Chapter 22 — Tricuspid and Pulmonic Valve Disease

📚 Guideline basis

Zoghbi WA, et al. Recommendations for Noninvasive Evaluation of Native Valvular Regurgitation (JASE 2017;30:303–71); Hahn RT, et al. extended TR grading scheme (massive/torrential); ASE 2025 Right Heart Guideline; 2025 ESC/EACTS Guidelines for the Management of Valvular Heart Disease, which upgrade transcatheter tricuspid valve intervention to Class IIa (LOE A) for high-risk symptomatic severe TR without severe pre-capillary pulmonary hypertension or RV dysfunction, and recommend the externally validated TRI-SCORE for perioperative risk assessment.

Why the tricuspid valve matters disproportionately in the ICU

Severe tricuspid regurgitation is the lesion most likely to be under-reported and most likely to corrupt other measurements. It:

• Invalidates thermodilution cardiac output by causing indicator recirculation across the incompetent valve, typically producing under- or over-estimation depending on the injection profile.
• Causes PASP underestimation. With a large regurgitant orifice, the RV and RA pressures equalise early and the RV–RA gradient falls. A "reassuring" TR velocity of 2.4 m/s in massive TR can coexist with severe pulmonary hypertension.
• Renders IVC-based assessment meaningless. The plethoric, non-varying IVC of severe TR reflects the valve, not the volume status.
• Drives venous congestion, and therefore renal and hepatic dysfunction, independently of cardiac output (Chapter 13).

Pathophysiology & Classification

The tricuspid annulus is larger, thinner, and more dynamic than the mitral annulus, and dilates preferentially in its anteroposterior dimension. Secondary TR is therefore self-perpetuating: annular dilatation begets regurgitation, which begets RV volume overload, which begets further annular dilatation.

Diagnostic Synthesis — tricuspid regurgitation

Severity grading

The extended massive and torrential grades exist because outcomes and transcatheter therapy decisions differ substantially within the old "severe" category.

The most reliable ICU parameters

1. Hepatic vein systolic flow reversal — specific for severe TR, obtainable from the same subcostal window used for the IVC, and unaffected by the acoustic problems that plague apical imaging in ventilated patients.
2. Vena contracta ≥ 0.7 cm in the RV-focused apical four-chamber view.
3. CW jet contour. A dense, triangular, early-peaking envelope with a low peak velocity indicates rapid RA–RV pressure equalisation — the signature of torrential TR.
4. Mechanism on 2D, particularly leaflet coaptation gap, flail segment, vegetation, or lead impingement.

Tricuspid stenosis

Rare; almost always rheumatic (nearly always with concomitant mitral disease) or carcinoid.

Gradients are strongly respiration- and rate-dependent; average across the respiratory cycle.

The pulmonic valve

Pulmonic regurgitation

Trivial PR is present in most normal adults. Its clinical value in the ICU is chiefly as a pressure estimator rather than as a lesion:

mPAP = 4 v²(PR early) + RAP

PADP = 4 v²(PR end) + RAP

The 2025 ASE diastolic guideline lists PR end-diastolic velocity ≥ 2 m/s, or PA diastolic pressure ≥ 16 mmHg, as a supplemental indicator of elevated left atrial pressure in the absence of pulmonary disease.

Severe PR: wide origin of the regurgitant jet occupying most of the RVOT, dense CW signal with steep deceleration and early termination of diastolic flow (pressure equalisation), pressure half-time < 100 ms, diastolic flow reversal in the main or branch pulmonary arteries, and RV volume overload. Common contexts are post-repair tetralogy of Fallot, post-valvotomy, endocarditis, and severe pulmonary hypertension.

Pulmonic stenosis

Causes: congenital (most), carcinoid, rheumatic (rare), and post-surgical conduit stenosis. Note that pulmonic stenosis or RVOT obstruction invalidates the standard PASP equation, because RV systolic pressure no longer equals pulmonary artery systolic pressure.

Carcinoid heart disease

Distinctive and worth recognising: thickened, retracted, fixed tricuspid and pulmonic leaflets producing combined regurgitation and stenosis in a plaque-like distribution, with right-sided chamber dilatation. Left-sided involvement implies a right-to-left shunt or bronchial carcinoid.

ICU-Specific Limitations

Therapeutic Logic

Secondary TR is a consequence, and in the ICU the treatment is almost always directed at the cause rather than the valve:

Support systemic diastolic pressure to maintain RV coronary perfusion, and avoid volume loading a dilated, regurgitant right ventricle — the additional preload passes back across the incompetent valve into the venous system rather than forward.

For the stabilised patient, the 2025 ESC/EACTS guidelines have moved transcatheter tricuspid intervention into the mainstream for high-risk symptomatic severe TR, explicitly conditioned on the absence of severe pre-capillary pulmonary hypertension and of significant RV dysfunction — both of which are echocardiographic determinations, making a careful RV assessment (Chapter 9) part of the eligibility question. TRI-SCORE is the recommended perioperative risk tool.

🛑 Critical pitfall: Reporting a normal PASP in a patient with torrential TR. The low RV–RA gradient reflects pressure equalisation across a wide-open valve, not a normal pulmonary circulation.

🛑 Critical pitfall: Using thermodilution cardiac output in severe TR without acknowledging the error. Cross-check with Doppler (RVOT or LVOT VTI).

🛑 Critical pitfall: Interpreting a plethoric, non-collapsing IVC in severe TR as hypervolaemia. It reflects the regurgitant valve; hepatic and portal venous Doppler give a better congestion assessment.

• 💡 Clinical pearl: Hepatic vein systolic flow reversal is the quickest specific sign of severe TR, obtainable from the subcostal window in seconds when the apical window is unusable.
• 💡 Clinical pearl: Functional TR that appears acutely in a ventilated patient is usually a marker of rising RV afterload. Look at the ventilator and the gas exchange before looking at the valve.
• 💡 Clinical pearl: In a patient with a pacing lead and new severe TR, image the lead's relationship to the septal leaflet from multiple windows; TEE or 3D imaging is often needed to demonstrate impingement.

References

1. Zoghbi WA, Adams D, Bonow RO, et al. Recommendations for noninvasive evaluation of native valvular regurgitation. J Am Soc Echocardiogr 2017;30:303–71.
2. Hahn RT, Zamorano JL. The need for a new tricuspid regurgitation grading scheme. Eur Heart J Cardiovasc Imaging 2017;18:1342–3.
3. American Society of Echocardiography. Guidelines for the echocardiographic assessment of the right heart in adults and special considerations in pulmonary hypertension. J Am Soc Echocardiogr 2025.
4. ESC/EACTS. 2025 Guidelines for the management of valvular heart disease. Eur Heart J 2025;46:4635–.
5. Dreyfus J, Audureau E, Bohbot Y, et al. TRI-SCORE: a new risk score for in-hospital mortality prediction after isolated tricuspid valve surgery. Eur Heart J 2022;43:654–62.