How does tricuspid regurgitation affect central venous pressure?

How Tricuspid Regurgitation Affects Central Venous Pressure

Tricuspid regurgitation increases central venous pressure by creating retrograde systolic flow from the right ventricle back into the right atrium during ventricular contraction, producing a prominent ventricular (V) wave and ultimately elevating mean CVP. 1

Mechanism of CVP Elevation in TR

The pathophysiology involves direct transmission of right ventricular systolic pressure into the venous system:

• Severe TR generates a prominent regurgitant pressure wave in the right atrium during systole, manifested as an elevated V wave on CVP tracings 1
• The V wave height correlates directly with TR severity, with systolic flow reversal in hepatic veins occurring when TR becomes severe (sensitivity 80% for severe TR) 1
• Mean CVP rises progressively as TR worsens due to volume overload and increased right atrial pressure from the regurgitant jet 1, 2

CVP Waveform Changes by TR Severity

The CVP waveform undergoes characteristic morphologic changes:

• In severe TR, the CVP waveform shows a truncated (notched) pattern with triangular contour and early peak velocity, indicating prominent regurgitant pressure transmission 1
• The difference between V wave and Y descent increases significantly with worsening TR (p=0.077), while C wave - Y descent and X descent - Y descent also show significant variation (p=0.0018 and 0.027 respectively) 3
• Ventricular waves in the IVC reach 14.9-16.2 mmHg in severe TR, confirming substantial pressure transmission into the central venous system 2

Hemodynamic Consequences

The elevated CVP from TR creates a cascade of adverse effects:

• Systolic hepatic vein flow reversal occurs in severe TR, representing retrograde flow during ventricular systole that can be visualized on color Doppler extending into the vena cava and hepatic veins 1
• Cardiac output decreases significantly with severe TR despite elevated filling pressures, as regurgitant volume reduces forward flow 2, 4
• Peripheral venous pressures can transmit as far as mid-calf level, causing pulsatile varicose veins and venous ulceration in severe cases 5

Clinical Implications for CVP Monitoring

When assessing CVP in TR patients:

• The X descent - Y descent difference has an AUC of 0.83 for distinguishing severe TR from none-to-moderate TR, making it a useful diagnostic parameter 3
• Marked respiratory variation in TR jet velocity (decreased with inspiration) suggests elevated RA pressure, corresponding to Kussmaul's sign on examination 1
• After successful TR reduction, CVP should decrease—failure of right atrial pressures to fall despite TR correction indicates advanced disease with high stressed blood volume or irreversible right ventricular dysfunction 4, 6

Important Caveats

Several factors complicate CVP interpretation in TR:

• Blunted systolic hepatic vein flow can occur from causes other than TR, including abnormal right atrial/RV compliance, atrial fibrillation, and elevated RA pressure from any etiology, reducing specificity 1
• In massive TR with near-equalization of RV and RA pressures, the TR jet velocity may be low (<2 m/s) despite severe regurgitation, so jet velocity alone does not indicate severity 1
• Patients in high cardiac output states (CI >2.6 L/min/m²) show less pronounced CVP reduction per unit decrease in regurgitant volume following TR treatment, indicating altered hemodynamic responses 4
• Elevated stressed blood volume (eSBV) predicts attenuated reduction in venous congestion after TR correction, with higher eSBV patients showing less improvement in right atrial pressures, edema, and ascites 6