consequences of the valvular disease
identify complications of IE
surveillance during and after therapy
If pathology found:
assessment of the degree
severity of valvular obstruction and/or regurgitation
evaluation of chamber dimensions
ventricular systolic function
estimation of the pulmonary pressures
Positive Echo for IE
Vegetations
Abscess formation
New partial dehiscence of prosthetic valve
Pseudoaneurysm
Leaflet perforation
Valve aneurysm/fistula
Modified Duke Criteria
Major Findings
+ blood cultures
Endocardial involvement
Positive echo findings
New regurgitation
Minor Findings
Predisposition (IV drug use, valve disease, etc)
Vascular phenomena (hemorrhages)
Fever ≥ 38° C
Immunological phenome (Osler’s nodes)
Definite
2 major
1 major + 3 minor
5 minor

Typical echocardiographic appearance of Vegetations
minimum size of a vegetation that is identifiable on transthoracic echocardiography is 3mm
located on the underside of the valve
atrial side of MV/TV
ventricular side of AV/PV
Where blood flows from
hypermobile, echogenic mass
independent high frequency motion (use m-mode to demonstrate)
acoustic properties
New: similar to myocardium
Old/healed: echogenic

Abscess
Complication of IE
Extension and penetration of infection to surrounding tissues
Contains pus
Non-pulsatile
Do not communicate with the circulation
Most common with prosthetic valve & AV IE
Pus-containing infection of the heart's myocardium or valve tissue

Embolic events
obstruction of a blood vessel by an infected thrombus/vegetation (septic emboli)
may cause injury by ischemia & infection
right side vegetation
goes to lungs
left side vegetation
goes to body & brain
life threatening
echo can play a key role in predicting embolic events
increased risk:
large mobile vegetation (> 10 mm)
vegetation on MV
↑ size of vegetation while antibiotic therapy is given
multivalvular infection
previous embolic event
infection w/specific organisms (Staph, strep, and Candida species)

Valve perforation
interruption of endocardial tissue continuity that can lead to valve perforating
hole in the body of the leaflet
color jet will arise from site other than valve tip

Valve aneurysm
weakening of valve tissue & loss of elastic components of valve
leads to a saccular outpouching of valvular tissue

Pseudoaneurysm
pulsatile
echo free space
with flow between the cavity and circulation

Fistula formation
communication between neighboring cavities via a perforation
communication confirmed by Doppler (treat as a shunt)
