10.2 Tricuspid-Valve Anatomy, Structure, and Function

Treat the valve and right heart as one functional unit

CCI task C7 requires assessment of tricuspid-valve structure and function. The apparatus includes a large nonplanar annulus, thin leaflets, chordae, papillary muscles, RA, RV, interventricular septum, and adjacent venae cavae and coronary sinus. The traditional leaflet names are anterior, septal, and posterior, but leaflet number, scalloping, and commissural pattern vary. The septal leaflet attaches near the septum; the anterior leaflet is usually the largest and most mobile; the posterior region is often more variable. A single 2-D slice rarely demonstrates all leaflets, so do not give a confident leaflet name merely because two lines appear in an apical image.

The annulus changes size and shape during the cardiac cycle. It contains more fibrous support near the septum and is more muscular along the free wall. Normal systolic annular contraction and leaflet coaptation limit regurgitation; RA or RV remodeling can flatten and enlarge the annulus, pull papillary muscles outward, increase tethering, and create a coaptation gap. Valve function therefore reflects both tissue integrity and the geometry generated by the chambers.

Build a reproducible multiplanar survey

Begin with the RV-focused apical four-chamber view rather than accepting a foreshortened standard view. Center the RV, show the apex and maximal basal diameter, and sweep or rotate through the valve. Parasternal RV-inflow imaging displays leaflet motion, chordae, inflow, and the RV free wall; parasternal short-axis imaging near the aortic valve provides a complementary commissural cut. Subcostal four-chamber and short-axis sweeps are valuable when apical alignment is poor and can show the septum, RA, IVC, and device course. Use zoom carefully: a close view improves tissue detail but may remove the landmarks needed for orientation.

Record color Doppler in more than one plane to locate systolic regurgitation and diastolic acceleration. Place PW Doppler at the leaflet tips when tricuspid inflow is needed, use low velocity scales and filters, and account for respiration and rhythm. CW across a regurgitant jet can support hemodynamic assessment, but the dedicated grading of TR belongs to an integrated protocol. Structural assessment should already describe the orifice, coaptation, jet origin, RA/RV response, IVC, hepatic-vein flow when obtained, RV systolic function, and estimated pulmonary pressure limitations.

Three-dimensional imaging is particularly useful for an en-face view of the annulus, commissural regions, coaptation defect, and relationship of a transvenous lead to leaflet tissue. Orient the dataset consistently and inspect multiplanar source images; rendered color can hide dropout. Thin leaflets, low volume rate, stitching, gain-dependent holes, acoustic shadow, and near-field artifact still limit 3-D certainty. A suspected lesion must persist in source planes and through appropriate frames.

Separate primary, functional, and device-related mechanisms

Primary tricuspid disease directly changes leaflet or chordal tissue. Examples include infective endocarditis, carcinoid retraction, rheumatic thickening and commissural fusion, prolapse or flail, trauma, and congenital disease such as Ebstein anomaly. Describe the visible abnormality and its motion rather than using regurgitation severity as proof of mechanism. A mobile mass, destroyed leaflet, acute flail segment, or suspected infection requires prompt communication through the laboratory pathway.

In ventricular functional TR, pulmonary hypertension, left-heart disease, RV disease, or RV volume overload produces RV and annular dilation with papillary displacement and systolic tethering. The leaflets may be structurally normal but fail to meet. In atrial functional TR, marked RA and annular dilation—often with long-standing atrial fibrillation—dominates, with comparatively less RV tethering early in the process. These categories can overlap; report observed annular size, tethering, coaptation gap, chamber geometry, pressure context, and RV function instead of forcing a label when mixed remodeling is present.

A cardiac implantable electronic-device lead may impinge on a leaflet, become entangled in chordae, adhere to tissue, perforate a leaflet, or indirectly contribute through remodeling. Its mere presence does not prove causation. Demonstrate temporal and spatial interaction in multiple 2-D planes or 3-D multiplanar reconstruction: does the lead prevent systolic closure, pin a leaflet, cross a commissure without restriction, or simply lie near the jet? Compare studies before and after implantation when available.

Ebstein anomaly illustrates why landmarks matter: apical displacement of the septal leaflet relative to the mitral insertion, atrialization of part of the RV, abnormal anterior-leaflet morphology, and right-heart dilation form a constellation. Do not diagnose it from apparent offset in a foreshortened image. Similarly, distinguish true thickening or a mass from reverberation by changing view, frequency, gain, and transducer position.

A useful final acquisition record states which views and leaflets were confidently demonstrated; annular size and contraction; leaflet thickness, mobility, and coaptation; chordal or papillary abnormality; mechanism of dysfunction; RA/RV size and RV function; pressure and volume-loading context; device relationship; and image limitations. This structural map makes later stenosis or regurgitation measurements interpretable.