TRICUSPID VALVE DISEASE (TVD) o Dyspnea

o hepatomegaly, ascites, and edema

- Advanced TS and/or TR = fatigue secondary to a low CO and
Tricuspid Stenosis
discomfort due to refractory edema, ascites, and marked
Etiology hepatomegaly.
- Much less prevalent than MS in North America and Western - Uncomfortable fluttering in the neck has been reported in
Europe patients with TV disease
- Generally rheumatic in origin
- More common in women than men Physical Findings:
- Does not occur as isolated lesion; assoc. with MS - Severe TS is assoc. w/ marked hepatic congestion, often
- Rheumatic TS commonly assoc. with tricuspid regurgitation resulting in cirrhosis, jaundice, serious malnutrition,
(TR) anasarca, and ascites
- The jugular veins are distended
- In patients with sinus rhythm
o giant a waves
o v waves are less conspicuous
o tricuspid obstruction impedes RA emptying during
diastole = slow y descent
o prominent presystolic pulsations of the enlarged liver
- Auscultation:
o OS of the tricuspid valve rarely heard ~0.06 s after
pulmonic valve closure.
o The diastolic murmur of TS
 Heard best along the L lower sternal border and over
the xiphoid process
 Most prominent during presystole in patients with
sinus rhythm
 Augmented during inspiration; reduced during
expiration
 particularly reduced during the strain phase of the
Valsalva maneuver, when tricuspid transvalvular
Pathology flow is reduced
- Commissure fusion
- In the case of rheumatic disease, mixed TS and TR may result Laboratory Examination
from fusion and shortening of the chordae tendineae + ECG:
commissure fusion = retraction of the valve leaflets. - RA enlargement
- Dilated RA and thickened in chronic TS - Tall, peaked P waves in lead II
- Chronic obstruction to RV filling often produces signs of - Prominent, upright P waves in lead V1
systemic venous congestion (ie. hepatomegaly and - Absence of RVH if pt has right-sided heart failure suspected
splenomegaly) to have MS should suggest assoc. TVD

Pathophysiology CXR:
- A diastolic pressure gradient between the RA AND RV - Combined TS and MS:
defines TS. o prominence of the RA and SVC w/o much PA
o Augmented when the transvalvular blood flow inc enlargement
during inspiration & declines on expiration o less evidence of pulmonary vascular congestion than
o Mean diastolic pressure gradient of 4 mmHg can elevate occurs in patients with isolated MS
the mean RA pressure = systemic venous congestion; o engorgement of the azygos vein
can cause…
 Hepatomegaly Transthoracic echocardiographic (TTE) examination:
 Ascites - Tricuspid valve is usually thickened and domes in diastole
 Edema - the transvalvular gradient can be estimated by continuous
- In patients with sinus rhythm: wave Doppler echocardiography.
o Tall RA a wave o Severe TS = valve area ≤1 cm2 or pressure half-time of
o Prolonged y descent ≥190 ms.
- CO at rest is usually depressed; fails to rise during exercise - The RA and IVC are enlarged
- The low CO is responsible for the normal or slightly elevated - Provides additional information regarding the severity of any
LA, PA & RV systolic pressures despite MS associated TR, mitral valve structure and function, LV and
- Presence of TS can mask the hemodynamic and clinical RV size and function, and PA pressure.
features of any associated MS
- Severe TS = valve area <1.0 cm2 Cardiac catheterization is not routinely necessary for assessment
of TS.

Clinical manifestations Treatment

Symptoms: - If w/ systemic venous congestion: salt restriction, bed rest,
- Development of MS generally precedes that of TS; initial sx and diuretic therapy
of pulmonary congestion and fatigue
- Severe TS: Surgical treatment:
- Preferably at the time of surgical mitral valvotomy or MVR  concomitant pressure load from PA HTN
for mitral valve disease  myocardial fibrosis from previous injury
- In patients with moderate or severe TS who have mean
diastolic pressure gradients > ~4 mmHg and tricuspid orifice Clinical manifestation
areas <1.5–2 cm2. Symptoms:
- May permit substantial improvement of tricuspid valve - Mild or moderate degrees of TR are usually well tolerated in
function. the absence of other hemodynamic disturbances.
- If repair cannot be accomplished= tricuspid valve - LV dysfunction (TR coexist w/ left-sided valve lesions)
replacement and/or PA HTN sx
- Mechanical valves in the tricuspid position are more prone to - Fatigue and exertional dyspnea due to reduced forward CO
thromboembolic complications are early sx of isolated, severe TR.
- PTBV for isolated severe TS without significant TR is very - As the disease progresses:
rarely performed. o RV function declines
o cervical pulsations
o abdominal fullness/bloating
Tricuspid Regurgitation o diminished appetite
Etiology o muscle wasting, although with progressive weight gain
- > 80% of TR cases are 2ry (functional) in nature o painful swelling of the lower extremities
- R/t tricuspid annular dilatation and leaflet tethering in the
setting of RV remodeling caused by pressure
Physical findings
and/or volume overload, myocardial infarction (MI) or
- Severe TR:
trauma
o Distended neck veins
- Secondary TR:
o Prominent c-v waves and rapid y descents (in the absence
o seen in the late stages of heart failure
of TS).
o due to rheumatic or congenital heart disease with severe
- May include marked hepatomegaly with systolic pulsations,
PA HTN (PA systolic pressure >55 mmHg)
ascites, pleural effusions, edema, and a positive hepatojugular
o can be caused by other types of left-sided valvular (e.g.,
reflux sign.
mitral regurgitation) or myocardial diseases (e.g., - Characteristic findings:
cardiomyopathies). o Prominent RV pulsation along the left parasternal region
o It is reversible in part if PA HTN can be relieved.
o blowing holosystolic murmur along the lower L sternal
o Can also develop from chronic RV apical pacing and
margin, w/c may be intensified during inspiration
dyssynchronous contraction; in some patients, the RV (Carvallo’s sign); reduced during expiration/strain phase
leads may also perforate or entrap the TV leaflets. of Valsalva maneuver
- TR can often emerge in the setting of new onset - Murmur of TR may sometimes be confused with that of MR
a-fib (AF) esp in elderly patients. unless attention is paid to its variation during the respiratory
- Rheumatic fever may produce primary TR, often associated cycle and extent of RV enlargement
with TS. - AF is usually present in the chronic phase
- Less commonly, primary TR results from congenitally
deformed tricuspid valves, and can occur with defects of the
AV canal, as well as with Ebstein’s malformation of the
tricuspid valve
Laboratory examination
Pathology ECG:
- Dilation and deformation of the tricuspid annulus - Inferior Q-wave MI suggestive of a prior RV MI, RVH, or a
- Valve leaflets appear stretched but pliable and normal in bizarre right BBB-type pattern with preexcitation in patients
appearance. with Ebstein’s anomaly.
- If TR is caused by carcinoid syndrome: white fibrous - Enlargement may be present in patients with sinus rhythm;
carcinoid plaques are found on the ventricular surfaces of the AF is frequently noted.
TV >> cusps to adhere to the underlying RV wall >> stents
the valve open CXR:
- RA and RV enlargement, depending on the chronicity and
Pathophysiology severity of TR
- Incompetent tricuspid valve allows blood to flow backward
from the RV into the RA TTE:
- The volume of back flow is dependent on the: - definitive with demonstration of RA dilation and RV volume
o driving pressure (i.e., RV systolic pressure) overload
o size of the regurgitant orifice - shows prolapsing, flail, scarred or displaced/tethered
- RV filling is increased during inspiration. tricuspid leaflets with annular dilatation
- Forward CO is reduced and does not augment with exercise. - Dx & assessment of TR = color flow Doppler imaging
- RA enlargement and elevation of the RA and JVP with - Severe TR is accompanied by hepatic vein systolic flow
prominent c-v waves in the pulse tracings. reversal.
- Progressively severe TR can lead to “ventricularization” of - Continuous wave Doppler of the TR velocity profile is useful
the RA wave form in estimating PA systolic pressure, except when the TR is
- Severe TR: very severe and the jet velocity is blunted by rapidly
o RV dilation (RV volume overload) increasing RA pressure.
o Eventual systolic dysfunction; progression can be - In patients with severe TR:
o CO is usually markedly reduced
accelerated by:
 o RA pressure pulse may not exhibit an x descent during
early systole
o RA pressre pulse may show a prominent c-v wave with a
rapid y descent.
- Elevated mean RA and RV end-diastolic pressures

Exercise testing can be used to assess functional capacity in

patients with asymptomatic severe TR.
Resources:
Harrisons
Schwartz