MD, MBA
Internal Medicine/ Critical Care Medicine
Hcor Research Institute / Einstein Hospital Israelita
Internal Medicine and Intensive Care Physician at Hospital Israelita Albert Einstein and HCor. PhD candidate at Faculdade Israelita Albert Einstein and clinical researcher at the Hospital Israelita Albert Einstein and the HCor Research Institute.
It is 2:15 AM in the ICU.
A 68-year-old man with ischemic cardiomyopathy (LVEF 25%), septic shock recovering from pneumonia, stage 3 AKI, and persistent atrial fibrillation is on low-dose norepinephrine. Over the past 24 hours he has received nearly 5 liters of intravenous fluid.
His blood pressure is 102/60 mmHg, heart rate 96/min, CVP 15 mmHg, urine output has fallen to 0.3 mL/kg/h, serum creatinine has risen from 1.3 to 2.1 mg/dL, and lactate has normalized. The team debates: does he need another fluid challenge, or are his kidneys now “drowning” in venous congestion?
Point-of-care ultrasound reveals a dilated IVC (2.5 cm) with minimal respiratory variation. Hepatic vein Doppler shows systolic flow reversal, portal vein pulsatility is 85%, and intrarenal venous Doppler demonstrates discontinuous monophasic flow — findings consistent with VExUS Grade 3.
A junior consultant declares confidently: “This is VExUS Grade 3. The patient is congested — let’s start aggressive diuresis.”
You pause.
The patient is mechanically ventilated with PEEP 12 cm H₂O, has moderate tricuspid regurgitation, chronic pulmonary hypertension, and long-standing RV dysfunction. NT-proBNP is markedly elevated. Lung ultrasound shows only scattered B-lines. Echocardiography reveals a dilated but contractile RV with estimated RA pressure of 15 mmHg.
Is VExUS truly diagnosing fluid overload — or merely reflecting elevated right atrial pressure from chronic RV disease and high PEEP? And should VExUS ever be interpreted in isolation, divorced from the hemodynamic and respiratory context around it?
The discussion shifts from pattern recognition to physiology.
(Click / Tap on Questions to Reveal Content)
Answer: This is one of the most important cognitive traps in critical care. If I were forced to trust only one measurement, I would choose VExUS over the absolute CVP value—but only as a marker of transmitted venous pressure, not as a diagnosis of fluid overload.That distinction is everything. VExUS extends the assessment beyond the right atrium by showing whether elevated right atrial pressure is actually being transmitted splanchnic circulation. Its physiological meaning is venous congestion, not circulating blood volume. If forced to choose one measurement, I would still take VExUS because it asks a more clinically relevant question.
Answer: My view is that a PEEP reduction is an excellent physiologic maneuver in selected patients, but it should not be part of a routine VExUS protocol. It is a dynamic test of cardiopulmonary interaction, not a prerequisite for interpreting venous congestion.It is best viewed as an adjunct when the physiology is ambiguous rather than a routine step before accepting a Grade 3 VExUS finding. The greatest diagnostic confidence still comes from integrating venous Doppler with right ventricular assessment and the broader cardiopulmonary context, rather than trying to “correct” VExUS for PEEP in every mechanically ventilated patient.
Answer: If I could choose only one bedside sign, it would be the jugular venous pressure (JVP), or its ultrasound equivalent. Creatinine is a delayed and nonspecific marker, whereas JVP provides real-time insight into whether the kidney is facing venous hypertension. A low JVP favors renal hypoperfusion and may support further volume assessment, while an elevated JVP makes venous congestion a much more likely cause of worsening kidney function. In short, creatinine reflects the consequence, whereas JVP helps identify the underlying physiology driving the AKI.Another alternative would be femoral vein Doppler evaluation.
Answer: I would almost never discard VExUS as “unusable.” I would discard the assumption that VExUS is a volume test. In patients with advanced chronic right-heart disease, VExUS remains an excellent indicator that the organs are exposed to elevated venous pressure. What it loses is specificity for how much of that pressure is due to excess volume versus fixed right-heart pathology. That distinction is resolved by integrating the evaluation of RV-PA coupling and to focus in more specific VExUS alterations, such as intrarenal venous doppler.
Answer: A diuretic challenge should be viewed as a physiologic test, not simply a way to assess urine output or kidney function. Although the Furosemide Stress Test is a validated tool for assessing tubular functional reserve and predicting progression of AKI, its purpose differs from a hemodynamic decongestive challenge. In the latter, the goal is to determine whether relieving venous congestion improves overall hemodynamics without compromising forward flow. Therefore, the response should be judged by integrated bedside findings, such as capillary refill, blood pressure, vasopressor requirement, LVOT VTI, JVP/VExUS, and RV performance, rather than early changes in urine output or creatinine alone, which lag behind physiology. A modest rise in creatinine should not outweigh evidence of improving perfusion and decongestion, whereas worsening tissue perfusion or hemodynamics should prompt reconsideration of the decongestive strategy.
Answer: A normal lactate indicates that global oxygen delivery is likely adequate, but it does not exclude organ-specific venous congestion. Renal perfusion depends on the pressure gradient between arterial inflow and renal venous pressure; therefore, elevated venous pressure can impair kidney function despite preserved systemic perfusion and normal lactate. In this setting, additional fluids may further increase renal venous hypertension and worsen AKI, whereas carefully relieving congestion can restore the renal perfusion gradient. In short, normal lactate reflects adequate global perfusion, not optimal renal hemodynamics.
Answer: A falling VExUS does not prove renal recovery, and a rising creatinine does not prove that decongestion has failed. They reflect different time scales: VExUS shows the current venous pressure load, whereas creatinine reflects accumulated renal injury. Importantly, serum creatinine may transiently increase in 20–40% of patients undergoing effective decongestive therapy, likely due to reduced intraglomerular filtration pressure and hemoconcentration rather than AKI. Therefore, the key question is whether physiology has improved: less congestion, preserved LVOT VTI/forward flow, stable vasopressor requirements, adequate tissue perfusion, and improving urine output. If these parameters are improving, an early rise in creatinine should not automatically prompt abandonment of the decongestive strategy.
Answer: I don’t actually have a personal MAP, norepinephrine dose, or lactate cutoff.I think that’s precisely where physiology gets oversimplified. A patient requiring norepinephrine is not automatically “too unstable” for decongestion, just as a patient with a VExUS Grade 3 is not automatically ready for aggressive fluid removal. The question I ask is ‘’ Is the circulation pressure-dependent, preload-dependent, or congestion-dependent at this moment?’’. Norepinephrine may be maintaining arterial pressure while decongestion relieves venous afterload. Those therapies are not inherently contradictory, actually, they can be complementary. The decision hinges on whether forward flow and tissue perfusion remain intact as congestion is relieved, not on crossing a predefined MAP, lactate, or vasopressor threshold.
