Chapter 13 — Venous Congestion and the VExUS Framework

📚 Guideline basis

Beaubien-Souligny W, Rola P, Haycock K, et al. Quantifying systemic congestion with point-of-care ultrasound: development of the venous excess ultrasound grading system (Ultrasound J 2020;12:16); ESICM 2025 recommendations on haemodynamic monitoring in shock, which reintroduce central venous pressure and add ultrasonographic detection of venous congestion; ASE 2025 right heart guideline for IVC and hepatic vein methodology.

Pathophysiology & Mechanisms

Resuscitation has historically been framed as a forward-flow problem. Venous congestion is the other half: organ perfusion is a pressure gradient, and raising the downstream pressure impairs it as effectively as lowering the upstream pressure.

Organ perfusion pressure = MAP - venous (or interstitial) pressure

Three mechanisms translate elevated venous pressure into organ injury:

1. Renal. The kidney is encapsulated. Rising renal venous pressure raises interstitial pressure within a non-compliant capsule, compressing tubules and peritubular capillaries, reducing transglomerular pressure and activating the renin–angiotensin system. Elevated central venous pressure predicts acute kidney injury independently of cardiac index across multiple cohorts — the observation that reframed congestion as a cause rather than a marker.
2. Hepatic. Sinusoidal congestion causes centrilobular hepatocyte injury, cholestasis and, with chronicity, fibrosis. The transaminase and bilirubin pattern of congestive hepatopathy differs from ischaemic hepatitis and is frequently misattributed.
3. Intestinal. Mucosal oedema impairs absorption and barrier function, contributing to feed intolerance and, plausibly, to bacterial translocation.

The clinical corollary: a positive cumulative fluid balance is not a benign accounting entry. The transition from a resuscitation phase to a de-resuscitation phase is a therapeutic decision, and venous Doppler is the instrument that informs it.

Why venous Doppler waveforms encode right atrial pressure

Venous flow toward the right atrium is pulsatile, shaped by atrial and ventricular events. As right atrial pressure and right ventricular stiffness rise, the systolic (x-descent) component of forward flow is progressively lost, and the waveform becomes increasingly pulsatile and eventually reversed. The same physics propagates upstream from hepatic vein to portal vein to intrarenal vein, and the number of beds showing an abnormal pattern grades the severity of the transmitted pressure.

Acquisition

An ECG trace or the simultaneous arterial signal is required for correct timing of hepatic and renal venous waveforms.

Diagnostic Synthesis — the VExUS grading system

The IVC is the gate. The system applies only when the IVC is dilated; a small IVC means congestion is not present regardless of the other waveforms.

Component patterns

Portal pulsatility index = ((V_max - V_min) / V_max) × 100%

Grading

📝 An inherited boundary discrepancy

The ASE right atrial pressure table (Chapter 9) partitions the IVC at ≤ 2.1 cm / > 2.1 cm; VExUS uses < 2.1 cm / ≥ 2.1 cm. At exactly 2.1 cm the two documents disagree. This is inherited from the source guidelines, not a transcription error, and it is clinically immaterial — but do not read either table as a typo of the other.

The system was developed and validated in a cardiac surgical cohort, where grade 3 congestion was associated with a substantially increased risk of subsequent acute kidney injury. Extension to general medical ICU populations is plausible but the validation is thinner.

The two distinct uses of the IVC

This book has criticised the IVC repeatedly, and the distinction matters:

The IVC is a bad preload-responsiveness test and a reasonable congestion screen. Most of the confusion in the literature stems from conflating those two roles.

ICU-Specific Limitations

⚠️ Evidence quality

VExUS is an observational grading system derived in a cardiac surgical population and associated with acute kidney injury. No randomised trial has shown that managing fluid according to VExUS improves outcomes. It should be used as one input into a de-resuscitation decision, alongside cardiac function, lung water, and the clinical trajectory — not as a target in itself.

Therapeutic Logic

Venous congestion assessment answers a different question from fluid responsiveness, and the two together define the decision space:

Decongestion targets and monitoring

Address the cause of the congestion, not only the volume. Congestion driven by acute cor pulmonale responds to RV-protective ventilation and PVR reduction far better than to diuresis (Chapter 32); congestion driven by severe tricuspid regurgitation responds to treating the driver of the TR; congestion driven by left heart failure responds to afterload reduction and diuresis.

🛑 Critical pitfall: Grading VExUS in a patient with severe tricuspid regurgitation. Hepatic vein systolic reversal is produced by the valve, and the score will overstate congestion. Assess the tricuspid valve before applying the system.

🛑 Critical pitfall: Using a plethoric IVC to conclude the patient is fluid unresponsive. Those are different questions; a dilated IVC in severe TR or acute cor pulmonale says nothing about the Frank–Starling position.

🛑 Critical pitfall: Diuresing a patient whose congestion is driven by a pressure-overloaded right ventricle without first addressing the afterload. Removing preload from an RV that is failing against high PVR can precipitate a fall in cardiac output.

• 💡 Clinical pearl: Hepatic vein Doppler is obtainable from the same subcostal window already used for the IVC and adds perhaps twenty seconds. It is the most informative single venous waveform and doubles as a severity marker for tricuspid regurgitation.
• 💡 Clinical pearl: Portal vein pulsatility is the most reproducible component for junior operators and is easily handed over as a trended number.
• 💡 Clinical pearl: Record a venous congestion assessment at the moment resuscitation stops working. The transition from giving fluid to removing it is the decision this chapter exists to inform, and it is usually made too late.

References

1. Beaubien-Souligny W, Rola P, Haycock K, et al. Quantifying systemic congestion with point-of-care ultrasound: development of the venous excess ultrasound grading system. Ultrasound J 2020;12:16.
2. Mullens W, Abrahams Z, Francis GS, et al. Importance of venous congestion for worsening of renal function in advanced decompensated heart failure. J Am Coll Cardiol 2009;53:589–96.
3. ESICM. 2025 recommendations on haemodynamic monitoring in shock. Intensive Care Med 2025.
4. 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.
5. Vieillard-Baron A, Millington SJ, Sanfilippo F, et al. A decade of progress in critical care echocardiography. Intensive Care Med 2019;45:770–88. PMID 30877351.